Global Epidemiology of Buruli Ulcer, 2010–2017, and Analysis of 2014 WHO Programmatic Targets

Omansen, Till F.; Erbowor-Becksen, Alfred; Yotsu, Rie Roselyne; Werf, Tjip S van der; Tiendrebeogo, Alexander; Grout, Lise; Asiedu, Kingsley

doi:10.3201/eid2512.190427

Cited by 42 publications

(37 citation statements)

References 34 publications

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“…270,271 However, despite a downward trend observed in the incidence of BU in the last two decades, the disease is currently gaining impetus in scattered worldwide foci. 272,273 Furthermore, many countries are still facing issues in detecting BU at the early stages and the antibiotherapy courses remain very long. 138 The factoring of these issues urges us to keep making strides in advancing our knowledge on BU so that the disease becomes truly negligible.…”

Section: Buruli Ulceromi C S and The Futu Rementioning

confidence: 99%

Genetics in the Host‐Mycobacterium ulcerans interaction

Fevereiro

Fraga

Pedrosa

2021

Immunological Reviews

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Buruli ulcer is an emerging infectious disease associated with high morbidity and unpredictable outbreaks. It is caused by Mycobacterium ulcerans, a slow-growing pathogen evolutionarily shaped by the acquisition of a plasmid involved in the production of a potent macrolide-like cytotoxin and by genome rearrangements and downsizing. These events culminated in an uncommon infection pattern, whereby M. ulcerans is both able to induce the initiation of the inflammatory cascade and the cell death of its proponents, as well as to survive within the phagosome and in the extracellular milieu.In such extreme conditions, the host is sentenced to rely on a highly orchestrated genetic landscape to be able to control the infection. We here revisit the dynamics of M. ulcerans infection, drawing parallels from other mycobacterioses and integrating the most recent knowledge on its evolution and pathogenicity in its interaction with the host immune response.

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Section: Buruli Ulceromi C S and The Futu Rementioning

confidence: 99%

Genetics in the Host‐Mycobacterium ulcerans interaction

Fevereiro

Fraga

Pedrosa

2021

Immunological Reviews

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“…The disease also occurs in the South-East of Australia ( Loftus et al, 2018 ; Organization, 2020 ; Simpson et al, 2019 ; Bratschi et al, 2013 ). The disease can affect all age groups and ethnicities ( Omansen et al, 2019a ).…”

Section: Introductionmentioning

confidence: 99%

High antibody titres induced by protein subunit vaccines usingMycobacterium ulceransantigens Hsp18 and MUL_3720 with a TLR-2 agonist fail to protect against Buruli ulcer in mice

Mangas

Tobias

Marion

et al. 2020

PeerJ

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Background Mycobacterium ulcerans is the causative agent of a debilitating skin and soft tissue infection known as Buruli ulcer (BU). There is no vaccine against BU. The purpose of this study was to investigate the vaccine potential of two previously described immunogenic M. ulcerans proteins, MUL_3720 and Hsp18, using a mouse tail infection model of BU. Methods Recombinant versions of the two proteins were each electrostatically coupled with a previously described lipopeptide adjuvant. Seven C57BL/6 and seven BALB/c mice were vaccinated and boosted with each of the formulations. Vaccinated mice were then challenged with M. ulcerans via subcutaneous tail inoculation. Vaccine performance was assessed by time-to-ulceration compared to unvaccinated mice. Results The MUL_3720 and Hsp18 vaccines induced high titres of antigen-specific antibodies that were predominately subtype IgG1. However, all mice developed ulcers by day-40 post-M. ulcerans challenge. No significant difference was observed in the time-to-onset of ulceration between the experimental vaccine groups and unvaccinated animals. Conclusions These data align with previous vaccine experiments using Hsp18 and MUL_3720 that indicated these proteins may not be appropriate vaccine antigens. This work highlights the need to explore alternative vaccine targets and different approaches to understand the role antibodies might play in controlling BU.

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“…The disease also occurs in Australia – primarily on the Bellarine and Mornington Peninsulas near the major metropolitan centre of Melbourne [10-12]. The disease can affect all age groups and ethnicities [13]. In Australia, ulcers are predominately reported on upper (27%) and lower limbs (70%) [14].…”

Section: Introductionmentioning

confidence: 99%

High antibody titres induced by protein subunit vaccines against Buruli ulcer using Mycobacterium ulcerans antigens Hsp18 and MUL_3720

Tobias

Marion

et al. 2020

Preprint

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24Background. Mycobacterium ulcerans is the causative agent of a debilitating skin and soft tissue 25 infection known as Buruli ulcer (BU). There is no vaccine against BU. The purpose of this study 26 was to investigate the vaccine potential of two previously described immunogenic M. 27 ulcerans proteins, MUL_3720 and Hsp18, using a mouse tail infection model of BU. 28 Methods. Recombinant versions of the two proteins were each electrostatically coupled with a 29 previously described lipopeptide adjuvant. Seven C57BL/6 and seven BALB/c mice were 30 vaccinated and boosted with each of the formulations. Vaccinated mice were then challenged 31 with M. ulcerans via subcutaneous tail inoculation. Vaccine performance was assessed by time-32 to-ulceration compared to unvaccinated mice. 33 Results. The MUL_3720 and Hsp18 vaccines induced high titres of antigen-specific antibodies 34 that were predominately subtype IgG 1 . However, all mice developed ulcers by day-40 post-M. 35 ulcerans challenge. No significant difference was observed in the time-to-onset of ulceration 36 between the experimental vaccine groups and unvaccinated animals.37

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Global Epidemiology of Buruli Ulcer, 2010–2017, and Analysis of 2014 WHO Programmatic Targets

Cited by 42 publications

References 34 publications

Genetics in the Host‐Mycobacterium ulcerans interaction

Genetics in the Host‐Mycobacterium ulcerans interaction

High antibody titres induced by protein subunit vaccines usingMycobacterium ulceransantigens Hsp18 and MUL_3720 with a TLR-2 agonist fail to protect against Buruli ulcer in mice

High antibody titres induced by protein subunit vaccines against Buruli ulcer using Mycobacterium ulcerans antigens Hsp18 and MUL_3720

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