Prevalence Of Quinolone Resistance Research Articles

Study of Plasmid-Mediated Quinolone Resistance in Klebsiella pneumoniae: Relation to Extended-Spectrum Beta-Lactamases

Klebsiella pneumoniae (K. pneumoniae) is an important pathogen associated with various infections. The emergence of antibiotic resistances, such as quinolone resistance and those due to extended-spectrum beta-lactamases (ESBL), reduces the available choices for treatment. The objectives of the current study include the evaluation of the prevalence of the plasmid-mediated quinolone resistance genes qepA, acrA, acrB, and aac(6’)-Ib-cr by polymerase chain reaction (PCR) in K. pneumoniae and the determination of the mechanism relating these genes to the ESBL phenotype and resistance to other groups of antibiotics. In total, 300 clinical isolates of K. pneumoniae were included in the study. Isolates were subjected to antibiotic sensitivity tests using the disc diffusion method. Quinolone resistance by the minimum inhibitory concentration method and detection of ESBL resistance by the double disc diffusion method were also determined. PCR analyses revealed the prevalence of acrA, aac(6’)-Ib-cr, acrB, and qepA in 74.3%, 73.7%, 71%, and 6.7% of the isolates, respectively. Quinolone-resistant isolates positive for plasmid-encoded genes represented 82.7% of K. pneumoniae isolates positive for ESBL activity. The results also showed that the isolates of K. pneumoniae carrying plasmid-encoded quinolone resistance genes had significantly increased resistance to amikacin, amoxicillin/clavulanate, gentamicin, and cefoxitin than those isolates without quinolone resistance genes. Therefore, there was a high prevalence of acrA, acrB, and aac(6’)-Ib-cr among K. pneumoniae and the prevalence of quinolone resistance was significantly associated with the ESBL resistance phenotype. Moreover, the presence of quinolone resistance genes was associated with resistance to aminoglycosides, namely amikacin and gentamicin.

Characterization of plasmid-mediated qnrA and qnrB genes among Enterobacteriaceae strains: quinolone resistance and ESBL production in Ismailia, Egypt

BackgroundPlasmid-mediated quinolone resistance genes (PMQR) are mainly associated with clinical isolates of Enterobacteriaceae and complicate treatment of infections caused by these isolates worldwide. Extended-spectrum-beta-lactamase (ESBL)-producing bacteria are resistant to common antibiotics and also through many mechanisms, ESBL could be disabling other types of antibiotics. This study aimed to assess the prevalence of quinolone resistance and ESBL among Enterobacteriaceae strains and investigated the presence of qnrA and qnrB genes in these strains which were isolated from urinary tract infections in Ismailia, Egypt. Ninety-four Enterobacteriaceae isolates were collected from cases of UTIs admitted to the intensive care unit, Suez-Canal University Hospitals, between October 2017 and January 2018. Antibacterial susceptibility was determined by the disk diffusion method. A polymerase chain reaction assay was used to detect qnrA and qnrB resistance genes in quinolone- and fluoroquinolone-resistant and ESBL strains. Also, ciprofloxacin MIC was determined by the agar dilution method.ResultsResistance rates were 59.6%, 54.3%, 53.2%, 53.2%, and 53.2% to NA, LEV, NOR, CIP, and FX, respectively. Of 56 NA-resistant isolates, 7 (12.5%) and 6 (10.7%) were positive for qnrA and qnrB, respectively, with only one isolate co-harboring both genes. ESBL-producing bacteria was 66.2% of isolates. The MICs for ciprofloxacin ranged from 32–256 μg/ml in ciprofloxacin-resistant isolates.ConclusionOur study shows high resistance rates of Enterobacteriaceae to quinolones and ESBL in our hospital which necessitate appropriate use of these antibiotics to reserve their application for therapy. The prevalence of quinolone-resistant and ESBL-producing Enterobacteriaceae was approximately 60% and 70% respectively.

