GL10

1: Institute of Tropical Medicine, Antwerp

Buruli ulcer (BU), caused by Mycobacterium ulcerans, is the third most significant mycobacterial disease after tuberculosis and leprosy. Though geographically restricted, BU remains endemic in 22 countries, with most cases in Africa and the Western Pacific. Children are predominantly affected in Africa, while adults are more commonly affected in Australia.

The disease primarily targets the skin through the action of mycolactone, a toxin that causes painless ulcers by suppressing immune responses and destroying tissue. Diagnosing BU is challenging due to its similarity to other skin conditions. The gold standard is IS2404-based PCR, known for its high sensitivity and specificity, but access is often limited in resource-poor settings.

Recent innovations aim to bring diagnostics closer to the point of care. Mobile qPCR platforms, like Biomeme, and LAMP (Loop-mediated isothermal amplification) assays, including heat-block and pocket-warmer formats, show promise. P-LAMP, incorporating a locked nucleic acid probe, enhances specificity and speed, though it requires further validation.

Efforts to detect mycolactone directly through TLC, ELISA, or lateral flow assays are ongoing but limited by technical and biochemical challenges. No validated serological test exists due to weak antibody responses and antigen cross-reactivity.

Treatment has evolved toward shorter, all-oral regimens. Telacebec (Q203), a new drug targeting the bacterial respiratory chain, shows strong potential, especially since M. ulcerans often lacks a backup oxidative pathway. Genetic studies suggest low risk of resistance.

In summary, BU diagnostics and treatment are advancing, with molecular tools and novel therapies offering hope for more accessible, effective care in endemic regions.