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Nat Commun. 2017 May 24;8:15483. doi: 10.1038/ncomms15483.

Evolutionary dynamics and genomic features of the Elizabethkingia anophelis 2015 to 2016 Wisconsin outbreak strain.

Author information

1
Institut Pasteur, Microbial Evolutionary Genomics, F-75724 Paris, France.
2
CNRS, UMR 3525, F-75724 Paris, France.
3
Institut Pasteur, Hub Bioinformatique et Biostatistique, C3BI, USR 3756 IP CNRS, F-75724 Paris, France.
4
CNRS, UMS 3601 IFB-Core, F- 91198 Gif-sur-Yvette, France.
5
Special Bacteriology Reference Laboratory, Bacterial Special Pathogens Branch, Division of High Consequence Pathogens and Pathology, Centers for Disease Control and Prevention, Atlanta, Georgia 30329, USA.
6
Centre for Systems Genomics, University of Melbourne, Parkville, Victoria 3010, Australia.
7
Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, Victoria 3010, Australia.
8
Wisconsin State Laboratory of Hygiene, Madison, Wisconsin 53718, USA.
9
CIP-Collection de l'Institut Pasteur, Institut Pasteur, F-75724 Paris, France.
10
Institut Pasteur, Pasteur International Bioresources network (PIBnet), Plateforme de Microbiologie Mutualisée (P2M), F-75724 Paris, France.
11
Division of Scientific Resources, Centers for Disease Control and Prevention, Atlanta, Georgia 30329, USA.
12
Epidemic Intelligence Service, Centers for Disease Control and Prevention, Atlanta, Georgia 30329, USA.
13
Division of Public Health, Wisconsin Department of Health Services, Madison, Wisconsin 53701, USA.
14
Division of Healthcare Quality Promotion, Centers for Disease Control and Prevention, Atlanta, Georgia 30329, USA.
15
Institut Pasteur, Molecular Prevention and Therapy of Human Diseases, F-75724 Paris, France.

Abstract

An atypically large outbreak of Elizabethkingia anophelis infections occurred in Wisconsin. Here we show that it was caused by a single strain with thirteen characteristic genomic regions. Strikingly, the outbreak isolates show an accelerated evolutionary rate and an atypical mutational spectrum. Six phylogenetic sub-clusters with distinctive temporal and geographic dynamics are revealed, and their last common ancestor existed approximately one year before the first recognized human infection. Unlike other E. anophelis, the outbreak strain had a disrupted DNA repair mutY gene caused by insertion of an integrative and conjugative element. This genomic change probably contributed to the high evolutionary rate of the outbreak strain and may have increased its adaptability, as many mutations in protein-coding genes occurred during the outbreak. This unique discovery of an outbreak caused by a naturally occurring mutator bacterial pathogen provides a dramatic example of the potential impact of pathogen evolutionary dynamics on infectious disease epidemiology.

PMID:
28537263
PMCID:
PMC5458099
DOI:
10.1038/ncomms15483
[Indexed for MEDLINE]
Free PMC Article

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