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首页> 外文期刊>Journal of medical bacteriology. >Molecular Detection of gyrA, parC and oprD Mutation in Pseudomonas aeruginosa Isolates from a University Hospital of Isfahan, Iran during 2016
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Molecular Detection of gyrA, parC and oprD Mutation in Pseudomonas aeruginosa Isolates from a University Hospital of Isfahan, Iran during 2016

机译：2016年伊朗伊斯法罕大学医院铜绿假单胞菌分离物中gyrA，parC和oprD突变的分子检测

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Background: Excessive use of broad-spectrum antibiotics in hospitals has led to the emergence of highly resistant strains of Pseudomonas aeruginosa. The main mechanism of resistance of this bacterium to fluoroquinolones and carbapenems are the modification of type II topoisomerases (DNA gyrase and topoisomerase IV) and alterations in the OprD porin, respectively. The aim of this study was to examine for the occurrence of mutations related to fluoroquinolone resistance of gyrA and parC genes and mutational inactivation of oprD gene of clinical isolates using DNA sequencing technique.Methods: A total of 60 P. aeruginosa isolates were collected from the hospitalized patients in the Intensive Care Units (ICUs) of Al-Zahra hospital located in Isfahan, Iran. The pattern of sensitivity to antibiotics was determined using CLSI disk diffusion and MIC methods. The assay was based on a DNA sequencing method using polymerase chain reaction (PCR) for amplification and sequencing of the selected genes.Results: The results show that replacement of Ile for Thr-83 in gyrA was the only replacement, while other substitutions not observed. No mutations were found in parC. The most frequent amino acid alterations were E185Q, P186G, and V189T, found in five resistance isolates, However, nucleotide insertions and deletions mutations not observed.Conclusion: Our study suggested that mutation of gyrA and oprD genes may play a minor role in fluoroquinolone and carbapenem resistance and other mechanisms may contribute to the fluoroquinolone and carbapenem resistance of P. aeruginosa.
机译：背景：医院中广泛使用广谱抗生素已导致出现高耐药铜绿假单胞菌菌株。该细菌对氟喹诺酮类和碳青霉烯类耐药的主要机制分别是II型拓扑异构酶（DNA旋转酶和拓扑异构酶IV）的修饰和OprD孔蛋白的改变。本研究的目的是利用DNA测序技术检测与gyrA和parC基因的氟喹诺酮耐药有关的突变的发生以及临床分离株oprD基因的突变失活的方法。方法：从分离的铜绿假单胞菌中共收集到60株分离的铜绿假单胞菌。伊朗伊斯法罕的Al-Zahra医院重症监护病房（ICU）的住院患者。使用CLSI磁盘扩散和MIC方法确定对抗生素的敏感性模式。该试验基于DNA测序方法，该方法使用聚合酶链反应（PCR）进行所选基因的扩增和测序。结果：结果表明，唯一的替代是在gyrA中用Ile替代Thr-83，而未观察到其他替代。 。在parC中未发现突变。结论：我们发现gyrA和oprD基因的突变可能在氟喹诺酮和氟喹诺酮中起次要的作用。在五个耐药菌株中发现的最常见的氨基酸改变是E185Q，P186G和V189T，但是未观察到核苷酸插入和缺失突变。碳青霉烯耐药性和其他机制可能有助于铜绿假单胞菌的氟喹诺酮和碳青霉烯耐药性。

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