Buruli ulcer is an indolent necrotizing disease of the skin and subcutaneous tissues caused by Mycobacterium ulcerans, leading to deep ulcerations and disability.
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name: Buruli ulcer
creation_date: '2026-01-26T15:56:41Z'
updated_date: '2026-04-11T01:06:52Z'
category: Infectious Disease
description: >-
Buruli ulcer is an indolent necrotizing disease of the skin and subcutaneous
tissues caused by Mycobacterium ulcerans, leading to deep ulcerations and
disability.
disease_term:
term:
id: MONDO:0000327
label: Buruli ulcer disease
preferred_term: Buruli ulcer disease
parents:
- Bacterial Infection
- Neglected tropical disease
infectious_agent:
- name: Mycobacterium ulcerans
infectious_agent_term:
preferred_term: Mycobacterium ulcerans
term:
id: NCBITaxon:1809
label: Mycobacterium ulcerans
description: Slow-growing mycobacterium that produces mycolactone toxin.
evidence:
- reference: PMID:21240839
reference_title: "Buruli ulcer: a review of in vitro tests to screen natural products for activity against Mycobacterium ulcerans."
supports: SUPPORT
snippet: "Buruli ulcer (BU), caused by Mycobacterium ulcerans"
explanation: The abstract identifies M. ulcerans as the cause of Buruli ulcer.
pathophysiology:
- name: Mycolactone-mediated tissue destruction
description: Mycolactone toxin leads to subcutaneous tissue destruction and immunosuppression, producing deep ulcers.
evidence:
- reference: PMID:30429139
reference_title: "Cutaneous Mycobacterial Infections."
supports: SUPPORT
snippet: "Mycobacterium ulcerans produces a mycolactone toxin that leads to subcutaneous tissue destruction and immunosuppression, resulting in deep ulcerations"
explanation: The abstract links mycolactone to tissue destruction and ulceration.
phenotypes:
- name: Skin ulcer
category: Dermatologic
frequency: VERY_FREQUENT
phenotype_term:
preferred_term: Skin ulcer
term:
id: HP:0200042
label: Skin ulcer
evidence:
- reference: PMID:19362692
reference_title: "Buruli ulcer."
supports: SUPPORT
snippet: "Buruli ulcer is an indolent necrotizing disease of the skin, subcutaneous tissue, and bone"
explanation: The disease is defined by necrotizing skin disease with ulceration.
treatments:
- name: Antimycobacterial therapy
description: Antimycobacterial therapy is effective for early lesions.
treatment_term:
preferred_term: Pharmacotherapy
term:
id: NCIT:C15986
label: Pharmacotherapy
evidence:
- reference: PMID:21240839
reference_title: "Buruli ulcer: a review of in vitro tests to screen natural products for activity against Mycobacterium ulcerans."
supports: SUPPORT
snippet: "While antimycobacterial therapy is often effective for the earliest nodular or ulcerative lesions"
explanation: The abstract describes antimycobacterial therapy effectiveness in early lesions.
- name: Surgical management
description: Surgery may be required for advanced ulcerated lesions.
treatment_term:
preferred_term: surgical procedure
term:
id: MAXO:0000004
label: surgical procedure
evidence:
- reference: PMID:21240839
reference_title: "Buruli ulcer: a review of in vitro tests to screen natural products for activity against Mycobacterium ulcerans."
supports: SUPPORT
snippet: "for advanced ulcerated lesions, surgery is sometimes necessary."
explanation: The abstract notes surgery for advanced lesions.
references:
- reference: DOI:10.1016/j.heliyon.2023.e22018
title: 'Buruli ulcer in Africa: Geographical distribution, ecology, risk factors, diagnosis, and indigenous plant treatment options – A comprehensive review'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: 'Buruli ulcer in Africa: Geographical distribution, ecology, risk factors, diagnosis, and indigenous plant treatment options – A comprehensive review'
supporting_text: 'Buruli ulcer in Africa: Geographical distribution, ecology, risk factors, diagnosis, and indigenous plant treatment options – A comprehensive review'
- reference: DOI:10.1038/s41598-024-70890-w
title: Pharmacokinetics of extended-release clarithromycin in patients with Mycobacterium ulcerans infection
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Pharmacokinetics of extended-release clarithromycin in patients with Mycobacterium ulcerans infection
supporting_text: Pharmacokinetics of extended-release clarithromycin in patients with Mycobacterium ulcerans infection
- reference: DOI:10.1101/2024.01.23.24301643
title: Towards a Buruli Ulcer Rapid Diagnostic Test that Targets Mycolactone
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: We report the development of a prototype rapid diagnostic test for Buruli ulcer, an ulcerative necrotizing skin disease caused by M. ulcerans .
supporting_text: We report the development of a prototype rapid diagnostic test for Buruli ulcer, an ulcerative necrotizing skin disease caused by M. ulcerans .
evidence:
- reference: DOI:10.1101/2024.01.23.24301643
reference_title: Towards a Buruli Ulcer Rapid Diagnostic Test that Targets Mycolactone
supports: SUPPORT
evidence_source: OTHER
snippet: We report the development of a prototype rapid diagnostic test for Buruli ulcer, an ulcerative necrotizing skin disease caused by M. ulcerans .
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.1111/bjd.19260
title: Are all Buruli ulcers caused by <i>Mycobacterium ulcerans</i> ?
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Are all Buruli ulcers caused by <i>Mycobacterium ulcerans</i> ?
supporting_text: Are all Buruli ulcers caused by <i>Mycobacterium ulcerans</i> ?
- reference: DOI:10.12788/cutis.1145
title: 'Buruli Ulcer Transmission: Environmental Pathways and Implications for Dermatologic Care'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: 'Buruli Ulcer Transmission: Environmental Pathways and Implications for Dermatologic Care'
supporting_text: 'Buruli Ulcer Transmission: Environmental Pathways and Implications for Dermatologic Care'
- reference: DOI:10.1371/journal.pntd.0011394
title: 'A human model of Buruli ulcer: The case for controlled human infection and considerations for selecting a Mycobacterium ulcerans challenge strain'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Critical knowledge gaps regarding infection withMycobacterium ulcerans, the cause of Buruli ulcer (BU), have impeded development of new therapeutic approaches and vaccines for prevention of this neglected tropical disease.
supporting_text: Critical knowledge gaps regarding infection withMycobacterium ulcerans, the cause of Buruli ulcer (BU), have impeded development of new therapeutic approaches and vaccines for prevention of this neglected tropical disease.
evidence:
- reference: DOI:10.1371/journal.pntd.0011394
reference_title: 'A human model of Buruli ulcer: The case for controlled human infection and considerations for selecting a Mycobacterium ulcerans challenge strain'
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: Critical knowledge gaps regarding infection withMycobacterium ulcerans, the cause of Buruli ulcer (BU), have impeded development of new therapeutic approaches and vaccines for prevention of this neglected tropical disease.
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.1371/journal.pntd.0011867
title: Amoxicillin/clavulanate in combination with rifampicin/clarithromycin is bactericidal against Mycobacterium ulcerans
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Buruli ulcer (BU) is a skin neglected tropical disease (NTD) caused by Mycobacterium ulcerans.
supporting_text: Buruli ulcer (BU) is a skin neglected tropical disease (NTD) caused by Mycobacterium ulcerans.
evidence:
- reference: DOI:10.1371/journal.pntd.0011867
reference_title: Amoxicillin/clavulanate in combination with rifampicin/clarithromycin is bactericidal against Mycobacterium ulcerans
supports: SUPPORT
evidence_source: OTHER
snippet: Buruli ulcer (BU) is a skin neglected tropical disease (NTD) caused by Mycobacterium ulcerans.
