Fluoroquinolone resistance determinants in carbapenem-resistant Escherichia coli isolated from urine clinical samples in Thailand

Abstract

Background Escherichia coli is the most common cause of urinary tract infections and has fluoroquinolone (FQ)-resistant strains, which are a worldwide concern. Objectives To characterize FQ-resistant determinants among 103 carbapenem-resistant E. coli (CREc) urinary isolates using WGS. Methods Antimicrobial susceptibility, biofilm formation, and short-read sequencing were applied to these isolates. Complete genome sequencing of five CREcs was conducted using short- and long-read platforms. Results ST410 (50.49%) was the predominant ST, followed by ST405 (12.62%) and ST361 (11.65%). Clermont phylogroup C (54.37%) was the most frequent. The genes NDM-5 (74.76%) and CTX-M-15 (71.84%) were the most identified. Most CREcs were resistant to ciprofloxacin (97.09%) and levofloxacin (94.17%), whereas their resistance rate to nitrofurantoin was 33.98%. Frequently, the gene aac(6′)-Ib (57.28%) was found and the coexistence of aac(6′)-Ib and blaCTX-M-15 was the most widely predominant. All isolates carried the gyrA mutants of S83L and D87N. In 12.62% of the isolates, the coexistence was detected of gyrA, gyrB, parC, and parE mutations. Furthermore, the five urinary CREc-complete genomes revealed that blaNDM-5 or blaNDM-3 were located on two plasmid Inc types, comprising IncFI (60%, 3/5) and IncFI/IncQ (40%, 2/5). In addition, both plasmid types carried other resistance genes, such as blaOXA-1, blaCTX-M-15, blaTEM-1B, and aac(6′)-Ib. Notably, the IncFI plasmid in one isolate carried three copies of the blaNDM-5 gene. Conclusions This study showed FQ-resistant determinants in urinary CREc isolates that could be a warning sign to adopt efficient strategies or new control policies to prevent further spread and to help in monitoring this microorganism.

SWOT and Root Cause Analyses of Antimicrobial Resistance to Oral Antimicrobial Treatment of Cystitis

“…Intriguingly, a third of patients with a resistant isolate did not have any documented risk factors for resistance [38]. Given that uropathogens endowed with specific virulence factors are also evidently surviving in hyperosmotic urine [17,18], it is likely that prior exposure to antibiotics give rise to microbial colonies with stimulated biochemical mechanisms that not only confers virulence but also predisposes to AMR [19,21] development.…”

“…Uropathogens exposed to below-MIC levels in urine bestow The infection of the urothelium can only occur after uropathogens successfully compete for available nutrients with the commensal microbiome [13] by employing mechanisms of commensalism [14], mutualism, and parasitism [15,16]. Many groups have suggested that the biochemical mechanisms driving the adaptability of uropathogens in the variable pH and osmolality of urine [17,18] are as dogged as the signaling pathways driving the gain of virulence [19][20][21] and antimicrobial resistance (AMR) [22]. From a clinical perspective, AMR refers to a microbial phenotype capable of surviving the exposure to a drug treatment course at a concentration anticipated to prevent its survival [20].…”

Emerging Trends in Quinolone Resistance among Urinary Pathogens: A Brief Review

“…These findings highlight the urgency for efficient strategies and control policies to mitigate the spread of fluoroquinolone-resistant CREc strains, offering valuable insights for ongoing efforts in monitoring and combating antimicrobial resistance. [23] The resistance patterns among Enterobacteriaceae isolated from urinary tract infections (UTIs) exhibited High rates of quinolone resistance among ESBL-producing isolates highlighting the increasing challenge of antibiotic resistance in this clinical context. The identification of PMQR genes, notably aac(6′)-Ibcr, in a significant proportion of samples, adds complexity to the resistance landscape.…”

The Impact of Urinary Catheterization on the Antibiotic Susceptibility of ESBL-Producing Enterobacterales: A Challenging Duo

“…ESBLs, typically encoded on plasmids, confer resistance to a broad spectrum of antibiotics, including most penicillins, cephalosporins, and aztreonam, through their enzymatic hydrolysis [2]. Additionally, while ESBLs do not directly deactivate non-beta-lactam agents, microorganisms carrying ESBLs often harbor genes that confer resistance to other antibiotics such as ciprofloxacin, gentamicin, or trimethoprim-sulfamethoxazole [3,4].…”