# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 1260 | 0 | 0.9582 | Isolation, Identification, and Antimicrobial Susceptibilities of Bacteria from the Conjunctival Sacs of Dogs with Bacterial Conjunctivitis in Different Regions of Wuhan, China. In order to investigate the bacterial species present in the conjunctival sacs of dogs with bacterial conjunctivitis in Wuhan (Hongshan District, Wuchang District, Jiangxia District, and Huangpi District) and their resistance to aminoglycoside antibiotics, samples of conjunctival sac secretions were collected from 56 dogs with bacterial conjunctivitis in various regions of Wuhan. Drug susceptibility testing for aminoglycoside antibiotics was performed on the most commonly isolated gram-positive and gram-negative bacteria. The expression of two aminoglycoside modifying enzyme genes, aacA-aphD and aac (6')-Ib, and three 16S rRNA methyltransferase genes, rmtB, rmtE and npmA, were analyzed by PCR. The results showed that a total of 123 bacterial strains were cultured from 56 conjunctival sac secretion samples, with Staphylococcus being the most commonly isolated species, followed by Escherichia. Among them, 14 strains of Staphylococcus pseudointermedius were not resistant to tobramycin, amikacin, gentamicin or neomycin, but the resistance rates to streptomycin and kanamycin were 35.71% and 42.86%, respectively. Among them, 14 Escherichia coli strains were not resistant to tobramycin and gentamicin, but they showed high resistance rates to neomycin and kanamycin (both at 50%). The detection rate of the aacA-aphD gene in Staphylococcus pseudointermedius strains was 100%. The detection rates of the rmtB gene and rmtE gene in Escherichia coli were 85.71% and 28.57%, respectively, while the aac(6')-Ib gene and npmA gene were not detected. | 2025 | 39852896 |
| 2282 | 1 | 0.9581 | Cross resistance of quinolone derivatives in gram-negative bacteria. A total of 127 Gram-negative bacteria resistant to nalidixic acid were isolated from as many patients affected by urinary tract infections and hospitalized in the first Clinic of Infectious Diseases, University of Naples. Enterobacteria were identified by Enterotube system (Roche) and API 20 system (Ayerst). Non-fermentative bacteria were identified by OXI/FERM system (Roche). The following bacteria were collected: Escherichia coli 50, Proteus spp. 35, Enterobacter agglomerans 12, Serratia sp. 5, Pseudomonas aeruginosa 25. The in vitro antibacterial activity of nalidixic acid and three other quinoline derivatives (pipemidic acid, oxolinic acid and ciprofloxacin) were studied by determining the MICs by a miniaturized dilution broth method. The MICs were compared to evaluate the eventual cross resistance to the drugs under examination within each bacterial species. The results showed that 23% of bacteria were resistant to nalidixic acid, pipemidic acid and oxolinic acid; 49.6% to nalidixic and pipemidic acid and 0.7% to nalidixic acid and oxolinic acid. On the other hand none of the bacteria were resistant to ciprofloxacin. The last showed very low MICs against all the bacteria under examination, including Pseudomonas and Serratia. The high antibacterial activity of ciprofloxacin even against bacteria highly resistant to the other quinolines could be due to a greater affinity of the target sites or to the better permeability of resistant strains to the newer drug or because it is unaffected until now by mutations of genes responsible for cross resistance. | 1985 | 3159488 |
| 5407 | 2 | 0.9579 | Resistance mechanisms and tedizolid susceptibility in clinical isolates of linezolid-resistant bacteria in Japan. OBJECTIVES: Studies combining linezolid resistance mechanisms and tedizolid susceptibility in linezolid-resistant clinical isolates are scarce. This study investigated the linezolid resistance mechanisms and tedizolid susceptibility of linezolid-resistant strains isolated clinically in Japan. METHODS: We analysed 25 linezolid-resistant strains of Enterococcus faecium and Enterococcus faecalis isolated from Japanese hospitals between 2015 and 2021. MICs of linezolid and tedizolid were determined using the agar plate dilution method. Each 23S rRNA copy was amplified by PCR, sequenced and analysed for mutations. The linezolid resistance genes cfr, poxtA, optrA, fexA and fexB were also detected by PCR. RESULTS: Drug susceptibility tests revealed that five linezolid-resistant E. faecium isolates had low (≤1 mg/L) tedizolid