Detection of qnr genes and gyrA mutation to quinolone phenotypic resistance of UTI pathogens in Bangladesh and the implications

Background: Plasmid-mediated quinolone-resistant (PMQR) genes and mutations within the quinolone resistance determining regions (QRDRs) resulted in the advent of quinolone-resistant pathogenic microbes. This research was designed to assess the roles of three PMQR genes, qnrA, qnrB, and qnrS, and any mutation in the gyrA gene in the QRDR as a process of quinolone/fluoroquinolone resistance to urinary tract infection (UTI) bacteria in Bangladesh to guide future management of UTIs. Methods: Pathogens from UTIs were isolated and identified, and their phenotype antibiotic susceptibilities were tested for lomefloxacin, ofloxacin, ciprofloxacin, and nalidixic acid. Polymerase chain reaction (PCR) detected the qnrA, qnrB, and qnrS genes. PCR and sequencing were performed to evaluate any mutation within the QRDRs of the gyrA gene. Results: Of 100 UTI bacteria, phenotypic resistance was observed in 95.0%, 89.0%, 83.0%, and 71.0% against lomefloxacin, nalidixic acid, ofloxacin, and ciprofloxacin, respectively. PMQR genes qnrS, qnrA, and qnrB genes were found in 54.0%, 1.0%, and 4.0% of isolates, respectively. Sequencing the gyrA gene revealed single mutation (Ser-83 to Leu) and double mutations (Ser-83 to Leu and Asp-87 to Asn). PMQR genes showed a statistically nonsignificant association with phenotypic resistance. Conclusions: This study confirms the presence of QRDR mutations that were independent of PMQR genes. Consequently, high resistance against quinolones among uropathogens is evident, and their future use needs to be moderated

Detection of mobile colistin-resistance gene variants (mcr-1 and mcr-2) in urinary tract pathogens in Bangladesh: the last resort of infectious disease management colistin efficacy is under threat

Background: Currently, colistin-resistant pathogens emerged has become a global health concern. This study assessed the distribution of mcr-1 to mcr-5 variants with the phenotypic colistin-resistance in bacterial isolates from urinary tract infection (UTI) patients in Bangladesh. Methods: A cross-sectional study was conducted between April 2017 and March 2018 to enroll uncomplicated UTI patients, and 142 urine samples were analyzed. Uropathogens were identified using the API-20E biochemical panel and 16s rRNA gene sequencing. Polymerase chain reactions detected the mcr gene variants in the UTI isolates. The phenotypic colistin-susceptibility was determined by the Kirby–Bauer disc-diffusion method and the minimal inhibitory concentration (MIC) measurement. Results: The combined carriage of mcr-1 and mcr-2 genes in 11.4% (14/123) of urinary tract pathogens. The mcr-positive pathogens include five Escherichia coli, three Klebsiella pneumoniae, three Pseudomonas putida, two Enterobacter cloacae, and one Enterobacter hormaechei. The mcr-positive variant showed significantly higher phenotypic colistin resistance with MIC between >16 μg/mL and >128 μg/mL (p< 0.001). Over 85% of colistin-resistant isolates showed MDR phenomena. Conclusions: The emergence of the clinical MDR pathogens with resistance to a highly selective drug may lead to a lack of treatment options for the infectious diseases and spread of infection to the unaffected cohorts

Detection of qnr genes and gyrA mutation to quinolone phenotypic resistance of UTI pathogens in Bangladesh and the implications : resistance UTI pathogens Bangladesh

Background: Plasmid-mediated quinolone resistance (PMQR) genes and mutations within the quin-olone resistance-determining regions (QRDRs) bequeath to the advent of quinolone-resistant path-ogenic microbes. This research was designed to assess the roles of three PMQR genes, qnrA, qnrB, and qnrS, and any mutation in the gyrA gene in the QRDR region as a process of quino-lone/fluoroquinolone resistance to urinary tract infection (UTI) bacteria in Bangladesh to guide fu-ture management of UTIs. Methods: Pathogens from UTIs were isolated and identified, and their phenotype antibiotic susceptibilities were tested for lomefloxacin, ofloxacin, ciprofloxacin, and na-lidixic acid. Polymerase chain reaction (PCR) detected the qnrA, qnrB, and qnrS genes. PCR and se-quencing were performed to evaluate any mutation within the QRDRs of the gyrA gene. Results: Of 100 UTI bacteria, phenotypic resistance was observed in 95.0%, 89.0%, 83.0%, and 71.0% against lomefloxacin, nalidixic acid, ofloxacin, and ciprofloxacin, respectively. PMQR genes: qnrS, qnrA, and qnrB genes were found in 54.0%, 1.0%, and 4.0% of isolates, respectively. Sequencing the gyrA gene revealed single mutation (Ser-83 to Leu) and double mutations (Ser-83 to Leu and Asp-87 to Asn). PMQR genes showed a statistically non-significant association with phenotypic resistance. Conclu-sions: This study confirms the presence of QRDR mutations that were independent of PMQR quino-lone resistance genes. Consequently, high resistance against quinolones among uropathogens is ev-ident, and their future use needs to be moderated