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

Authors: Perrin, Amandine and Larsonneur, Elise and Nicholson, Ainsley C and Edwards, David J and Gundlach, Kristin M and Whitney, Anne M and Gulvik, Christopher A and Bell, Melissa E and Rendueles, Olaya and Cury, Jean and Hugon, Perrine and Clermont, Dominique and Enouf, Vincent and Loparev, Vladimir and Juieng, Phalasy and Monson, Timothy and Warshauer, David and Elbadawi, Lina I and Walters, Maroya Spalding and Crist, Matthew B and Noble-Wang, Judith and Borlaug, Gwen and Rocha, Eduardo P C and Criscuolo, Alexis and Touchon, Marie and Davis, Jeffrey P and Holt, Kathryn E and McQuiston, John R and Brisse, Sylvain

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.

Journal: Nature communications
DOI: 10.1038/ncomms15483
Year: 2017

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