MICs. Resistance mechanisms included the G2576T mutation in 23S rRNA, the T2504A mutation and the resistance genes optrA, fexA and fexB. The T2504A mutation was identified in one E. faecium isolate, which exhibited linezolid and tedizolid MICs of 64 and 32 mg/L, respectively. CONCLUSIONS: Some linezolid-resistant isolates demonstrated low (≤1 mg/L) tedizolid MICs. To determine whether tedizolid susceptibility testing should be performed on linezolid-resistant isolates, more linezolid-resistant isolates should be collected and tested for tedizolid MICs. Tedizolid MICs were 2-3 doubling dilutions lower than linezolid MICs. The results of this study suggest that future research should investigate whether the T2504A mutation contributes to tedizolid resistance. To our knowledge, this is the first study to report tedizolid susceptibility in E. faecium with the T2504A mutation and in isolate harbouring this mutation. | 2025 | 40463587 |
| 2475 | 3 | 0.9577 | Examination of single and multiple mutations involved in resistance to quinolones in Staphylococcus aureus by a combination of PCR and denaturing high-performance liquid chromatography (DHPLC). Detection of DNA sequence variation is fundamental to the identification of the genomic basis of phenotypic variability. Denaturing high-performance liquid chromatography (DHPLC) is a novel technique that has been used to detect mutations in human DNA. We report on the first study to use this technique as a tool to detect mutations in genes encoding antibiotic resistance in bacteria. Three methicillin-sensitive and three methicillin-resistant clinical Staphylococcus aureus isolates, susceptible to ciprofloxacin (MIC | 2002 | 12407120 |
| 829 | 4 | 0.9576 | Loop-mediated isothermal amplification assay for 16S rRNA methylase genes in Gram-negative bacteria. Using the loop-mediated isothermal amplification (LAMP) method, we developed a rapid assay for detection of 16S rRNA methylase genes (rmtA, rmtB, and armA), and investigated 16S rRNA methylase-producing strains among clinical isolates. Primer Explorer V3 software was used to design the LAMP primers. LAMP primers were prepared for each gene, including two outer primers (F3 and B3), two inner primers (FIP and BIP), and two loop primers (LF and LB). Detection was performed with the Loopamp DNA amplification kit. For all three genes (rmtA, rmtB, and armA), 10(2) copies/tube could be detected with a reaction time of 60 min. When nine bacterial species (65 strains saved in National Institute of Infectious Diseases) were tested, which had been confirmed to possess rmtA, rmtB, or armA by PCR and DNA sequencing, the genes were detected correctly in these bacteria with no false negative or false positive results. Among 8447 clinical isolates isolated at 36 medical institutions, the LAMP method was conducted for 191 strains that were resistant to aminoglycosides based on the results of antimicrobial susceptibility tests. Eight strains were found to produce 16S rRNA methylase (0.09%), with rmtB being identified in three strains (0.06%) of 4929 isolates of Enterobacteriaceae, rmtA in three strains (0.10%) of 3284 isolates of Pseudomonas aeruginosa, and armA in two strains (0.85%) of 234 isolates of Acinetobacter spp. At present, the incidence of strains possessing 16S rRNA methylase genes is very low in Japan. However, when Gram-negative bacteria showing high resistance to aminoglycosides are isolated by clinical laboratories, it seems very important to investigate the status of 16S rRNA methylase gene-harboring bacilli and monitor their trends among Japanese clinical settings. | 2014 | 25179393 |
| 1250 | 5 | 0.9570 | Distribution of 16S rRNA methylases among different species of Gram-negative bacilli with high-level resistance to aminoglycosides. 16S rRNA methylases confer high-level resistance to most aminoglycosides in Gram-negative bacteria. Seven 16S rRNA methylase genes, armA, rmtA, rmtB, rmtC, rmtD, rmtE and npmA, have been identified since 2003. We studied the distribution of methylase genes in more than 200 aminoglycoside-resistant Gram-negative clinical isolates collected in 2007 at our hospital in Shanghai, China. 16S rRNA methylase genes were amplified by polymerase chain reaction (PCR) among 217 consecutive clinical isolates of Gram-negative bacilli resistant to gentamicin and amikacin by a disk diffusion method. 