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Buruli Ulcer

Infectious Diseases · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

A lesion in the skin and subcutaneous tissues due to infections by mycobacterium ulcerans.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (747 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

A lesion in the skin and subcutaneous tissues due to infections by mycobacterium ulcerans. It was first reported in Uganda, Africa.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Ulcer, Buruli; Buruli Ulcer Disease; Buruli Ulcer Diseases; Disease, Buruli Ulcer; Diseases, Buruli Ulcer; Ulcer Disease, Buruli; Ulcer Diseases, Buruli; Infections, Mycobacterium ulcerans.

Where it fits in the MeSH classification

Broader topics
Mycobacterium Infections, Nontuberculous; Skin Ulcer

Related concepts

  • Mycobacterium Ulcerans

Research landscape

PubMed indexes 808 records tagged with the MeSH heading “Buruli Ulcer” (counts retrieved 2026-10-29). 227 of them (28.1%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 481 records.

Reviews account for 88 records (10.9%) and meta-analyses for 3. Randomized controlled trials number 10 (1.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 0 records; 2000-2009: 100 records; 2010-2019: 481 records; 2020 onward: 227 records0through 19991002000-20094812010-20192272020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19990
2000-2009100
2010-2019481
2020 onward227
Share of records by publication typeReviews: 10.9 percent; Meta-analyses: 0.4 percent; Randomized controlled trials: 1.2 percentReviews10.9% (88)Meta-analyses0.4% (3)Randomized controlled trials1.2% (10)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 808 PubMed records
TypeRecordsShare
Reviews8810.9%
Meta-analyses30.4%
Randomized controlled trials101.2%

Method: PubMed query "Buruli Ulcer"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.

Reading the evidence in infectious diseases

Infectious disease evidence combines microbiology, epidemiology and clinical trials. Laboratory studies identify pathogens and how they cause harm; surveillance and outbreak investigations describe who is affected and how infection spreads; trials establish whether treatments and vaccines work. Results depend on place and time, because pathogens evolve and resistance patterns and population immunity change. Check when and where the data were collected, how cases were defined and how up to date the evidence is.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Distribution of Mycobacterium ulcerans in buruli ulcer endemic and non-endemic aquatic sites in Ghana
Williamson HR, Benbow ME, Nguyen KD, Beachboard DC, Kimbirauskas RK, McIntosh MD, et al.
2008Research article
Design not recorded in structured metadata
108cc by
PMID 18365034 · DOI · PMC2268743
Risk of Buruli ulcer and detection of Mycobacterium ulcerans in mosquitoes in southeastern Australia
Lavender CJ, Fyfe JA, Azuolas J, Brown K, Evans RN, Ray LR, et al.
2011Research article
Design not recorded in structured metadata
74cc by
PMID 21949891 · DOI · PMC3176747
Targeting the Mycobacterium ulcerans cytochrome bc1:aa3 for the treatment of Buruli ulcer
Scherr N, Bieri R, Thomas SS, Chauffour A, Kalia NP, Schneide P, et al.
2018Research article
Design not recorded in structured metadata
64cc by
PMID 30560872 · DOI · PMC6299076
Epidemiology of Buruli Ulcer in Victoria, Australia, 2017-2022
Ravindran B, Hennessy D, O'Hara M, Tay EL, Banuve RS, McVernon J, et al.
2025Review article
Design not recorded in structured metadata
7cc by
PMID 40023793 · DOI · PMC11878321

Distribution of Mycobacterium ulcerans in buruli ulcer endemic and non-endemic aquatic sites in Ghana [1]

Research article Williamson HR, Benbow ME, Nguyen KD, Beachboard DC, Kimbirauskas RK, McIntosh MD, et al. · · 2008 · cited 108 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Mycobacterium ulcerans, the causative agent of Buruli ulcer, is an emerging environmental bacterium in Australia and West Africa.
Closing excerpt
These findings imply that focal demography, along with patterns of human water contact, may play a major role in transmission of Buruli ulcer.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (235 words)

Mycobacterium ulcerans, the causative agent of Buruli ulcer, is an emerging environmental bacterium in Australia and West Africa. The primary risk factor associated with Buruli ulcer is proximity to slow moving water. Environmental constraints for disease are shown by the absence of infection in arid regions of infected countries. A particularly mysterious aspect of Buruli ulcer is the fact that endemic and non-endemic villages may be only a few kilometers apart within the same watershed. Recent studies suggest that aquatic invertebrate species may serve as reservoirs for M. ulcerans, although transmission pathways remain unknown. Systematic studies of the distribution of M. ulcerans in the environment using standard ecological methods have not been reported. Here we present results from the first study based on random sampling of endemic and non-endemic sites. In this study PCR-based methods, along with biofilm collections, have been used to map the presence of M. ulcerans within 26 aquatic sites in Ghana. Results suggest that M. ulcerans is present in both endemic and non-endemic sites and that variable number tandem repeat (VNTR) profiling can be used to follow chains of transmission from the environment to humans. Our results suggesting that the distribution of M. ulcerans is far broader than the distribution of human disease is characteristic of environmental pathogens. These findings imply that focal demography, along with patterns of human water contact, may play a major role in transmission of Buruli ulcer.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 18365034 · DOI · PMC2268743

