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

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.

The antibiotic resistance and pathogenicity of a multidrug‐resistant Elizabethkingia anophelis isolate

“…For example, all 51 E. anophelis isolates from South Korea were immediately sensitive or sensitive to piperacillin or piperacillin–tazobactam (Han et al, ). Furthermore, 25 Wisconsin outbreak strains were also susceptible to piperacillin–tazobactam tested by Kirby Bauer disk diffusion method (Perrin et al, ). The same observations were reported in E. anophelis EM361‐97 isolated from Taiwan (Lin, Lai, Yang, Huang, & Lin, ).…”

“…However, the antibiograms in various Elizabethkingia isolates are often controversially reported. For instance, most of the 100 E. anophelis strains isolated from Korea as well as strain EM361‐97 from Taiwan were resistant to ciprofloxacin and levofloxacin, while most of the Wisconsin outbreak strains were susceptible to these quinolone drugs (Han et al, ; Lin et al, ; Perrin et al, ). These variations stress that different origins of Elizabethkingia isolates may evolve different antibiotic resistance mechanisms.…”

“…In this mobile genetic element, both relaxase and integrase (TIGR02249) were predicted (Figure A2). The CSID 3000521207, one present representative isolate of the outbreak in Wisconsin, had the integrative and conjugative element ICEEa1 (Perrin et al, ). ICEEa1 consists of VirD4 ATPase (T4CP), relaxase, integrase, and several Tra proteins.…”

“…Taiwan were resistant to ciprofloxacin and levofloxacin, while most of the Wisconsin outbreak strains were susceptible to these quinolone drugs (Han et al, 2017;Lin et al, 2017;Perrin et al, 2017). These variations stress that different origins of Elizabethkingia isolates may evolve different antibiotic resistance mechanisms.…”

Potential for transmission ofElizabethkingia anophelisbyAedes albopictusand the role of microbial interactions in Zika virus competence

“…Our findings bear clinical significance as E. anophelis has been identified as a cause of sepsis in adults and children, as well as a cause of neonatal meningitis [9]. By 2016, E. anophelis had caused an outbreak in Central African Republic [6], Singapore [7] and two outbreaks in the Midwest, United States that resulted in morbidity and mortality of ~ 30% [8–10]. The Midwest outbreak occurred primarily in community settings [8] and despite extensive investigations, no point source of infection has been identified in either the Midwest or Singapore outbreaks [9,10].…”