Buruli ulcer ( Mycobacterium ulcerans infection)

• Published in: Transactions of the Royal Society of Tropical Medicine and Hygiene 2008-10, Vol.102 (10), p.969-978
• Main Authors: Walsh, Douglas S., Portaels, Françoise, Meyers, Wayne M.
• Format: Article
• Language: English
• Subjects: Adolescent; Africa - epidemiology; Bacterial diseases; Biological and medical sciences; Buruli ulcer; Buruli Ulcer - epidemiology; Buruli Ulcer - microbiology; Buruli Ulcer - prevention & control; Child; Emerging diseases; Female; General aspects; Human bacterial diseases; Humans; Infection; Infectious diseases; Male; Medical sciences; Mycobacteria; Mycobacterium Infections, Nontuberculous - epidemiology; Mycobacterium Infections, Nontuberculous - microbiology; Mycobacterium Infections, Nontuberculous - pathology; Mycobacterium Infections, Nontuberculous - prevention & control; Mycobacterium ulcerans; Review; Tuberculosis and atypical mycobacterial infections
• ISSN: 0035-9203; 1878-3503
• DOI: 10.1016/j.trstmh.2008.06.006

Mycobacterium ulcerans is an emerging infection that causes indolent, necrotizing skin lesions known as Buruli ulcer (BU). Bone lesions may include reactive osteitis or osteomyelitis beneath skin lesions, or metastatic osteomyelitis from lymphohematogenous spread of M. ulcerans. Pathogenesis is related to a necrotizing and immunosuppressive toxin produced by M. ulcerans, called mycolactone. The incidence of BU is highest in children up to 15 years old, and is a major public health problem in endemic countries due to disabling scarring and destruction of bone. Most patients live in West Africa, but the disease has been confirmed in at least 30 countries. Treatment options for BU are antibiotics and surgery. BCG vaccination provides short-term protection against M. ulcerans infection and prevents osteomyelitis. HIV infection may increase risk for BU, and renders BU highly aggressive. Unlike leprosy and tuberculosis, BU is related to environmental factors and is thus considered non-communicable. The most plausible mode of transmission is by skin trauma at sites contaminated by M. ulcerans. The reemergence of BU around 1980 may be attributable to environmental factors such as deforestation, artificial topographic alterations and increased manual agriculture of wetlands. The first cultivation of M. ulcerans from nature was reported in 2008.