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Buruli Ulcer

GMJ News knowledge hub · last reviewed August 2026 · Georgian Medical Journal

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Buruli ulcer — caused by Mycobacterium ulcerans — produces painless necrotising skin ulcers that can be massive, deforming and permanently disabling, making it one of the most destructive mycobacterial diseases after tuberculosis and leprosy: approximately 2,700 cases are officially reported per year (substantially underreported) across 33 endemic countries, predominantly in West and Central Africa (WHO). A major 2023 advance: WHO now recommends fully oral rifampicin + clarithromycin for 8 weeks — replacing the previous IV amikacin combination and enabling community-level treatment for the first time. The mechanism of painlessness — mycolactone toxin destroying tissue AND locally suppressing immunity — is unique in infectious diseases.

Key messages

Painless ulcers — mycolactone explains why
Buruli ulcer (Mycobacterium ulcerans) produces uniquely painless necrotising ulcers — because mycolactone toxin not only destroys tissue but also locally suppresses the immune response and blocks pain signalling. This painlessness delays presentation and allows lesions to reach enormous size.
2023 breakthrough — fully oral treatment
WHO now recommends rifampicin + clarithromycin (fully oral, 8-week course) for Buruli ulcer — replacing the previous regimen (rifampicin + IV amikacin) that required parenteral treatment and hospital admission. This enables community-level treatment for the first time.
Endemic in West Africa, Central Africa, Australia
Buruli ulcer is endemic across 33 countries — predominantly West Africa (Ivory Coast, Ghana, Benin, Cameroon) and Central Africa, with Australia (North Queensland, Victoria) as a high-income country hotspot. Approximately 2,700 cases are officially reported per year — substantially underreported.
Category 3 WHO NTD — significant disability
Without treatment, Buruli ulcer causes massive tissue destruction, bone involvement (osteomyelitis), and permanent functional disability (contractures, lymphoedema, loss of limb). With early treatment, healing occurs in 6-12 weeks and disability is minimised.
Transmission unknown
The mode of M. ulcerans transmission to humans remains unclear — one of the key unanswered questions in tropical medicine. Water, aquatic insects (water bugs), contaminated soil and possibly direct contact with infected animals have all been proposed.
Early detection is critical
Early-stage Buruli ulcer (non-ulcerative plaque, papule or oedema) responds better to antibiotics and has lower disability. Late-stage ulcerative disease (especially with bone involvement) is harder to treat and causes more disability.

Key statistics

~2,700
officially reported cases/year (substantially underreported)
WHO 2023
33
endemic countries
WHO
2023
year WHO recommended fully oral rifampicin + clarithromycin
WHO
8 weeks
standard antibiotic treatment duration
WHO
Unknown
mode of transmission (a key open question)
WHO
Ivory Coast
highest national Buruli ulcer burden globally
WHO

Buruli ulcer cases by country — WHO officially reported 2022

Source: WHO. West Africa dominates. Australia is the highest-income country with significant BU burden.

Glossary of key terms

Mycobacterium ulcerans
WHOA slow-growing environmental mycobacterium — a relative of M. tuberculosis and M. leprae. Its unique virulence factor is the production of mycolactone — a polyketide toxin that destroys tissue, suppresses local immunity and inhibits pain signalling. Found in aquatic environments in endemic areas.
Mycolactone
WHO/ResearchThe polyketide toxin produced by M. ulcerans — responsible for the characteristic features of Buruli ulcer: (1) tissue necrosis (destroys fat cells and other tissues); (2) local immunosuppression (prevents immune cell recruitment to the lesion — explaining the lack of acute inflammation); and (3) pain suppression (inhibits pain signalling — explaining the characteristic painlessness).
Rifampicin + clarithromycin (oral)
WHO 2023The WHO-recommended treatment since 2023 — rifampicin 10mg/kg/day + clarithromycin 7.5mg/kg twice daily, both oral, for 8 weeks. Replaces the previous standard of rifampicin + IV amikacin (requiring hospital-based parenteral treatment). Oral treatment enables decentralised community-level treatment — dramatically improving access in remote endemic areas.
Osteomyelitis in Buruli ulcer
WHOBone involvement — occurring in approximately 10-15% of Buruli ulcer cases — significantly worsens outcomes and disability. M. ulcerans invades underlying bone from large ulcers, causing osteomyelitis (bone infection) that requires prolonged antibiotic treatment and may necessitate surgery. Detection by X-ray is important for staging and treatment planning.
Categories of BU lesions
WHOThree WHO categories of BU severity: Category 1 (small — <5cm); Category 2 (moderate — 5-15cm); Category 3 (severe — >15cm, multifocal lesions, or affecting functionally important areas like the face, breast, genitalia, or involving bone). Category determines treatment complexity and disability risk.
BCG and Buruli ulcer
WHOBCG vaccination (given for TB prevention) provides partial, temporary protection against Buruli ulcer (approximately 50-70% for 6 months). BCG is therefore given to children at risk of BU in endemic areas. A specific Buruli ulcer vaccine is not available.

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NTDsTuberculosis (related mycobacterium)Leprosy (mycobacterial NTD)DisabilityWASHMycobacterial AMR

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