Correlation between ability of biofilm formation with their responsible genes and MDR pattetns in clinical and environmental Acinetobacter baumannii isolates

Correlation between ability of biofilm formation with their responsible genes and MDR pattetns in clinical and environmental Acinetobacter baumannii isolates
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DOI:
10.1016/j.micpath.2017.04.039
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发表时间:
2017-07-01
影响因子:
3.8
通讯作者:
Bagheri, Kamran Pooshang
Bagheri, Kamran Pooshang
中科院分区:
医学3区
文献类型:
--
作者:
Bardbari, Ali Mohammadi;Arabestani, Mohammad Reza;Bagheri, Kamran Pooshang

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鲍曼不动杆菌形成生物被膜的潜力和表现出多种抗生素耐药性可能是其在医院环境中存活的原因。因此,本研究旨在确定生物膜形成能力与生物膜相关基因频率与抗生素耐药表型之间的相关性,以及它们在临床和环境分离株中的模式分类。收集鲍曼不动杆菌并通过API 20 NE鉴定。药敏试验采用纸片扩散法和微量肉汤稀释法。采用微量滴定板法进行生物膜形成试验。PCR扩增OXA分型及生物膜相关基因Bla(OXA-51)、Bla(OXA-23)、Bla(OXA-24)、Bla(OXA-58)、bap、bla(PER-1)、ompA。临床分离株鲍曼不动杆菌检出率(100%)高于环境分离株(81.2%)(P < 0.05)。在10种耐药类型中,临床和环境分离株的主要耐药模式为耐药I型(分别为85.3%和78.1%)。Bla(OXA-23)基因频率在临床分离株(85.3%)和环境分离株(68.7%)之间差异有统计学意义(p < 0.05)。临床分离株和环境分离株中强生物被膜菌的检出率分别为31.2%和58.7%。临床分离株和环境分离株中ompA、bla(PER-1)和bap基因的频率分别为100%、533%、82.7%和100%、37.5%、84.4%。统计学分析显示MDR菌株的频率与生物膜形成能力之间存在显著相关性(p = 0.008)。MDR I型菌株的高频率表明医院环境中已发生较早的暴发,目前正在形成地方性菌株。如果临床分离株和环境分离株的I型频率和生物膜形成能力没有差异,则这是代表细菌从环境传播到患者的风险较高的临界点。所得数据将有助于改进消毒策略,以更好地控制医院感染。一个占主导地位的耐药模式已显示在临床和环境分离株。bla(OXA-23)在临床分离株和环境分离株中的频率差异有统计学意义。bap基因在A.鲍曼不动杆菌分离株与生物膜形成有关。多重耐药与生物膜形成之间存在显着相关性。与环境样品相比,临床分离株具有更高的形成强生物膜的能力。(C)2017爱思唯尔有限公司版权所有
Acinetobacter baumannii potential to form biofilm and exhibit multiple antibiotic resistances may be responsible in its survival in hospital environment. Accordingly, our study was aimed to determine the correlation between ability of biofilm formation and the frequency of biofilm related genes with antibiotic resistance phenotypes, and also the categorization of their patterns in clinical and environmental isolates.A total of 75 clinical and 32 environmental strains of the A. baumannii were collected and identified via API 20NE. Antibiotic susceptibility was evaluated by disk diffusion and microdilution broth methods. Biofilm formation assay was performed by microtiter plate method. OXA types and biofilm related genes including Bla(OXA-51), Bla(OXA-23), Bla(OXA-24), Bla(OXA-58), bap, bla(PER-1), and ompA were amplified by PCR.The rate of MDR A. baumannii in clinical isolates (100%) was higher than environmental (81.2%) isolates (p < 0.05). Among 10 antibiotypes; the predominant resistance pattern in clinical and environmental isolates was antibiotypes I (85.3 and 78.1%, respectively). Analysis of the frequency of Bla(OXA-23) gene revealed a statistically significant difference between clinical (85.3%) and environmental (68.7%) isolates (p < 0.05). The prevalence of strong biofilm producers in clinical and environmental isolates were 31.2% 58.7%, respectively. In the clinical and environmental isolates, the frequencies of ompA, bla(PER-1) and bap genes were 100%, 533%, 82.7% and 100%, 37.5%, 84.4% respectively. Statistical analysis revealed a significant correlation between the frequency of MDR isolates and biofilm formation ability (p = 0.008).The high frequency of antibiotype I would be indicated that an outbreak has been happened earlier and an endemic strain is currently being settled in the hospital environment. It would be suggested that if there was no difference in the frequency of pattern I and biofilm formation ability between clinical and environmental isolates, it is a critical point representing the higher risk of bacterial transmission from environment to the patients. The resulting data would be assisted in the improvement of disinfection strategies to better control of nosocomial infections. One dominant resistance pattern has shown among clinical and environmental isolates. The frequency of bla(OXA-23) had significant difference between clinical and environmental isolates. The presence of bap gene in the A. baumannii isolates was associated with biofilm formation. There was a significant correlation between multiple drug resistance and biofilm formation. The clinical isolates had a higher ability to form strong biofilms compared to the environmental samples. (C) 2017 Elsevier Ltd. All rights reserved.