|
|
|
Search published articles |
|
|
Showing 2 results for Fluoroquinolone
Roqiyeh Nouri, Mohammad Ahangarzadeh Rezaee , Alka Hasani, Mohammad Aghazadeh, Mohammad Asgharzadeh, Morteza Ghojazadeh, Volume 16, Issue 2 (7-2016)
Abstract
Background & objectives: Fluoroquinolones have important role in treatment of P. aeruginosa infections. The main mechanism of fluoroquinolones resistance in P. aeruginosa is mutations in the quinolone-resistance-determining region (QRDR) of gyrA and parC genes. The aim of this study was to investigate the role of these mutations in ciprofloxacin resistance in different clinical isolates of P. aeruginosa.
Methods: A total of 75 clinical P. aeruginosa isolates were collected from different university-affiliated hospitals in Tabriz. Minimum inhibitory concentrations (MICs) of ciprofloxacin were evaluated by Etest assay. DNA sequences of the QRDR of gyrA and parC were determined by dideoxy chain termination method.
Results: From 75 isolates, 77.33% were resistant to ciprofloxacin. No amino acid changes were detected in gyrA or parC genes of the ciprofloxacin susceptible isolates. Thr-83→Ile substitution in gyrA was observed in all ciprofloxacin resistant isolates. About 90% of them had Ser-87→Leu substitution in parC. Geometric mean MICs of ciprofloxacin were different for various clinical isolates of P. aeruginosa which had the same situation in type and location of gyrA and parC mutations. Moreover, the geometric mean MIC in isolates from urine was significantly (p<0.05) higher than isolates from tracheal aspirates.
Conclusion: Mutations in gyrA and parC genes are the major mechanisms for ciprofloxacin resistance in clinical isolates of P. aeruginosa. Moreover, the role of different effective factors in fluoroquinolone resistance can be different in various clinical isolates of P. aeruginosa.
Maryam Nazari, Nilofar Saeli, Mohsen Arzanlou, Saghar Jafari-Ramedani, Hafez Mirzanejad-Asl, Farzad Khademi, Aida Alinezhad, Volume 24, Issue 1 (4-2024)
Abstract
Background: Antibiotic resistance represents a critical global concern within the medical community, posing significant challenges in the treatment of infections caused by drug-resistant pathogens. Over the years, broad-spectrum fluoroquinolones have been extensively used to treat infections caused by both Gram-positive and Gram-negative bacteria, including Pseudomonas aeruginosa. In this study, we decided to assess the prevalence of plasmid-mediated quinolone resistance mechanisms among clinical isolates of P. aeruginosa in Ardabil hospitals.
Methods: We analyzed a total of 200 clinical isolates of P. aeruginosa, collected between June 2019 and May 2023. The antibiotic resistance profiles of these strains against various fluoroquinolone antibiotics were determined using the disk diffusion method. Additionally, we investigated the presence of qnrA, qnrB, qnrC, qnrD, and qnrS genes through polymerase chain reaction (PCR) analysis. Furthermore, we assessed the expression levels of efflux pump genes and outer membrane porin genes using the quantitative reverse transcription PCR (qRT-PCR) in fluoroquinolone-resistant P. aeruginosa strains.
Results: Our findings revealed that 69% of P. aeruginosa strains were resistant to fluoroquinolones. The resistance rates for different fluoroquinolones were as follows: ciprofloxacin 55.5%, ofloxacin 62%, norfloxacin 53.5%, lomefloxacin 55.3%, and levofloxacin 55.5%. Notably, 78.9% of these strains exhibited multidrug resistance (MDR). Among the qnr genes, qnrB was the most prevalent (2.9%). No other qnr genes were identified. Interestingly, 75% of P. aeruginosa strains carrying the qnrB gene showed overexpression of efflux pump genes, while 100% exhibited down-regulation of the oprD gene.
Conclusion: Given the high prevalence of fluoroquinolone-resistant P. aeruginosa clinical isolates in Ardabil hospitals and the multifactorial nature of resistance, continuous monitoring of antibiotic resistance trends and understanding the underlying resistance mechanisms are crucial for selecting appropriate treatment strategies.
|
|