Buruli ulcer (BU) is a necrotising infection of skin and soft tissue caused by the bacterium Mycobacterium ulcerans and is the third most common mycobacterial disease worldwide after tuberculosis and leprosy. It mainly affects children living in rural and remote regions of Africa but is endemic in 33 countries, including South and Central America, Asia and Australasia. The prevalence of BU is increased in people infected with HIV infection (63, 64) and it has been reported in travellers to endemic areas (65). The mode of transmission to humans remains unknown but it may be via skin contact with contaminated soils or water, or the bite of a vector like a mosquito or water-bug (66, 67).
The classic lesion is a painless ulcer, usually on the limbs, which slowly progresses. However non-ulcerative forms can occur that include papules, nodules, plaques and aggressive oedematous lesions that present as cellulitis (68). Patients with HIV infection have more severe lesions with an increased incidence of multiple and non-ulcerative lesions. There also appears to be an increased mortality in HIV-infected patients with BU (64, 69). The incubation period is estimated on average to be 4-5 months (70).
Diagnosis is best made by performing an IS2404 PCR of lesion fluid or tissue, although biopsy specimens can be examined for acid-fast bacilli and sent for mycobacterial cultures (71).
Combination antibiotic therapy for BU should be commenced before starting ART and given for 8 weeks duration. The recommended combination is rifampicin (10mg/kg daily up to 600mg) plus clarithromycin (7.5 mg/kg twice daily up to 600mg), although due to drug interactions this regimen should be used with caution when used with efavirenz. An alternative regimen is rifampicin plus moxifloxacin (400mg once daily). Rapid ART initiation (preferably within 2 weeks) for those not on ART is recommended to all BU–HIV coinfected patients, regardless of clinical stage and CD4+ T cell count (72).