Prevalence of Plasmid-Mediated Quinolone Resistance in Multidrug-Resistant Gram Negative Bacilli in Egypt

Resistance to quinolone has increased significantly and one of the most reasons is plasmid-mediated quinolone resistance (PMQR). The aim of this study is to detect the prevalence of PMQR in multidrug-resistant (MDR) Gram negative bacilli and to characterize these resistance genes. A total of 420 Gram negative bacilli clinical isolates were collected from patients attending Misr children hospital. Isolates were identified by biochemical reactions, while antimicrobial susceptibility testingwas done by Kirby-Bauer disk diffusion method. Minimum inhibitory concentrations (MIC) of ciprofloxacin were detected by E-test, whereas combined test method was used to detect extended-spectrum β-lactamase (ESBL) production. QnrA, qnrB, and qnrS genes were determined by multiplex polymerase chain reaction (PCR). MDRGram negative bacilli represented 68% (268/420); most of them were recovered from blood culture specimens (21%).Among these MDR isolates21%(60/268) were ciprofloxacin resistant; with MICs >32µg/ml in 95% of the isolates.ESBL production was detected in 11.7% of the studied isolates. The qnr genes were detected in 60%. QnrS and qnrB were the detected genes in 77.8% and 16.7% of the isolates respectively. Both qnrB and qnrS genes were determined simultaneously in 5.5%.QnrB gene was found alone in only one isolate (14.3%) that was ESBL-producer. The most MDR isolates were recovered from blood culture; this confirms the occurrence of these superbugs and their ability to cause life threatening infections. The prevalence of quinolone resistant Gram negative bacilli clinical isolates is high. The mostly prevalent PMQR gene is qnrS followed by qnrB.

Prevalence of Quinolone Resistance in Enterobacteriaceae from Sierra Leone and the Detection of qnrB Pseudogenes and Modified LexA Binding Sites.

A collection of 74 Enterobacteriaceae isolates found in Bo, Sierra Leone, were tested for quinolone antibiotic susceptibility and resistance mechanisms. The majority of isolates (62%) were resistant to quinolones, and 61% harbored chromosomal gyrA and/or parC mutations. Plasmid-mediated quinolone resistance genes were ubiquitous, with qnrB and aac(6')-Ib-cr being the most prevalent. Mutated LexA binding sites were found in all qnrB1 genes, and truncated qnrB pseudogenes were found in the majority of Citrobacter isolates.

Carriage of Class 1 and 2 Integrons in Quinolone, Extended-Spectrum-β-Lactamase-Producing and Multi Drug Resistant E.coli and K.pneumoniae: High Burden of Antibiotic Resistance.

The study aimed at assessing any association between quinolone resistance, MDR and ESBL production and their relation with the presence of integrons in Esherichia coli and Klebsiella pneumoniae. E.coli and K.pneumoniae isolated from various clinical infections were fully identified and analyzed for being quinolone resistant. These isolates were further tested for ESBL production, multi drug resistance and carriage of integrons. In total, 135 isolates were confirmed as quinolone resistant. K.pneumoniae was observed as potent ESBL producer in comparison to E.coli. Ciprofloxacin resistance in both organisms was related significantly with the presence of integron class 1, co-presence of class 1 and 2 as well as to the presence of ESBL production (p< 0.001). However, nalidixic acid resistance was related significantly (p< 0.01) with only integron class 1 and to the presence of ESBL production. Class 1 and 2 integrons were found in 73.5% of MDR isolates with 13.2% of them possessing both intI1 and intI2 genes. Prevalence of quinolone resistance together with ESBL production and MDR in E.coli and K.pneumoniae has contributed to the emergence of antibacterial resistance burden. The higher integron prevalence in our isolates advocates the potentiality of these isolates as a source for dissemination of resistance determinants.

