Abstract
Extended-spectrum β-lactamase (ESBL)-producing Escherichia coli isolates are known to tolerate superior quinolone antimicrobials compared with other antibacterial agents. Among the clones belonging to sequence type (ST) 131 by multilocus sequence typing, the involvement of the H30-Rx subclone has been reported worldwide with various fimH genes encoding type 1 pili. We investigated 83 isolates of ESBL-producing E. coli and performed antimicrobial susceptibility test, CH (fumC/fimH) ST131 by typing the specific PCR. Moreover, mutation analysis of genes involved in quinolone antibiotic resistance (gyrA and parC) and ESBL genotypes were determined. As a result, 54 of 83 isolates (65.1%) of CH40-30 clones corresponding to ST131-fimH30 were detected, and all were resistant to levofloxacin. Mutations associated with this resistance were common, and included S83L and D87N of gyrA and S80I and E84V of parC. Subclone analysis revealed a high proportion of fimH30-non-Rx (40 isolates, 74.1%). Each subclone was characterized by ESBL genotype, and the CTX-M-15 type was mainly seen for fimH30-Rx, with the CTX-M-14 type or CTX-M-27 type seen for fimH30-non-Rx. This study suggests that an increase in ESBL-producing quinolone-resistant E. coli in a city hospital in Hyogo, Japan, was caused by the spread of subclones belonging to fimH30-non-Rx of ST131.
Highlights
Escherichia coli is a causative microorganism of infectious diseases, such as those of the urinary tract and bloodstream
It is reported that quinolone-resistant ST131-fimH30 has spread before the acquisition of ESBL-producing genes as a reason why various ESBL-producing genes are found in quinolone-resistant clones [1]
FimH30 subclone fimH30-Rx is characterized by CTX-M-15-type ESBL production of the CTX-M-1 group, with specific amino acid substitutions (Ser83Leu and Asp87Asn in gyrA, and Ser80Ile and Glu84Val in parC) in quinolone resistance-determining regions (QRDRs) of quinolone resistance
Summary
Escherichia coli is a causative microorganism of infectious diseases, such as those of the urinary tract and bloodstream. According to research by Japan Nosocomial Infections. Surveillance, the resistance rate of E. coli to cefotaxime (CTX) in Japan was 9% in 2008 and reached 26% in 2016 [2]. The main antimicrobial resistance mechanism of E. coli is the inactivation of antimicrobials by isolates with extended-spectrum β-lactamase (ESBL) production. ESBL genotypes include TEM and SHV types, but those most widely spread around the world are CTX-M types. The resulting rise in infection caused by the escalation of ESBL-producing bacteria has necessitated an increase in the use of carbapenems, which are first-line drugs, but are treated as final choices because of their broad spectrum; this, increases the risk of developing further resistant bacterial isolates [5]
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