Comparative analysis of the complete genome of KPC-2-producing Klebsiella pneumoniae Kp13 reveals remarkable genome plasticity and a wide repertoire of virulence and resistance mechanisms.
Comparative analysis of the complete genome of KPC-2-producing Klebsiella pneumoniae Kp13 reveals remarkable genome plasticity and a wide repertoire of virulence and resistance mechanisms.
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DOI：
10.1186/1471-2164-15-54
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发表时间：
2014-01-22
期刊：
影响因子：
4.4
通讯作者：
Nicolás MF
中科院分区：
文献类型：
--
作者：
Ramos PI;Picão RC;Almeida LG;Lima NC;Girardello R;Vivan AC;Xavier DE;Barcellos FG;Pelisson M;Vespero EC;Médigue C;Vasconcelos AT;Gales AC;Nicolás MF
肺炎克雷伯菌是一种与医院和社区获得性感染相关的重要机会性病原体。肺炎克雷伯菌基因组中存在广泛的毒力和抗微生物药物耐药性基因，这可能对治疗某些菌株引起的感染构成额外的挑战。肺炎克雷伯菌Kp13是一种多重耐药菌株，导致巴西南部一所教学医院发生大规模院内疫情。Kp13产生肺炎克雷伯菌碳青霉烯酶（KPC-2），但与属于ST 258和ST 11的分离株无关，ST 258和ST 11是产生kpc的肺炎克雷伯菌在全球传播的主要聚集群。在本报告中，我们对Kp13与以下三个肺炎克雷伯菌基因组：MGH 78578、NTUH-K2044和342进行了基因组比较。我们完全确定了肺炎克雷伯菌Kp13的基因组，包括1条染色体（5.3 Mbp）和6个质粒（0.43 Mbp）。在菌株Kp13中鉴定出几个毒力和抗性决定因素。具体来说，我们检测了6种β -内酰胺酶（SHV-12、OXA-9、TEM-1、CTX-M-2、SHV-110和KPC-2）的编码基因，以及8个粘附素相关的基因簇，包括编码1型（film）和3型（mrk）纤维粘附素的区域。还检测到rmtG质粒16S rRNA甲基转移酶基因，以及属于五个不同家族的外排泵。在OmpK35孔蛋白编码基因上游发现突变，可能影响其表达。相对于比较菌株的snp分析显示，141个突变落在与耐药相关的CDSs内，这也可能影响Kp13的生活方式。最后，在一个可塑性区域内确定了合成叶尔辛吸素铁载体的遗传装置。染色体结构分析允许检测Kp13相对于比较菌株的13个差异区域。我们的研究结果表明，发生在许多层次上的可塑性（从整个基因组片段到单个核苷酸碱基）可能对肺炎克雷伯菌Kp13的生活方式起作用，并表明全基因组测序对研究细菌病原体的重要性。在比较的细菌中，一般的染色体结构在一定程度上是保守的，重组事件导致基因组片段的增加/损失似乎是推动这些菌株进化的原因。
Klebsiella pneumoniae is an important opportunistic pathogen associated with nosocomial and community-acquired infections. A wide repertoire of virulence and antimicrobial resistance genes is present in K. pneumoniae genomes, which can constitute extra challenges in the treatment of infections caused by some strains. K. pneumoniae Kp13 is a multidrug-resistant strain responsible for causing a large nosocomial outbreak in a teaching hospital located in Southern Brazil. Kp13 produces K. pneumoniae carbapenemase (KPC-2) but is unrelated to isolates belonging to ST 258 and ST 11, the main clusters associated with the worldwide dissemination of KPC-producing K. pneumoniae. In this report, we perform a genomic comparison between Kp13 and each of the following three K. pneumoniae genomes: MGH 78578, NTUH-K2044 and 342. We have completely determined the genome of K. pneumoniae Kp13, which comprises one chromosome (5.3 Mbp) and six plasmids (0.43 Mbp). Several virulence and resistance determinants were identified in strain Kp13. Specifically, we detected genes coding for six beta-lactamases (SHV-12, OXA-9, TEM-1, CTX-M-2, SHV-110 and KPC-2), eight adhesin-related gene clusters, including regions coding for types 1 (fim) and 3 (mrk) fimbrial adhesins. The rmtG plasmidial 16S rRNA methyltransferase gene was also detected, as well as efflux pumps belonging to five different families. Mutations upstream the OmpK35 porin-encoding gene were evidenced, possibly affecting its expression. SNPs analysis relative to the compared strains revealed 141 mutations falling within CDSs related to drug resistance which could also influence the Kp13 lifestyle. Finally, the genetic apparatus for synthesis of the yersiniabactin siderophore was identified within a plasticity region. Chromosomal architectural analysis allowed for the detection of 13 regions of difference in Kp13 relative to the compared strains. Our results indicate that the plasticity occurring at many hierarchical levels (from whole genomic segments to individual nucleotide bases) may play a role on the lifestyle of K. pneumoniae Kp13 and underlie the importance of whole-genome sequencing to study bacterial pathogens. The general chromosomal structure was somewhat conserved among the compared bacteria, and recombination events with consequent gain/loss of genomic segments appears to be driving the evolution of these strains.
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