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.1371/journal.pntd.0013509
title: 'Territorial and gender-linked risk factors for Buruli ulcer in Southern Benin: A case-control study using geographic and behavioral surveying'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: The manuscript examines the risk factors associated with Buruli ulcer in endemic regions of Benin, focusing on community practices, agricultural activities, and age and gender disparities.
supporting_text: The manuscript examines the risk factors associated with Buruli ulcer in endemic regions of Benin, focusing on community practices, agricultural activities, and age and gender disparities.
evidence:
- reference: DOI:10.1371/journal.pntd.0013509
reference_title: 'Territorial and gender-linked risk factors for Buruli ulcer in Southern Benin: A case-control study using geographic and behavioral surveying'
supports: SUPPORT
evidence_source: OTHER
snippet: The manuscript examines the risk factors associated with Buruli ulcer in endemic regions of Benin, focusing on community practices, agricultural activities, and age and gender disparities.
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.1371/journal.pntd.0013684
title: 'Risk factors for Buruli ulcer disease in Ghana: A matched case-control study in four selected endemic districts of Eastern and Oti Regions'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Buruli ulcer disease (BUD) remains a poorly understood neglected tropical disease (NTD).
supporting_text: Buruli ulcer disease (BUD) remains a poorly understood neglected tropical disease (NTD).
evidence:
- reference: DOI:10.1371/journal.pntd.0013684
reference_title: 'Risk factors for Buruli ulcer disease in Ghana: A matched case-control study in four selected endemic districts of Eastern and Oti Regions'
supports: SUPPORT
evidence_source: OTHER
snippet: Buruli ulcer disease (BUD) remains a poorly understood neglected tropical disease (NTD).
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.31128/ajgp-08-23-6914
title: An overview of Buruli ulcer in Australia
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: An overview of Buruli ulcer in Australia
supporting_text: An overview of Buruli ulcer in Australia
- reference: DOI:10.3310/nihropenres.13332.1
title: 'Buruli-RifDACC: Evaluation of the efficacy and cost-effectiveness of high-dose versus standard-dose rifampicin on outcomes in Mycobacterium ulcerans disease, a protocol for a randomised controlled trial in Ghana'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Buruli ulcer (BU) can lead to disfiguring ulcers and permanent disability.
supporting_text: Buruli ulcer (BU) can lead to disfiguring ulcers and permanent disability.
evidence:
- reference: DOI:10.3310/nihropenres.13332.1
reference_title: 'Buruli-RifDACC: Evaluation of the efficacy and cost-effectiveness of high-dose versus standard-dose rifampicin on outcomes in Mycobacterium ulcerans disease, a protocol for a randomised controlled trial in Ghana'
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: Buruli ulcer (BU) can lead to disfiguring ulcers and permanent disability.
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.3390/life15071096
title: 'Mycobacterium Ulcerans Ulcer: Current Trends in Antimicrobial Management and Reconstructive Surgical Strategies'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Mycobacterium ulcerans causes Buruli ulcer (BU), a necrotizing skin disease endemic in over 30 countries.
supporting_text: Mycobacterium ulcerans causes Buruli ulcer (BU), a necrotizing skin disease endemic in over 30 countries.
evidence:
- reference: DOI:10.3390/life15071096
reference_title: 'Mycobacterium Ulcerans Ulcer: Current Trends in Antimicrobial Management and Reconstructive Surgical Strategies'
supports: SUPPORT
evidence_source: OTHER
snippet: Mycobacterium ulcerans causes Buruli ulcer (BU), a necrotizing skin disease endemic in over 30 countries.
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.3390/ph17060691
title: 'Formulation and Stability of a 1% Clarithromycin-Based Topical Skin Cream: A New Option to Treat Buruli Ulcers?'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: There are more than 170 known species of non-tuberculous mycobacteria, and some are responsible for serious diseases in people infected with them.
supporting_text: There are more than 170 known species of non-tuberculous mycobacteria, and some are responsible for serious diseases in people infected with them.
evidence:
- reference: DOI:10.3390/ph17060691
reference_title: 'Formulation and Stability of a 1% Clarithromycin-Based Topical Skin Cream: A New Option to Treat Buruli Ulcers?'
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: There are more than 170 known species of non-tuberculous mycobacteria, and some are responsible for serious diseases in people infected with them.
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.3390/toxins16120528
title: 'Exploring Mycolactone—The Unique Causative Toxin of Buruli Ulcer: Biosynthetic, Synthetic Pathways, Biomarker for Diagnosis, and Therapeutic Potential'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Mycolactone is a complex macrolide toxin produced by Mycobacterium ulcerans, the causative agent of Buruli ulcer.
supporting_text: Mycolactone is a complex macrolide toxin produced by Mycobacterium ulcerans, the causative agent of Buruli ulcer.
evidence:
- reference: DOI:10.3390/toxins16120528
reference_title: 'Exploring Mycolactone—The Unique Causative Toxin of Buruli Ulcer: Biosynthetic, Synthetic Pathways, Biomarker for Diagnosis, and Therapeutic Potential'
supports: SUPPORT
evidence_source: OTHER
snippet: Mycolactone is a complex macrolide toxin produced by Mycobacterium ulcerans, the causative agent of Buruli ulcer.
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
- reference: DOI:10.5694/mja2.52591
title: 'Management of <i>Mycobacterium ulcerans</i> infection (Buruli ulcer) in Australia: consensus statement'
found_in:
- Buruli_Ulcer-deep-research-falcon.md
findings:
- statement: Buruli ulcer, caused by Mycobacterium ulcerans, is increasing in incidence and spreading to new areas in southeast Australia.
supporting_text: Buruli ulcer, caused by Mycobacterium ulcerans, is increasing in incidence and spreading to new areas in southeast Australia.
evidence:
- reference: DOI:10.5694/mja2.52591
reference_title: 'Management of <i>Mycobacterium ulcerans</i> infection (Buruli ulcer) in Australia: consensus statement'
supports: SUPPORT
evidence_source: OTHER
snippet: Buruli ulcer, caused by Mycobacterium ulcerans, is increasing in incidence and spreading to new areas in southeast Australia.
explanation: Deep research cited this publication as relevant literature for Buruli Ulcer.
Buruli ulcer (BU) is a necrotizing infection of skin and subcutaneous tissue caused by Mycobacterium ulcerans, typically beginning as a painless pre-ulcerative lesion (papule, nodule, plaque, or oedema) that can progress to a necrotic ulcer with undermined edges and substantial tissue loss, scarring, and disability if untreated or treated late (akolgo2024exploringmycolactone—theunique pages 1-3, muhi2023ahumanmodel pages 1-2, anthony2024buruliulcertransmission pages 1-2). BU is categorized by WHO as a neglected tropical disease and is geographically focal, with highest burden in West/Central Africa and important endemic foci in Australia (akolgo2024exploringmycolactone—theunique pages 3-4, muhi2023ahumanmodel pages 1-2).
Evidence retrieved in-session supports the following identifiers/classifications: - MeSH (condition/descriptor ID): D054312 “Buruli Ulcer” (ClinicalTrials.gov record) (NCT00321178 chunk 2). - WHO clinical lesion categories (severity by size/complexity): Category I (<5 cm), Category II (5–15 cm), Category III (>15 cm and/or critical sites/complex disease) (anthony2024buruliulcertransmission pages 1-2, obrien2024anoverviewof pages 1-2).
Not located in retrieved sources: ICD-10/ICD-11 codes, Orphanet (ORPHA) identifier, and MONDO ID were not present in the retrieved full-text excerpts and therefore cannot be populated from the present evidence set.
Synonyms/alternative names include Mycobacterium ulcerans disease and historical regional names Bairnsdale ulcer, Searls ulcer, and Daintree ulcer (NCT00321178 chunk 2, akolgo2024exploringmycolactone—theunique pages 3-4).
