Abstract
A previous survey for clinical cases of Buruli ulcer (BU) in the Mapé Basin of Cameroon suggested that, compared to older age groups, very young children may be less exposed to Mycobacterium ulcerans. Here we determined serum IgG titres against the 18 kDa small heat shock protein (shsp) of M. ulcerans in 875 individuals living in the BU endemic river basins of the Mapé in Cameroon and the Densu in Ghana. While none of the sera collected from children below the age of four contained significant amounts of 18 kDa shsp specific antibodies, the majority of sera had high IgG titres against the Plasmodium falciparum merozoite surface protein 1 (MSP-1). These data suggest that exposure to M. ulcerans increases at an age which coincides with the children moving further away from their homes and having more intense environmental contact, including exposure to water bodies at the periphery of their villages.
Highlights
It has been established that the chronic necrotizing skin disease Buruli ulcer (BU) is caused by the emerging pathogen Mycobacterium ulcerans, the mode(s) of transmission and environmental reservoirs are still unknown
In accordance with these findings, data of the present seroepidemiological study indicate that children,4 years old are less exposed to M. ulcerans than older children
Age distribution of BU incidence and M. ulcerans 18 kDa shsp specific serum IgG responses among individuals living in the Mape Basin of Cameroon
Summary
It has been established that the chronic necrotizing skin disease BU is caused by the emerging pathogen Mycobacterium ulcerans, the mode(s) of transmission and environmental reservoirs are still unknown. Comparative genetic studies have revealed that M. ulcerans has diverged from the fish pathogen M. marinum. In addition to M. ulcerans strains isolated from human lesions, which belong either to the classical or to the ancestral lineage [3], other mycolactoneproducing mycobacteria (MPM) have been identified as fish and frog pathogens and given diverse species names [4,5,6,7]. In African endemic settings both the physical environment and organisms such as amoeba, insects, fish and frogs have been proposed as possible environmental reservoirs of the pathogen [9]. The distribution pattern of lesions is not indicative for a particular route of infection [11] and a genetic fingerprinting study of M. ulcerans isolates has revealed a highly focal transmission pattern, which excludes certain modes of transmission [12]
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