Risk of Buruli ulcer and detection of Mycobacterium ulcerans in mosquitoes in southeastern Australia [2]

Research article Lavender CJ, Fyfe JA, Azuolas J, Brown K, Evans RN, Ray LR, et al. · · 2011 · cited 74 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundBuruli ulcer (BU) is a destructive skin condition caused by infection with the environmental bacterium, Mycobacterium ulcerans.
Closing excerpt
This has implications for the development of intervention strategies to control and prevent BU.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (212 words)

BackgroundBuruli ulcer (BU) is a destructive skin condition caused by infection with the environmental bacterium, Mycobacterium ulcerans. The mode of transmission of M. ulcerans is not completely understood, but several studies have explored the role of biting insects. In this study, we tested for an association between the detection of M. ulcerans in mosquitoes and the risk of BU disease in humans in an endemic area of southeastern Australia.Methodology/principal findingsAdult mosquitoes were trapped in seven towns on the Bellarine Peninsula in Victoria, Australia, from December 2004 to December 2009 and screened for M. ulcerans by real-time PCR. The number of laboratory-confirmed cases of BU in permanent residents of these towns diagnosed during the same period was tallied to determine the average cumulative incidence of BU in each location. Pearson's correlation coefficient (r) was calculated for the proportion of M. ulcerans-positive mosquitoes per town correlated with the incidence of BU per town. We found a strong dose-response relationship between the detection of M. ulcerans in mosquitoes and the risk of human disease (r, 0.99; 95% CI, 0.92-0.99; p Conclusions/significanceThe results of this study strengthen the hypothesis that mosquitoes are involved in the transmission of M. ulcerans in southeastern Australia. This has implications for the development of intervention strategies to control and prevent BU.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 21949891 · DOI · PMC3176747

Targeting the Mycobacterium ulcerans cytochrome bc1:aa3 for the treatment of Buruli ulcer [3]

Research article Scherr N, Bieri R, Thomas SS, Chauffour A, Kalia NP, Schneide P, et al. · · 2018 · cited 64 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Mycobacterium ulcerans is the causative agent of Buruli ulcer, a neglected tropical skin disease that is most commonly found in children from West and Central Africa.
Closing excerpt
ulcerans replicating in vitro and in mice, making the drug a promising candidate for Buruli ulcer treatment.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)

Mycobacterium ulcerans is the causative agent of Buruli ulcer, a neglected tropical skin disease that is most commonly found in children from West and Central Africa. Despite the severity of the infection, therapeutic options are limited to antibiotics with severe side effects. Here, we show that M. ulcerans is susceptible to the anti-tubercular drug Q203 and related compounds targeting the respiratory cytochrome bc1:aa3. While the cytochrome bc1:aa3 is the primary terminal oxidase in Mycobacterium tuberculosis, the presence of an alternate bd-type terminal oxidase limits the bactericidal and sterilizing potency of Q203 against this bacterium. M. ulcerans strains found in Buruli ulcer patients from Africa and Australia lost all alternate terminal electron acceptors and rely exclusively on the cytochrome bc1:aa3 to respire. As a result, Q203 is bactericidal at low dose against M. ulcerans replicating in vitro and in mice, making the drug a promising candidate for Buruli ulcer treatment.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30560872 · DOI · PMC6299076

Epidemiology of Buruli Ulcer in Victoria, Australia, 2017-2022 [4]

Review article Ravindran B, Hennessy D, O'Hara M, Tay EL, Banuve RS, McVernon J, et al. · · 2025 · cited 7 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Buruli ulcer (BU) is a rare, neglected tropical disease caused by Mycobacterium ulcerans that can lead to severe skin ulcers.
Closing excerpt
The expansion of BU-endemic areas throughout Victoria remains a public health concern and calls for targeted action, particularly for patients and clinicians in new BU-endemic areas.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)

