Initial adherence of EPEC, EHEC and VTEC to host cells

Initial adherence to host cells is the first step of the infection of enteropathogenic Escherichia coli (EPEC), enterohaemorrhagic Escherichia coli (EHEC) and verotoxigenic Escherichia coli (VTEC) strains. The importance of this step in the infection resides in the fact that (1) adherence is the first contact between bacteria and intestinal cells without which the other steps cannot occur and (2) adherence is the basis of host specificity for a lot of pathogens. This review describes the initial adhesins of the EPEC, EHEC and VTEC strains. During the last few years, several new adhesins and putative colonisation factors have been described, especially in EHEC strains. Only a few adhesins (BfpA, AF/R1, AF/R2, Ral, F18 adhesins) appear to be host and pathotype specific. The others are found in more than one species and/or pathotype (EPEC, EHEC, VTEC). Initial adherence of EPEC, EHEC and VTEC strains to host cells is probably mediated by multiple mechanisms

Aflatoxin Exposure from Milk in Rural Kenya and the Contribution to the Risk of Liver Cancer

Milk is an important commodity in Kenya; the country has the largest dairy herd and highest per capita milk consumption in East Africa. As such, hazards in milk are of concern. Aflatoxin M1 (AFM1) is a toxic metabolite of aflatoxin B1 (AFB1) excreted in milk by lactating animals after ingesting AFB1-contaminated feeds. This metabolite is injurious to human health, but there is little information on the risk to human health posed by AFM1 in milk in rural Kenya. To fill this gap, a quantitative risk assessment (QRA) applying probabilistic statistical tools to quantify risks was conducted. This assessed the risk of liver cancer posed by AFM1 in milk, assuming 10-fold lower carcinogenicity than AFB1. Data from four agro–ecological zones in Kenya (semi-arid, temperate, sub-humid and humid) were used. We estimated that people were exposed to between 0.3 and 1 ng AFM1 per kg body weight per day through the consumption of milk. The annual incidence rates of cancer attributed to the consumption of AFM1 in milk were 3.5 × 10−3 (95% CI: 3 × 10−3–3.9 × 10−3), 2.9 × 10−3 (95% CI: 2.5 × 10−3–3.3 × 10−3), 1.4 × 10−3 (95% CI: 1.2 × 10−3–1.5 × 10−3) and 2.7 × 10−3 (95% CI: 2.3 × 10−3–3 × 10−3) cancers per 100,000 in adult females, adult males, children 6–18 years old, and in children less than five years old, respectively. Our results show that aflatoxin exposure from milk contributes relatively little to the incidence of liver cancer. Nonetheless, risk managers should take action based on cumulative exposure from all sources of aflatoxins

Aflatoxin Exposure from Milk in Rural Kenya and the Contribution to the Risk of Liver Cancer

Milk is an important commodity in Kenya; the country has the largest dairy herd and highest per capita milk consumption in East Africa. As such, hazards in milk are of concern. Aflatoxin M-1 (AFM(1)) is a toxic metabolite of aflatoxin B-1 (AFB(1)) excreted in milk by lactating animals after ingesting AFB(1)-contaminated feeds. This metabolite is injurious to human health, but there is little information on the risk to human health posed by AFM(1) in milk in rural Kenya. To fill this gap, a quantitative risk assessment (QRA) applying probabilistic statistical tools to quantify risks was conducted. This assessed the risk of liver cancer posed by AFM(1) in milk, assuming 10-fold lower carcinogenicity than AFB(1). Data from four agro-ecological zones in Kenya (semi-arid, temperate, sub-humid and humid) were used. We estimated that people were exposed to between 0.3 and 1 ng AFM(1) per kg body weight per day through the consumption of milk. The annual incidence rates of cancer attributed to the consumption of AFM(1) in milk were 3.5 x 10(-3) (95% CI: 3 x 10(-3)-3.9 x 10(-3)), 2.9 x 10(-3) (95% CI: 2.5 x 10(-3)-3.3 x 10(-3)), 1.4 x 10(-3) (95% CI: 1.2 x 10(-3)-1.5 x 10(-3)) and 2.7 x 10(-3) (95% CI: 2.3 x 10(-3)-3 x 10(-3)) cancers per 100,000 in adult females, adult males, children 6-18 years old, and in children less than five years old, respectively. Our results show that aflatoxin exposure from milk contributes relatively little to the incidence of liver cancer. Nonetheless, risk managers should take action based on cumulative exposure from all sources of aflatoxins