Buruli ulcer

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Cases of Buruli ulcer reported to the World Health Organization in 2018. Color indicates case number: yellow, (1–150) Dem. Rep. Congo, Gabon, Guinea, Togo; orange (151–300), Benin, Cameroon, Côte d'Ivoire; light red (301–450), Liberia, Nigeria; dark red (451+), Ghana. Not shown are Australia (358), Papua New Guinea (12) and Japan (3).
  • Skin infection caused by Mycobacterium ulcerans
  • Named for Buruli district in Uganda
  • Begins as a localized lesion and progresses to extensive ulceration


  • Most frequent in humid, rural, tropical regions with limited access to medical care


  • Mode of transmission is not fully understood, but linked to contaminated water [1]
  • Human to human transmission is rare


  • Caused by Mycobacterium ulcerans, a slow growing mycobacterium that can be cultured in vitro at 29-33C
  • Mycobacterium ulcerans is capable of producing mycolactone, a cytotoxin that induces necrosis and ulceration
  • Effect of mylactone includes cell structural deformation and apoptosis of several cell types, including immune cells

Clinical Features

Early signs of Buruli ulcer: painless swollen bumps (top); plaque (bottom-left); and widespread swelling of the lower arm (bottom-right).
Later signs of a buruli ulcer: early ulcer (top-left); larger ulcer across the lower arm and wrist (top-right), and a large ulcer on the thigh (bottom).
  • Usually begins as a painless nodule <5cm in diameter, but also may initially present as papules, plaques, or edematous lesions
  • Limbs are most frequently involved, although it may also affect the head, neck, trunk, and genitals
  • Initial lesion usually breaks down after days to weeks, forming an ulcer with characteristic undermined edges
  • Ulceration tends to progress slowly and painlessly, usually systemic symptoms are not present unless there is secondary bacterial infection
  • However, some individuals may present with an initial edematous lesion that will have relatively rapid progression leading to ulceration within a few days, these patients also often have pain and a low grade fever
  • Superficial lesions can progress to deeper tissues (i.e. tendons, bones)

Differential Diagnosis

Travel-related skin conditions

See also domestic U.S. ectoparasites


  • There are several options for laboratory evaluation, but in endemic regions diagnosis is often made by clinical diagnosis due to limited resources

Laboratory Testing[2] [3]

  • Acid fast staining – does not rule out other related infections such as mycobacterium tuberculosis, sensitivity is approximately 40%
  • Culture – mycobacterium ulcerans grows slowly in laboratory (positive results require 6 weeks or more), sensitivity is approximately 60%
  • Histology – sensitivity up to 82%
  • PCR – sensitivity 70-80%


  • Antibiotic therapy
  • Most cases will heal with antibiotics alone, but healing is often incomplete until after antibiotic therapy
  • Surgical debridement can be considered to remove necrotic tissue


  • Discharge


  1. Raghunathan PL, Whitney EA, Asamoa K, et al. Risk factors for Buruli ulcer disease (Mycobacterium ulcerans Infection): results from a case-control study in Ghana. Clin Infect Dis. 2005;40(10):1445-1453. doi:10.1086/429623
  2. Phillips R, Horsfield C, Kuijper S, et al. Sensitivity of PCR targeting the IS2404 insertion sequence of Mycobacterium ulcerans in an Assay using punch biopsy specimens for diagnosis of Buruli ulcer. J Clin Microbiol. 2005;43(8):3650-3656. doi:10.1128/JCM.43.8.3650-3656.2005
  3. Phillips RO, Sarfo FS, Osei-Sarpong F, et al. Sensitivity of PCR targeting Mycobacterium ulcerans by use of fine-needle aspirates for diagnosis of Buruli ulcer. J Clin Microbiol. 2009;47(4):924-926. doi:10.1128/JCM.01842-08
  4. O'Brien DP, Jenkin G, Buntine J, et al. Treatment and prevention of Mycobacterium ulcerans infection (Buruli ulcer) in Australia: guideline update. Med J Aust. 2014;200(5):267-270. doi:10.5694/mja13.11331