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Buruli ulcer (Mycobacterium ulcerans infection)

Tjip S van der Werf, MD, PhD
Ymkje Stienstra, MD, PhD
Section Editor
C Fordham von Reyn, MD
Deputy Editor
Elinor L Baron, MD, DTMH


Buruli ulcer is a disabling skin infection caused by Mycobacterium ulcerans. It is named for the Buruli district in Uganda, a region where many of the early cases in the literature were described [1-4]. Buruli ulcer begins as localized skin lesions that progress to extensive ulceration, leading to functional disability, loss of economic productivity, and social stigma [5-8]. Since the 1998 World Health Organization (WHO) Buruli ulcer initiative, there has been increased attention to research efforts for treatment and control of Buruli ulcer [9-11].


Mycobacterium ulcerans is the third most common mycobacterial infection worldwide (after tuberculosis and leprosy) [12,13]. Buruli ulcer due to M. ulcerans mainly affects individuals in humid, rural, tropical regions with limited access to medical care. It has been reported in about 33 (mostly tropical) countries, with the greatest frequency in Africa, particularly in the West African countries of Côte d'Ivoire, Ghana, and Bénin (20 to 158 cases per 100,000) [14-21]. Cases have also been described in other locales including Mexico, South America, Papua New Guinea, and Australia (where the disease is known as Bairnsdale ulcer) [22-26]. In Victoria, Australia, and in Japan [27], transmission has been observed in moderate, nontropical climates.

The peak age group in West Africa studies is 5 to 15 years, although Buruli ulcer can affect any age group [19,28,29]. In Japan, the median age is 40 to 57 years [30], and, in Australia, the median age is 50 to 66 years [24]. The disease has a low mortality rate, but its disabling sequelae have an enormous physical and socioeconomic impact on affected individuals.

Transmission — The mode of M. ulcerans transmission is not fully understood, although the disease is known to be linked to contaminated water [31-38]. Areas affected by Buruli ulcer disease are located near stagnant or slow-moving water, and outbreaks appear to be related to environmental changes (deforestation, agriculture, hydraulic installations) involving surface water [16,31,36,39]. Buruli ulcers have been observed more frequently during the rainy season in Africa, and exposure may occur in muddy farming fields [23,40,41].

Transmission of the organism is probably via skin trauma. In an experimental guinea pig model, direct inoculation of skin abrasions with M. ulcerans failed to result in development of Buruli ulcer lesions [42]. Insects may also play a role in some cases [43,44] though not in all foci where transmission occurs [45]. Water insects (Naucoris and Belostoma spp) have been implicated in laboratory transmission of infection, but their potential role as vectors [33] has been questioned by studies in West Africa [46,47]. In Australia, salt marsh mosquitoes appear to have positive polymerase chain reaction (PCR) signals [35,36,48], while the highest quantitative signals (by real-time PCR) from the environment were obtained from fecal pellets of possums living in trees in the foci of transmission in Victoria [49]. Intermediate hosts including aquatic animals may also play a role [33-35,50,51]; amebae have also been implicated [52], but their role in transmission is limited [53]. Human-to-human transmission is rare [54,55]. Only once has the causative organism been isolated by culture from the environment [43].

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Literature review current through: Oct 2017. | This topic last updated: Dec 15, 2016.
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