Genomic Analysis of the Emergence and Rapid Global Dissemination of the Clonal Group 258 Klebsiella pneumoniae Pandemic.
Genomic Analysis of the Emergence and Rapid Global Dissemination of the Clonal Group 258 Klebsiella pneumoniae Pandemic.
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DOI：
10.1371/journal.pone.0133727
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Limbago BM
中科院分区：
文献类型：
--
作者：
Bowers JR;Kitchel B;Driebe EM;MacCannell DR;Roe C;Lemmer D;de Man T;Rasheed JK;Engelthaler DM;Keim P;Limbago BM
产生KPC碳青霉烯酶的耐多药肺炎克雷伯菌已在世界各地迅速蔓延，在有限的抗菌治疗选择下造成严重的卫生保健相关感染。产生kpc的肺炎克雷伯菌的传播主要归因于单一优势菌株ST258的扩增。在这项研究中，我们利用17年来从20个国家收集的167株ST258及其克隆群CG258的全基因组序列分析，探讨了ST258及其克隆群CG258的系统发育关系和进化。我们的研究结果表明，一个共同的ST258祖先在1995年左右从其多样化的亲本克隆群体中出现，并且可能在传播之前获得了bla KPC。在过去的20年里，尽管ST258的附属元件多样性和荚膜多糖合成位点的分化，但它仍然保持着高度克隆性。除了产生ST258的大型重组事件外，很少有突变将其与克隆群区分开来。然而，一个突变发生在一个全局转录调节因子中。外膜蛋白序列的表征显示ST258中包含一个截断的OmpK35和修饰的OmpK37。我们的工作阐明了ST258致病成功的潜在基因组贡献者，帮助我们更好地了解该菌株的全球传播，并确定了ST258特有的遗传标记。
Multidrug-resistant Klebsiella pneumoniae producing the KPC carbapenemase have rapidly spread throughout the world, causing severe healthcare-associated infections with limited antimicrobial treatment options. Dissemination of KPC-producing K. pneumoniae is largely attributed to expansion of a single dominant strain, ST258. In this study, we explore phylogenetic relationships and evolution within ST258 and its clonal group, CG258, using whole genome sequence analysis of 167 isolates from 20 countries collected over 17 years. Our results show a common ST258 ancestor emerged from its diverse parental clonal group around 1995 and likely acquired bla KPC prior to dissemination. Over the past two decades, ST258 has remained highly clonal despite diversity in accessory elements and divergence in the capsule polysaccharide synthesis locus. Apart from the large recombination event that gave rise to ST258, few mutations set it apart from its clonal group. However, one mutation occurs in a global transcription regulator. Characterization of outer membrane protein sequences revealed a profile in ST258 that includes a truncated OmpK35 and modified OmpK37. Our work illuminates potential genomic contributors to the pathogenic success of ST258, helps us better understand the global dissemination of this strain, and identifies genetic markers unique to ST258.