AI Article Synopsis

  • The study examines the global spread of E. coli ST131 and its role in the rise of extended-spectrum β-lactamases (ESBL) in patients at a French University hospital between 2015-2017.
  • It found that 17.5% of ESBL-producing E. coli were part of the ST131 clonal group, with the majority being from the fimH30 subtype, carrying various ESBL genes.
  • Risk factors identified for infection or colonization included previous infections and community acquisition, highlighting the challenge in recognizing shared risk factors for this widespread clonal group.

Article Abstract

The worldwide spread of E. coli ST131 has significantly contributed to the dissemination of E. coli producing extended-spectrum β-lactamases (ESBL). In a French University hospital, we assessed the molecular features of ESBL-producing E. coli and identified risk factors in patients for colonization or infection with E. coli ST131. Over a 2-year period (2015-2017), each patient with at least one clinical isolate or one screening isolate positive with ESBL-producing E. coli were included (n = 491). The ST131 clonal group accounted for 17.5% (n = 86) of all ESBL-producing E. coli and represented 57.3% isolates of phylogroup B2. FimH-based sub-typing showed that 79.1% (68/86) of ST131 isolates were fimH30, among which 67.6% (n = 46), 20.6% (n = 14) and 11.8% (n = 8) isolates harbored genes encoding the ESBL CTX-M-15, CTX-M-27, and CTX-M-14, respectively. The multivariate analysis identified two factors independently associated with ST131 ESBL-producing E. coli isolates: infection (Odds ratio [OR] = 1.887, 95% confidence interval [CI]: 1.143-3.115; p = 0.013) and community acquisition (OR = 2.220, 95% CI: 1.335-3.693; p = 0.002). In conclusion, our study confirmed the predominance of ST131 clonal group among ESBL-producing E. coli and the difficulty to identify common risk factors associated with carriage of this pandemic clonal group.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7952690PMC
http://dx.doi.org/10.1038/s41598-021-85116-6DOI Listing

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