Department of Medical Biotechnology and Laboratory Science, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-Shan, Taoyuan 333, Taiwan.
Int J Antimicrob Agents. 2012 Mar;39(3):217-22. doi: 10.1016/j.ijantimicag.2011.09.023. Epub 2011 Nov 10.
Between 2003 and 2009, the prevalence of extensively drug-resistant Pseudomonas aeruginosa (XDR-PA) increased significantly in northern Taiwan from 1.0% to 2.1%. Molecular methods were used to investigate the genetic relatedness and carbapenem resistance mechanisms of a collection of 203 non-repetitive XDR-PA isolates available for study. Using pulsed-field gel electrophoresis (PFGE), 52 genotypes were observed; one predominant genotype (pulsotype 1) was found in 57.6% of the isolates. Polymerase chain reaction (PCR), sequencing and quantitative reverse-transcriptase PCR analyses demonstrated that one horizontally acquired mechanism [metallo-β-lactamase (MBL) genes] and two mutational mechanisms (efflux and porins) accounted for the carbapenem resistance. The most predominant horizontally acquired mechanism was carriage of bla(VIM-3), which was found in 61.1% of isolates. Decreased expression of oprD was the most prevalent mutational mechanism and was found in 70.0% of the XDR-PA isolates, whereas overexpression of mexA was found in 27.6% of the isolates. The highlight of this study was the discovery of statistically significant relationships between certain horizontally acquired and mutational resistance mechanisms and their contribution to carbapenem susceptibility. MBL-producers expressed significantly lower MexAB and higher OprD than non-MBL-producers. Amongst isolates without an acquired β-lactamase gene, oprD expression was significantly reduced, whilst expression of efflux pumps was increased. Reduced OprD expression alone or the production of VIM-type MBLs showed similar contributions to a low to intermediate MIC(50) (minimum inhibitory concentration for 50% of the organisms) for carbapenems. Isolates with reduced OprD expression that simultaneously harboured bla(VIM) exhibited high levels of resistance to carbapenems, which implied that these two mechanisms had a synergistic effect on the MICs.
2003 年至 2009 年间,台湾北部地区广泛耐药铜绿假单胞菌(XDR-PA)的流行率从 1.0%显著上升至 2.1%。采用分子方法对 203 株非重复 XDR-PA 分离株的遗传相关性和碳青霉烯类耐药机制进行了研究。利用脉冲场凝胶电泳(PFGE)观察到 52 种基因型;发现一种主要基因型(脉冲型 1)存在于 57.6%的分离株中。聚合酶链反应(PCR)、测序和实时定量逆转录-PCR 分析表明,一种水平获得的机制(金属β-内酰胺酶(MBL)基因)和两种突变机制(外排泵和孔蛋白)导致了碳青霉烯类耐药。最主要的水平获得机制是携带 bla(VIM-3),在 61.1%的分离株中发现。OprD 表达下调是最常见的突变机制,在 70.0%的 XDR-PA 分离株中发现,而 mexA 过度表达在 27.6%的分离株中发现。本研究的重点是发现某些水平获得和突变耐药机制之间存在统计学显著关系及其对碳青霉烯类药物敏感性的贡献。MBL 生产者表达的 MexAB 显著低于非 MBL 生产者,OprD 表达显著高于非 MBL 生产者。在没有获得性β-内酰胺酶基因的分离株中, oprD 表达显著降低,而外排泵表达增加。单独降低 OprD 表达或产生 VIM 型 MBLs 对碳青霉烯类药物的 MIC50(最低抑菌浓度的 50%)表现出相似的低至中等水平的贡献。同时存在 oprD 表达降低和 bla(VIM)携带的分离株对碳青霉烯类药物表现出高水平的耐药性,这意味着这两种机制对 MIC 具有协同作用。