Yes / Buruli ulcer (BU) is an insidious neglected tropical disease. Cases are reported around the world but the rural regions of West and
Central Africa are most affected. How BU is transmitted and spreads has remained a mystery, even though the causative agent,
Mycobacterium ulcerans, has been known for more than 70 years. Here, using the tools of population genomics, we reconstruct the
evolutionaryhistoryofM. ulceransbycomparing165isolatesspanning48yearsandrepresenting11endemiccountriesacrossAfrica.
The genetic diversity of African M. ulcerans was found to be restricted due to the bacterium’s slow substitution rate coupled with its
relatively recent origin. We identified two specific M. ulcerans lineages within the African continent, and inferred that M. ulcerans
lineage Mu_A1 existed in Africa for several hundreds of years, unlike lineage Mu_A2, which was introduced much more recently,
approximately during the 19th century. Additionally, we observed that specific M. ulcerans epidemic Mu_A1 clones were introduced
during the same time period in the three hydrological basins that were well covered in our panel. The estimated time span of the
introduction events coincides with the Neo-imperialism period, during which time the European colonial powers divided the African
continent among themselves. Using this temporal association, and in the absence of a known BU reservoir or—vector on the
continent, we postulate that the so-called "Scramble for Africa" played a significant role in the spread of the disease across the
continent. / K.V. was supported by a PhD-grant of the Flemish Interuniversity Council—University Development Cooperation (Belgium). B.d.J. and C.M. were supported by the European Research Council-INTERRUPTB starting grant (no. 311725). T.P.S. was supported by a fellowship from the National Health and Medical Research Council of Australia (1105525). Funding for this work was provided by the Department of Economy, Science and Innovation of the Flemish Government, the Stop Buruli Consortium supported by the UBS Optimus Foundation, and the Fund for Scientific Research Flanders (Belgium) (FWO grant no. G.0321.07N). The computational resources used in this work were provided by the HPC core facility CalcUA and VSC (Flemish Supercomputer Center), funded by the University of Antwerp, the Hercules Foundation and the Flemish Government—department EWI. Aspects of the research in Cameroon and Benin were funded by the Raoul Follereau Fondation France.
| Identifer | oai:union.ndltd.org:BRADFORD/oai:bradscholars.brad.ac.uk:10454/17302 |
| Date | 24 September 2019 |
| Creators | Vandelannoote, K., Meehan, Conor J., Eddyani, M., Affolabi, D., Phanzu, D.M., Eyangoh, S., Jordaens, K., Portaels, F., Mangas, K., Seemann, T., Marsollier, L., Marion, E., Chauty, A., Landier, J., Fontanet, A., Leirs, H., Stinear, T.P., de Jong, B.C. |
| Source Sets | Bradford Scholars |
| Language | English |
| Detected Language | English |
| Type | Article, Published version |
| Rights | © The Author(s) 2017. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited., CC-BY-NC |
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