Escherichia coli sequence type 131 H30 is the main driver of emerging extended-spectrum-β-lactamase-producing E. coli at a tertiary care center

James R. Johnson, Brian Johnston, Paul Thuras, Bryn Launer, Evgeni V. Sokurenko, Loren G. Miller

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5 Scopus citations

Abstract

The H30 strain of Escherichia coli sequence type 131 (ST131-H30) is a recently emerged, globally disseminated lineage associated with fluoroquinolone resistance and, via its H30Rx subclone, the CTX-M-15 extended-spectrum betalactamase (ESBL). Here, we studied the clonal background and resistance characteristics of 109 consecutive recent E. coli clinical isolates (2015) and 41 historical ESBLproducing E. coli blood isolates (2004 to 2011) from a public tertiary care center in California with a rising prevalence of ESBL-producing E. coli isolates. Among the 2015 isolates, ST131, which was represented mainly by ST131-H30, was the most common clonal lineage (23% overall). ST131-H30 accounted for 47% (8/17) of ESBLproducing, 47% (14/30) of fluoroquinolone-resistant, and 33% (11/33) of multidrugresistant isolates. ST131-H30 also accounted for 53% (8/14) of dually fluoroquinoloneresistant, ESBL-producing isolates, with the remaining 47% comprised of diverse clonal groups that contributed a single isolate each. ST131-H30Rx, with CTX-M-15, was the major ESBL producer (6/8) among ST131-H30 isolates. ST131-H30 and H30Rx also dominated (46% and 37%, respectively) among the historical ESBL-producing isolates (2004 to 2011), without significant temporal shifts in relative prevalence. Thus, this medical center's recently emerging ESBL-producing E. coli strains, although multiclonal, are dominated by ST131-H30 and H30Rx, which are the only clonally expanded fluoroquinolone-resistant, ESBL-producing lineages. Measures to rapidly and effectively detect, treat, and control these highly successful lineages are needed.

Original languageEnglish (US)
Article numbere00314-16
JournalmSphere
Volume1
Issue number6
DOIs
StatePublished - Nov 1 2016

Bibliographical note

Funding Information:
This material is based on work supported by the Office of Research and Development, Medical Research Service, Department of Veterans Affairs, via grant no. 1 I01 CX000192 01 (J.R.J.), and by NIH grant no. R01AI106007 (E.V.S.). The sponsors had no involvement in the conduct of the study, data analysis, manuscript preparation, or decision to publish. The opinions expressed here are strictly those of the authors and do not represent those of the federal government, any of its branches, or the authors' respective institutions. J.R.J. has received contracts, grants, or consultancies from Actavis, ICET, Jannsen, Merck, and Tetraphase. J.R.J. and E.V.S. have patent applications pertaining to tests for specific E. coli strains. E.V.S. is a founder and major shareholder in ID Genomics, Inc. L.M. has received contracts, grants, or consultancies from Cubist, Durata, Gilead Sciences, Tetraphase, and Theravance. The other authors report no conflicts of interest. This work, including the efforts of James R. Johnson, was funded by Department of Veterans Affairs (1 I01 CX000192 01). This work, including the efforts of Evgeni V. Sokurenko, was funded by HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) (R01AI106007)

Publisher Copyright:
© 2016 Johnson et al.

Keywords

  • Antimicrobial resistance
  • Clonality
  • Escherichia coli infections
  • Extended-spectrum β-lactamase
  • Fluoroquinolone resistance
  • Molecular epidemiology
  • Phylogenetic analysis
  • ST131
  • ST131-H30

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