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在意大利中部多次暴发疫情的多重耐药鲍曼不动杆菌流行株中,碳青霉烯酶基因模式发生变化。

Changing carbapenemase gene pattern in an epidemic multidrug-resistant Acinetobacter baumannii lineage causing multiple outbreaks in central Italy.

机构信息

Istituto Nazionale per le Malattie Infettive Lazzaro Spallanzani I.R.C.C.S., Rome, Italy.

出版信息

J Antimicrob Chemother. 2011 Jan;66(1):54-61. doi: 10.1093/jac/dkq407. Epub 2010 Nov 18.

DOI:10.1093/jac/dkq407
PMID:21088019
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3031335/
Abstract

OBJECTIVES

infections caused by multidrug-resistant (MDR) Acinetobacter baumannii are a challenging problem worldwide. Here, the molecular epidemiology and the genetic basis of antibiotic resistance in 111 MDR A. baumannii strains isolated from June 2005 to March 2009 from infected patients in 10 intensive care units (ICUs) in central Italy were investigated.

METHODS

epidemiological typing was performed by random amplification of polymorphic DNA, PCR-based sequence grouping and macrorestriction analysis. MICs of antibiotics were determined by the broth microdilution method. Genes for OXA carbapenemases, metallo-β-lactamases and the CarO porin were searched for by PCR.

RESULTS

molecular genotyping identified one predominant A. baumannii lineage, related to the international clonal lineage II, accounting for 95.6% of isolates. Isolates referable to this lineage were recovered from all ICUs surveyed and were resistant to nearly all classes of antimicrobials, with the exception of tigecycline and colistin. A high percentage (60.5%) of A. baumannii isolates showed elevated resistance to imipenem (MICs ≥  128 mg/L), concomitant with resistance to meropenem. Carbapenem resistance was associated with the presence of either bla(OXA-58)-like (22.8%) or bla(OXA-23)-like (71.1%) carbapenemase genes. Molecular typing showed that the epidemic lineage encoding OXA-23 emerged in 2007 and displaced a genetically related clone encoding OXA-58 that had been responsible for previous ICU outbreaks in the same region.

CONCLUSIONS

emergence of the OXA-23 epidemic lineage could result from selective advantage conferred by the bla(OXA-23)-like determinant, which provides increased resistance to carbapenems.

摘要

目的

多重耐药(MDR)鲍曼不动杆菌引起的感染是一个全球性的挑战。本研究调查了 2005 年 6 月至 2009 年 3 月期间,来自意大利中部 10 个重症监护病房(ICU)感染患者的 111 株 MDR 鲍曼不动杆菌菌株的分子流行病学和抗生素耐药的遗传基础。

方法

采用随机扩增多态性 DNA、基于 PCR 的序列分组和宏限制分析进行流行病学分型。采用肉汤微量稀释法测定抗生素的 MIC。通过 PCR 检测 OXA 碳青霉烯酶、金属β-内酰胺酶和 CarO 孔蛋白基因。

结果

分子基因分型确定了一种主要的鲍曼不动杆菌谱系,与国际克隆谱系 II 有关,占分离株的 95.6%。从所有调查的 ICU 中均分离到属于该谱系的菌株,对除替加环素和黏菌素以外的几乎所有类别的抗菌药物均具有耐药性。60.5%的鲍曼不动杆菌分离株对亚胺培南的耐药性升高(MICs≥128mg/L),同时对美罗培南耐药。碳青霉烯类耐药与 bla(OXA-58)样(22.8%)或 bla(OXA-23)样(71.1%)碳青霉烯酶基因的存在相关。分子分型显示,编码 OXA-23 的流行谱系于 2007 年出现,并取代了先前在同一地区导致 ICU 暴发的遗传相关克隆,该克隆编码 OXA-58。

结论

OXA-23 流行谱系的出现可能是由于 bla(OXA-23)样决定簇赋予的选择优势所致,该决定簇增加了对碳青霉烯类的耐药性。

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