After tuberculosis and leprosy, Buruli ulcer (BU), caused by M. ulcerans, is the third most common mycobacterial disease, and Western Africa is the world region most affected by this chronic necrotising disease of the skin and the subcutaneous tissue. M. ulcerans is unique among mycobacterial pathogens in that it is mainly extracellular and produces a plasmid-encoded toxin with a polyketide-derived macrolide structure, named mycolactone.
Symptoms and Treatment
Mycolactone is believed to play a central role in determining the extracellular localization of the bacteria and modulation of immunological responses to M. ulcerans. Clinical lesions usually start as painless nodules and if left untreated lead to massive destruction of skin and sometimes bone. While surgery has traditionally been the only recommended treatment for BU, in 2004 WHO published provisional guidelines recommending treatment with a combination of rifampicin and streptomycin for 8 weeks.
We developed a broad research portfolio comprising clinical, field and laboratory studies.
The goals of our research are to
- improve understanding of the pathogenesis, immunology and transmission of Buruli ulcer,
- develop methods for early diagnosis, and
- investigate prospects for improving therapy and vaccine development.
Eddyani M, Affolabi D, Ablordey A, Eyangoh S, Pluschke G. Laboratory investigations in Buruli ulcer. In: Nunzi E,Massone C,Portaels F, eds. Leprosy and Buruli ulcer: a practical guide, 443-454. Cham: Springer Nature, 2022. DOI: 10.1007/978-3-030-89704-8_41
Hall B.S et al. Inhibition of the SEC61 translocon by mycolactone induces a protective autophagic response controlled by EIF2S1-dependent translation that does not require ULK1 activity. Autophagy. 2022;18(4):841-859. DOI: 10.1080/15548627.2021.1961067
Hsieh L.T et al. Aberrant stromal tissue factor localisation and mycolactone-driven vascular dysfunction, exacerbated by IL-1β, are linked to fibrin formation in Buruli ulcer lesions. PLoS Pathog. 2022;18:e1010280. DOI: 10.1371/journal.ppat.1010280
Leuenberger A et al. Perceived water-related risk factors of Buruli ulcer in two villages of south-central Côte d’Ivoire. PLoS Negl Trop Dis. 2022;16(12):e0010927. DOI: 10.1371/journal.pntd.0010927
Pluschke G, Röltgen K. Overview: development of drugs against Mycobacterium ulcerans. In: Pluschke G,Röltgen K, eds. Mycobacterium ulcerans:, 185-187. New York, NY: Humana, 2022. (Methods in molecular biology: 2387). DOI: 10.1007/978-1-0716-1779-3_17
Portaels F, Pluschke G. History and geographic distribution of Buruli ulcer. In: Nunzi E,Massone C,Portaels F, eds. Leprosy and Buruli ulcer: a practical guide, 421-430. Cham: Springer Nature, 2022. DOI: 10.1007/978-3-030-89704-8_39
Röltgen K, Johnson P.D.R, Pluschke G. Epidemiology of Buruli ulcer. In: Nunzi E,Massone C,Portaels F, eds. Leprosy and Buruli ulcer. A practical guide, 541-550. Cham: Springer Nature, 2022. DOI: 10.1007/978-3-030-89704-8_47
Röltgen K, Pluschke G. Overview: Mycobacterium ulcerans disease (Buruli ulcer). In: Pluschke G,Röltgen K, eds. Mycobacterium ulcerans:, 3-6. New York, NY: Humana, 2022. (Methods in molecular biology: 2387). DOI: 10.1007/978-1-0716-1779-3_1
Toppino S et al. Skin wounds in a rural setting of Côte d'Ivoire: population-based assessment of the burden and clinical epidemiology. PLoS Negl Trop Dis. 2022;16(10):e0010608. DOI: 10.1371/journal.pntd.0010608
Please H.R et al. Chronic wounds in Sierra Leone: searching for Buruli ulcer, a NTD caused by Mycobacterium ulcerans, at Masanga Hospital. PLoS Negl Trop Dis. 2021;15(10):e0009862. DOI: 10.1371/journal.pntd.0009862