A compact identifiers/synonyms summary is provided here:
| Item | Value | Source | URL / publication date |
|---|---|---|---|
| Disease name | Buruli ulcer (BU) (akolgo2024exploringmycolactone—theunique pages 1-3, muhi2023ahumanmodel pages 1-2) | Akolgo et al., Exploring Mycolactone—The Unique Causative Toxin of Buruli Ulcer; Muhi et al., A human model of Buruli ulcer | https://doi.org/10.3390/toxins16120528 (Dec 2024); https://doi.org/10.1371/journal.pntd.0011394 (Jun 2023) |
| Synonyms / alternative names | Mycobacterium ulcerans disease; Bairnsdale ulcer; Searls ulcer; Daintree ulcer (NCT00321178 chunk 2, akolgo2024exploringmycolactone—theunique pages 3-4) | ClinicalTrials.gov BURULICO protocol; Akolgo et al. | NCT00321178 / ClinicalTrials.gov (2006); https://doi.org/10.3390/toxins16120528 (Dec 2024) |
| Causative agent | Mycobacterium ulcerans (environmental nontuberculous mycobacterium) (akolgo2024exploringmycolactone—theunique pages 1-3, anthony2024buruliulcertransmission pages 1-2) | Akolgo et al.; Anthony et al., Buruli ulcer transmission: environmental pathways and implications for dermatologic care | https://doi.org/10.3390/toxins16120528 (Dec 2024); https://doi.org/10.12788/cutis.1145 (Dec 2024) |
| MeSH condition ID | D054312 (“Buruli Ulcer”) (NCT00321178 chunk 2) | ClinicalTrials.gov BURULICO protocol | NCT00321178 / ClinicalTrials.gov (2006) |
| WHO lesion category I | Lesion diameter <5 cm (anthony2024buruliulcertransmission pages 1-2, obrien2024anoverviewof pages 1-2) | Anthony et al.; O'Brien et al., An overview of Buruli ulcer in Australia | https://doi.org/10.12788/cutis.1145 (Dec 2024); https://doi.org/10.31128/ajgp-08-23-6914 (Sep 2024) |
| WHO lesion category II | Lesion diameter 5–15 cm (anthony2024buruliulcertransmission pages 1-2, obrien2024anoverviewof pages 1-2) | Anthony et al.; O'Brien et al. | https://doi.org/10.12788/cutis.1145 (Dec 2024); https://doi.org/10.31128/ajgp-08-23-6914 (Sep 2024) |
| WHO lesion category III | Lesion diameter >15 cm and/or lesions at critical sites or involving bone/joint/other clinically complex disease (anthony2024buruliulcertransmission pages 1-2, obrien2024anoverviewof pages 1-2) | Anthony et al.; O'Brien et al. | https://doi.org/10.12788/cutis.1145 (Dec 2024); https://doi.org/10.31128/ajgp-08-23-6914 (Sep 2024) |
| WHO reported new cases in 2023 | 1,952 total new cases from 12 countries; 1,573 in the African Region; 379 in the Western Pacific Region (akolgo2024exploringmycolactone—theunique pages 3-4) | Akolgo et al. | https://doi.org/10.3390/toxins16120528 (Dec 2024) |
Table: This table compiles high-yield identifiers, synonyms, classification details, and recent WHO surveillance figures for Buruli ulcer using only evidence retrieved in the session. It is useful as a compact reference for nomenclature and disease-level knowledge base fields.
BU is caused by infection with the environmental, nontuberculous mycobacterium Mycobacterium ulcerans (akolgo2024exploringmycolactone—theunique pages 1-3, anthony2024buruliulcertransmission pages 1-2).
A central driver of BU pathology is the diffusible macrolide toxin mycolactone, encoded on plasmid pMUM001 (anthony2024buruliulcertransmission pages 1-2, akolgo2024exploringmycolactone—theunique pages 1-3).
BU acquisition is strongly associated with water-rich environments (e.g., swamps, ponds, marshes) and water-contact activities; transmission pathways appear to vary by geography and remain incompletely defined (anthony2024buruliulcertransmission pages 1-2, akolgo2024exploringmycolactone—theunique pages 4-6).
Quantified modifiable risk factors were identified in a recent matched case-control study in Ghana: - Farming without adequate protective clothing: aOR 3.02 (gohoho2025riskfactorsfor pages 13-15) - Living near waterbodies: aOR 4.45 (gohoho2025riskfactorsfor pages 13-15)
A separate case-control study in Benin (2025) also highlighted elevated odds for specific water-exposure behaviors (e.g., bathing; frequenting irrigation canals) with odds ratios in the ~3–5 range depending on subgroup/territory (johnson2025territorialandgenderlinked pages 9-12).
In the Ghana matched case-control study, the following were associated with reduced odds: - Applying alcohol to injuries: aOR 0.17 (gohoho2025riskfactorsfor pages 13-15) - Being married: aOR 0.32 (gohoho2025riskfactorsfor pages 13-15)
No robust human genetic susceptibility loci or gene–environment interaction datasets were retrieved in-session. Current evidence emphasizes an environmental reservoir with toxin-mediated pathogenesis rather than a defined Mendelian genetic architecture (muhi2023ahumanmodel pages 1-2, akolgo2024exploringmycolactone—theunique pages 4-6).
Early BU can present as papule, nodule, plaque, or oedematous lesions, with eventual ulceration characterized by a necrotic base and undermined edges (obrien2024anoverviewof pages 1-2, anthony2024buruliulcertransmission pages 1-2, muhi2023ahumanmodel pages 1-2). In Australia, oedematous BU was reported to account for ~8% of cases and is described as the most rapidly progressive/destructive form; multiple lesions occur in ~5% of cases (obrien2024anoverviewof pages 1-2).
BU lesions are painless in most cases, consistent with mycolactone-mediated hypoesthesia/analgesia; pain and fever may suggest secondary bacterial infection (obrien2024anoverviewof pages 1-2, anthony2024buruliulcertransmission pages 1-2).
Severe disease can extend to deeper structures including bone (osteomyelitis), and complications include scarring, joint contractures, deformity, and functional impairment (obrien2024anoverviewof pages 1-2, anthony2024buruliulcertransmission pages 1-2, muhi2023ahumanmodel pages 1-2).
A clinical image panel of classic forms (nodule, plaque, oedema, small ulcer) is available from a 2024 review:
Incubation can be prolonged (reported average 4–5 months in Victoria, Australia) with slow progression from pre-ulcerative lesions to ulceration (muhi2023ahumanmodel pages 1-2). Progression from nodule to ulcer has been described as ranging from weeks to months (anthony2024buruliulcertransmission pages 1-2).
WHO categories are used clinically to stratify severity by lesion size and complexity: category I (<5 cm), II (5–15 cm), III (>15 cm and/or critical sites/complex disease) (anthony2024buruliulcertransmission pages 1-2, obrien2024anoverviewof pages 1-2).
BU can cause cosmetic deformity, functional impairment, psychological impact, and substantial economic burden, especially when diagnosis/treatment is delayed or when lesions are large/complex (obrien2024anoverviewof pages 1-2, boakyeappiah2023currentprogressand pages 1-5).
Suggested HPO term mappings consistent with the retrieved clinical descriptions: - Papule; Nodule; Plaque; Localized edema (oedema form) (obrien2024anoverviewof pages 1-2, anthony2024buruliulcertransmission pages 1-2) - Skin ulcer; Skin necrosis; Undermined ulcer edge (obrien2024anoverviewof pages 1-2, anthony2024buruliulcertransmission pages 1-2) - Hypoesthesia / decreased pain sensation (painless lesion) (anthony2024buruliulcertransmission pages 1-2) - Fever (secondary infection context) (obrien2024anoverviewof pages 1-2) - Osteomyelitis (obrien2024anoverviewof pages 1-2, anthony2024buruliulcertransmission pages 1-2) - Joint contracture / decreased range of motion; Impaired mobility (muhi2023ahumanmodel pages 1-2) - Abnormal scarring / disfigurement (akolgo2024exploringmycolactone—theunique pages 1-3, muhi2023ahumanmodel pages 1-2)
BU is an infectious disease; no human causal genes/variants were identified in the retrieved evidence.
A key pathogen genetic determinant is the plasmid-encoded mycolactone biosynthetic machinery (pMUM001) (anthony2024buruliulcertransmission pages 1-2).
