Buruli ulcer is an infectious disease caused by Mycobacterium ulcerans, from the same family of bacteria which causes tuberculosis and leprosy. The infection causes painless swelling, with lesions developing in the skin later on. Further progression of this bacteria produces toxins that suppress the immune system and destroy skin, underlying tissue and bone, causing severe deformities. It predominantly affects the limbs^[1].

Buruli ulcer was first described in 1948 from the Bairnsdale district in south-east Australia.

Buruli ulcer is an infectious disease caused by the tuberculous agent Mycobacterium ulcerans. The infection causes painless swelling, with lesions developing in the skin later on.

The diagnosis of Buruli ulcer is usually based on the characteristic appearance of the ulcer in an endemic area. If there is any doubt about the diagnosis, then PCR using the IS2404 target is helpful, but this is not specific for M. ulcerans. The Ziehl-Neelsen stain is only 40–80% sensitive, and culture is 20–60% sensitive.

Antibiotics currently play little part in the treatment of Buruli ulcer. Recommended drugs include rifampin, streptomycin and dapsone.

Treatment is by surgical excision (removal) of the lesion, which may be only a minor operation and very successful if undertaken early. Advanced disease may require prolonged treatment with extensive skin grafting. Surgical practice can be dangerous and scarcely available in affected third world countries.