16S rRNA methylase genes were present in 97.5% (193/198) of clinical isolates highly resistant to amikacin (≥512 μg/ml), with armA and rmtB detected in 67.2 and 30.3% of strains, respectively, while no 16S rRNA methylase genes were detected in 19 strains with amikacin minimum inhibitory concentration (MIC) ≤256 μg/ml. armA or rmtB genes were detected in 100% of 104 strains of Enterobacteriaceae, and these two genes were equally represented (49 vs. 55 strains). Genes for armA or rmtB were detected in 94.7% (89/94) of Acinetobacter baumannii and Pseudomonas aeruginosa strains, and armA was predominant (84 vs. 5 strains with rmtB). No rmtA, rmtC, rmtD or npmA genes were found. Enterobacterial repetitive intergenic consensus sequence (ERIC-PCR) indicated that armA and rmtB genes were spread by both horizontal transfer and clonal dissemination. | 2010 | 20614151 |
| 1249 | 6 | 0.9569 | High-Level Resistance to Aminoglycosides due to 16S rRNA Methylation in Enterobacteriaceae Isolates. Introduction: High-level aminoglycoside resistance due to methylase genes has been reported in several countries. The purpose of this study was to investigate the diversity of the genes encoding 16S rRNA methylase and their association with resistance phenotype in Enterobacteriacae isolates. Materials and Methods: Based on sampling size formula, from February to August 2014, a total of 307 clinical Enterobacteriaceae isolates were collected from five hospitals in northwest Iran. The disk diffusion method for amikacin, gentamicin, tobramycin, kanamycin, and streptomycin, as well as the minimum inhibitory concentration (MIC) for aminoglycosides (except streptomycin), was used. Six 16S rRNA methylase genes (armA, npmA, and rmtA-D) were screened by PCR and sequencing assays. Results: In this study, 220 (71.7%) of 307 isolates were aminoglycoside resistant and 40 isolates (18.2%, 40/220) were positive for methylase genes. The frequency of armA, rmtC, npmA, rmtB, and rmtA genes was 9.5%, 4.5%, 3.6%, 2.3%, and 1%, respectively. The rmtD gene was not detected in the tested bacteria. Sixty percent of positive methylase gene isolates displayed high-level resistance (MIC ≥512 μg/mL to amikacin and kanamycin; and MIC ≥128 μg/mL to gentamicin and tobramycin). Conclusions: The prevalence of resistance to aminoglycoside in Iran is high. Furthermore, there is a statistically significant association between amikacin and kanamycin resistance with the presence of rmtC and rmtB genes. | 2019 | 31211656 |
| 2288 | 7 | 0.9569 | Resistance of Stenotrophomonas maltophilia to Fluoroquinolones: Prevalence in a University Hospital and Possible Mechanisms. OBJECTIVE: The purpose of this study was to investigate the clinical distribution and genotyping of Stenotrophomonas maltophilia, its resistance to antimicrobial agents, and the possible mechanisms of this drug resistance. METHODS: S. maltophilia isolates were collected from clinical specimens in a university hospital in Northwestern China during the period between 2010 and 2012, and were identified to the species level with a fully automated microbiological system. Antimicrobial susceptibility testing was performed for S. maltophilia with the Kirby-Bauer disc diffusion method. The minimal inhibitory concentrations (MICs) of norfloxacin, ofloxacin, chloramphenicol, minocycline, ceftazidime, levofloxacin and ciprofloxacin against S. maltophilia were assessed using the agar dilution method, and changes in the MIC of norfloxacin, ciprofloxacin and ofloxacin were observed after the addition of reserpine, an efflux pump inhibitor. Fluoroquinolone resistance genes were detected in S. maltophilia using a polymerase chain reaction (PCR) assay, and the expression of efflux pump smeD and smeF genes was determined using a quantitative fluorescent (QF)-PCR assay. Pulsed-field gel electrophoresis (PFGE) was employed to genotype identified S. maltophilia isolates. RESULTS: A total of 426 S. maltophilia strains were isolated from the university hospital from 2010 to 2012, consisting of 10.1% of total non-fermentative bacteria. The prevalence of norfloxacin, ciprofloxacin and ofloxacin resistance was 32.4%, 21.9% and 13.2% in the 114 S. maltophilia isolates collected from 2012, respectively. Following reserpine treatment, 19 S. maltophilia isolates positive for efflux pump were identified, and high expression of smeD and smeF genes was detected in two resistant isolates. gyrA, parC, smeD, smeE and smeF genes were detected in all 114 S. maltophilia isolates, while smqnr gene was found in 25.4% of total isolates. Glu-Lys mutation (GAA-AAA) was detected at the 151th amino acid of the gyrA gene, while Gly-Arg mutation (GGC-CGC) was found at the 37th amino acid of the parC gene. However, no significant difference was observed in the prevalence of gyrA or parC mutation between fluoroquinolone-resistant and -susceptible isolates (p> 0.05). The smqnr gene showed 92% to 99% heterogenicity among the 14 S. maltophilia clinical isolates. PFGE of 29 smqnr gene-positive S. maltophilia clinical isolates revealed 25 PFGE genotypes and 28 subgenotypes. CONCLUSIONS: Monitoring the clinical distribution and antimicrobial resistance of S. maltophilia is of great significance for the clinical therapy of bacterial infections. Reserpine is effective to inhibit the active efflux of norfloxacin, ciprofloxacin and ofloxacin on S. maltophilia and reduce MIC of fluoroquinolones against the bacteria. The expression of efflux pump smeD and smeF genes correlates with the resistance of S. maltophilia to fluoroquinolones. | 2015 | 25985315 |
| 2338 | 8 | 0.9568 | Characterization of disinfectant susceptibility profiles among clinical isolates of Acinetobacter baumannii in Ardabil, Iran. Antimicrobial disinfectants have been extensively used to control hospital-acquired infections worldwide. Prolonged exposure to bacteria could promote resistance to antimicrobial disinfectants. This study evaluated the antimicrobial activity of four commonly used disinfectants; triclosan, chlorhexidine digluconate, benzalkonium chloride, and formaldehyde against Acinetobacter baumannii clinical isolates. This study also determined the prevalence and association of efflux pumps encoding genes qacE, qacED1, emrA, and aceI with tolerance to disinfectants. A total of 100 A. baumannii isolates were included in the current study. The antimicrobial disinfectants' minimum inhibitory concentration (MIC) was determined using an agar dilution method. Genes involved in resistance to disinfectants were investigated by PCR method. The benzalkonium chloride MICs ranged between 32 and 128 μg mL-1, chlorhexidine digluconate 8-64 μg mL-1, triclosan 1-32 μg mL-1, and formaldehyde 128 μg mL-1. Overall, the highest MIC90 value was identified for formaldehyde (128 μg mL-1), followed by benzalkonium chloride and chlorhexidine digluconate (64 μg mL-1, each one) and triclosan (4 μg mL-1). In the present study, the qacE, qacED1, emrA, and aceI genes were found in 91%, 55%, 100%, and 88% of isolates, respectively. The qacG gene was not identified in our A. baumannii isolates. The qacED1 gene was associated with higher MICs for all disinfectants tested (P < 0.05), while the qacE and aceI genes were associated with higher MICs for benzalkonium chloride and chlorhexidine. This study indicated that triclosan is the most effective disinfectant against A. baumannii isolates. | 2023 | 38063878 |
| 2446 | 9 | 0.9567 | Low selection of topoisomerase mutants from strains of Escherichia coli harbouring plasmid-borne qnr genes. OBJECTIVES: To investigate mutations in the type II topoisomerase genes in quinolone-resistant mutants selected from bacteria harbouring plasmid-borne qnr genes. METHODS: Mutants were selected by nalidixic acid, ciprofloxacin and moxifloxacin from two Escherichia coli reference strains and corresponding transconjugants harbouring qnrA1, qnrA3, qnrB2 or qnrS1 genes. RESULTS: The proportion of resistant mutants selected by the three quinolones was, respectively, in the same range for qnr-positive transconjugants and reference strains. Only 20% (65/329) of the mutants selected from the transconjugants showed a gyrase mutation, whereas 79% (94/119) of those from the reference strains without a qnr gene did (P < 0.0001). At four times the MIC of the selector quinolone, gyrA mutants represented 49% and 95% of the mutants selected with nalidixic acid, 4% and 94% with ciprofloxacin and 0% and 54% with moxifloxacin for qnr-positive transconjugants and reference strains, respectively. Mutations within gyrA were distributed at codon 87 (D87G, H, N or Y) and at codon 83 (S83L) with three novel mutations (gyrA Ser83stop, gyrA Asp82Asn and gyrB insertion of Glu at 465) and three rare mutations (gyrA Gly81Asp, gyrA Asp82Gly and gyrA Ser431Pro), mainly obtained from reference strains after moxifloxacin selection. Strikingly, none of the mutants selected by moxifloxacin from qnr-positive transconjugants harboured a mutation in the topoisomerase genes. CONCLUSIONS: Topoisomerase mutants are rarely selected by ciprofloxacin and moxifloxacin from strains harbouring qnr. This suggests that the quinolone resistance-determining region domains are protected from quinolones by the Qnr protein and consequently other mechanisms are developed to acquire a further step of fluoroquinolone resistance. | 2008 | 18325893 |
