Explore the vast range of titles available.

Previous studies have reported the occurrence of transferable quinolone resistance determinants in environmental Escherichia coli . However, little is known about their vectors and genetic contexts. To gain insights into these genetic characteristics, we analyzed the complete genomes of 53 environmental E. coli isolates containing one or more transferable quinolone resistance determinants, including 20 sequenced in this study and 33 sourced from RefSeq. The studied genomes carried the following transferable quinolone resistance determinants alone or in combination: aac(6′)-Ib-cr , oqxAB , qepA1 , qnrA1 , qnrB4 , qnrB7 , qnrB19 , qnrD1 , qnrS1 , and qnrS2 , with qnrS1 being predominant. These resistance genes were detected on plasmids of diverse replicon types; however, aac(6′)-Ib-cr , qnrS1 , and qnrS2 were also detected on the chromosome. The genetic contexts surrounding these genes included not only those found in clinical isolates but also novel contexts, such as qnrD1 embedded within a composite transposon-like structure bounded by Tn 3 -derived inverted-repeat miniature elements (TIMEs). This study provides deep insights into mobile genetic elements associated with transferable quinolone resistance determinants, highlighting the importance of genomic surveillance of antimicrobial-resistant bacteria in the environment.

Background Fluoroquinolones are commonly recommended as treatment for urinary tract infections (UTIs). The development of resistance to these agents, particularly in gram-negative microorganisms complicates treatment of infections caused by these organisms. This study aimed to investigate antimicrobial resistance of different Enterobacteriaceae species isolated from hospital- acquired and community-acquired UTIs against fluoroquinolones and correlate its levels with the existing genetic mechanisms of resistance. Methods A total of 440 Enterobacteriaceae isolates recovered from UTIs were tested for antimicrobial susceptibility. Plasmid-mediated quinolone resistance (PMQR) genes and mutations in the quinolone resistance-determining regions (QRDRs) of gyrA and parC genes were examined in quinolone-resistant strains. Results About (32.5%) of isolates were resistant to quinolones and (20.5%) were resistant to fluoroquinolones. All isolates with high and intermediate resistance phenotypes harbored one or more PMQR genes. Q nrB was the most frequent gene (62.9%) of resistant isolates. Co-carriage of 2 PMQR genes was detected in isolates (46.9%) with high resistance to ciprofloxacin (CIP) (MICs > 128 μg/mL), while co-carriage of 3 PMQR genes was detected in (6.3%) of resistant isolates (MICs > 512 μg/mL). Carriage of one gene only was detected in intermediate resistance isolates (MICs of CIP = 1.5–2 μg/mL). Neither qnrA nor qnrC genes were detected. The mutation at code 83 of gyrA was the most frequent followed by Ser80-Ile in p arC gene, while Asp-87 Asn mutation of gyr A gene was the least, where it was detected only in high resistant E. coli isolates (MIC ≥128 μg/mL). A double mutation in gyrA (Lys154Arg and Ser171Ala) was observed in high FQs resistant isolates (MIC of CIP < 128 μg/mL). Conclusion FQs resistance is caused by interact between PMQR genes and mutations in both gyrA and parC genes while a mutation in one gene only can explain quinolone resistance. Accumulation of PMQR genes and QRDR mutations confers high resistance to FQs.

