Molecular epidemiology of a clonal outbreak of multidrug-resistant Acinetobacter baumannii in a university hospital in Italy.
Molecular epidemiology of a clonal outbreak of multidrug-resistant Acinetobacter baumannii in a university hospital in Italy.
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意大利一所大学医院多重耐药鲍曼不动杆菌克隆暴发的分子流行病学。
DOI：
10.1111/j.1469-0691.2006.01675.x
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
R. Utili
中科院分区：
文献类型：
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作者：
R. Zarrilli;R. Casillo;A. D. Popolo;M. Tripodi;M. Bagattini;S. Cuccurullo;V. Crivaro;E. Ragone;A. Mattei;Nicola Galdieri;Maria Triassi;R. Utili
本研究调查了 2003 年 6 月至 2004 年 6 月期间意大利那不勒斯一家三级医院发生的多重耐药鲍曼不动杆菌克隆爆发的分子流行病学。从 74 名患者体内分离出鲍曼不动杆菌，其中 38 人被感染，36 人被定植。 33 名患者患有呼吸机相关性肺炎，3 名患者患有医院获得性肺炎，2 名患者患有败血症。对 45 种鲍曼不动杆菌分离株的基因型分析揭示了两种不同的脉冲场凝胶电泳 (PFGE) 模式。其中，PFGE 模式 1 以来自 44 名患者的分离株为代表，与 2002 年那不勒斯另一家医院分离出的流行鲍曼不动杆菌克隆相同。所有 PFGE 1 型鲍曼不动杆菌分离株均表现出相同的多重耐药性抗体型，其特征是对所有测试的抗菌药物（包括碳青霉烯类药物）具有耐药性，但粘菌素除外。在这些分离株中，200 mM NaCl 对 OXA 酶的抑制使亚胺培南 MIC 降低多达四倍。抗菌素耐药基因的分子分析表明，所有 PFGE 1 型鲍曼不动杆菌分离株均含有 1 类整合子，其中包含 aacA4、orfX 和 bla(OXA-20) 基因盒、ampC 基因和 bla(OXA-51) 样等位基因。此外，在 PFGE 1 型（而非 PFGE 2 型）鲍曼不动杆菌分离株的 30 kb 质粒中鉴定出 bla(OXA-58) 样基因，该基因被调节元件 ISAba2 和 ISAba3 包围。因此，选择产生 OXA-58 型碳青霉烯水解苯唑西林酶的单个鲍曼不动杆菌克隆是导致鲍曼不动杆菌数量增加的原因。该医院发生鲍曼不动杆菌感染。
This study investigated the molecular epidemiology of a clonal outbreak of multidrug-resistant Acinetobacter baumannii that occurred between June 2003 and June 2004 in a tertiary-care hospital in Naples, Italy. A. baumannii was isolated from 74 patients, of whom 38 were infected and 36 were colonised. Thirty-three patients had ventilator-associated pneumonia, three had hospital-acquired pneumonia, and two had sepsis. Genotypic analysis of 45 available A. baumannii isolates revealed two distinct pulsed-field gel electrophoresis (PFGE) patterns. Of these, PFGE pattern 1 was represented by isolates from 44 patients and was identical to that of an epidemic A. baumannii clone isolated in another hospital of Naples during 2002. All A. baumannii isolates of PFGE type 1 showed identical multiresistant antibiotypes, characterised by resistance to all antimicrobial agents tested, including carbapenems, with the exception of colistin. In these isolates, inhibition of OXA enzymes by 200 mM NaCl reduced the imipenem MIC by up to four-fold. Molecular analysis of antimicrobial resistance genes showed that all A. baumannii isolates of PFGE type 1 harboured a class 1 integron containing the aacA4, orfX and bla(OXA-20) gene cassettes, an ampC gene and a bla(OXA-51)-like allele. Moreover, a bla(OXA-58)-like gene surrounded by the regulatory elements ISAba2 and ISAba3 was identified in a 30-kb plasmid from A. baumannii isolates of PFGE type 1, but not PFGE type 2. Thus, selection of a single A. baumannii clone producing an OXA-58-type carbapenem-hydrolysing oxacillinase was responsible for the increase in the number of A. baumannii infections that occurred in this hospital.