No relevant host epigenetic or chromosomal abnormality evidence was retrieved in-session.
Multiple sources emphasize BU’s association with aquatic and swampy environments and possible involvement of aquatic organisms and insects in ecology/transmission (anthony2024buruliulcertransmission pages 1-2, oseiowusu2023buruliulcerin pages 5-7). M. ulcerans DNA has been detected in fish, water insects, and snails; aquatic insects and mosquitoes have been studied as possible vectors (anthony2024buruliulcertransmission pages 1-2).
Farming without protective clothing and proximity to water bodies are associated with increased odds, while injury cleansing with alcohol is associated with reduced odds (gohoho2025riskfactorsfor pages 13-15).
Environmental exposure and inoculation (likely through skin breaches in aquatic-associated settings) is followed by local infection with M. ulcerans (anthony2024buruliulcertransmission pages 1-2, akolgo2024exploringmycolactone—theunique pages 4-6). Disease progression is driven by mycolactone, which mediates: - Cytotoxic tissue necrosis → necrotic ulcers and undermined edges (akolgo2024exploringmycolactone—theunique pages 1-3, anthony2024buruliulcertransmission pages 1-2) - Immune suppression → reduced inflammatory signs and impaired local control (muhi2023ahumanmodel pages 1-2, akolgo2024exploringmycolactone—theunique pages 4-6) - Analgesia/hypoesthesia → typically painless lesions despite extensive tissue damage (anthony2024buruliulcertransmission pages 1-2)
A major mechanism is mycolactone binding and inhibition of the Sec61 translocon, blocking protein translocation into the endoplasmic reticulum and suppressing cytokine production including IL-2 and IFN-γ (muhi2023ahumanmodel pages 1-2, muhi2023ahumanmodel pages 12-13). Additional proposed targets/mechanisms include WASP/N-WASP inhibition, angiotensin II type 2 receptor (AT2R) signaling in analgesia, and mTOR inhibition (akolgo2024exploringmycolactone—theunique pages 1-3, anthony2024buruliulcertransmission pages 1-2).
Mycolactone affects multiple mammalian cell types including macrophages, fibroblasts, keratinocytes, dendritic cells, and T cells (akolgo2024exploringmycolactone—theunique pages 4-6). Suggested Cell Ontology (CL) mappings include macrophage; fibroblast; keratinocyte; dendritic cell; T cell.
Based on described mechanisms: - Immune effector process / cytokine production - Protein targeting to ER / protein translocation - Apoptotic process - Inflammatory response regulation
No transcriptomic/proteomic/metabolomic profiling datasets were retrieved in-session.
Primary involvement is skin and subcutaneous tissue, often on distal limbs around joints; severe disease can involve bone (osteomyelitis) and joints (obrien2024anoverviewof pages 1-2, anthony2024buruliulcertransmission pages 1-2). Suggested UBERON mappings: skin; subcutaneous adipose tissue; lower limb; upper limb; bone tissue.
The Sec61 target localizes to the endoplasmic reticulum membrane, consistent with an ER protein translocation blockade mechanism (muhi2023ahumanmodel pages 1-2).
WHO-reported notifications for 2023 were 1,952 new cases from 12 countries, with 1,573 in the African Region and 379 in the Western Pacific Region (akolgo2024exploringmycolactone—theunique pages 3-4). Burden remains concentrated in West/Central Africa, with notable endemicity in Ghana, Benin, Côte d’Ivoire, and DRC (akolgo2024exploringmycolactone—theunique pages 3-4). Australia has an important endemic focus with older median age at diagnosis (66 years) and increasing recognition/spread to new areas (obrien2024anoverviewof pages 1-2).
Historical global estimates cited in a 2023 review were about 5,000–6,000 cases/year during 2004–2010 (muhi2023ahumanmodel pages 1-2).
BU affects all ages, but age patterns differ by geography (children often affected in Africa; adults more frequently in Australia) (akolgo2024exploringmycolactone—theunique pages 1-3, obrien2024anoverviewof pages 1-2).
PCR is emphasized as the preferred confirmatory test. In Australia-specific guidance, PCR on an ulcer swab is considered the diagnostic test of choice, while tissue biopsy is recommended when disease is non-ulcerated because swabs from non-ulcerative lesions can be falsely negative (obrien2024anoverviewof pages 1-2).
An Australian consensus statement further specifies IS2404-targeted PCR on ulcer swabs as the primary confirmatory test, provides swab/biopsy technique guidance, and notes culture can take up to 12 weeks and is less sensitive than PCR (muhi2025managementofmycobacterium pages 2-3).
A structured diagnostics summary is provided here:
| Diagnostic modality | Typical specimen type(s) | What it detects / target | Practical notes | Quantitative / performance details | Source URL / date |
|---|---|---|---|---|---|
| Real-time PCR (preferred confirmatory test) | Ulcer swab; tissue biopsy for non-ulcerative lesions | M. ulcerans DNA; IS2404 is the primary confirmatory target in recent guidance | Diagnostic test of choice because of speed and accuracy; specifically request M. ulcerans PCR. Swabs from non-ulcerative lesions have a high false-negative rate, so biopsy is recommended for early/pre-ulcerative or PCR-negative suspicious lesions. Optimal ulcer swab technique is around the undermined edge with visible material; saline may improve yield. (obrien2024anoverviewof pages 1-2, muhi2025managementofmycobacterium pages 2-3, anthony2024buruliulcertransmission pages 1-2) | WHO reports about 70% of notified cases are PCR-confirmed. False negatives are particularly noted in early/pre-ulcerative lesions and in children. (muhi2025managementofmycobacterium pages 2-3, anthony2024buruliulcertransmission pages 1-2) | https://doi.org/10.31128/ajgp-08-23-6914 (Sep 2024); https://doi.org/10.5694/mja2.52591 (Feb 2025); https://doi.org/10.12788/cutis.1145 (Dec 2024) |
| Ulcer swab PCR workflow | Ulcer swab | Same as above | Best for open ulcers; easy, rapid, field-practical. For ulcers, swab the undermined edge rather than superficial debris. (obrien2024anoverviewof pages 1-2, muhi2025managementofmycobacterium pages 2-3) | No sensitivity value provided in retrieved texts, but repeatedly described as primary/most accurate routine confirmatory approach for ulcers. (obrien2024anoverviewof pages 1-2, muhi2025managementofmycobacterium pages 2-3) | https://doi.org/10.31128/ajgp-08-23-6914 (Sep 2024); https://doi.org/10.5694/mja2.52591 (Feb 2025) |
| Biopsy PCR | Punch or skin biopsy from center of non-ulcerated lesions or ulcer margin | M. ulcerans DNA; IS2404-targeted PCR in recent consensus guidance | Recommended when lesions are non-ulcerative, early, or when swab PCR is negative but suspicion remains. Fresh tissue should not be placed in preservative; transport in saline-moistened gauze/drops of saline to avoid dehydration. (muhi2025managementofmycobacterium pages 2-3, lim2025mycobacteriumulceransulcer pages 7-9) | No formal sensitivity value provided in retrieved texts; emphasized as necessary to reduce false negatives in pre-ulcerative disease. (muhi2025managementofmycobacterium pages 2-3, lim2025mycobacteriumulceransulcer pages 7-9) | https://doi.org/10.5694/mja2.52591 (Feb 2025); https://doi.org/10.3390/life15071096 (Jul 2025) |
