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Abstract Fluoroquinolone-resistant (FQs-R) microorganisms causing infectious complications after ultrasound-guided needle biopsy of the prostate (TRUS-BP) have become an important challenge in healthcare settings globally, questioning the continued utility of FQ as the preferred prophylactic agent. This study aimed to characterize molecular mechanisms of resistance on FQs-R E. coli isolated from the enteric microbiota of patients undergoing (TRUS-BP) and to highlight their impact on Minimum Inhibitory Concentrations (MICs). From February 2016 to December 2018, the incidence of rectal carriage of Qs-FQs resistant Enterobacterales detected from rectal swabs of patients before undergoing (TRUS-BP) was 61.06% (80/131) all related to E. coli species. Based on the MICs range of Qs (24–256 mg/L) and FQs (0.24–128 mg/L) breakpoint by EUCAST, we categorized these E. coli isolates into three resistance profiles (I, II, and III) associated with the patterns of chromosomal mutations in the quinolone resistance-determining regions (QRDRs) of gyrA and parC and the plasmid-mediated quinolone resistance encoding genes (PMQRs) detected by PCR-based assay and sequencing; MICs increase in an escalation step according to the co-occurrence of multiple molecular mechanisms. The mutation of the gyrA gene was the most frequent on codons (Ser83Leu/Thr/Tyr/Trp and Asp87Asn); mutation on the parC gene was the least on codons (Ser80Iso/Leu and Glu84 Val/Gly/Lys). PMQRs genes (4 qnrB ,7 qnrS, and one aac(6’)-Ib-cr) were determined within 15% of the isolates. Allelic variation allows us to report earliest the qnrB81 determinant in an E. coli isolate. Among isolates (35%) belonged to the notorious ST131 lineage. The phylogenetic group showed a predominance of B2 group (51, 25%), however (PFGE) revealed a high level of clonal variability. Worrying incidence of FQs-R E. coli isolates in the rectal flora of our local population showed the potential to cause post-infection. FQ resistance is a complex interplay between mutations in the QRDRs and PMQR determinants that impact MICs. The importance of intestinal microbiota as a reservoir of resistant strains and pandemic clones encourages driving mitigation challenges to characterize molecular mechanisms of antimicrobial resistance to adapt prophylactic therapy, control infection, and ensure epidemiological monitoring.

Fluoroquinolone-resistant (FQs-R) microorganisms causing infectious complications after ultrasound-guided needle biopsy of the prostate (TRUS-BP) have become an important challenge in healthcare settings globally, questioning the continued utility of FQ as the preferred prophylactic agent. This study aimed to characterize molecular mechanisms of resistance on FQs-R E. coli isolated from the enteric microbiota of patients undergoing (TRUS-BP) and to highlight their impact on Minimum Inhibitory Concentrations (MICs). From February 2016 to December 2018, the incidence of rectal carriage of Qs-FQs resistant Enterobacterales detected from rectal swabs of patients before undergoing (TRUS-BP) was 61.06% (80/131) all related to E. coli species. Based on the MICs range of Qs (24–256 mg/L) and FQs (0.24–128 mg/L) breakpoint by EUCAST, we categorized these E. coli isolates into three resistance profiles (I, II, and III) associated with the patterns of chromosomal mutations in the quinolone resistance-determining regions (QRDRs) of gyrA and parC and the plasmid-mediated quinolone resistance encoding genes (PMQRs) detected by PCR-based assay and sequencing; MICs increase in an escalation step according to the co-occurrence of multiple molecular mechanisms. The mutation of the gyrA gene was the most frequent on codons (Ser83Leu/Thr/Tyr/Trp and Asp87Asn); mutation on the parC gene was the least on codons (Ser80Iso/Leu and Glu84 Val/Gly/Lys). PMQRs genes (4 qnrB ,7 qnrS, and one aac(6’)-Ib-cr) were determined within 15% of the isolates. Allelic variation allows us to report earliest the qnrB81 determinant in an E. coli isolate. Among isolates (35%) belonged to the notorious ST131 lineage. The phylogenetic group showed a predominance of B2 group (51, 25%), however (PFGE) revealed a high level of clonal variability. Worrying incidence of FQs-R E. coli isolates in the rectal flora of our local population showed the potential to cause post-infection. FQ resistance is a complex interplay between mutations in the QRDRs and PMQR determinants that impact MICs. The importance of intestinal microbiota as a reservoir of resistant strains and pandemic clones encourages driving mitigation challenges to characterize molecular mechanisms of antimicrobial resistance to adapt prophylactic therapy, control infection, and ensure epidemiological monitoring. [ABSTRACT FROM AUTHOR]