Prevalence of Antibiotic-Resistant Bacteria on Rectal Swabs and Factors Affecting Resistance to Antibiotics in Patients Undergoing Prostate Biopsy

PurposeThe prevalence of antibiotic-resistant bacteria on rectal swabs in patients undergoing transrectal ultrasound (TRUS)-guided prostate biopsy and the factors affecting resistance to antibiotics were evaluated.Materials and MethodsTwo hundred twenty-three men who underwent TRUS-guided prostate biopsy from November 2011 to December 2012 were retrospectively evaluated. Rectal swabs were cultured on MacConkey agar to identify antibiotic-resistant bacteria in rectal flora before TRUS-guided prostate biopsy. All patients were admitted and received intravenous antibiotics before prostate biopsy. Clinical variables including underlying disease, infectious complications, and antibiotics associated with resistance were evaluated. Logistic regression was used to determine the factors influencing antibiotic resistance.ResultsOf the 233 patients, 161 had positive rectal cultures. Escherichia coli was cultured in 130 (80.7%) and Klebsiella pneumonia in 16 (9.9%). The prevalence of quinolone resistance was 16.8% and the prevalence of extended-spectrum beta-lactamase (ESBL) positivity was 9.3%. A previous history of prostatitis was correlated with quinolone resistance and ESBL positivity (both p=0.001). The factors affecting quinolone resistance in the univariate analysis were a previous history of prostatitis (p=0.003) and previous exposure to antibiotics (p=0.040). Only a previous history of prostatitis was statistically significant in the multivariate analysis (p=0.014). Four patients had infectious complications.ConclusionsThe prevalence of quinolone resistance was 16.8% in rectal swabs performed before TRUS-guided prostate biopsy. A previous history of prostatitis was influential. In patients with a history of prostatitis, selection of prophylactic antibiotics before the biopsy may be reconsidered.

Prevalence of quinolone resistance and mutations in the topoisomerase genes in Salmonella enterica serotype Enteritidis isolates from Serbia

The prevalence of quinolone resistance was studied in Salmonella enterica serotype Enteritidis isolates collected during 2005–2010 in Southern Bačka County, Serbia. A total of 878 clinical isolates were examined, among which 19 (2.2%) nalidixic acid (NAL)-resistant S. Enteritidis were detected by selection on agar plates containing 64mg/L NAL. Antimicrobial susceptibility of the isolates was tested by the agar dilution method. According to Clinical and Laboratory Standards Institute (CLSI) breakpoints, ciprofloxacin (CIP) resistance was not present in the strains. Multiple drug resistance was rare, and resistance to NAL was most often present as a single resistance property. All but one NAL-resistant S. Enteritidis showed reduced susceptibility to CIP [i.e. minimum inhibitory concentration (MIC)≥0.125mg/L]. This isolate of human origin had a CIP MIC of 0.064mg/L and DNA sequencing revealed that it contained an Asp87Gly gyrA mutation. Most of the remaining isolates had MICs for NAL and CIP of 256mg/L and 0.256mg/L, respectively. Mutations in the Asp87 codon resulted in substitutions to Asn in most of the isolates, but Asp87Gly and Ser83Phe exchanges were also detected. No mutations were present in the gyrB, parC or parE genes. Although CIP resistance was absent, reduced susceptibility characterised by mutations in gyrA was apparent among S. Enteritidis isolates from Serbia.

Antimicrobial resistance in non-typhi Salmonella enterica isolated from humans and poultry in Palestine

The efficacy of chemotherapy can be compromised by drug resistance.This study was undertaken to describe the resistance profiles and fluoroquinolone resistance mechanism of non-typhoidal Salmonella (NTS) isolated from humans and poultry in West Bank, Palestine. One hundred and fifty-one isolates of NTS, obtained from humans (71) and poultry (80), collected between September 2005 and January 2007, were tested for susceptibility to ampicillin, gentamicin, tetracycline ceftriaxone, nalidixic acid and ciprofloxacin. Mutation patterns within gyrA were determined by direct sequencing or by digestion of PCR-amplified DNA fragments with the restriction enzyme HinfI. Resistance rates among human and poultry isolates were respectively 59% and 51% for ampicillin, 31% and 10% for gentamicin, 59% and 80% for tetracycline, 59% and 45% for nalidixic acid, and 30% and 15% for ciprofloxacin. All the isolates were susceptible to ceftriaxone. Mutations at positions 83 and/or 87 were detected in gyrA of isolates with resistance to nalidixic acid. Isolates which were resistant to nalidixic acid but susceptible to ciprofloxacin had a single gyr A gene mutation at point 87.This gene mutation was sufficient to induce a new phenotype (6 isolates) with decreased susceptibility to ciprofloxacin. Mutations in gyrA at positions 83 or 87 were the most prevalent mutation pattern of fluoroquinolone resistant NTS isolates but other unknown mechanisms are also present. Continued surveillance of antimicrobial resistance among NTS isolates is needed to mitigate the increasing prevalence of quinolone resistance.

