背景:氨基糖苷类已成为治疗铜绿假单胞菌引起的医院感染的基石超过80年。然而,不断升级的抵抗带来了重大挑战。因此,本研究旨在调查伊朗铜绿假单胞菌临床分离株中氨基糖苷类耐药的普遍模式;以及在转诊到Ardabil医院的患者中观察到的潜在耐药机制.
方法:对来自5家医院的200株分离株进行了评价。铜绿假单胞菌对妥布霉素的耐药谱,阿米卡星,和奈替米星是使用圆盘扩散法测定的。氨基糖苷抗性分离株形成生物膜的能力通过表型测定进行评估。并使用基因扩增技术证实了结果。使用聚合酶链反应(PCR)检测与氨基糖苷抗性相关的基因的存在。进行定量逆转录PCR(qRT-PCR)以测量编码MexXY-OprM外排泵和PhoPQ双组分系统(TCS)的基因的表达水平。
结果:氨基糖苷类耐药铜绿假单胞菌的患病率为48%,94.7%的患者表现出多药耐药(MDR)。所有耐氨基糖苷的铜绿假单胞菌菌株均表现出生物膜形成能力,并具有与生物膜产生相关的所有基因。在编码16SrRNA甲基化酶和氨基糖苷修饰酶的9个基因中,在这些分离物中检测到三个基因:aac(6')-Ib(85.4%),蚂蚁(2\'\')-Ia(18.7%),和aph(3')-VI(3.1%)。此外,所有耐氨基糖苷的铜绿假单胞菌分离株都携带mexY和phoP基因,尽管mexY和phoP的表达水平分别为75%和87.5%,分别。
结论:鉴于氨基糖苷类耐药铜绿假单胞菌菌株的患病率相当高,有必要采取紧急措施,向使用新型氨基糖苷类过渡,并对耐药模式保持警惕。
BACKGROUND: Aminoglycosides have been a cornerstone of the treatment of nosocomial infections caused by Pseudomonas aeruginosa for over 80 years. However, escalating emergence of resistance poses a significant challenge. Therefore, this study aimed to investigate the prevailing patterns of
aminoglycoside resistance among clinical isolates of P. aeruginosa in Iran; as well as the underlying resistance mechanisms observed in patients referred to Ardabil hospitals.
METHODS: A total of 200 isolates from five hospitals were evaluated. The resistance profiles of P. aeruginosa isolates to tobramycin, amikacin, and netilmicin were determined using the disk diffusion method. The capacity of
aminoglycoside-resistant isolates to form biofilms was assessed through a phenotypic assay, and the results were confirmed using the gene amplification technique. The presence of genes associated with aminoglycoside resistance was detected using polymerase chain reaction (PCR). Quantitative reverse transcription PCR (qRT-PCR) was performed to measure the expression levels of genes encoding the MexXY-OprM efflux pump and PhoPQ two-component system (TCS).
RESULTS: The prevalence of aminoglycoside-resistant P. aeruginosa isolates was 48%, with 94.7% demonstrating multidrug resistance (MDR). All
aminoglycoside-resistant P. aeruginosa strains exhibited biofilm-forming capabilities and harbored all the genes associated with biofilm production. Among the nine genes encoding 16S rRNA methylase and
aminoglycoside-modifying enzymes, three genes were detected in these isolates: aac(6\')-Ib (85.4%), ant(2\'\')-Ia (18.7%), and aph(3\')-VI (3.1%). Additionally, all
aminoglycoside-resistant P. aeruginosa isolates carried mexY and phoP genes, although the expression levels of mexY and phoP were 75% and 87.5%, respectively.
CONCLUSIONS: Given the considerably high prevalence of aminoglycoside-resistant P. aeruginosa strains, urgent measures are warranted to transition towards the use of novel aminoglycosides and to uphold vigilant surveillance of resistance patterns.