| 5229 | 10 | 0.9567 | Paradoxical High-Level Spiramycin Resistance and Erythromycin Susceptibility due to 23S rRNA Mutation in Streptococcus constellatus. Objectives: The aim of the study was to characterize phenotypically and genotypically an uncommon mechanism of resistance to macrolides, lincosamides, and streptogramins (MLS) in a Streptococcus milleri group clinical isolate. Materials and Methods: The isolate UCN96 was recovered from an osteoradionecrosis wound, and was identified using the matrix assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry and the partial sequencing of the sodA gene. Antimicrobial susceptibility testing were carried out by the disk diffusion method and minimal inhibitory concentrations (MICs) were determined by the broth microdilution technique. PCR screening was performed for MLS resistance genes described in Gram-positive bacteria. Specific mutations in the ribosomal proteins L3-, L4-, and L22-encoding genes were also screened and those in domain V of the 23S rRNA gene (rrl). The number of mutated copies of the rrl gene was determined using amplification-refractory mutation system quantitative-polymerase chain reaction (qPCR) analysis. Results: The clinical isolate UCN96 was unambiguously identified as Streptococcus constellatus. It was susceptible to all macrolides and lincosamides (ML) antibiotics except spiramycin (MIC >256 mg/L) while it was also resistant to streptogramins. Screening for all acquired resistance genes was negative and no mutation was found in genes coding for L3, L4, and L22 ribosomal proteins. Of interest, a single mutation, A2062C (according to Escherichia coli numbering), was detected in the domain V of 23S rRNA. Conclusion: Mutations at the position 2062 of 23S rRNA have been detected once in Streptococcus pneumoniae, and not yet in other Streptococcus spp. This mechanism is very likely uncommon in Gram-positive bacteria because different copies of 23S rRNA operons should be mutated for development of such a resistance pattern. | 2020 | 32031922 |
| 2445 | 11 | 0.9567 | Isolation and characterisation of carbapenem-resistant Xanthomonas citri pv. mangiferaeindicae-like strain gir from the faecal material of giraffes. The purpose of this study was to determine if giraffes (Giraffa camelopardalis) living in captivity at the Jacksonville Zoo and Gardens, Jacksonville, FL were colonised with carbapenem-resistant bacteria and, if found, to identify underlying genetic mechanisms contributing to a carbapenem-resistant phenotype. Faecal samples from seven giraffes were examined for carbapenem-resistant bacteria. Only one isolate (a Xanthomondaceae) was found to be carbapenem-resistant by antibiotic susceptibility testing. This isolate was selected for additional characterization, including whole genome sequencing (WGS). Based on average nucleotide identity, the bacterium was identified as Xanthomonas citri pv. mangiferaeindicae-like strain gir. Phenotypic carbapenemase tests and PCR for the most common carbapenemase genes produced negative results, suggesting that carbapenem resistance was mediated by another mechanism. Resistance gene profile analysis of WGS results confirmed these results. Among identified resistance genes, a chromosomal class A beta-lactamase with 71% identity to the penP beta-lactamase gene from Xanthomonas citri ssp. citri was identified, which could contribute to a carbapenem-resistant phenotype. | 2020 | 31485840 |
| 2096 | 12 | 0.9564 | Investigation of isepamicin in vitro efficiency in Gram negative bacteria efficacy of isepamicin. CONTEXT: Isepamicin is a new semisynthetic aminoglycoside derived from gentamicin B and it is effective against Gram negative bacteria. Antibiotic resistance is an emerging problem and new options need for the treatment of infections caused by Gram negative bacteria. AIMS: In this study we aimed to investigate the in vitro efficiency in carbapenem susceptible and nonsusceptible Enterobacterales and Pseudomonas aeruginosa. METHODS AND MATERIAL: A total of 214 isolates of Gram-negative bacteria (Enterobacterales n = 129 and P. aeruginosa n = 85). Identification of the bacteria was tested in Vitek MS (Biomeriux, France). Susceptibility of isepamicin, amikacin, gentamicin, tobramycin and netilmicin was determined by Kirby Bauer disc diffusion method. The breakpoints for susceptibility to isepamicin, amikacin, gentamicin, streptomycin, tobramycin and netilmicin were evaluated according to the Comité de l'Antibiogramme dela Société Française de Microbiologie (CA-SFM) and EUCAST, respectively. Aminoglycoside modifying enzyme (AME) genes were investigated by multiplex PCR method. RESULTS: Isepamicin susceptibility was determined as 92.3% for Enterobacterales and 67% for P. aeruginosa and 94.4% for carbapenem resistant Enterobacterales. The most common AME gene was aac (6')-Ib in both Enterobacterales (76%) and P. aeruginosa (14.1%). Seven of the isepamicin intermediate or resistant isolates were positive aac (6')-Ib in Enterobacterales and P. aeruginosa. CONCLUSIONS: In this study, isepamicin showed good efficiency against both susceptible and carbapenem nonsusceptible Enterobacterales. But amikacin was prior to isepamicin P. aeruginosa isolates. Isepamicin could be a therapeutic option for the infections caused by Enterobacterales. | 2021 | 33610258 |
| 2211 | 13 | 0.9563 | The molecular analysis of antibiotic resistance and identification of the aerobic bacteria isolated from pleural fluids obtained from patients. OBJECTIVE: Pleural effusion is a common clinical condition due to various etiological causes. Infectious pleural effusion can be seen in 20-40% of patients. In this study, follow-up of patients admitted to our hospital and diagnosed with pleural effusion are reported. It was aimed to investigate the prevalence of bacteria isolated from patients with pleural effusion and their antibiotic resistance profiles. MATERIALS AND METHODS: The pleural fluids obtained from the patients during surgical operations were analyzed microbiologically. Conventional culture, Vitek 2, 16S rRNA, and single Polymerase Chain Reaction (sPCR) were used for microbiological analysis. RESULTS: Twenty-two (12.2%) bacteria were isolated from 180 patients. The most prominent of them were 16 (8.8%) Klebsiella pneumoniae strains. As for the antibiotic sensitivity, gram-negative bacteria showed the highest sensitivity to colistin, while Gram-positive bacteria showed sensitivity to different antibiotics. In 16S rRNA PCR, 22 samples were found to be positive. In the analysis of antibiotic resistance genes, the OXA-48 gene was determined as the highest. CONCLUSIONS: In our region, it is essential to perform a microbiological analysis of the sample in patients with pleural effusion. It was thought that revealing both the phenotype and genotype of the antibiotic resistance of the patients was important in terms of treatment. In hospital surveillance, it was considered important to reveal and record the resistance gene profiles of the patients. | 2022 | 36263534 |
| 1173 | 14 | 0.9563 | Investigation of plasmid-mediated quinolone resistance in Pseudomonas aeruginosa clinical isolates. AIMS: To investigate plasmid-mediated quinolone resistance in clinical isolates of Pseudomonas aeruginosa with the polymerase chain reaction (PCR). The plasmid-mediated quinolone resistance genes have been identified in many bacteria within the Enterobactericeae family, they have not been detected in P. aeruginosa isolates. Subjects and Methods : Identification of the isolates and testing of antibiotic susceptibility was performed in Vitek2 Compact (Biomeriux, France) and Phoinex (BD, USA) automated systems. Screening for the qnrA, qnrB, qnrS, qnrC, aac (6')-Ib-cr and qepA genes was carried out by PCR amplification and aac (6')-Ib-cr DNA sequencing. RESULTS: The qnr and the qepA genes were not detected in any of P. aeruginosa isolates. The aac (6')-Ib gene was detected in six of the isolates and positive isolates for aac (6')-Ib were sequenced for detection of the aac (6')-Ib-cr variant but aac (6')-Ib-cr was not detected in any isolates. CONCLUSIONS: Plasmid-mediated quinolone resistance genes have so far not been identified in P. aeruginosa isolates. However, qnrB have detected in P. florescens and P. putida isolates. This is the first study conducted on the qnrA, qnrB, qnrS and qnrC genes as well as the qepA and aac (6')-Ib-cr genes in P. aeruginosa clinical isolates. | 2014 | 25008822 |
