Tahbaz S V, Azimi L, Lari A R
Department of Microbiology, Islamic Azad University, North Tehran Branch, Tehran, Iran.
Pediatric Infections Research Centre, Research Institute for Children's Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Ann Burns Fire Disasters. 2019 Jun 30;32(2):115-121.
Clinical isolates of Acinetobacter baumannii have a tendency to develop antimicrobial resistance against commonly prescribed antimicrobial agents, including aminoglycoside agents, particularly in hospitalized patients worldwide. Resistance mechanisms of the bacterium to aminoglycosides are diverse and commonly involve production of aminoglycoside-modifying enzymes and efflux systems. The aim of this study was to investigate the frequency of gene encoding aminoglycoside-modifying enzymes and expression level of adeB efflux gene in A. baumannii isolates recovered from burn wound colonization. A total of 47 clinical isolates of A. baumannii were obtained from burned patients admitted to the Burns Teaching Hospital, Tehran, in 2018. Standard antimicrobial susceptibility screening was performed to determine resistance pattern. A polymerase chain reaction (PCR) assay was performed to determine aminoglycoside-modifying genes ACC(6'), aph(3')-Via, aph(3')-IIb, aadA1, aphA1 and aph6. Semi-quantitative RT-PCR was also carried out to quantify the expression level of the adeB gene. According to the results of the present study, the acc(6') was the predominant aminoglycoside-modifying enzyme gene (80.9%), followed by aph(3')-via, aph6, aph(3')-IIb and aphA1, which was detected in 59.6%, 42.6%, 14.9% and 14.9% of isolates, respectively. None of the A. baumannii isolates harboured the aadA1 gene. The up regulation of adeB gene expression was observed in 63.8% of strains. Moreover, we indicated that there is a relationship between adeB expression and high resistance to gentamicin. Our results revealed that aminoglycoside resistance could be explained by the production of one or a combination of known aminoglycoside-modifying enzymes rather than overexpression of adeB.
鲍曼不动杆菌的临床分离株往往会对常用的抗菌药物产生耐药性，包括氨基糖苷类药物，在全球范围内的住院患者中尤其如此。该细菌对氨基糖苷类药物的耐药机制多种多样，通常涉及氨基糖苷类修饰酶的产生和外排系统。本研究的目的是调查从烧伤创面定植中分离出的鲍曼不动杆菌菌株中编码氨基糖苷类修饰酶的基因频率以及adeB外排基因的表达水平。2018年，从德黑兰烧伤教学医院收治的烧伤患者中总共获得了47株鲍曼不动杆菌临床分离株。进行标准抗菌药物敏感性筛选以确定耐药模式。采用聚合酶链反应（PCR）检测法来确定氨基糖苷类修饰基因ACC(6')、aph(3')-Via、aph(3')-IIb、aadA1、aphA1和aph6。还进行了半定量逆转录PCR以量化adeB基因的表达水平。根据本研究结果，acc(6')是主要的氨基糖苷类修饰酶基因（80.9%），其次是aph(3')-via、aph6、aph(3')-IIb和aphA1，分别在59.6%、42.6%、14.9%和14.9%的分离株中检测到。所有鲍曼不动杆菌分离株均未携带aadA1基因。在63.8%的菌株中观察到adeB基因表达上调。此外，我们表明adeB表达与对庆大霉素的高耐药性之间存在关联。我们的结果显示，氨基糖苷类耐药性可以通过一种或多种已知的氨基糖苷类修饰酶的产生来解释，而不是adeB的过表达。
