Ghaffari Lashkenari Erfan, Mir Maryam Sadat, Mohammadi Mohsen, Javadi Kasra, Halaji Mehrdad
Student Research Committee, Babol University of Medical Sciences, Babol, Iran.
Non-Communicable Pediatric Diseases Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, I.R. Iran.
Microb Drug Resist. 2025 Sep 10. doi: 10.1177/10766294251377378.
Fluoroquinolone resistance in , particularly uropathogenic (UPEC), is a growing concern worldwide. This study investigates the association between mutations in the and genes and fluoroquinolone resistance in UPEC isolates from Urine samples in Iran. In total, 150 UPEC isolates were collected, and then, 12 ciprofloxacin-resistant isolates were selected for molecular analysis. Antimicrobial susceptibility testing was performed using the disk diffusion method, and minimum inhibitory concentrations (MICs) of ciprofloxacin were determined by microbroth dilution. Polymerase chain reaction and sequencing were used to detect mutations in the quinolone resistance-determining regions (QRDRs) of and . All isolates had MIC >4 and were resistant to all four fluoroquinolones and quinolones tested, including ciprofloxacin, norfloxacin, ofloxacin, and nalidixic acid. All isolates harbored mutations in both genes. The most frequent mutations in were Ser-83→Leu and Asp-87→Asn, found in 100% of isolates. Similarly, mutations in , including Ser-80→Ile (83.3%) and Glu-84→Val (58.3%), were prevalent. Additional nucleotide substitutions in both genes were observed. These mutations likely contribute to the high-level fluoroquinolone resistance observed in the isolates. The results of this study confirm that mutations in the and genes primarily drive fluoroquinolone resistance in UPEC isolates. The presence of specific alterations within the QRDRs significantly reduces bacterial susceptibility to fluoroquinolones, contributing to the persistence and spread of resistant strains. Identifying these mutations provides critical insights into resistance mechanisms, which can aid in developing more effective antimicrobial therapy strategies.
氟喹诺酮耐药性,尤其是尿路致病性大肠埃希菌(UPEC)的耐药性,在全球范围内日益受到关注。本研究调查了伊朗尿液样本中UPEC分离株中gyrA和parC基因的突变与氟喹诺酮耐药性之间的关联。总共收集了150株UPEC分离株,然后选择12株对环丙沙星耐药的分离株进行分子分析。采用纸片扩散法进行药敏试验,通过微量肉汤稀释法测定环丙沙星的最低抑菌浓度(MIC)。使用聚合酶链反应和测序检测gyrA和parC喹诺酮耐药决定区(QRDR)的突变。所有分离株的MIC均>4,并且对所测试的所有四种氟喹诺酮类和喹诺酮类药物耐药,包括环丙沙星、诺氟沙星、氧氟沙星和萘啶酸。所有分离株在两个基因中均存在突变。gyrA中最常见的突变是Ser-83→Leu和Asp-87→Asn,在100%的分离株中发现。同样,parC中的突变,包括Ser-80→Ile(83.3%)和Glu-84→Val(58.3%)也很普遍。在两个基因中还观察到其他核苷酸替换。这些突变可能导致分离株中观察到的高水平氟喹诺酮耐药性。本研究结果证实,gyrA和parC基因中的突变主要导致UPEC分离株对氟喹诺酮耐药。QRDR内特定改变的存在显著降低了细菌对氟喹诺酮的敏感性,有助于耐药菌株的持续存在和传播。识别这些突变可为耐药机制提供关键见解,有助于制定更有效的抗菌治疗策略。