| Fine-needle aspirate (FNA) / punch biopsy qPCR | FNA or 3 mm punch biopsy | IS2404 and KR qPCR used in reported series | Useful in non-ulcerative disease and in some research/diagnostic series. (combe2020areallburuli pages 4-6, lim2025mycobacteriumulceransulcer pages 19-20) | Example qPCR-positive lesion: IS2404 Ct ~23.64, KR Ct ~25 with culture positivity; high Ct values (~41 and ~38.87) associated with culture negativity and absence of M. ulcerans by metabarcoding. (combe2020areallburuli pages 4-6) | https://doi.org/10.1111/bjd.19260 (Jul 2020); https://doi.org/10.3390/life15071096 (Jul 2025) |
| Microscopy / acid-fast smear | Swab smear; tissue material | Acid-fast bacilli (Ziehl-Neelsen / BAAR) | Available and historically used, but less emphasized than PCR in current practice. (combe2020areallburuli pages 4-6, anthony2024buruliulcertransmission pages 1-2) | No sensitivity/specificity values provided in retrieved texts. (combe2020areallburuli pages 4-6, anthony2024buruliulcertransmission pages 1-2) | https://doi.org/10.1111/bjd.19260 (Jul 2020); https://doi.org/10.12788/cutis.1145 (Dec 2024) |
| Mycobacterial culture | Swab- or biopsy-derived material; Lowenstein-Jensen medium commonly cited | Viable M. ulcerans growth | Definitive but slow and less sensitive than PCR; useful for confirmation and research/isolate recovery. (obrien2024anoverviewof pages 1-2, muhi2025managementofmycobacterium pages 2-3, combe2020areallburuli pages 4-6) | Results may take up to 12 weeks in recent consensus guidance; one report incubated cultures up to 9 months at 30°C. (muhi2025managementofmycobacterium pages 2-3, combe2020areallburuli pages 4-6) | https://doi.org/10.31128/ajgp-08-23-6914 (Sep 2024); https://doi.org/10.5694/mja2.52591 (Feb 2025); https://doi.org/10.1111/bjd.19260 (Jul 2020) |
| Histopathology | Tissue biopsy | Tissue changes of BU: necrosis/chronic inflammation; granuloma formation may be seen | Supports diagnosis and helps exclude alternatives, especially when PCR is negative or lesion is atypical. (muhi2025managementofmycobacterium pages 2-3, siirin2024towardsaburuli pages 1-5) | No sensitivity values provided; consensus notes granuloma formation is seen more often in ulcers than in pre-ulcerative lesions. (muhi2025managementofmycobacterium pages 2-3) | https://doi.org/10.5694/mja2.52591 (Feb 2025); https://doi.org/10.1101/2024.01.23.24301643 (Jan 2024 preprint) |
| Mass spectrometry for mycolactone | Tissue extracts / lesion-derived material | Mycolactone biomarker | Attractive because mycolactone is unique to M. ulcerans, but cost and instrumentation limit point-of-care use in endemic settings. (akolgo2024exploringmycolactone—theunique pages 18-20) | Detects mycolactone with observed [M+Na]+ at m/z 765.6. (akolgo2024exploringmycolactone—theunique pages 18-20) | https://doi.org/10.3390/toxins16120528 (Dec 2024) |
| Anti-mycolactone monoclonal antibody ELISA | Lesion-associated material / research assay formats | Mycolactone via competitive immunoassay | Demonstrates feasibility of toxin detection; translation to simple field LFA is technically difficult because mycolactone is light-sensitive, amphiphilic, aggregates, and binds serum proteins. (akolgo2024exploringmycolactone—theunique pages 18-20) | Competitive ELISAs reached low-nanogram sensitivity. (akolgo2024exploringmycolactone—theunique pages 18-20) | https://doi.org/10.3390/toxins16120528 (Dec 2024) |
| Mycolactone lateral flow immunoassay (early/prototype reports) | Lesion material | Mycolactone | Conceptually promising for point-of-care use, but older prototype LFIA evidence was very limited. (akolgo2024exploringmycolactone—theunique pages 18-20) | Review notes only a single case-report prototype in earlier literature. (akolgo2024exploringmycolactone—theunique pages 18-20) | https://doi.org/10.3390/toxins16120528 (Dec 2024) |
| Aptamer-based mycolactone assay | Swab-based samples in pilot study | Mycolactone-binding nucleic acid aptamers | Experimental and not yet adequate as a stand-alone clinical test. (akolgo2024exploringmycolactone—theunique pages 18-20) | Pilot case-control study on swabs (n=41 suspected BU patients) showed 50% sensitivity. (akolgo2024exploringmycolactone—theunique pages 18-20) | https://doi.org/10.3390/toxins16120528 (Dec 2024) |
| Prototype rapid mycolactone lateral flow test with immunomagnetic concentration | Swab-collected wound exudate from open lesions | Mycolactone using anti-mycolactone monoclonal antibody + magnetic gold nanoshells | Designed as a low-infrastructure rapid test; requires only a magnetic rack and no powered instrumentation. Procedure can be completed in about 2 hours. Particularly aimed at point-of-care use from wound swabs. (siirin2024towardsaburuli pages 1-5) | Detection limit 3.5-7 ng of mycolactone collected on a swab. (siirin2024towardsaburuli pages 1-5) | https://doi.org/10.1101/2024.01.23.24301643 (Jan 2024 preprint) |
| Other emerging assays | Variable | LAMP, antigen detection, mycolactone TLC-based methods | LAMP is highlighted as a promising point-of-care nucleic-acid alternative; antigen detection and TLC-based mycolactone assays remain under development. (anthony2024buruliulcertransmission pages 1-2, siirin2024towardsaburuli pages 1-5) | No robust field performance metrics provided in retrieved texts. (anthony2024buruliulcertransmission pages 1-2, siirin2024towardsaburuli pages 1-5) | https://doi.org/10.12788/cutis.1145 (Dec 2024); https://doi.org/10.1101/2024.01.23.24301643 (Jan 2024 preprint) |
Table: This table summarizes routine and emerging diagnostic approaches for Buruli ulcer, including specimen selection, confirmatory PCR practices, conventional pathology/microbiology, and new mycolactone-based assays. It is useful for quickly comparing test targets, practical limitations, and the most clinically relevant workflow notes.
Mycolactone is increasingly positioned as a biomarker for point-of-care diagnostics; a 2024 prototype rapid test uses immunomagnetic concentration plus lateral flow detection and can detect 3.5–7 ng of mycolactone on a swab in ~2 hours without powered instrumentation (siirin2024towardsaburuli pages 1-5).
With effective antibiotic therapy, BU cure rates are high; a recent review reports cure rates exceeding 90% in patients completing therapy (lim2025mycobacteriumulceransulcer pages 4-6). Delayed diagnosis/treatment is associated with higher risk of extensive necrosis, scarring, contractures, deformity, and long-term disability (muhi2023ahumanmodel pages 1-2, obrien2024anoverviewof pages 1-2).
WHO-preferred treatment is an 8-week all-oral regimen of rifampicin plus clarithromycin combined with wound care, with dosing summarized in recent reviews (rifampicin 10 mg/kg daily; clarithromycin 7.5 mg/kg twice daily) (lim2025mycobacteriumulceransulcer pages 2-4, saezlopez2024amoxicillinclavulanateincombination pages 1-2).
A structured treatment and trials summary is provided here:
| Treatment / implementation | Regimen or intervention | Real-world use / status | Key evidence / outcomes | Trial ID / endpoint | URL / publication date |
|---|---|---|---|---|---|
| Standard first-line all-oral therapy | Rifampicin 10 mg/kg once daily (max 600 mg) + clarithromycin 7.5 mg/kg twice daily (max 500 mg BID) for 8 weeks | Current WHO-preferred regimen; widely used in endemic settings and Australia; often combined with wound dressings and selective surgery | Oral RC8 largely replaced streptomycin-containing regimens because of non-inferior healing and less injection toxicity; cure rates exceed 90% in patients completing therapy; shorter 6-week courses may be considered for small lesions in selected settings (lim2025mycobacteriumulceransulcer pages 2-4, lim2025mycobacteriumulceransulcer pages 6-7, lim2025mycobacteriumulceransulcer pages 4-6) | Historical phase II/III non-inferiority evidence vs SR8; endpoint: healing without recurrence and without excision surgery at 12 months (NCT01659437 chunk 1) | https://doi.org/10.3390/life15071096 (Jul 2025); https://clinicaltrials.gov/study/NCT01659437 (2012) |
| Historical injectable regimen | Rifampicin 10 mg/kg oral daily + streptomycin 15 mg/kg IM daily for 8 weeks | Former standard since 2004; now largely replaced where all-oral therapy is available | Effective but limited by injection logistics and streptomycin-associated ototoxicity; used as comparator in WHO-sponsored trial (lim2025mycobacteriumulceransulcer pages 2-4, NCT01659437 chunk 1) | NCT01659437; primary endpoint: healing without recurrence and without excision surgery at 12 months (NCT01659437 chunk 1) | https://clinicaltrials.gov/study/NCT01659437 (2012); https://doi.org/10.3390/life15071096 (Jul 2025) |
| Adjunct wound care and selective surgery | Standard wound cleaning, moist dressings, possible grafting/debridement; surgery for extensive, function-threatening, or reconstructive indications | Real-world routine supportive care across endemic programs and Australian practice | Wound care remains integral to management; surgery is now adjunctive rather than primary therapy, but still important for large lesions, tissue loss, or function-preserving reconstruction (lim2025mycobacteriumulceransulcer pages 4-6, saezlopez2024amoxicillinclavulanateincombination pages 1-2) | NCT05169554 defines cure as lesion healing without recurrence and without excision surgery at 12 months (NCT05169554 chunk 1) | https://doi.org/10.3390/life15071096 (Jul 2025); https://clinicaltrials.gov/study/NCT05169554 (2021) |
| Pharmacokinetic consideration | Rifampicin + clarithromycin, including clarithromycin extended-release evaluation | Important for dose optimization in clinical practice and trials | Rifampicin induces CYP3A4 and lowers clarithromycin exposure; extended-release clarithromycin did not clearly improve PK advantage; higher failure risk has been noted in heavier patients, supporting ongoing dose-optimization work (klis2024pharmacokineticsofextendedrelease pages 5-6, lim2025mycobacteriumulceransulcer pages 4-6) | NCT01659437 PK substudy; endpoints included Cmax, AUC0-24, t1/2, CL/F, V/F (klis2024pharmacokineticsofextendedrelease pages 5-6) | https://doi.org/10.1038/s41598-024-70890-w (Aug 2024); https://doi.org/10.3390/life15071096 (Jul 2025) |
| Beta-lactam add-on to shorten therapy | Rifampicin + clarithromycin + amoxicillin/clavulanate; investigational 4-week regimen vs standard 8-week RC8 | Active multicenter phase II trial in West Africa | In vitro time-kill assays showed RIF+AMX/CLV and RIF+CLA+AMX/CLV were bactericidal and more effective than RIF+CLA alone, supporting treatment-shortening strategy (saezlopez2024amoxicillinclavulanateincombination pages 1-2) | NCT05169554; endpoint: cure (healing without recurrence and without excision surgery) at 12 months; PK and bacterial clearance substudies included (NCT05169554 chunk 1) | https://doi.org/10.1371/journal.pntd.0011867 (Apr 2024); https://clinicaltrials.gov/study/NCT05169554 (2021) |
| High-dose rifampicin + DACC dressings | Higher-than-standard rifampicin dose + dialkylcarbamoyl chloride-coated dressings | Phase 3 protocol in Ghana; implementation-focused strategy aiming at faster bacterial clearance and cost-effectiveness | Rationale is that rifampicin is the key drug and higher doses may improve healing; DACC dressings irreversibly bind bacteria on wound surfaces and may improve wound management (amoako2023burulirifdaccevaluationof pages 1-3) | PACTR202011867644311; primary endpoint: mean time to clearance of viable mycobacteria (amoako2023burulirifdaccevaluationof pages 1-3) | https://doi.org/10.3310/nihropenres.13332.1 (Nov 2023) |
| Telacebec (Q203) | Oral telacebec monotherapy or Q203-containing ultrashort regimens | Emerging experimental therapy; active phase 2 trial in Australia | Preclinical studies show extraordinary potency, with Q203-containing regimens rendering nearly all mouse footpads culture-negative after 2 weeks and suggesting potential 1-2 week oral cures (lim2025mycobacteriumulceransulcer pages 6-7) | NCT06481163; phase 2 recruiting trial of telacebec in adults with Buruli ulcer (lim2025mycobacteriumulceransulcer pages 6-7) | https://clinicaltrials.gov/study/NCT06481163 (2024); https://doi.org/10.3390/life15071096 (Jul 2025) |
| Thermotherapy | Local heat therapy integrated with wound management | Investigated as adjunct/alternative in field and community programs | Reported phase II cure rates >80% in one trial/reviewed experience; evidence remains less mature than antibiotic regimens (lim2025mycobacteriumulceransulcer pages 4-6) | NCT03969940 (withdrawn community-level thermotherapy study); NCT03957447 (observational integrated thermotherapy program) (lim2025mycobacteriumulceransulcer pages 4-6) | https://doi.org/10.3390/life15071096 (Jul 2025); https://clinicaltrials.gov/study/NCT03969940 (2019); https://clinicaltrials.gov/study/NCT03957447 (2019) |
| Topical clarithromycin formulation | 1% clarithromycin skin cream | Experimental formulation; not standard of care | Stable for at least 60 days, including at 40°C, supporting feasibility for low-resource settings and future topical treatment development (amoako2023burulirifdaccevaluationof pages 1-3) | No NCT provided in retrieved evidence (amoako2023burulirifdaccevaluationof pages 1-3) | https://doi.org/10.3390/ph17060691 (May 2024) |
Table: This table summarizes current standard, historical, adjunctive, and emerging Buruli ulcer treatments, including dosing, real-world implementation, and active/recent clinical trials. It is useful for comparing established care with treatment-shortening and next-generation strategies.
No licensed BU vaccine is available; prevention currently emphasizes early detection and treatment, plus reducing high-risk exposures and addressing skin injury care in endemic settings (boakyeappiah2023currentprogressand pages 1-5, gohoho2025riskfactorsfor pages 13-15). Epidemiological evidence supports public health messaging about protective clothing and safer water-contact practices in high-risk agricultural/wetland settings (johnson2025territorialandgenderlinked pages 9-12).
BCG provides partial/transient protection and remains a baseline comparator in animal studies; no experimental strategy has clearly surpassed BCG in the cited vaccine review chapter (boakyeappiah2023currentprogressand pages 1-5). Vaccine development is complicated by mycolactone-mediated immunosuppression, but mycolactone-directed strategies are under investigation (boakyeappiah2023currentprogressand pages 14-17).
Australian data implicate native possums as natural hosts, with geographic linkage to human cases (muhi2023ahumanmodel pages 1-2). Environmental and animal-associated evidence includes M. ulcerans DNA detection in aquatic organisms and insects (anthony2024buruliulcertransmission pages 1-2, oseiowusu2023buruliulcerin pages 5-7). A broader set of mycolactone-producing mycobacteria includes amphibian-associated strains (e.g., frog pathogen ecovar liflandii) referenced in ecology reviews (oseiowusu2023buruliulcerin pages 20-21).
Mouse models are used for immunologic mechanism and therapeutic evaluation. For example, IFN-γ knockout mice show reduced capacity to control infection and more rapid progression, supporting a role for IFN-γ-mediated immunity in BU (muhi2023ahumanmodel pages 1-2). Mycolactone alone can reproduce BU-like lesions in animal models, supporting toxin-driven pathology (akolgo2024exploringmycolactone—theunique pages 4-6).
A vaccine-focused expert review emphasizes that mycolactone “is cytotoxic and immunosuppressive and causes vascular dysfunction in infected skin,” and that its Sec61 targeting is a major advance in pathogenesis understanding (boakyeappiah2023currentprogressand pages 1-5). A clinical overview for Australian primary care stresses that PCR is central for diagnosis and that non-ulcerative disease requires biopsy due to swab false negatives (obrien2024anoverviewof pages 1-2).
