Dissemination of Mycobacterium abscessus via global transmission networks.

Authors
Ruis, Christopher 
Bryant, Josephine M 
Bell, Scott C 
Thomson, Rachel 
Davidson, Rebecca M 

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Article
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Abstract

Mycobacterium abscessus, a multidrug-resistant nontuberculous mycobacterium, has emerged as a major pathogen affecting people with cystic fibrosis (CF). Although originally thought to be acquired independently from the environment, most individuals are infected with one of several dominant circulating clones (DCCs), indicating the presence of global transmission networks of M. abscessus. How and when these clones emerged and spread globally is unclear. Here, we use evolutionary analyses of isolates from individuals both with and without CF to reconstruct the population history, spatiotemporal spread and recent transmission networks of the DCCs. We demonstrate synchronous expansion of six unrelated DCCs in the 1960s, a period associated with major changes in CF care and survival. Each of these clones has spread globally as a result of rare intercontinental transmission events. We show that the DCCs, but not environmentally acquired isolates, exhibit a specific smoking-associated mutational signature and that current transmission networks include individuals both with and without CF. We therefore propose that the DCCs initially emerged in non-CF populations but were then amplified and spread through the CF community. While individuals with CF are probably the most permissive host, non-CF individuals continue to play a key role in transmission networks and may facilitate long-distance transmission.

Publication Date
2021-10
Online Publication Date
2021-09-20
Acceptance Date
2021-08-18
Keywords
Cystic Fibrosis, Genome, Bacterial, Global Health, Humans, Lung, Mutation, Mycobacterium Infections, Nontuberculous, Mycobacterium abscessus, Phylogeny, Smokers
Journal Title
Nature Microbiology
Journal ISSN
2058-5276
2058-5276
Volume Title
6
Publisher
Nature Research
Sponsorship
Wellcome Trust (107032/Z/15/Z)
Wellcome Trust (110224/Z/15/Z)
Funding for this work was provided by The Wellcome Trust (investigator award no. 107032/Z/15/Z to R.A.F.), Fondation Botnar (Programme grant no. 6063) and the UK CF Trust (Innovation Hub award no. 001; Strategic Research Centre award no. 010). M.S., N.A.H. and R.M.D. acknowledge the Cystic Fibrosis Foundation for funding.