CAS Key Laboratory of Genome Sciences & Information, Beijing Institute of Genomics, Chinese Academy of Sciences, China National Center for Bioinformation, Beijing, China; University of Chinese Academy of Sciences, Beijing, China.
CAS Key Laboratory of Genome Sciences & Information, Beijing Institute of Genomics, Chinese Academy of Sciences, China National Center for Bioinformation, Beijing, China.
J Glob Antimicrob Resist. 2020 Sep;22:426-433. doi: 10.1016/j.jgar.2020.04.009. Epub 2020 Apr 18.
We investigated the pathogenesis of a patient with severe acute pancreatitis by comprehensively analysing a rare carbapenem-resistant hypervirulent K1/ST1265 Klebsiella pneumoniae (CR-HvKP) strain.
We conducted virulence and multidrug-resistance phenotypic characterization and identified a CR-HvKP strain from the patient. It was subjected to Pacbio sequencing, and subsequent analysis of virulence, resistance genes and mobile genetic elements.
We described the phenotype and genotype of a rare CR-HvKP strain with an untypeable bla-harboured conjugative plasmid and a pLVPK-like virulent plasmid. Resistance gene analysis showed that the untypeable bla-harboured plasmid was formed by IS26-mediated recombination of bla-embedded transposon Tn6500 into pCN061p4 from Escherichia coli. Interestingly, it had an R-M system that might protect plasmid from cleavage. This may facilitate the stabilization of plasmids in bacteria in the event of missing CR-plasmid during transmission. Virulence gene analysis indicated 78 virulence genes on the genome, including 67 on the chromosome (37 in high-pathogenic island) and 11 on the pLVPK-like virulence plasmid (harbouring rmpA/rmpA2). Further phylogenetic analysis revealed that the CR-HvKP evolved from HvKP through acquiring an antimicrobial-resistance plasmid.
Our research, to our knowledge, first reported a ST1265/K1 CR-HvKP strain with an untypeable bla-harboured plasmid. The trend that HvKP could evolve into CR-HvKP by obtaining stabilized/conjugative bla-carrying plasmids is a considerable threat to public health and should be closely supervised.
通过综合分析一株罕见的耐碳青霉烯高毒力 K1/ST1265 肺炎克雷伯菌（CR-HvKP），研究 1 例重症急性胰腺炎患者的发病机制。
对患者分离的一株耐碳青霉烯高毒力肺炎克雷伯菌进行毒力和多重耐药表型特征分析，并进行 Pacbio 测序，随后对毒力基因、耐药基因和移动遗传元件进行分析。
我们描述了一株罕见的耐碳青霉烯高毒力肺炎克雷伯菌的表型和基因型，该菌含有一个无法分型的 bla 基因携带的可接合质粒和一个 pLVPK 样毒力质粒。耐药基因分析表明，无法分型的 bla 基因携带质粒是由 bla 基因插入转座子 Tn6500 通过 IS26 介导重组插入大肠杆菌 pCN061p4 形成的。有趣的是，它含有一个 R-M 系统，可能保护质粒免受切割。这可能有助于在传代过程中缺失 CR 质粒时稳定细菌中的质粒。毒力基因分析表明，基因组上有 78 个毒力基因，包括染色体上的 67 个（高致病性岛 37 个）和 pLVPK 样毒力质粒上的 11 个（携带 rmpA/rmpA2）。进一步的系统发育分析表明，该耐碳青霉烯高毒力肺炎克雷伯菌是由高毒力肺炎克雷伯菌通过获得一个抗菌药物耐药质粒进化而来的。
据我们所知，本研究首次报道了一株 ST1265/K1 耐碳青霉烯高毒力肺炎克雷伯菌，携带无法分型的 bla 基因的可接合质粒。高毒力肺炎克雷伯菌通过获得稳定/可接合的 bla 基因携带质粒进化为耐碳青霉烯高毒力肺炎克雷伯菌的趋势对公共健康构成了相当大的威胁，应密切监测。