Several required ontology identifiers (ICD-10/ICD-11, Orphanet ORPHA, MONDO) and GBD-style incidence/prevalence per 100,000 and DALYs were not found within the retrieved in-session texts. These fields should be completed via direct ontology/registry lookups or additional targeted literature retrieval outside the present evidence set.
References
(akolgo2024exploringmycolactone—theunique pages 1-3): Gideon Atinga Akolgo, Kingsley Bampoe Asiedu, and Richard Kwamla Amewu. Exploring mycolactone—the unique causative toxin of buruli ulcer: biosynthetic, synthetic pathways, biomarker for diagnosis, and therapeutic potential. Toxins, 16:528, Dec 2024. URL: https://doi.org/10.3390/toxins16120528, doi:10.3390/toxins16120528. This article has 3 citations.
(muhi2023ahumanmodel pages 1-2): Stephen Muhi, Joshua Osowicki, Daniel O’Brien, Paul D. R. Johnson, Sacha Pidot, Marcel Doerflinger, Julia L. Marshall, Marc Pellegrini, James McCarthy, and Timothy P. Stinear. A human model of buruli ulcer: the case for controlled human infection and considerations for selecting a mycobacterium ulcerans challenge strain. PLOS Neglected Tropical Diseases, 17:e0011394, Jun 2023. URL: https://doi.org/10.1371/journal.pntd.0011394, doi:10.1371/journal.pntd.0011394. This article has 8 citations and is from a domain leading peer-reviewed journal.
(anthony2024buruliulcertransmission pages 1-2): Michelle R. Anthony, Christopher Farkouh, P. Abdi, and Qasiar Ali Khan. Buruli ulcer transmission: environmental pathways and implications for dermatologic care. Cutis, 114 6:184-186, Dec 2024. URL: https://doi.org/10.12788/cutis.1145, doi:10.12788/cutis.1145. This article has 1 citations and is from a peer-reviewed journal.
(akolgo2024exploringmycolactone—theunique pages 3-4): Gideon Atinga Akolgo, Kingsley Bampoe Asiedu, and Richard Kwamla Amewu. Exploring mycolactone—the unique causative toxin of buruli ulcer: biosynthetic, synthetic pathways, biomarker for diagnosis, and therapeutic potential. Toxins, 16:528, Dec 2024. URL: https://doi.org/10.3390/toxins16120528, doi:10.3390/toxins16120528. This article has 3 citations.
(NCT00321178 chunk 2): BURULICO Drug Trial Study Protocol: RCT SR8/SR4+CR4, GHANA. University Medical Center Groningen. 2006. ClinicalTrials.gov Identifier: NCT00321178
(obrien2024anoverviewof pages 1-2): Daniel P O'Brien, Christopher Chun Wen Wong, and Stephen Muhi. An overview of buruli ulcer in australia. Australian journal of general practice, 53 9:671-674, Sep 2024. URL: https://doi.org/10.31128/ajgp-08-23-6914, doi:10.31128/ajgp-08-23-6914. This article has 5 citations.
(NCT01659437 chunk 1): Tjip van der Werf. WHO Drug Study for Buruli Ulcer - Comparison of SR8 and CR8. University Medical Center Groningen. 2012. ClinicalTrials.gov Identifier: NCT01659437
(akolgo2024exploringmycolactone—theunique pages 4-6): Gideon Atinga Akolgo, Kingsley Bampoe Asiedu, and Richard Kwamla Amewu. Exploring mycolactone—the unique causative toxin of buruli ulcer: biosynthetic, synthetic pathways, biomarker for diagnosis, and therapeutic potential. Toxins, 16:528, Dec 2024. URL: https://doi.org/10.3390/toxins16120528, doi:10.3390/toxins16120528. This article has 3 citations.
(gohoho2025riskfactorsfor pages 13-15): Mawuli Gohoho, Samuel Adolf Bosoka, George Sarpong Agyemang, Sorengmen Amos Ziema, James Alorwu, Hudatu Ahmed, Christian Atsu Gohoho, Isaac Annobil, Nana Konama Kotey, and John Owusu Gyapong. Risk factors for buruli ulcer disease in ghana: a matched case-control study in four selected endemic districts of eastern and oti regions. PLOS Neglected Tropical Diseases, 19:e0013684, Nov 2025. URL: https://doi.org/10.1371/journal.pntd.0013684, doi:10.1371/journal.pntd.0013684. This article has 0 citations and is from a domain leading peer-reviewed journal.
(johnson2025territorialandgenderlinked pages 9-12): Harvey Johnson, Alexandra Boccarossa, Esai Anagonou, Télésphore Brou, Perin Catraye, Sébastien Fleuret, Estelle Marion, and Matthieu Eveillard. Territorial and gender-linked risk factors for buruli ulcer in southern benin: a case-control study using geographic and behavioral surveying. PLOS Neglected Tropical Diseases, 19:e0013509, Sep 2025. URL: https://doi.org/10.1371/journal.pntd.0013509, doi:10.1371/journal.pntd.0013509. This article has 2 citations and is from a domain leading peer-reviewed journal.
(akolgo2024exploringmycolactone—theunique media 536a767e): Gideon Atinga Akolgo, Kingsley Bampoe Asiedu, and Richard Kwamla Amewu. Exploring mycolactone—the unique causative toxin of buruli ulcer: biosynthetic, synthetic pathways, biomarker for diagnosis, and therapeutic potential. Toxins, 16:528, Dec 2024. URL: https://doi.org/10.3390/toxins16120528, doi:10.3390/toxins16120528. This article has 3 citations.
(boakyeappiah2023currentprogressand pages 1-5): Justice Boakye-Appiah, Belinda Hall, Rajko Reljic, and Rachel E. Simmonds. Current progress and prospects for a buruli ulcer vaccine. Vaccines for Neglected Pathogens: Strategies, Achievements and Challenges, pages 71-95, Jan 2023. URL: https://doi.org/10.1007/978-3-031-24355-4_5, doi:10.1007/978-3-031-24355-4_5. This article has 5 citations.
(oseiowusu2023buruliulcerin pages 5-7): Jonathan Osei-Owusu, Owusu Fordjour Aidoo, Fatima Eshun, David Sewordor Gaikpa, Aboagye Kwarteng Dofuor, Bright Yaw Vigbedor, Bernard Kofi Turkson, Kingsley Ochar, John Opata, Maxwell Jnr. Opoku, Kodwo Dadzie Ninsin, and Christian Borgemeister. Buruli ulcer in africa: geographical distribution, ecology, risk factors, diagnosis, and indigenous plant treatment options – a comprehensive review. Heliyon, 9:e22018, Nov 2023. URL: https://doi.org/10.1016/j.heliyon.2023.e22018, doi:10.1016/j.heliyon.2023.e22018. This article has 8 citations.
(muhi2023ahumanmodel pages 12-13): Stephen Muhi, Joshua Osowicki, Daniel O’Brien, Paul D. R. Johnson, Sacha Pidot, Marcel Doerflinger, Julia L. Marshall, Marc Pellegrini, James McCarthy, and Timothy P. Stinear. A human model of buruli ulcer: the case for controlled human infection and considerations for selecting a mycobacterium ulcerans challenge strain. PLOS Neglected Tropical Diseases, 17:e0011394, Jun 2023. URL: https://doi.org/10.1371/journal.pntd.0011394, doi:10.1371/journal.pntd.0011394. This article has 8 citations and is from a domain leading peer-reviewed journal.
(muhi2025managementofmycobacterium pages 2-3): Stephen Muhi, Victoria RV Cox, Matthew O'Brien, Jonathan T Priestley, Jodie Hill, Adrian Murrie, Anthony McDonald, Peter Callan, Grant A Jenkin, N Deborah Friedman, Kasha P Singh, Callum Maggs, Peter Kelley, Eugene Athan, Paul DR Johnson, and Daniel P O'Brien. Management of mycobacterium ulcerans infection (buruli ulcer) in australia: consensus statement. The Medical Journal of Australia, 222:571-578, Feb 2025. URL: https://doi.org/10.5694/mja2.52591, doi:10.5694/mja2.52591. This article has 6 citations.
