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PubMed1976

Experimental acute aflatoxicosis in mink (Mustela vison).

Susceptibility of mink to intoxication by aflatoxins was studied by giving mink single doses (300, 600, and 900 mug of aflatoxins B1 and G1 (40:60)/kg of body weight) and observing them for 8 weeks. One, 2, and 4 of 5 mink in each group died within 4 days after ingesting the small, medium, and large doses, respectively. Enlarged liver with pale yellow to yellowish pink spots was the most consistent lesion observed in mink that died of acute aflatoxicosis. Some lobules of liver also appeared hemorrhagic and fragile, whereas others showed fatty metamorphosis. Histopathologic examination of the liver showed different degrees of fat infiltration, bile duct proliferation, and necrosis of liver cells. Hematologically, mink that survived were not appreciably different from control mink in terms of hemoglobin content, packed cell volume, and white blood cell count. Liver specimen from aflatoxin-treated mink contained more fat, was larger, and contained less protein, RNA and DNA than did liver from control mink. Aflatoxin residue (only B1 ) was recovered from liver of 6 mink and were between 0.1 and 7.6 mug of the original dose.

Animals↗
PubMed1967

The effect of the aflatoxins B1, G1, and G2 on protein and nucleic acid synthesis in rat liver.

A comparison has been made of the difference spectra obtained by causing various aflatoxins (B(1), G(1) and G(2)) to interact with calf-thymus DNA. The effect of these toxins on RNA and protein synthesis by rat-liver slices has been measured. The extent of their inhibitory action on the synthetic reactions was proportional to the degree of spectral shift obtained with their interaction with DNA. It is proposed that their toxicity depends on this interaction. It was demonstrated that the RNA polymerase of nucleoli isolated from the livers of aflatoxin B(1)-poisoned rats was inhibited. This finding is in agreement with the proposed mechanism for the hepatotoxic action of aflatoxin.

Aflatoxins↗
PubMed2005

Aflatoxin levels in maize and maize products during the 2004 food poisoning outbreak in Eastern Province of Kenya.

BACKGROUND: On 10th May, 2004 food samples suspected to have caused acute poisoning in Makueni district were received at the National Public Health Laboratory Services (NPHLS). On analysis, they were found to be highly contaminated with aflatoxin B1. More cases of poisoning were reported in the district and in neighbouring districts of Kitui, Machakos and Thika. As at 20th July, 2004 the Ministry of Health was aware of 317 cases of which 125 resulted in deaths. OBJECTIVE: To assess the magnitude of aflatoxin contamination of maize and maize products in the affected areas. DESIGN: Random environmental sampling of maize and maize products and case/control samples of the same in the affected regions and subsequent determination of aflatoxin levels using immunoaffinity coupled with solution fluorometry. SETTING: National Public Health Laboratory Services, Ministry of Health, Kenya, from May to August, 2004. SUBJECTS: A total of 480 samples comprising 362 random environmental samples, 26 cases and 92 controls were collected and analysed. The foods analysed included maize grains, maize flour and dehulled dry maize, traditionally known as muthokoi. RESULTS: Forty six point four per cent of the environmental samples, 15% of cases and 29.3% of controls were within the maximum permissible limit of 20 microg implying that over 50% (54.4) of the total did not comply and would be regarded as unfit for human consumption. 6.9% of the environmental samples, 57.7% of cases and 21.7 of controls had levels beyond 1000 microg/Kg. The amount of aflatoxin observed in the food samples had a range of 0-58,000 microg/Kg. CONCLUSION: The population in the affected region was exposed to high levels of aflatoxin. There is need to address the issue of pre and post harvest handling of grain and establishing monitoring and surveillance for early detection and intervention.

Acute Disease↗
PubMed1989

Aflatoxicosis in cattle pastured in a field of sweet corn.

Aflatoxicosis was diagnosed in a small herd of cattle having access to moldy, unharvested sweet corn. Necropsy of 1 cow that died revealed anasarca and a pale tan liver. In this cow, microscopic examination revealed edema of all soft tissues and liver lesions consistent with aflatoxicosis. Samples of corn taken from the field contained 2,365 ng of aflatoxin/g of corn. Weather conditions were conducive to the formation of aflatoxins by Aspergillus flavus and A parasiticus.

Animal Feed↗
PubMed2006

Mycotoxins in pet food: a review on worldwide prevalence and preventative strategies.

Mycotoxins contaminate cereal grains worldwide, and their presence in pet food has been a potential health threat to companion animals. Aflatoxins, ochratoxin A, and Fusarium mycotoxins have been found in both raw ingredients and final products of pet food around the globe. Aflatoxin, a hepatotoxin and carcinogen, has caused several food poisoning outbreaks in dogs, and aflatoxin content is regulated in pet food in many countries. Ochratoxin A and Fusarium mycotoxins including trichothecenes, zearalenone, and fumonisins may have chronic effects on the health of companion animals. Grain processing, sampling error, analytical methods, conjugated mycotoxins, storage conditions, and synergistic interactions are common challenges faced by the pet food industry. Food-processing techniques such as sieving, washing, pearling, ozonation, and acid-based mold inhibition reduce the mycotoxin content of cereal grains. Dietary supplementation with large neutral amino acids, antioxidants, and omega-3 polysaturated fatty acids as well as inclusion of mycotoxin-sequestering agents and detoxifying microbes may ameliorate the harmful effects of mycotoxins in contaminated pet food.

