Abstract
Background. Escherichia coli sequence type ST131 (O25:H4), associated with the CTX-M-15 extended-spectrum β-lactamase, has emerged internationally as a multidrug-resistant pathogen but has received little attention in the United States. Methods. From the SENTRY and Meropenem Yearly Susceptibility Test Information Collection (MYSTIC) surveillance programs, 127 E. coli clinical isolates from hospitalized patients across the United States in 2007, stratified by extended-spectrum cephalosporin and fluoroquinolone phenotype and bla CTX-M-15 genotype, were assessed for phylogenetic group, ST131 status, susceptibility profile, virulence genotype, gyrA and parC sequence, and pulsed-field gel electrophoresis profile. Results. The 54 identified ST131 isolates (all fluoroquinolone resistant) accounted for an estimated 17% of the source populations, including 67%-69% of isolates resistant to extended-spectrum cephalosporins or fluoroquinolones, 55% of those resistant to both fluoroquinolones and trimethoprim-sulfamethoxazole, and 52% of multidrug-resistant isolates. Their distinctive virulence profiles were more extensive compared with other antimicrobial- resistant isolates but similarly extensive compared with antimicrobial-susceptible isolates. Pulsed-field profiling suggested ongoing dissemination among locales, with concentration of blaCTX-M-15 within specific ST131 lineages. A historical ST131 isolate lacked the 2007 ST131 isolates' conserved fluoroquinolone resistance-associated single-nucleotide polymorphisms in gyrA and parC. Conclusions. A single E. coli clonal group, ST131, probably caused the most significantly antimicrobial- resistant E. coli infections in the United States in 2007, thereby constituting an important new public health threat. Enhanced virulence and/or antimicrobial resistance compared with other E. coli, plus ongoing dissemination among locales, may underlie ST131's success. Urgent investigation of the sources and transmission pathways of ST131 is needed to inform mitigation efforts.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 286-294 |
| Number of pages | 9 |
| Journal | Clinical Infectious Diseases |
| Volume | 51 |
| Issue number | 3 |
| DOIs | |
| State | Published - Aug 1 2010 |
Bibliographical note
Funding Information:Financial support. This material is based on work supported by Office of Research and Development, Medical Research Service, Department of Veterans Affairs (J.R.J.). The study sponsor had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript.