Buruli ulcer A31.1

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 13.03.2021

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Synonym(s)

Buruli ulcer; mycobacterium ulcerans

History
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Cook 1897; Kleinschmidt 1935; McCallum 1948

Definition
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Common tropical infectious disease caused by Mycobacterium ulcerans a"non-tuberculous mycobacterium" (NTM).

Pathogen
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Mycobacterium ulcerans a non-tuberculous mycobacterium (NTM) that is the only mycobacterium that is obligately pathogenic. It grows in vitro at 30-35 °C. Infection remains confined to the (cool) skin (probably because of the limited temperature optimum). Unique among mycobacteria is the production of exotoxins(mycolactones) with immunosuppressive effects (this explains, among other things, the persistent and destructive course of the infection).

Occurrence/Epidemiology
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After tuberculosis and leprosy, Buruli ulcer is the third most common mycobacterial disease in immunocompetent individuals (Manry J 2020). Endemic occurrence in tropical and subtropical areas. High incidence and prevalence (up to 16% of the population) in endemic areas.

Affected regions: West and Central Africa, Australia, Papua New Guinea, Malaysia, Sri Lanka and South America.

In Australia, M. ulcerans has been detected in clinically healthy koalas and oppossums.

Etiopathogenesis
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Infection with M. ulcerans. Transmission route is unclear, but contaminated soil, contaminated water, plants, insects (e.g. bugs), aerosols or human contact are discussed (some authors deny this). Apparently, the most important risk factor is contact with slow-flowing waters. The pathogens enter the host through micro-injuries.

Manifestation
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Women and children between 5 and 15 years are preferentially affected.

Localization
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Leg or trunk

Clinical features
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Incubation period: 2 to 14 weeks.

At the site of inoculation (pathogen penetrates through small injuries of the skin), a painless, small, subcutaneous, reddish, hyperpigmented and scaly nodule is formed. Centrally, the skin blisters and shines.

Formation of an indurated oedema. After weeks to months ulcer formation. Progressive growth in size of the ulcer. Ulcers may cover up to 15% of the body surface.

Deeply undermined ulcer margins are typical; spontaneous remission with scarring and corresponding loss of function is possible. Patients do not show any systemic signs of infection!

Deep fascia, nerves, muscles and bones are often involved.

Regression or progression possible, with extensive ulceration that may involve an entire limb.

Histology
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Granulomatous dermatitis with giant cells of Langerhans. Acanthosis, hyperkeratosis.

Diagnosis
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Typical clinic with exorbitantly large ulcers; microbiological detection of M. ulcerans(Ziehl-Neelsen preparation) from culture of necrotic tissue from the ulcer base; molecular biological detection by PCR.

Therapy
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Early detection is important! Therapeutic options are limited. In the early stage, the disease can be cured by excision. Larger lesions should be excised as extensively as possible and treated by transplantation.

Effects of chemotherapeutic agents have been disappointing so far. Antimycobacterial drugs (e.g. rifampicin 10 mg/kg bw/day p.o.) alone are only promising for preulcerative lesions or smallest ulcers, but are not sufficient for larger lesions.

WHO recommendation: Rifampicin in combination with streptomycin (clarithromycin) + necessary surgical measures.

Hyperthermia has been experimentally proven as a procedure.

Postoperative physiotherapy to prevent loss of function or contractures.

Progression/forecast
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Development of larger necroses possible; mutating contractures, possibly metastatic bone lesions. Carcinomatous degeneration possible.

Note(s)
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Buruli is a district in Uganda. In the tropics, sufferers are often ostracized, which is why the disease is hidden for a long time under appropriately long clothing and thus only diagnosed at a very advanced stage.

Literature
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  1. Addy JH (1995) The problem of Buruli-Ulcer in Ghana. Ghana Med J 29: 587-588
  2. Cook A (1970) Mengo Hospital notes 1897, Makerere Medical School Library. Br Med J 2: 378-379
  3. Kaloga M et al (2015) Squamous cell carcinoma secondary to Buruli ulcer in West Africa. Ann Dermatol Venereol doi: 10.1016/j.annder.2015.10.577
  4. McCallum et al (1948) A new mycobacterial infection in man. J Bacteriol 60: 93-122
  5. Manry J (2020) Human genetics of Buruli ulcer. Hum Genet 139:847-853.
  6. Peters F et al. (2016) Germ or no germ: challenges in the diagnosis of mycobacterial infections of the skin. J Dtsch Dermatol Ges 14:1227-1236.
  7. Pszolla N et al (2003) Buruli ulcer: a systemic disease. Clin Infect Dis 37: e78-82.
  8. Simpson H et al.(2019) Mapping the global distribution of Buruli ulcer: a systematic review with evidence consensus. Lancet Glob Health 7:e912-e922.

  9. Tabah EN et al. (2016) Buruli ulcer in Cameroon: the development and impact of the National Control Programme. PLoS Negl Trop Dis 10: e0004224
  10. Thomssen J (2002) Buruli ulcer. A mycobacterial skin disease. Dermatologist 53: 334-337
  11. van der Werf TS et al (2003) Mycolactones and Mycobacterium ulcerans disease. Lancet 362: 1062-1064
  12. van der Werft TS et al (1999) Mycobacterium ulcerans infection. Lancet 354: 1013-1015

Incoming links (2)

Buruli ulcer; Onchocerciasis;

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

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Last updated on: 13.03.2021