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<p>Virulence plasmids are key drivers of hypervirulence in <i>Klebsiella pneumoniae</i>. Here, we report a systematic analysis of chromosomal integration of a p17-15vir-derived fragment carrying virulence (<i>rmpA2</i> and <i>iutA</i>-<i>iucABCD</i>) and resistance genes in nine <i>bla</i><sub>KPC−2</sub>-positive ST11-KL47 carbapenem-resistant <i>K. pneumoniae</i> (CRKP) isolates. Of these, seven exhibited a hypervirulent phenotype in a mouse infection model. Nanopore sequencing analysis revealed that these virulence-associated integration regions could be classified into three distinct groups based on their structural patterns. Notably, we investigated the mechanisms underlying the formation of the integration region and proposed an IS<i>26</i>-mediated model for the integration of virulence gene-carrying plasmid fragment into the chromosome. Besides, IS<i>Kpn1</i> was identified for the first time as a preferred insertion hotspot. Both <i>bla</i><sub>KPC−2</sub> and <i>rmpA2</i> demonstrated stable persistence in these isolates without antibiotic selection pressure, and group I integration regions displayed the capability to form circular intermediates. These findings provide critical insights into the virulence plasmid fragment integrated into their chromosomes and underscore the importance of surveillance for such hybrid threats.</p>

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ST11 carbapenem-resistant Klebsiella pneumoniae integrates virulence plasmid fragments into the chromosome via insertion sequence

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月11日

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  • Xu Liu,
  • Lijuan Xu,
  • Huiyue Dong,
  • Shangshang Qin,
  • Yan Li,
  • Hong Yao

摘要

Virulence plasmids are key drivers of hypervirulence in Klebsiella pneumoniae. Here, we report a systematic analysis of chromosomal integration of a p17-15vir-derived fragment carrying virulence (rmpA2 and iutA-iucABCD) and resistance genes in nine blaKPC−2-positive ST11-KL47 carbapenem-resistant K. pneumoniae (CRKP) isolates. Of these, seven exhibited a hypervirulent phenotype in a mouse infection model. Nanopore sequencing analysis revealed that these virulence-associated integration regions could be classified into three distinct groups based on their structural patterns. Notably, we investigated the mechanisms underlying the formation of the integration region and proposed an IS26-mediated model for the integration of virulence gene-carrying plasmid fragment into the chromosome. Besides, ISKpn1 was identified for the first time as a preferred insertion hotspot. Both blaKPC−2 and rmpA2 demonstrated stable persistence in these isolates without antibiotic selection pressure, and group I integration regions displayed the capability to form circular intermediates. These findings provide critical insights into the virulence plasmid fragment integrated into their chromosomes and underscore the importance of surveillance for such hybrid threats.