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Mycobacterium ulcerans causes indolent, necrotizing cutaneous lesions known as Buruli ulcers, an appellation given by Dodge and Lunn who described the first large epidemic, located in Buruli County (now called Nakasongola), Uganda. Today, M ulcerans infections are recognized to present a spectrum of clinical disease: nodules, plaques, severe edemas, and massive ulcers in the skin, and osteomyelitis. Buruli ulcer, after tuberculosis and leprosy, is the third most common and perhaps least understood major mycobacterial infection. In contrast to tuberculosis and leprosy, Buruli ulcer is closely related to environmental factors.

Since 1998, the World Health Organization (WHO) has recognized Buruli ulcer as a reemerging infectious disease in West and Central Africa with an important public health impact. In endemic countries, Buruli ulcer is a major public health and psychosocial problem because of potential disabling sequelae. The disease tends to afflict children in those countries in which it is highly endemic.


M ulcerans is strongly acid-fast, with an optimal growth temperature of 30°C to 32°C on routine mycobacteriologic media such as Löwenstein-Jensen medium. The organism is a slow grower, often requiring several months of incubation to achieve isolation in primary culture. Microaerophilic conditions promote the growth of M ulcerans, and the organism is strikingly sensitive to temperatures of 37°C or higher. After a multitude of attempts to cultivate the organism from the environment by many investigators over half a century, the first isolation of M ulcerans from nature was reported in 2008. The development of polymerase chain reaction (PCR) techniques specific for M ulcerans facilitated detection of DNA in the environment in Australia and West Africa, although the significance of environmental M ulcerans DNA remains unclear.

Modes of transmission to humans have not been delineated completely; however, the most plausible route is by trauma at sites of skin recently contaminated by M ulcerans. Many patients give a history of specific antecedent penetrating trauma at the site of the initial lesion, which may include wounds from a gunshot or land mine, thrown stones, human bite, and hypodermic injection. Nonpenetrating trauma may also provoke lesions at the site of injury. Additionally, the organism may be spread by aerosol from the surface of ponds or be carried by fomites or insects to skin surfaces.

Globally, the highest incidence of Buruli ulcer is in West and Central Africa, followed by Australia, where one endemic focus is in a tropical region (Queensland), yet a larger focus is located in a temperate climate (Victoria). The greatest number of reported patients live in West Africa (Benin, Cóte d’Ivoire, and Ghana), with 2200 Buruli case notifications from 12 countries received by WHO in 2014. Other known endemic countries include Angola, Cameroon, Democratic Republic of Congo, Equatorial Guinea, French Guiana, Gabon, Kenya, Malaysia, Papua New Guinea, Peru, Suriname, Togo, and Uganda. In some West African countries, the number of Buruli ulcer patients exceeds those ...

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