Will a Reduction in Community Prescribing of Quinolones Decrease the Prevalence of Quinolone Resistance?

Will a Reduction in Community Prescribing of Quinolones Decrease the Prevalence of Quinolone Resistance?

Prevalence of qnr genes in Salmonella in France

To detect the qnrA, qnrB and qnrS genes among Salmonella isolates received at the French National Reference Centre for Salmonella in Paris, France. Antibiotic susceptibility was determined by disc diffusion for 499 Salmonella isolates including 320 Salmonella Typhimurium, 100 Salmonella Enteritidis and 79 Salmonella Hadar collected in 2002. Amplification with specific primers of qnrA, qnrB and qnrS genes was performed for all Salmonella Typhimurium, Salmonella Enteritidis and Salmonella Hadar isolates resistant to quinolones and for 17 additional isolates that produced expanded-spectrum beta-lactamases (ESBLs). Prevalence of quinolone resistance was 3.75%, 11% and 79.7% for Salmonella Typhimurium, Salmonella Enteritidis and Salmonella Hadar serovars, respectively. A single isolate (0.2%) was qnrA-positive (QnrA1 determinant) being a Salmonella serovar Concord carrying also the ESBL gene bla(CTX-M-15). This strain was probably from East Africa. No qnrB or qnrS genes were identified. Whereas plasmid-mediated quinolone resistance of the Qnr type is emerging in Enterobacteriaceae worldwide, it remains rare in Salmonella in France.

Emergence of quinolone resistance among viridans group streptococci isolated from the oropharynx of neutropenic peripheral blood stem cell transplant patients receiving quinolone antimicrobial prophylaxis

In neutropenic patients receiving quinolone prophylaxis, bacteremia with viridans group streptococci resistant to quinolones is a known complication. The frequency of occurrence of quinolone-resistant organisms colonizing the oropharynx during antibacterial prophylaxis with a quinolone is not well defined. In 48 patients undergoing hematopoietic stem cell transplantation, the prevalence of quinolone resistance in viridans group streptococci colonizing the oropharynx before and during antibacterial prophylaxis with gatifloxacin or moxifloxacin (most with concomitant penicillin) was determined. For quinolone-resistant isolates, mutations in the genes gyrA and parC, which confer resistance to quinolones, were analyzed. Seventy-four isolates before and 27 isolates during quinolone use were recovered from patients' oropharynxes. The numbers of susceptible isolates recovered before versus during quinolone use were as follows: 52 (70%) versus three (11%) for ciprofloxacin, 66 (89%) versus eight (30%) for levofloxacin, 66 (89%) versus ten (37%) for gatifloxacin, and 67 (91%) versus 11 (41%) for moxifloxacin (p<0.0001). Mutations in gyrA and/or parC were detected in quinolone-resistant isolates. Quinolone-resistant viridans group streptococci are frequently found in the oropharynx of neutropenic patients after a brief (median, 8 days) exposure to gatifloxacin or moxifloxacin.

Genetic relatedness and quinolone resistance of Campylobacter jejuni strains isolated in 2002 in Hong Kong.

Pulsed-field gel electrophoresis fingerprints of 98 Campylobacter jejuni isolates from patients (85) and chicken carcasses (13) in Hong Kong in 2002 demonstrated high genetic diversity. The prevalence of quinolone resistance among the isolates was 85.9%, and replacement of the threonine-86 residue in the gyrase subunit A was the major resistance mechanism.