Fluoroquinolone-resistant is considered a serious public health problem and has been put on the WHO global priority list of antibiotic-resistant bacteria. This study was aimed to investigate the fluoroquinolone resistance in and its relevant genetic mechanisms. isolates that were isolated from diarrheal patient's feces in Ningbo China from 2011 to 2018 were tested for susceptibility to ampicillin, gentamicin, tetracycline, nalidixic acid, ciprofloxacin, and cefotaxime. Genes related to quinolone resistance were amplified by PCR. A total of 118 isolates were collected, including 76 isolates, 40 isolates, and 2 isolates. Ciprofloxacin susceptibility test identified 10 (9%) susceptible, 65 (55%) intermediate, and 43 (36%) resistant isolates. Of 76 isolates, 37 were ciprofloxacin resistant, a prevalence significantly higher than 6 of 40 isolates ( =0.01). The isolates collected during 2014-2018 displayed a significant increase in the prevalence of ciprofloxacin resistance ( =0.05) than those collected during 2011-2013. All the ciprofloxacin-intermediate and resistant isolates had mutations of (S83L) and (S80I), whereas only the ciprofloxacin-resistant isolates had (D87N) mutation and gene. Additionally, 30% of the ciprofloxacin-resistant isolates were positive for gene. This study shows the currently increasing prevalence of ciprofloxacin resistance. The reduced fluoroquinolone susceptibility is highly associated with (S83L) and (S80I) mutations, while the fluoroquinolone resistance is highly associated with (D87N) mutation, gene and perhaps gene.

Background Transferrable mechanisms of quinolone resistance (TMQR) can lead to fluoroquinolone non-susceptibility in addition to chromosomal mechanisms. Some evidence suggests that fluoroquinolone resistance is increasing among the pediatric population. We sought to determine the occurrence of TMQR genes among quinolone-resistant E. coli and K. pneumoniae causing urinary tract infections among Nepalese outpatient children (< 18 years) and identify molecular characteristics of TMQR-harboring isolates. Methods We performed antimicrobial susceptibility testing, phenotypic extended-spectrum β-lactamase (ESBL) and modified carbapenem inactivation method tests, and investigated the presence of six TMQR genes ( qnrA , qnrB , qnrS , aac(6’)-Ib-cr , oqxAB, qepA ), three ESBL genes ( bla CTX−M , bla TEM , bla SHV ), and five carbapenemase genes ( bla NDM , bla OXA−48 , bla KPC , bla IMP , bla VIM ). The quinolone resistance-determining region (QRDR) of gyrA and parC were sequenced for 35 TMQR-positive isolates. Results A total of 74/147 (50.3%) isolates were TMQR positive by multiplex PCR [ aac(6’)-Ib-cr in 48 (32.7%), qnrB in 23 (15.7%), qnrS in 18 (12.3%), qnrA in 1 (0.7%), and oqxAB in 1 (0.7%) isolate]. The median ciprofloxacin minimum inhibitory concentration of TMQR-positive isolates (64 µg/mL) was two-fold higher than those without TMQR (32 µg/mL) (p = 0.004). Ser-83→Leu and Asp-87→Asn in GyrA and Ser-80→Ile in ParC were the most common QRDR mutations (23 of 35). In addition, there was a statistically significant association between TMQR and two β-lactamase genes; bla CTX−M (p = 0.037) and bla TEM (p = 0.000). Conclusion This study suggests a high prevalence of TMQR among the quinolone-resistant E. coli and K. pneumoniae isolates causing urinary tract infection in children in this area of Nepal and an association with the carriage of ESBL gene. This is a challenge for the management of urinary infections in children. Comprehensive prospective surveillance of antimicrobial resistance in these common pathogens will be necessary to devise strategies to mitigate the emergence of further resistance.

Actinobacillus pleuropneumoniae is a pathogen that infects pigs and poses a serious threat to the pig industry. The emergence of quinolone-resistant strains of A.pleuropneumoniae further limits the choice of treatment. However, the mechanisms behind quinolone resistance in A.pleuropneumoniae remain unclear. The genomes of a ciprofloxacin-resistant strain, A. pleuropneumoniae SC1810 and its isogenic drug-sensitive counterpart were sequenced and analyzed using various bioinformatics tools, revealing 559 differentially expressed genes. The biological membrane, plasmid-mediated quinolone resistance genes and quinolone resistance-determining region were detected. Upregulated expression of efflux pump genes led to ciprofloxacin resistance. The expression of two porins, OmpP2B and LamB, was significantly downregulated in the mutant. Three nonsynonymous mutations in the mutant strain disrupted the water–metal ion bridge, subsequently reducing the affinity of the quinolone–enzyme complex for metal ions and leading to cross-resistance to multiple quinolones. The mechanism of quinolone resistance in A. pleuropneumoniae may involve inhibition of expression of the outer membrane protein genes ompP2B and lamB to decrease drug influx, overexpression of AcrB in the efflux pump to enhance its drug-pumping ability, and mutation in the quinolone resistance-determining region to weaken the binding of the remaining drugs. These findings will provide new potential targets for treatment.