(lim2025mycobacteriumulceransulcer pages 7-9): Bryan Lim, Omar Shadid, Jennifer Novo, Yi Mon, Ishith Seth, Gianluca Marcaccini, Roberto Cuomo, Daniel P. O’Brien, and Warren M. Rozen. Mycobacterium ulcerans ulcer: current trends in antimicrobial management and reconstructive surgical strategies. Life, 15:1096, Jul 2025. URL: https://doi.org/10.3390/life15071096, doi:10.3390/life15071096. This article has 1 citations.
(combe2020areallburuli pages 4-6): M. Combe, P. Couppié, R. Blaizot, A. Valentini, and R.E. Gozlan. Are all buruli ulcers caused by mycobacterium ulcerans ? British Journal of Dermatology, 183:968-970, Jul 2020. URL: https://doi.org/10.1111/bjd.19260, doi:10.1111/bjd.19260. This article has 5 citations and is from a highest quality peer-reviewed journal.
(lim2025mycobacteriumulceransulcer pages 19-20): Bryan Lim, Omar Shadid, Jennifer Novo, Yi Mon, Ishith Seth, Gianluca Marcaccini, Roberto Cuomo, Daniel P. O’Brien, and Warren M. Rozen. Mycobacterium ulcerans ulcer: current trends in antimicrobial management and reconstructive surgical strategies. Life, 15:1096, Jul 2025. URL: https://doi.org/10.3390/life15071096, doi:10.3390/life15071096. This article has 1 citations.
(siirin2024towardsaburuli pages 1-5): Marina Siirin, Bijan Pedram, Maria J. Gonzalez-Moa, Louisa Warryn, Rie Yotsu, Jean M. Saunders, Aaron E. Saunders, Richard K. Baldwin, Jessica L. Porter, Timothy P. Stinear, Israel Cruz-Mata, Dziedzom Komi de Souza, Gerd Pluschke, and Marco A. Biamonte. Towards a buruli ulcer rapid diagnostic test that targets mycolactone. MedRxiv, Jan 2024. URL: https://doi.org/10.1101/2024.01.23.24301643, doi:10.1101/2024.01.23.24301643. This article has 1 citations.
(akolgo2024exploringmycolactone—theunique pages 18-20): Gideon Atinga Akolgo, Kingsley Bampoe Asiedu, and Richard Kwamla Amewu. Exploring mycolactone—the unique causative toxin of buruli ulcer: biosynthetic, synthetic pathways, biomarker for diagnosis, and therapeutic potential. Toxins, 16:528, Dec 2024. URL: https://doi.org/10.3390/toxins16120528, doi:10.3390/toxins16120528. This article has 3 citations.
(lim2025mycobacteriumulceransulcer pages 4-6): Bryan Lim, Omar Shadid, Jennifer Novo, Yi Mon, Ishith Seth, Gianluca Marcaccini, Roberto Cuomo, Daniel P. O’Brien, and Warren M. Rozen. Mycobacterium ulcerans ulcer: current trends in antimicrobial management and reconstructive surgical strategies. Life, 15:1096, Jul 2025. URL: https://doi.org/10.3390/life15071096, doi:10.3390/life15071096. This article has 1 citations.
(lim2025mycobacteriumulceransulcer pages 2-4): Bryan Lim, Omar Shadid, Jennifer Novo, Yi Mon, Ishith Seth, Gianluca Marcaccini, Roberto Cuomo, Daniel P. O’Brien, and Warren M. Rozen. Mycobacterium ulcerans ulcer: current trends in antimicrobial management and reconstructive surgical strategies. Life, 15:1096, Jul 2025. URL: https://doi.org/10.3390/life15071096, doi:10.3390/life15071096. This article has 1 citations.
(saezlopez2024amoxicillinclavulanateincombination pages 1-2): Emma Sáez-López, Ana Cristina Millán Placer, A. Quintana, and Santiago Ramón-García. Amoxicillin/clavulanate in combination with rifampicin/clarithromycin is bactericidal against mycobacterium ulcerans. PLOS Neglected Tropical Diseases, 18:e0011867, Apr 2024. URL: https://doi.org/10.1371/journal.pntd.0011867, doi:10.1371/journal.pntd.0011867. This article has 5 citations and is from a domain leading peer-reviewed journal.
(NCT05169554 chunk 1): Beta-Lactam Containing Regimen for the Shortening of Buruli Ulcer Disease Therapy. Fundacion Agencia Aragonesa para la Investigacion y Desarrollo (ARAID). 2021. ClinicalTrials.gov Identifier: NCT05169554
(amoako2023burulirifdaccevaluationof pages 1-3): Yaw Ampem Amoako, Abigail Agbanyo, Jacob Novignon, Lucy Owusu, Joseph Tuffour, Adwoa Asante-Poku, Yohannes Hailemichael, Iris Mosweu, Ruth Canter, Charles Opondo, Elizabeth Allen, Catherine Pitt, Dorothy Yeboah-Manu, Stephen L. Walker, Michael Marks, and Richard Odame Phillips. Buruli-rifdacc: evaluation of the efficacy and cost-effectiveness of high-dose versus standard-dose rifampicin on outcomes in mycobacterium ulcerans disease, a protocol for a randomised controlled trial in ghana. NIHR Open Research, 2:59, Nov 2023. URL: https://doi.org/10.3310/nihropenres.13332.1, doi:10.3310/nihropenres.13332.1. This article has 4 citations.
(lim2025mycobacteriumulceransulcer pages 6-7): Bryan Lim, Omar Shadid, Jennifer Novo, Yi Mon, Ishith Seth, Gianluca Marcaccini, Roberto Cuomo, Daniel P. O’Brien, and Warren M. Rozen. Mycobacterium ulcerans ulcer: current trends in antimicrobial management and reconstructive surgical strategies. Life, 15:1096, Jul 2025. URL: https://doi.org/10.3390/life15071096, doi:10.3390/life15071096. This article has 1 citations.
(klis2024pharmacokineticsofextendedrelease pages 5-6): Sandor-Adrian Klis, Ymkje Stienstra, Kabiru M. Abass, Justice Abottsi, Samuel O. Mireku, Jan-Willem Alffenaar, and Tjip S. van der Werf. Pharmacokinetics of extended-release clarithromycin in patients with mycobacterium ulcerans infection. Scientific Reports, Aug 2024. URL: https://doi.org/10.1038/s41598-024-70890-w, doi:10.1038/s41598-024-70890-w. This article has 1 citations and is from a peer-reviewed journal.
(boakyeappiah2023currentprogressand pages 14-17): Justice Boakye-Appiah, Belinda Hall, Rajko Reljic, and Rachel E. Simmonds. Current progress and prospects for a buruli ulcer vaccine. Vaccines for Neglected Pathogens: Strategies, Achievements and Challenges, pages 71-95, Jan 2023. URL: https://doi.org/10.1007/978-3-031-24355-4_5, doi:10.1007/978-3-031-24355-4_5. This article has 5 citations.
(oseiowusu2023buruliulcerin pages 20-21): Jonathan Osei-Owusu, Owusu Fordjour Aidoo, Fatima Eshun, David Sewordor Gaikpa, Aboagye Kwarteng Dofuor, Bright Yaw Vigbedor, Bernard Kofi Turkson, Kingsley Ochar, John Opata, Maxwell Jnr. Opoku, Kodwo Dadzie Ninsin, and Christian Borgemeister. Buruli ulcer in africa: geographical distribution, ecology, risk factors, diagnosis, and indigenous plant treatment options – a comprehensive review. Heliyon, 9:e22018, Nov 2023. URL: https://doi.org/10.1016/j.heliyon.2023.e22018, doi:10.1016/j.heliyon.2023.e22018. This article has 8 citations.