Background. Extraintestinal Escherichia coli infections are increasingly challenging due to emerging antimicrobial resistance, including resistance to extended-spectrum beta-lactams and fluoroquinolones. Sequence type 131 (ST131) is a leading contributor. Methods. Three hundred sixty E. coli clinical isolates from across the United States (2011-2012), selected randomly from the SENTRY collection within 3 resistance categories (extended-spectrum cephalosporin [ECS]-reduced susceptibility [RS]; fluoroquinolone- resistant, ESC-susceptible; and fluoroquinolone-susceptible, ESC-susceptible) were typed for phylogroup, sequence type complex (STc), subsets thereof, virulence genotype, O type, and beta-lactamase genes. Molecular results were compared with susceptibility profile, specimen type, age, and sex. Results. Phylogroup B2 accounted for most isolates, especially fluoroquinolone-resistant isolates (83%). Group B2-derived ST131 and its H30 subclone (divided between H30Rx and H30R1) predominated, especially among ESC-RS and fluoroquinolone-resistant isolates. In contrast, among fluoroquinolone-susceptible isolates, group B2-derived STc73 and STc95 predominated. Within each resistance category, ST131 isolates exhibited more extensive resistance and/or virulence profiles than non-ST131 isolates. ST131-H30 was distributed broadly by geographical region, age, and specimen type and exhibited distinctive beta-lactamase genes. Back-calculations indicated that within the source population ST131 accounted for 26.4% of isolates overall (vs 17% in 2007), including 19.8% ST131-H30, 13.2% ST131-H30R1, and 6.6% each ST131-H30Rx and non-H30 ST131. Conclusions. ST131-H30, with its ESC resistance-associated H30Rx subset, caused most antimicrobial-resistant E. coli infections across the United States in 2011-2012 and, since 2007, increased in relative prevalence by > 50%. Focused attention to this strain could help combat the current E. coli resistance epidemic.
Bibliographical noteFunding Information:
Financial support. This material is based on work supported by an investigator-initiated grant from Merck and by Office of Research and Development, Medical Research Service, Department of Veterans Affairs (grant 1 I01 CX000192 01; both to J. R. J.). Potential conflicts of interest. J. R. J. has received contracts, grants, or consultancies from Achaogen, Actavis, Jannsen, Merck, and Tetraphase, and has patent applications pertaining to tests for specific E. coli strains. M. C. is an employee of JMI Laboratories, which was contracted to perform services in 2016 for Achaogen, Actelion, Allecra, Allergan, Ampliphi, API, Astellas, AstraZeneca, Basilea, Bayer, BD, Biomodels, Cardeas, CEM-102 Pharma, Cempra, Cidara, Cormedix, CSA Biotech, Cubist, Debiopharm, Dipexium, Duke, Durata, Entasis, Fortress, Fox Chase Chemical, GSK, Medpace, Melinta, Merck, Micurx, Motif, N8 Medical, Nabriva, Nexcida, Novartis, Paratek, Pfizer, Polyphor, Rempex, Scynexis, Shionogi, Spero Therapeutics, Symbal Therapeutics, Synolgoic, TGV Therapeutics, The Medicines Company, Theravance, ThermoFisher, Venatorx, Wockhardt, and Zavante. Additionally, some JMI employees are advisors/consultants for Allergan, Astellas, Cubist, Pfizer, Cempra, and Theravance. All other authors: no reported conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.
- Antimicrobial resistance
- Escherichia coli infections
- Extended-spectrum beta-lactamases
- Fluoroquinolone resistance