Non-typhoidal salmonellosis remains a pressing public health problem worldwide. Quinolones, particularly fluoroquinolones, are widely used to treat various infections, including non-typhoidal salmonellosis, which can be a serious illness. The emergence of fluoroquinolone-resistant Salmonella has resulted in treatment failure and high mortality rates. In this study, we estimated the presence of plasmid-mediated quinolone resistance (PMQR) genes in Salmonella enterica isolated from human salmonellosis patients in South Korea from 2016 to 2019. We evaluated the association of these genes with fluoroquinolone susceptibility. Antimicrobial susceptibility tests for Salmonella isolates were performed using the Vitek II system, and the minimum inhibitory concentrations (MIC) of ciprofloxacin and levofloxacin were determined using the E-test method. Plasmid-mediated quinolone resistance (PMQR) genes were detected by PCR amplification and quinolone resistance-determining regions (QRDRs) of the gyrA and parC genes were analyzed following Sanger sequencing of the PCR products. Thirty-four Salmonella strains with reduced susceptibility to fluoroquinolones (ciprofloxacin MIC ≥ 0.125 µg/mL and levofloxacin MIC ≥ 0.25 µg/mL) were selected from 208 human clinical Salmonella isolates. Among them, 22 Salmonella strains harbored one PMQR gene ( qnrA , qnrB , or qnrS ), and three Salmonella strains carried two PMQR genes ( qnrS and aac(6′)-Ib-cr or qnrA and qnrB ). qnrS was the most common PMQR gene. Serotyping revealed that Salmonella 4,[5]12:i:- (32.4%, 11/34) and Salmonella Typhimurium (29.4%, 10/34) were the two most predominant serovars, and Multi-locus sequence typing (MLST) showed that ST19 and ST34 were the most frequent sequence types. In conclusion, qnr gene-positive Salmonella 4,[5],12:i:- and Salmonella Typhimurium were the main serovars responsible for reduced susceptibility to fluoroquinolones. Therefore, our findings suggest that PMQR-positive Salmonella strains, which can be isolated from various samples including human, food, and the environment, should be carefully monitored.

Quinolone resistance in bacterial pathogens has primarily been associated with mutations in the quinolone resistance-determining regions (QRDRs) of bacterial type-II topoisomerases, which are DNA gyrase and topoisomerase IV. Depending on the position and type of the mutation (s) in the QRDRs, bacteria either become partially or completely resistant to quinolone. QRDR mutations have been identified and characterized in Salmonella enterica isolates from around the globe, particularly during the last decade, and efforts have been made to understand the propensity of different serovars to carry such mutations. Because there is currently no thorough analysis of the available literature on QRDR mutations in different Salmonella serovars, this review aims to provide a comprehensive picture of the mutational diversity in QRDRs of Salmonella serovars, summarizing the literature related to both typhoidal and non-typhoidal Salmonella serovars with a special emphasis on recent findings. This review will also discuss plasmid-mediated quinolone-resistance determinants with respect to their additive or synergistic contributions with QRDR mutations in imparting elevated quinolone resistance. Finally, the review will assess the contribution of membrane transporter-mediated quinolone efflux to quinolone resistance in strains carrying QRDR mutations. This information should be helpful to guide the routine surveillance of foodborne Salmonella serovars, especially with respect to their spread across countries, as well as to improve laboratory diagnosis of quinolone-resistant Salmonella strains.