Aflatoxins↗
PubMedDate not supplied

Effect of aflatoxicosis on the kinetic behaviour of ceftiofur in chickens.

The kinetic behaviour of ceftiofur sodium was studied in aflatoxin treated chickens for 30 days and in non-treated chickens, following oral, intramuscular and intravenous administrations of 10 mg kg(-1) bodyweight of ceftiofur. Aflatoxicosis resulted in a more significant decrease in ceftiofur serum concentration in the treated than in non-treated chickens following oral and intravenous administrations. The kinetic behaviour showed that following intravenous injection the elimination half life time t0.5 (el) was significantly shorter in the treated chickens (1.75+/-0.03 hours) than in non-treated chickens (4.23+/-0.05 hours). Following oral administration, the kinetic behaviour revealed a longer absorption half-life [t0.5 (ab), 62.74+/-1.59 minutes] in the treated chickens than in non-treated (50.46+/-5.07 minutes), with lower Cmax 23.25+/-0.42 microg ml(-1) at long tmax (3.05+/-0.07 hour) in treated chickens than in non-treated (Cmax 27.83+/-1.28 at tmax 2.39+/-0.07 hours).

Animals↗
PubMed1998

Liquid chromatography-mass spectrometry in forensic and clinical toxicology.

This paper reviews liquid chromatographic-mass spectrometric (LC-MS) procedures for the identification and/or quantification of drugs of abuse, therapeutic drugs, poisons and/or their metabolites in biosamples (whole blood, plasma, serum, urine, cerebrospinal fluid, vitreous humor, liver or hair) of humans or animals (cattle, dog, horse, mouse, pig or rat). Papers published from 1995 to early 1997, which are relevant to clinical toxicology, forensic toxicology, doping control or drug metabolism and pharmacokinetics, were taken into consideration. They cover the following analytes: amphetamines, cocaine, lysergide (LSD), opiates, anabolics, antihypertensives, benzodiazepines, cardiac glycosides, corticosteroids, immunosuppressants, neuroleptics, non-steroidal anti-inflammatory drugs (NSAID), opioids, quaternary amines, xanthins, biogenic poisons such as aconitines, aflatoxins, amanitins and nicotine, and pesticides. LC-MS interface types, mass spectral detection modes, sample preparation procedures and chromatographic systems applied in the reviewed papers are discussed. Basic information about the biosample assayed, work-up, LC column, mobile phase, interface type, mass spectral detection mode, and validation data of each procedure is summarized in tables. Examples of typical LC-MS applications are presented.

Animals↗
PubMed2001

Foodborne diseases in Kenya.

OBJECTIVES: To determine the occurrence of foodborne disease outbreaks in Kenya and the efforts employed to combat them. DESIGN: Cross-sectional survey. SETTING: Forty two districts in Kenya between 1970 and 1993. STUDY SUBJECTS: Foodborne disease outbreak episodes due to Staphylococcus aureus, Clostridium perfringens, Clostridium botulinum, Bacillus cereus, Escherichia coli, Campylobacter jejuni, Yersinia enterocolitica, Listera monocytogenes, chemicals, aflatoxin, plant and animal poisons. OUTCOME MEASURES: Number and aetiological causes of foodborne disease outbreaks reported in the study period. RESULTS: Thirty seven food poisoning outbreaks were reported to the Ministry of Health from various parts of the country in the study period 1970 to 1993, and only 13 of these involving a total of 926 people were confirmed to be due to particular aetiological agents. Foods that were involved included milk and milk products, meat and meat products, maize flour, bread, scones and other wheat products, vegetables and lemon pie pudding. A high number of food poisoning cases were treated as outpatients in various health facilities. CONCLUSION: Under-reporting, inadequate investigation of outbreaks and inadequate diagnostic facilities suggest that foodborne disease outbreaks are more than is recorded by the Ministry of Health.

Animals↗
PubMed1989

Aflatoxicosis in Iowa swine: eight cases (1983-1985).

During 1983, 1984, and 1985, aflatoxicosis was diagnosed in 8 Iowa swine herds after the herds were fed corn from the 1983 corn crop. As a result of the diagnosis, the associated environmental conditions, clinical signs of aflatoxicosis, macroscopic and microscopic lesions, aflatoxin concentrations detected in feeds, and management of affected swine were reviewed. Concentrations of aflatoxin in shelled corn and complete feed were as high as 2,020 ng and 1,200 ng of aflatoxin (B1 and B2)/g of feed, respectively. Clinical signs of aflatoxicosis included decreased feed consumption and weight loss. Some pigs died acutely, but death often was preceded by a period of clinical disease. Greater morbidity and mortality were observed in swine herds that consumed greater concentrations of aflatoxin.

Aflatoxins↗