| 2345 | 15 | 0.9563 | The Frequency of Occurrence of Resistance and Genes Involved in the Process of Adhesion and Accumulation of Biofilm in Staphylococcus aureus Strains Isolated from Tracheostomy Tubes. Background: Bacterial biofilm on the surface of tracheostomy tubes (TTs) is a potential reservoir of potentially pathogenic bacteria, including S. aureus. For this reason, our study aimed to investigate biofilm production in vitro and the presence of icaAD and MSCRAMM genes in clinical S. aureus strains derived from TTs, with respect to antibiotic resistance and genetic variability. Methods: The clonality of the S. aureus strains was analyzed by the PFGE method. The assessment of drug resistance was based on the EUCAST recommendations. The isolates were evaluated for biofilm production by the microtiter plate method and the slime-forming ability was tested on Congo red agar (CRA). The presence of icaAD genes was investigated by PCR and MSCRAMM genes were detected by multiplex PCR. Results: A total of 60 patients were enrolled in the study. One TT was obtained from each patient (n = 60). Twenty-one TTs (35%) were colonized with S. aureus. A total of 24 strains were isolated as 3 patients showed colonization with 2 SA clones (as confirmed by PFGE). PFGE showed twenty-two unique molecular profiles. Two isolates (8%) turned out to be MRSA, but 50% were resistant to chloramphenicol, 25% to erythromycin and 8% to clindamycin (two cMLS(B) and four iMLS(B) phenotypes were detected). The microtiter plate method with crystal violet confirmed that 96% of the strains were biofilm formers. Representative strains were visualized by SEM. All isolates had clfAB, fnbA, ebpS and icaAD. Different MSCRAMM gene combinations were observed. Conclusions: the present study showed that the S. aureus isolated from the TTs has a high diversity of genotypes, a high level of antibiotic resistance and ability to produce biofilm. | 2022 | 35744728 |
| 2478 | 16 | 0.9562 | Study on the resistance mechanism via outer membrane protein OprD2 and metal β-lactamase expression in the cell wall of Pseudomonas aeruginosa. The aim of the present study was to evaluate the imipenem-resistant mechanism via the outer membrane protein (OMP) OprD2 and metal β-lactamase expression in the cell wall of Pseudomonas aeruginosa. The Pseudomonas aeruginosa was clinically separated and validated by VITEK-2 full-automatic bacteria analyzer. Drug resistance, sensitive antibiotics and minimum inhibitory concentration (MIC) were tested using the drug sensitivity analysis system. The phenotype positive strains of MBL genes were screened using the Kirby-Bauer diffusion method by adding metal ion-chelating agent EDTA on the imipenem susceptibility paper. IMP-1, VIM-1 and SPM metaloenzyme genes were tested by polymerase chain reaction (PCR)-telomeric repeat amplification protocol (TRAP). The OMP OprD2 genes were tested by PCR-TRAP, and the protein expression was tested using western blot analysis. The location of OMP OprD2 was confirmed using the sodium salicylate inhibition test. The results showed that 80 portions (40%) of MBL-positive strains were screened out of 200 specimens. Imipenem-resistant Pseudomonas aeruginosa (IRPA) and MIC values were significantly higher than quality control bacteria and control bacteria (P<0.05). A total of 35 cases with IMP-1 positive, 20 with VIM-1 positive, 16 with SPM positive, 5 with 2 positive genes and 4 with 3 positive genes were screened among MBL positive strains. A total of 150 portions (75%) of OprD2 deficiencies were screened from 200 specimens. The standard strains and sensitive strains showed OprD2 protein bands at 45 kDa while no OprD2 protein bands appeared in OprD2 deficiency strains. It was in accordance with gene detection. In conclusion, OMP OprD2 deficiency and MBL phenotype positivity may be important mechanisms of IRPA. | 2016 | 27882088 |
| 2139 | 17 | 0.9562 | Study of Some Resistance Genes in Clinical Proteus mirabilis. Proteus mirabilis belongs to the family Enterobacteriaceae and is capable of transforming in shape from rod to elongated and swarming motility by flagella. It is an opportunity for bacteria and can cause different clinical diseases. Therefore, this study aimed to assay and detect a sequence of genes that encode for antibiotic resistance in multidrug resistance clinical isolates of Proteus mirabilis, including blaTEM, aac(6')-Ib, qnrA, IntI2, IntI1 and secondly to investigate the relationship in the phylogenetic tree among these genes in Iraq comparison with global strains in NCBI. The study included the identifying of 500 clinical samples depending on morphological