The aim of this study was to determinate the prevalence of in retail foods and its resistance to quinolones in retail foods in Lanzhou, People's Republic of China. In this work, 2,182 food samples, collected from March 2015 to December 2018, were analyzed to detect and then analyzed for serotype distribution, quinolone resistance, and quinolone-resistant gene detection. The findings demonstrate that the overall prevalence of in these food categories was low. A total of 41 (1.9%) of 2,182 food samples were found to be positive for . Ten distinct serovars were identified, and Derby, Anatum, and Enteritidis were the most prevalent serovars. According to the broth microdilution test, the resistance percentages were 90.2% to nalidixic acid, 39.0% to enrofloxacin, 41.5% to ciprofloxacin, 29.3% to ofloxacin, and 26.8% to levofloxacin. Among the quinolone-resistant isolates, 12 strains had a single mutation in at codon 83 (Ser→Phe) or codon 87 (Asp→Asn or Asp→Gly). Five isolates had one mutation (Ser80→Arg) and one or two hot spot mutations. genes were found in seven isolates (five and two ), and the gene in seven isolates. Two isolates carry both and genes. Based on these results, a low prevalence of contamination in retail foods was found, but it might play a potential risk factor in the spread of quinolone-resistant strains in the Lanzhou region.

is an important pathogenic bacterium in causing urinary tract infection. With the overuse of antibiotics, bacteria resistant to quinolones combined with carbapenems are increasing. In this study, we investigated the epidemiology, molecular characteristics, drug resistance of multidrug-resistant ( ) isolated from urine samples. It provides theoretical basis for the treatment of urinary tract infection by clinicians. Fifty-one strains of were obtained from urine samples collected between 2012 and 2017 in total. All the strains are multi-drug resistant bacteria. This paper used multilocus sequence typing (MLST) to determine molecular epidemiological typing. We performed antimicrobial susceptibility testing and investigated quinolones and carbapenems resistance genes. The strains which we collected were resistant to ciprofloxacin and Levofloxacin. In an epidemiological analysis using MLST, 86.27% (44/51) of isolates were confirmed to be ST11. The main carbapenem resistance gene was KPC-19, 78.43(40/51). Among the quinolone resistance genes, the major resistance genes were aac(6')-Ib-cr, oqxA and oqxB. The main molecular epidemiological types we detected was ST11. The main resistance gene of carbapenems was KPC-19. The quinolone resistance genes are mainly . The experimental results can help control the use of quinolones and carbapenems, and we could provide rational drug use basis for clinicians to treat urinary tract infection. For , a combination of multiple antibiotics is necessary.

Background & objectives: Infection from fluoroquinolone-resistant extra-intestinal Escherichia coli is a global concern. In this study, isolation and characterization of fluoroquinolone-resistant extra-intestinal E. coli isolates obtained from hospital samples were undertaken to detect plasmid-mediated quinolone resistance (PMQR) genes. Methods: Forty three isolates of E. coli obtained from patients with extra-intestinal infections were subjected to antibiogram to detect fluoroquinolone resistance. The mechanism of fluoroquinolone resistance was determined by the detection of PMQR genes and mutations in quinolone resistance determining region (QRDR). Results: Of the 43 isolates, 36 were resistant to nalidixic acid (83.72%) and 28 to ciprofloxacin (65.11%). Eight E. coli isolates showed total resistance to both the antimicrobials without any minimum inhibitory concentration. The detection of PMQR genes with qnr primers showed the presence of qnrA in two, qnrB in six and qnrS in 21 isolates. The gene coding for quinolone efflux pump (qepA) was not detected in any of the isolates tested. The presence of some unexpressed PMQR genes in fluoroquinolone sensitive isolates was also observed. Interpretation & conclusions: The detection of silent PMQR genes as observed in the present study presents a risk of the transfer of the silent resistance genes to other microorganisms if present in conjugative plasmids, thus posing a therapeutic challenge to the physicians. Hence, frequent monitoring is to be done for all resistance determinants.