Abrupt emergence of a single dominant multidrug-resistant strain of Escherichia coli

James R. Johnson, Veronika Tchesnokova, Brian Johnston, Connie Clabots, Pacita L. Roberts, Mariya Billig, Kim Riddell, Peggy Rogers, Xuan Qin, Susan Butler-Wu, Lance B. Price, Maliha Aziz, Marie Hélène Nicolas-Chanoine, Chitrita Debroy, Ari Robicsek, Glen Hansen, Carl Urban, Joanne Platell, Darren J. Trott, George ZhanelScott J. Weissman, Brad T. Cookson, Ferric C. Fang, Ajit P. Limaye, Delia Scholes, Sujay Chattopadhyay, David C. Hooper, Evgeni V. Sokurenko

Research output: Contribution to journalArticlepeer-review

215 Scopus citations


Background. Fluoroquinolone-resistant Escherichia coli are increasingly prevalent. Their clonal origins-potentially critical for control efforts-remain undefined.Methods. Antimicrobial resistance profiles and fine clonal structure were determined for 236 diverse-source historical (1967-2009) E. coli isolates representing sequence type ST131 and 853 recent (2010-2011) consecutive E. coli isolates from 5 clinical laboratories in Seattle, Washington, and Minneapolis, Minnesota. Clonal structure was resolved based on fimH sequence (fimbrial adhesin gene: H subclone assignments), multilocus sequence typing, gyrA and parC sequence (fluoroquinolone resistance-determining loci), and pulsed-field gel electrophoresis.Results. Of the recent fluoroquinolone-resistant clinical isolates, 52% represented a single ST131 subclonal lineage, H30, which expanded abruptly after 2000. This subclone had a unique and conserved gyrA/parC allele combination, supporting its tight clonality. Unlike other ST131 subclones, H30 was significantly associated with fluoroquinolone resistance and was the most prevalent subclone among current E. coli clinical isolates, overall (10.4%) and within every resistance category (11%-52%).Conclusions. Most current fluoroquinolone-resistant E. coli clinical isolates, and the largest share of multidrug-resistant isolates, represent a highly clonal subgroup that likely originated from a single rapidly expanded and disseminated ST131 strain. Focused attention to this strain will be required to control the fluoroquinolone and multidrug-resistant E. coli epidemic.

Original languageEnglish (US)
Pages (from-to)919-928
Number of pages10
JournalJournal of Infectious Diseases
Issue number6
StatePublished - 2013

Bibliographical note

Funding Information:
Potential conflicts of interest. The following authors report these conflicts of interest: F. C. F.: Consultancy, research grants, and educational presentations with Cepheid. D. C. H.: Research grant from Rib-X Pharmaceuticals, consultancies with Fab Pharma and Pfizer, speakers bureau with Pfizer. J. R. J.: Research grants and contracts from Merck, Rochester Medical, and Syntiron; patent pending for detection of the H30 ST131 subclone. L. B. P.: Patent pending for detection of the H30 ST131 subclone. M.-H. N.-C.: Expert testimony for Region Wallon; research grant from Direction de la Recherche Clinique AP-HP; lectures for Novar-tis; travel reimbursement for 2012 ICAAC speaker. E. V. S.: Research grant from Group Health; patent pending for detection of the H30 ST131 subclone. D. T.: Research grant from ARC Linkage; consultancy from Pfizer and Bayer; speaker for Bayer Animal Health. C. U.: Consultancy with Pfizer, lecture/speaker for Forest Pharmaceuticals, Cubist, and Pfizer. G. Z.: Research grants from Achaogen, Merck, Pfizer, Cubist, Affi-nium, and Sunovion. All other authors report no potential conflicts.

Funding Information:
Financial support. This material is based upon work supported by Office of Research and Development, Medical Research Service, Department of Veterans Affairs, Merit Review grant 1 I01 CX000192 01 ( J. R. J.), and NIH ARRA award 1RC4AI092828 (E. V. S.).


  • CTX-M-15
  • Escherichia coli infections
  • FimH
  • antimicrobial resistance
  • extended-spectrum β-lactamase
  • fluoroquinolone resistance
  • molecular epidemiology
  • multidrug resistance
  • multilocus sequence typing
  • sequence type ST131


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