Buruli ulcer (BU) is a disease of the skin and subcutaneous tissues caused by Mycobacterium ulcerans, a slow-growing environmental bacterium that grows optimally at temperatures from 30C - 33C

The restricted growth temperature is thought to limit infection to the cooler parts of the body; most ulcers occur on the extremities; lesions on the lower extremities are almost twice as common as those on the upper (Marston et al. 1995, WHO 2000). The disease affects all age groups, but children under the age of 15 years are predominantly affected. There are no sex differences in the distribution, but BU commonly affects rural communities with limited access to health care.

Buruli ulcer can present itself in several ways. The infection may begin with a painless, raised skin lesion or papule or with a hard sub-cutaneous nodule (Figure 1a). Infection extends from the skin into the subcutaneous tissue and often invades underlying muscle tissue. In other cases it presents as an extensive area of edema or swelling (Figure 1b). Tissue underlying these areas of edema is necrotic and the edematous region usually breaks down to form a large ulcer (Figure 1c). The disease also can present as a firm, painless plaque of a well-demarcated lesion of irregular edges with a reddened or discolored appearance (Figure 1d). (To see additional pictures of Buruli ulcer infection, please see our image gallery). Ulceration can be extensive and disfiguring, often affecting 50% or more of a limb

The mainstay of treatment is surgical excision of the lesion. This is both costly and dangerous, leading to the loss of considerable amounts of tissues or disability. Lesions are often extensive because many patients do not seek medical authorities until there is considerable tissue destruction (Thanjaraj et al. 1999, WHO 2000). Early detection of nodules and surgical excision of small lesions could prevent complications (WHO 2000). Several antimycobacterial agents have in vitro activity, but no single compound has proven regularly useful for treatment (WHO 2001). Current research indicates that a combination of amikacin or streptomycin and rifampicin can kill M.ulcerans cultured from human lesions (Johnson et al 2005). Heat treatment and hyperbaric oxygen therapy have also has clinical success, but are not practical for use in rural areas.

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Figure 1.Clinical symptoms of Buruli ulcer disease.(a) nodule on abdomen of a young child, (b)non-ulcerative edematous swelling of child’s hand, (c), ulcer covering most of a young child’s arm, (d) a plaque.