Abstract

BackgroundEscherichia coli (E. coli) is known to cause urinary tract infection (UTI) and meningitis in neonates, as well as existing as a commensal flora of the human gut. Extended-spectrum β-lactamase (ESBL)-producing E. coli has increased in the community with the spread of CTX-M type ESBL-producing sequence type 131 (ST131)-O25-H30Rx E. coli clone. The role of ESBL-producing E. coli in female genital tract infection has not been elucidated. The clinical and molecular features of E. coli isolated from community-onset female genital tract infections were evaluated to elucidate the current burden in the community, focusing on the highly virulent and multidrug-resistant ST131 clone.MethodsWe collected and sequenced 91 non-duplicated E. coli isolates from the female genital tract of 514 patients with community-onset vaginitis. ESBL genotypes were identified by PCR and confirmed to be ESBL-producers by sequencing methods. ST131 clones were screened by PCR for O16-ST131 and O25b-ST131. Pulsed-field gel electrophoresis (PFGE) and PCR-based replicon typing (PBRT) were conducted in ESBL producers. Independent clinical risk factors associated with acquiring ESBL-producing E. coli and ST131 clone were analyzed using multivariate logistic regression analysis.ResultsOf the 514 consecutive specimens obtained from the infected female genital tract, 17.7% (91/514) had E. coli infection, of which 19.8% (18/91) were ESBL producers. CTX-M-15 was the most common type (n = 15). O25b-ST131 and O16-ST131 clones accounted for 15.4% (14/91) and 6.6% (6/91), respectively. In plasmid analysis, ten isolates succeeded in conjugation and plasmid types were IncFII (n = 4), IncFI (n = 3), IncI1-Iγ (n = 3) with one non-typable case. Compared to ESBL-nonproducing E. coli, ESBL-producing E. coli acquisition was strongly associated with recurrent vaginitis (OR 40.130; 95% CI 9.980–161.366), UTI (OR 18.915; 95% CI 5.469–65.411), and antibiotics treatment (OR 68.390; 95% CI 14.870–314.531).ConclusionA dominant clone of CTX-M type ESBL-producing E. coli in conjugative plasmids seems to be circulating in the community and considerable number of ST131 E. coli in the genital tract of Korean women was noted. Sustained monitoring of molecular epidemiology and control of the high-risk group is needed to prevent ESBL-producing E. coli from spreading throughout the community.

Highlights

  • Escherichia coli (E. coli) is known to cause urinary tract infection (UTI) and meningitis in neonates, as well as existing as a commensal flora of the human gut

  • We focused on the highly virulent and multidrug-resistant sequence type 131 (ST131) clone because it could be another indicator of the spread in the community and an emerging public health threat

  • Of the 514 consecutive specimens obtained from the infected female genital tract, 17.7% (91/514) had E. coli infection, of which 19.8% (18/91) were ESBL producers

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Summary

Introduction

Escherichia coli (E. coli) is known to cause urinary tract infection (UTI) and meningitis in neonates, as well as existing as a commensal flora of the human gut. The role of ESBL-producing E. coli in female genital tract infection has not been elucidated. Escherichia coli (E. coli) is known to cause urinary tract infection (UTI), surgical site infection, and meningitis in neonates, as well as existing as a commensal flora of the human gut [1, 2]. Colonization or infection of extended-spectrum-β-lactamase (ESBL)-producing E. coli has remarkably increased in the community, mostly due to the spread of high virulent and multidrug-resistant sequence type 131 (ST131) E. coli clone [6,7,8]. The presence of ESBL-producing E. coli in female genital tract infections are scarcely identified within our knowledge

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