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首页> 外文期刊>Gut Pathogens >KPC-mediated resistance in Klebsiella pneumoniae in two hospitals in Padua, Italy, June 2009-December 2011: massive spreading of a KPC-3-encoding plasmid and involvement of non-intensive care units
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KPC-mediated resistance in Klebsiella pneumoniae in two hospitals in Padua, Italy, June 2009-December 2011: massive spreading of a KPC-3-encoding plasmid and involvement of non-intensive care units

机译：2009年6月至2011年12月，意大利帕多瓦州两家医院的肺炎克雷伯菌肺炎克雷伯菌介导的耐药性：编码KPC-3的质粒的大规模传播和非重症监护病房的参与

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Background Klebsiella pneumoniae carbapenemases (KPCs) producing bacteria have emerged as a cause of multidrug-resistant nosocomial infections worldwide. KPCs are plasmid-encoded enzymes capable of hydrolysing a broad spectrum of beta-lactams, including carbapenems and monobactams, therefore worryingly limiting antimicrobial treatment options. Analysis of circulating bacterial strains and KPC alleles may help understanding the route of KPC dissemination and therefore help containing the infection. Methods KPC-producing Klebsiella pneumoniae dissemination in two 1580- and 300- bed hospitals in Padua, Italy, from initial outbreak in 2009 to late 2011 was analysed. Molecular and clinical epidemiology, including bacterial strains, KPC-encoding plasmid sequences and associated resistance genes, involved hospital wards and relocation of patients were described. Routine antimicrobial susceptibility testing and MIC of carbapenems on clinical isolates were performed. Detection of resistance genes was obtained by PCR and sequencing. MLST, PFGE and ERIC were used for molecular genotyping. Plasmid analysis was obtained by digestion with restriction enzymes and deep sequencing. Results KPC-positive clinical samples were isolated from nearly 200 patients. In the initial outbreak intensive care units were almost exclusively involved, while medical, surgical and long-term wards were successively massively concerned. Analysis of KPC alleles, plasmids and bacterial sequence types (STs) indicated that during the initial outbreak KPC-3 in ST258 and KPC-2 in ST147 were each confined in one of the two surveilled hospitals. While KPC-2 dissemination was effectively contained, KPC-3 in ST258 cross-spreading was observed. The simultaneous presence of two carbapenemases, VIM-1 and KPC-2, in the same isolate was also observed in three patients. Total sequencing of plasmid content of two KPC-3 strains showed novel association of resistance plasmids. Conclusions The acquired molecular epidemiology demonstrated that 1) both acquisitions from outward sources and patient relocation within the hospitals were responsible for the observed spreading; 2) KPC-3-encoding Klebsiella pneumoniae ST258 prevailed over other strains. In addition, the described massive transfer of KPC-mediated resistance to non-intensive care units may anticipate spreading of resistance to the non-hospitalized population. Therefore, genotypic analysis alongside phenotypic identification of carbapenemase producers, also at the carriage state, is advisable to prevent and contain further carbapenemase resistance dissemination.
机译：背景技术产生细菌的肺炎克雷伯菌肺炎克雷伯菌（KPCs）已成为全球范围内多重耐药性医院感染的原因。 KPC是能够水解广谱β-内酰胺（包括碳青霉烯和单bactam）的质粒编码酶，因此令人担忧地限制了抗菌药物的治疗选择。分析循环细菌菌株和KPC等位基因可能有助于了解KPC的传播途径，从而有助于控制感染。方法分析了2009年最初爆发至2011年末期间在意大利帕多瓦的两家拥有1580张床和300张床的医院中传播的KPC产生的肺炎克雷伯菌。分子和临床流行病学，包括细菌菌株，编码KPC的质粒序列和相关的耐药基因，涉及医院病房和患者的安置。对临床分离株进行了常规抗菌药敏试验和碳青霉烯类药物的MIC。通过PCR和测序获得抗性基因的检测。 MLST，PFGE和ERIC用于分子基因分型。通过用限制酶消化和深度测序获得质粒分析。结果从近200名患者中分离出KPC阳性临床样品。在最初的暴发中，重症监护室几乎全都参与其中，而医疗，外科和长期病房相继受到广泛关注。对KPC等位基因，质粒和细菌序列类型（ST）的分析表明，在最初暴发期间，ST258中的KPC-3和ST147中的KPC-2分别被限制在两家接受监视的医院之一。尽管有效地控制了KPC-2的传播，但观察到ST258交叉传播中的KPC-3。在三名患者中还观察到在同一分离物中同时存在两种碳青霉烯酶（VIM-1和KPC-2）。两种KPC-3菌株的质粒含量的总测序表明抗性质粒具有新型关联。结论获得性分子流行病学表明：1）从外部来源获得的信息以及医院内部患者的重新安置均与观察到的传播有关; 2）编码KPC-3的肺炎克雷伯菌ST258胜过其他菌株。此外，KPC介导的耐药性向非重症监护病房的大规模转移可能会导致耐药性向非住院患者的传播。因此，建议将碳青霉烯酶生产者进行基因型分析和表型鉴定，即使在运输状态下，也应防止和抑制进一步的碳青霉烯酶耐药性传播。

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