Introduction

The deleterious effects of mycotoxins were reported as early as 857 AD and very serious epidemics of ergotism occurred from the late 900s to the 1800s, but most Kenyans are neither fully aware of nor appreciative of the magnitude of the dangers that can result from consuming mycotoxin-contaminated food. This ignorance remains even though Kenya has experienced two outbreaks of aflatoxins food poisoning between April 2004 and September 2005, in which 125 and 16 people died, respectively (Nyikal et al., 2004; Azziz-Baumgartner et al., 2005; Lewis et al., 2005). The villages in the affected districts are remote and cases were reported from across a large geographic area. The limited medical facilities in this region probably means that some patients did not reach health facilities for diagnosis and treatment before they died and that the true magnitude of these outbreaks was probably considerably greater and the death toll much higher than has been documented.

The 2004 and 2005 cases were not the first aflatoxicosis outbreaks to be reported in Kenya or in that part of the country. Kenya has previously had sporadic outbreaks of afla-toxicosis, but the earlier outbreaks were more limited in the area and the number of people affected much smaller. The last major reported outbreak of aflatoxicosis in Kenya occurred in 1981 (Ngindu et al., 1982) in which a total of 20 people died. Yet to this day, maize grain harvested from the fields routinely is sorted into clean grain, which is consumed by the family and sold for between 16 and 22 Kenyan shillings per kilo, while moldy and discolored grain is fed to livestock or sold at a price that is about half that for the clean grain. The price per kilogram of both clean and discolored moldy grain depends on the season. During prolonged drought periods, the price of both grades of maize can more than double. Depending on the poverty level of the household, during a severe famine moldy grain may be mixed with clean grain and cooked for consumption by the family.

During the 2004 and 2005 outbreaks, the area involved was large; ~40,000 sq. km covering six districts in the Eastern province (Machakos, Kitui, Mwingi, Makueni, Embu and Mbeere) and one district (Thika) in the Central Province of Kenya, although > 87% of the cases were reported from only four districts (Machakos, Kitui, Thika and Makueni). Among the questions that need answers are:

• What was the extent of the problem? i.e., how widespread is aflatoxin contamination of maize in the distribution market channels?

• What was the source of the contaminated maize? Was it home grown? Was it sourced from other parts of the country? Was it imported?

• What were the risk factors associated with the outbreak?

• What types of toxins and fungal species were involved in the outbreak?

A series of studies were undertaken to answer these questions. The descriptive epidemiology investigations conducted in May 2004 resulted in a hypothesis relating aflatoxin content to the methods of harvesting, preparing and storing the maize grain. Based on this hypothesis two other concurrent studies - an assessment of market maize and case control studies were undertaken (Lewis et al, 2005).

The 2004 and 2005 outbreaks affected mainly young adults, some livestock and domesticated animals. The patients were aged between 1.3 years and 80 years with a mean age of 22.5 years. However, in some instances all of the adult members of one household were affected. There were cases of recurrence in some patients who were discharged back into the community. These recurrent cases indicated that contaminated maize remained present in the local communities.

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