Buruli ulcer (BU) is a rare, neglected tropical disease caused by Mycobacterium ulcerans that can lead to severe skin ulcers. To determine the epidemiology of BU in Victoria, Australia, during 2017-2022 we analyzed surveillance data. A total of 1,751 cases of BU were notified; 968 (55%) patients were male and 781 (45%) female (2 were missing sex data), and 984 (56%) resided in established BU-endemic areas, although an increasing number were in new BU-endemic areas. Most cases (83%, 1,301) were classified as category I. Multivariate modeling demonstrated that factors for severe BU included being male, being older, and living in a new BU-endemic or non-BU-endemic area. A relatively shorter interval between first visit to a clinician and receipt of diagnosis was protective against severe disease. The expansion of BU-endemic areas throughout Victoria remains a public health concern and calls for targeted action, particularly for patients and clinicians in new BU-endemic areas.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40023793 · DOI · PMC11878321

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Buruli ulcer: reductive evolution enhances pathogenicity of Mycobacterium ulcerans [5]
    Demangel C, Stinear TP, Cole ST · Nat Rev Microbiol · 2009 · cited 132 times (Europe PMC)
  • Research article Buruli ulcer [6]
    Portaels F, Silva MT, Meyers WM · Clin Dermatol · 2009 · cited 119 times (Europe PMC)
  • Research article Recent advances: role of mycolactone in the pathogenesis and monitoring of Mycobacterium ulcerans infection/Buruli ulcer disease [7]
    Sarfo FS, Phillips R, Wansbrough-Jones M, Simmonds RE · Cell Microbiol · 2016 · cited 71 times (Europe PMC)
  • Research article Sec61 blockade by mycolactone: A central mechanism in Buruli ulcer disease [8]
    Demangel C, High S · Biol Cell · 2018 · cited 67 times (Europe PMC)
  • Research article Pathogenetic mechanisms of the intracellular parasite Mycobacterium ulcerans leading to Buruli ulcer [9]
    Silva MT, Portaels F, Pedrosa J · Lancet Infect Dis · 2009 · cited 65 times (Europe PMC)
  • Research article Buruli ulcer (Mycobacterium ulcerans infection) [10]
    Walsh DS, Portaels F, Meyers WM · Trans R Soc Trop Med Hyg · 2008 · cited 57 times (Europe PMC)

References

  1. Williamson HR, Benbow ME, Nguyen KD, Beachboard DC, Kimbirauskas RK, McIntosh MD, et al.. Distribution of Mycobacterium ulcerans in buruli ulcer endemic and non-endemic aquatic sites in Ghana. . 2008. PMID 18365034 · DOI · PMC2268743
  2. Lavender CJ, Fyfe JA, Azuolas J, Brown K, Evans RN, Ray LR, et al.. Risk of Buruli ulcer and detection of Mycobacterium ulcerans in mosquitoes in southeastern Australia. . 2011. PMID 21949891 · DOI · PMC3176747
  3. Scherr N, Bieri R, Thomas SS, Chauffour A, Kalia NP, Schneide P, et al.. Targeting the Mycobacterium ulcerans cytochrome bc1:aa3 for the treatment of Buruli ulcer. . 2018. PMID 30560872 · DOI · PMC6299076
  4. Ravindran B, Hennessy D, O'Hara M, Tay EL, Banuve RS, McVernon J, et al.. Epidemiology of Buruli Ulcer in Victoria, Australia, 2017-2022. . 2025. PMID 40023793 · DOI · PMC11878321
  5. Demangel C, Stinear TP, Cole ST. Buruli ulcer: reductive evolution enhances pathogenicity of Mycobacterium ulcerans. Nat Rev Microbiol. 2009. PMID 19079352 · DOI
  6. Portaels F, Silva MT, Meyers WM. Buruli ulcer. Clin Dermatol. 2009. PMID 19362692 · DOI
  7. Sarfo FS, Phillips R, Wansbrough-Jones M, Simmonds RE. Recent advances: role of mycolactone in the pathogenesis and monitoring of Mycobacterium ulcerans infection/Buruli ulcer disease. Cell Microbiol. 2016. PMID 26572803 · DOI · PMC4705457
  8. Demangel C, High S. Sec61 blockade by mycolactone: A central mechanism in Buruli ulcer disease. Biol Cell. 2018. PMID 30055020 · DOI
  9. Silva MT, Portaels F, Pedrosa J. Pathogenetic mechanisms of the intracellular parasite Mycobacterium ulcerans leading to Buruli ulcer. Lancet Infect Dis. 2009. PMID 19850228 · DOI
  10. Walsh DS, Portaels F, Meyers WM. Buruli ulcer (Mycobacterium ulcerans infection). Trans R Soc Trop Med Hyg. 2008. PMID 18657836 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-29.

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At a glance

808
PubMed records on this heading
28%
published since 2020
88
review articles
10
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

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