and biochemical tests and confirming Proteus mirabilis diagnosis by the VITEK-2 Compact system. The confirmed isolates of Proteus mirabilis were 95 clinical isolates (19%). Antibiotic susceptibility test of all these isolates was done using twelve antibiotics tested using Amoxicillin, Aztreonam, Imipenem, Cefoxitin, Amikacin, Ceftazidem, Ciprofloxacin, Nalidixic acid, Gentamicin, Sulphamethazol-trimethoprim, Cefotaxime, Amoxicillin-clavulanic acid. The results showed that multidrug resistance Proteus mirabilis isolates contained the genes in different levels as follow blaTEM gene (90%), aac(6')-Ib gene (80%) ,IntI1 gene (100%), IntI2 gene (80%). These genes were sequenced and detected phylogenetic relationships among these genes and global genes were documented in NCBI. The results showed that some Iraqi isolates contain genetic variation compared to global strains. Therefore, this variation was detected and registered in NCBI of all five antibiotic resistance genes mentioned above and accepted under accession numbers of aacIb gene (LC613168.1), blaTEM gene (LC613166.1), IntI1 gene (LC613169.1), IntI2 gene (LC613170.1). | 2022 | 37274906 |
| 2194 | 18 | 0.9562 | Detection of Antiseptic-Resistance Genes in Pseudomonas and Acinetobacter spp. Isolated From Burn Patients. BACKGROUND: Quaternary ammonium compounds (QAC), which contain benzalkonium chloride as the most widely used agent, are employed as wound and skin antiseptics, as well as disinfectants in hospitals. The resistance mechanism to disinfectants is usually determine by genes which are related to resistance to quaternary ammonium compounds, namely, qacE, qacΔE1, qacΔE1 that are found in Gram-negative bacteria. OBJECTIVES: The aim of this study was to determine the incidence of antiseptic resistance genes, qacE and qacΔE1, in clinical isolates of Pseudomonas aeruginosa and Acinetobacter bumanii. MATERIALS AND METHODS: In this study, 83 clinical isolates of Pseudomonas aeruginosa, and 5 isolates of Acinetobacter baumannii from burn hospitals in Tehran and Isfahan provinces in 2010-2011, were tested by the PCR method. RESULTS: Out of the 83 clinical isolates of Pseudomonas aeruginosa, 49 isolates (50%) had the qacE gene, and 76 isolates (91.5%) had the qacΔE1 gene. In addition, in 5 isolates of Acinetobacter bumanii, 2 isolates (40%) had the qacE gene, and 4 isolates (80%) had the qacΔE1 gene. CONCLUSIONS: This study shows that the genes which harbored resistance to quaternary ammonium compound antiseptics are widespread among Pseudomonas aeruginosa and Acinetobacter bumanii isolates in burn patients. | 2014 | 24872941 |
| 2448 | 19 | 0.9562 | Emerging coexistence of three PMQR genes on a multiple resistance plasmid with a new surrounding genetic structure of qnrS2 in E. coli in China. BACKGROUND: Quinolones are commonly used for treatment of infections by bacteria of the Enterobacteriaceae family. However, the rising resistance to quinolones worldwide poses a major clinical and public health risk. This study aimed to characterise a novel multiple resistance plasmid carrying three plasmid-mediated quinolone resistance genes in Escherichia coli clinical stain RJ749. METHODS: MICs of ceftriaxone, cefepime, ceftazidime, ciprofloxacin, and levofloxacin for RJ749 and transconjugant c749 were determined by the Etest method. Conjugation was performed using sodium azide-resistant E. coli J53 strain as a recipient. The quinolone resistance-determining regions of gyrA, gyrB, parC, and parE were PCR-amplified. RESULTS: RJ749 was highly resistant to quinolones, while c749 showed low-level resistance. S1-nuclease pulsed-field gel electrophoresis revealed that RJ749 and c749 both harboured a plasmid. PCR presented chromosomal mutation sites of the quinolone resistance-determining region, which mediated quinolone resistance. The c749 genome comprised a single plasmid, pRJ749, with a multiple resistance region, including three plasmid-mediated quinolone resistance (PMQR) genes (aac (6')-Ib-cr, qnrS2, and oqxAB) and ten acquired resistance genes. One of the genes, qnrS2, was shown for the first time to be flanked by two IS26s. Three IS26-mediated circular molecules carrying the PMQR genes were detected. CONCLUSIONS: We revealed the coexistence of three PMQR genes on a multiple resistance plasmid and a new surrounding genetic structure of qnrS2 flanked by IS26 elements. IS26 plays an important role in horizontal spread of quinolone resistance. | 2020 | 32293532 |