Multiple major disease-associated clones of Legionella pneumophila have emerged recently and independently

Sophia David, Christophe Rusniok, Massimo Mentasti, Laura Gomez-Valero, Simon R. Harris, Pierre Lechat, John Lees, Christophe Ginevra, Philippe Glaser, Laurence Ma, Christiane Bouchier, Anthony Underwood, Sophie Jarraud, Timothy Harrison, Julian Parkhill*, Carmen Buchrieser

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

51 Citations (Scopus)

Abstract

Legionella pneumophila is an environmental bacterium and the leading cause of Legionnaires' disease. Just five sequence types (ST), from more than 2000 currently described, cause nearly half of disease cases in northwest Europe. Here, we report the sequence and analyses of 364 L. pneumophila genomes, including 337 from the five disease-associated STs and 27 representative of the species diversity. Phylogenetic analyses revealed that the five STs have independent origins within a highly diverse species. The number of de novo mutations is extremely low with maximum pairwise single-nucleotide polymorphisms (SNPs) ranging from 19 (ST47) to 127 (ST1), which suggests emergences within the last century. Isolates sampled geographically far apart differ by only a few SNPs, demonstrating rapid dissemination. These five STs have been recombining recently, leading to a shared pool of allelic variants potentially contributing to their increased disease propensity. The oldest clone, ST1, has spread globally; between 1940 and 2000, four new clones have emerged in Europe, which show long-distance, rapid dispersal. That a large proportion of clinical cases is caused by recently emerged and internationally dispersed clones, linked by convergent evolution, is surprising for an environmental bacterium traditionally considered to be an opportunistic pathogen. To simultaneously explain recent emergence, rapid spread and increased disease association, we hypothesize that these STs have adapted to new man-made environmental niches, which may be linked by human infection and transmission.

Original languageEnglish
Pages (from-to)1555-1564
Number of pages10
JournalGenome Research
Volume26
Issue number11
DOIs
Publication statusPublished - Nov 2016

Bibliographical note

Funding Information:
Work in the C.B. laboratory is financed by the Institut Pasteur, the Institut Carnot-Pasteur MI, the French Region Ile de France (DIM Malinf), the Agence Nationale de la Recherche (ANR) Grant No. ANR-10-LABX-62-IBEID, the ANR-10-PATH-004 project, in the frame of ERA-Net PathoGenoMics, and the Fondation pour la Recherche M?dicale (FRM) Grant No. DEQ20120323697. We thank M. Tichit and M. Hunt for their technical support. The Plate-forme G?nomique is a member of "France G?nomique" consortium (ANR10-INBS-09-08).Work at the Sanger Institute is funded by The Wellcome Trust Grant No. 098051.

Publisher Copyright:
© 2016 David, al.; Published by Cold Spring Harbor Laboratory Press.

Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.

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