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Objective <p>Hypervirulent <i>Klebsiella pneumoniae</i> (hvKp)–associated pyogenic liver abscess is most commonly linked to K1/K2 capsule serotypes and canonical lineages such as ST23, ST65, and ST86. Reports of hvKp outside these lineages remain rare but carry significant public health implications. We investigated an unusual case of liver abscess in an immunocompetent patient caused by hvKp sequence type 111 (ST111).</p> Methods <p>Five isolates (KP1–KP5) recovered from a patient with pyogenic liver abscess were characterized by antimicrobial susceptibility testing, whole-genome sequencing, and pulsed-field gel electrophoresis. To investigate the contribution of the virulence plasmid to the host strain, CRISPR/Cas9-mediated plasmid curing was performed, followed by functional analyses including phenotypic characterization and a murine infection model. In addition, comparative genomic analyses were conducted to elucidate the epidemiological relationships and genetic determinants underlying hypervirulence.</p> Results <p>The five isolates recovered from the patient were genetically identical. Genomic analysis identified a 181&#xa0;kb IncHI1B/IncFIB virulence plasmid encoding rmpADC and the salmochelin cluster (iroBCDN), but lacking iuc and rmpA2. Remarkably, the plasmid also carried the yersiniabactin locus (ybt), typically chromosomal in origin. Comparative genomics revealed that similar ST111 strains have been reported exclusively in China, suggesting clonal expansion of a previously unrecognized hvKp lineage. Functional assays demonstrated that plasmid curing abolished the hypermucoviscous phenotype, reduced capsule production, and completely attenuated virulence in murine models, confirming the plasmid as the principal driver of hypervirulence. Interestingly, plasmid loss enhanced biofilm formation and alleviated growth burden, indicating fitness trade-offs associated with virulence.</p> Conclusion <p>This study describes a rare case of hvKp ST111 liver abscess and identifies a novel plasmid conferring hypervirulence. These findings broaden the recognized diversity of hvKp and highlight that non-canonical lineages can acquire potent virulence determinants capable of causing severe disease. Ongoing clinical and genomic surveillance is essential to detect and contain emerging hvKp clones before widespread dissemination.</p>

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Emergence of hypervirulent Klebsiella pneumoniae ST111 with a novel virulence plasmid causing pyogenic liver abscess

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月22日

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  • Liya Feng,
  • Ke Liu,
  • Yuheng Liu,
  • Lu Ouyang,
  • Xiutao Dong,
  • Zongguo Sun,
  • Liang Chen,
  • Xiaohong Shi,
  • Mingju Hao

摘要

Objective

Hypervirulent Klebsiella pneumoniae (hvKp)–associated pyogenic liver abscess is most commonly linked to K1/K2 capsule serotypes and canonical lineages such as ST23, ST65, and ST86. Reports of hvKp outside these lineages remain rare but carry significant public health implications. We investigated an unusual case of liver abscess in an immunocompetent patient caused by hvKp sequence type 111 (ST111).

Methods

Five isolates (KP1–KP5) recovered from a patient with pyogenic liver abscess were characterized by antimicrobial susceptibility testing, whole-genome sequencing, and pulsed-field gel electrophoresis. To investigate the contribution of the virulence plasmid to the host strain, CRISPR/Cas9-mediated plasmid curing was performed, followed by functional analyses including phenotypic characterization and a murine infection model. In addition, comparative genomic analyses were conducted to elucidate the epidemiological relationships and genetic determinants underlying hypervirulence.

Results

The five isolates recovered from the patient were genetically identical. Genomic analysis identified a 181 kb IncHI1B/IncFIB virulence plasmid encoding rmpADC and the salmochelin cluster (iroBCDN), but lacking iuc and rmpA2. Remarkably, the plasmid also carried the yersiniabactin locus (ybt), typically chromosomal in origin. Comparative genomics revealed that similar ST111 strains have been reported exclusively in China, suggesting clonal expansion of a previously unrecognized hvKp lineage. Functional assays demonstrated that plasmid curing abolished the hypermucoviscous phenotype, reduced capsule production, and completely attenuated virulence in murine models, confirming the plasmid as the principal driver of hypervirulence. Interestingly, plasmid loss enhanced biofilm formation and alleviated growth burden, indicating fitness trade-offs associated with virulence.

Conclusion

This study describes a rare case of hvKp ST111 liver abscess and identifies a novel plasmid conferring hypervirulence. These findings broaden the recognized diversity of hvKp and highlight that non-canonical lineages can acquire potent virulence determinants capable of causing severe disease. Ongoing clinical and genomic surveillance is essential to detect and contain emerging hvKp clones before widespread dissemination.