Fluoroquinolone-resistant escherichia coli sequence type 131 isolates causing bloodstream infections in a canadian region with a centralized laboratory system: Rapid emergence of the H30-RX sublineage

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Abstract

A population-based surveillance study was designed to describe the clinical features and characteristics of sequence type 131 (ST131) and its H30 and H30-Rx sublineages among fluoroquinolone-resistant (FQ-R) Escherichia coli isolates that caused bloodstream infections (BSIs) in a Canadian region with a centralized laboratory system over an 11-year period (2000 to 2010). Nonrepeat isolates from true incident cases were included. Established PCR methods were used to define ST131, its H30 and H30-Rx sublineages, extended-spectrum μ-lactamase and AmpC production, and plasmid-mediated quinolone resistance determinants. A total of 677 Calgary residents with incident BSIs due to FQ-R E. coli were identified; the majority presented with health care-Associated upper urinary tract infections (UTIs). There was a rise in FQ-R over the 11-year period because of an increase in ST131 toward the end of the study period (2008 to 2010) that was due to a rapid influx of the H30-Rx sublineage. We identified the association of H30-Rx with primary sepsis, upper UTIs as a complication of prostate biopsies, multidrug resistance, and the presence of bla CTX-M-15 and aac(6=)-lb-cr. E. coli ST131 H30-Rx has established itself as a major drug-resistant sublineage in Calgary, posing an important new public health threat within our region. We urgently need well-designed epidemiological and molecular studies to further understand the dynamics of transmission, risk factors, and reservoirs of H30-Rx.© 2014, American Society for Microbiology. All Rights Reserved.

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CITATION STYLE

APA

Peirano, G., & Pitout, J. D. D. (2014). Fluoroquinolone-resistant escherichia coli sequence type 131 isolates causing bloodstream infections in a canadian region with a centralized laboratory system: Rapid emergence of the H30-RX sublineage. Antimicrobial Agents and Chemotherapy, 58(5), 2699–2703. https://doi.org/10.1128/AAC.00119-14

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