RT Journal
A1 David, Sophia
A1 Rusniok, Christophe
A1 Mentasti, Massimo
A1 Gomez-Valero, Laura
A1 Harris, Simon R.
A1 Lechat, Pierre
A1 Lees, John
A1 Ginevra, Christophe
A1 Glaser, Philippe
A1 Ma, Laurence
A1 Bouchier, Christiane
A1 Underwood, Anthony
A1 Jarraud, Sophie
A1 Harrison, Timothy G.
A1 Parkhill, Julian
A1 Buchrieser, Carmen
T1 Multiple major disease-associated clones of Legionella pneumophila have emerged recently and independently
JF Genome Research 
JO Genome Research 
YR 2016 
FD November 01 
VO 26 
IS 11 
SP 1555 
OP 1564 
DO 10.1101/gr.209536.116 
UL http://genome.cshlp.org/content/26/11/1555.abstract 
AB 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.