In April 2004, one of the largest aflatoxicosis outbreaks occurred in rural Kenya, resulting in 317 cases and 125 deaths. Aflatoxin-contaminated homegrown maize was the source of the outbreak, but the extent of regional contamination and status of maize in commercial markets (market maize) were unknown. We conducted a cross-sectional survey to assess the extent of market maize contamination and evaluate the relationship between market maize aflatoxin and the aflatoxicosis outbreak. We surveyed 65 markets and 243 maize vendors and collected 350 maize products in the most affected districts. Fifty-five percent of maize products had aflatoxin levels greater than the Kenyan regulatory limit of 20 ppb, 35% had levels > 100 ppb, and 7% had levels > 1,000 ppb. Makueni, the district with the most aflatoxicosis case-patients, had significantly higher market maize aflatoxin than did Thika, the study district with fewest case-patients (geometric mean aflatoxin = 52.91 ppb vs. 7.52 ppb, p = 0.0004). Maize obtained from local farms in the affected area was significantly more likely to have aflatoxin levels > 20 ppb compared with maize bought from other regions of Kenya or other countries (odds ratio = 2.71; 95% confidence interval, 1.12–6.59). Contaminated homegrown maize bought from local farms in the affected area entered the distribution system, resulting in widespread aflatoxin contamination of market maize. Contaminated market maize, purchased by farmers after their homegrown supplies are exhausted, may represent a source of continued exposure to aflatoxin. Efforts to successfully interrupt exposure to aflatoxin during an outbreak must consider the potential role of the market system in sustaining exposure.

Consecutive outbreaks of acute aflatoxicosis in Kenya in 2004 and 2005 caused > 150 deaths. In response, the Centers for Disease Control and Prevention and the World Health Organization convened a workgroup of international experts and health officials in Geneva, Switzerland, in July 2005. After discussions concerning what is known about aflatoxins, the workgroup identified gaps in current knowledge about acute and chronic human health effects of aflatoxins, surveillance and food monitoring, analytic methods, and the efficacy of intervention strategies. The workgroup also identified public health strategies that could be integrated with current agricultural approaches to resolve gaps in current knowledge and ultimately reduce morbidity and mortality associated with the consumption of aflatoxin-contaminated food in the developing world. Four issues that warrant immediate attention were identified: a) quantify the human health impacts and the burden of disease due to aflatoxin exposure; b) compile an inventory, evaluate the efficacy, and disseminate results of ongoing intervention strategies; c) develop and augment the disease surveillance, food monitoring, laboratory, and public health response capacity of affected regions; and d) develop a response protocol that can be used in the event of an outbreak of acute aflatoxicosis. This report expands on the workgroup’s discussions concerning aflatoxin in developing countries and summarizes the findings.

Maize contaminated with aflatoxins has been implicated in deadly epidemics in Kenya three times since 1981, but the fungi contaminating the maize with aflatoxins have not been characterized. Here we associate the S strain of Aspergillus flavus with lethal aflatoxicoses that took more than 125 lives in 2004.The 2004 outbreak of acute aflatoxicosis in Kenya was one of the most severe episodes of human aflatoxin poisoning in history. A total of 317 cases were reported by 20 July 2004, with a case fatality rate of 39% (1,26). This epidemic resulted from ingestion of contaminated maize (22). However, identities of the fungi causing the contamination remain unclear.Aflatoxins are carcinogenic metabolites produced by several Aspergillus species (4, 28). Aflatoxin-producing fungi vary widely in many characteristics, including virulence for crops and aflatoxin-producing capacity (10). A. flavus and A. parasiticus are most commonly implicated as causal agents of aflatoxin contamination. A. flavus has two morphotypes, the typical or L strain (sclerotia of Ͼ400 m in diameter) and the S strain (sclerotia of Ͻ400 m in diameter) (10, 18). S-strain isolates produce more aflatoxins than L-strain isolates, on average (10). Many L-strain isolates produce no aflatoxins ("atoxigenic") (7). All members of A. flavus lack the ability to synthesize G aflatoxins due to a 0.8-to 1.5-kb deletion in the 28-gene aflatoxin biosynthesis cluster (15). In contrast to cases in the United States, studies conducted in West Africa found that an unnamed taxon (sometimes called strain S BG ) is commonly implicated in contamination events (12). Strain S BG is morphologically similar to the S strain of A. flavus, but DNAbased phylogenies reveal strain S BG to be a distinct species ancestral to both A. flavus and A. parasiticus (14, 16). In order to determine the primary causal agent(s) of the 2004 contamination events in Kenya, we considered both fungal aflatoxinproducing potential and frequency of occurrence in the contaminated crop (7).Representative maize samples were collected from major agricultural markets and storage facilities of the most affected Kenyan districts by the National Public Health Laboratory Services in Nairobi, Kenya, during the 2004 outbreak (24). Samples were screened for aflatoxin content, and only B aflatoxins were detected (22,24). Subsamples (n ϭ 104; average weight ϭ 87.5 g; range of contamination ϭ 0.27 to 4,400 ppb total aflatoxin) were imported to the United States from the National Public Health Laboratory Services for fungal analyses. Fungi were isolated from the maize by using the dilution plate technique on modified rose Bengal agar (8). Isolates were classified into species and strains by observing colony characteristics and sclerotial and conidial morphologies after subculturing on 5/2 agar (5% V8 juice; 2% agar; pH 5.2) (10). Isolations were repeated two to four times to verify results. Isolates from each sample were collected from at least two isolations. Quantities of Aspergillus section Flavi isolates in maize w...

Objectives: During January–June 2004, an aflatoxicosis outbreak in eastern Kenya resulted in 317 cases and 125 deaths. We conducted a case–control study to identify risk factors for contamination of implicated maize and, for the first time, quantitated biomarkers associated with acute aflatoxicosis.Design: We administered questionnaires regarding maize storage and consumption and obtained maize and blood samples from participants.Participants: We recruited 40 case-patients with aflatoxicosis and 80 randomly selected controls to participate in this study.Evaluations/Measurements: We analyzed maize for total aflatoxins and serum for aflatoxin B1–lysine albumin adducts and hepatitis B surface antigen. We used regression and survival analyses to explore the relationship between aflatoxins, maize consumption, hepatitis B surface antigen, and case status.Results: Homegrown (not commercial) maize kernels from case households had higher concentrations of aflatoxins than did kernels from control households [geometric mean (GM) = 354.53 ppb vs. 44.14 ppb; p = 0.04]. Serum adduct concentrations were associated with time from jaundice to death [adjusted hazard ratio = 1.3; 95% confidence interval (CI), 1.04–1.6]. Case patients had positive hepatitis B titers [odds ratio (OR) = 9.8; 95% CI, 1.5–63.1] more often than controls. Case patients stored wet maize (OR = 3.5; 95% CI, 1.2–10.3) inside their homes (OR = 12.0; 95% CI, 1.5–95.7) rather than in granaries more often than did controls.Conclusion: Aflatoxin concentrations in maize, serum aflatoxin B1–lysine adduct concentrations, and positive hepatitis B surface antigen titers were all associated with case status.Relevance: The novel methods and risk factors described may help health officials prevent future outbreaks of aflatoxicosis.