Escherichia coli sequence type ST131 as the major cause of serious multidrug-resistant E. coli infections in the United States.
BACKGROUND
Escherichia coli sequence type ST131 (O25:H4), associated with the CTX-M-15 extended-spectrum beta-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 bla(CTX-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.
Johnson
James R
JR
Infectious Diseases,VA Medical Center, Minneapolis, MN 55417, USA. johns007@umn.edu
Johnston
Brian
B
Clabots
Connie
C
Kuskowski
Michael A
MA
Castanheira
Mariana
M
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D015373:Bacterial Typing Techniques; D002511:Cephalosporins / Q000494:pharmacology; D016000:Cluster Analysis; D016172:DNA Fingerprinting; D027081:DNA Gyrase / Q000235:genetics; D027101:DNA Topoisomerase IV / Q000235:genetics; D004269:DNA, Bacterial / Q000235:genetics; D024901:Drug Resistance, Multiple, Bacterial; D016521:Electrophoresis, Gel, Pulsed-Field; D004926:Escherichia coli / Q000145:classification* / Q000187:drug effects* / Q000235:genetics / Q000302:isolation & purification; D004927:Escherichia coli Infections / Q000453:epidemiology* / Q000382:microbiology*; D029968:Escherichia coli Proteins / Q000096:biosynthesis / Q000235:genetics; D024841:Fluoroquinolones / Q000494:pharmacology; D005838:Genotype; D006801:Humans; D008826:Microbial Sensitivity Tests; D017720:Molecular Epidemiology; D017422:Sequence Analysis, DNA; D014481:United States / Q000453:epidemiology; D037521:Virulence Factors / Q000235:genetics; D001618:beta-Lactamases / Q000096:biosynthesis
D000900:Anti-Bacterial Agents; D002511:Cephalosporins; D004269:DNA, Bacterial; D029968:Escherichia coli Proteins; D024841:Fluoroquinolones; D037521:Virulence Factors; D001618:beta-Lactamases; D027101:DNA Topoisomerase IV; D027081:DNA Gyrase