Buruli ulcer

Background

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

Epidemiology

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

Transmission

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

Microbiology

• 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

• Eumycetoma
• Pyoderma gangrenosum
• Venous stasis ulcer
• Diabetic skin ulceration
• Squamous cell carcinoma

Travel-related skin conditions

• Papules
  • Insect bites
  • Scabies
  • Seabather's eruption
  • Cercarial dermatitis (Swimmer's Itch)
• Macular
  • Chikungunya
• Sub Q Swelling and Nodules
  • Myiasis
  • Tungiasis
  • Loa loa
  • African Trypanosomiasis
  • Onchocerciasis
• Ulcers
  • Tropical pyoderma
  • Leishmaniasis
  • Mycobacterium marinum
  • Buruli ulcer
  • Dracunculiasis (Guinea Worm disease)
• Linear and Migratory Lesions
  • Cutaneous larvae migrans
  • Photodermatitis

See also domestic U.S. ectoparasites

Evaluation

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

Laboratory Testing

• 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%

Management

• Antibiotic therapy
  • Guided by severity of lesions
  • Most commonly 8 weeks of rifampin and clarithromycin
• 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

Disposition

• Discharge