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<p>Bacterial pathogens adapt to host niches because of selective within-host pressures, an evolutionary process that offers invaluable insights into host-pathogen interactions. Here, we retrospectively track the evolution of a single multiresistant <i>Klebsiella pneumoniae</i> clone in 110 patients over a 5-year nosocomial outbreak. We combine comparative genomics with phenotypic characterization of mucoviscosity, serum survival, iron utilization, biofilm formation, and infection potential in <i>Galleria mellonella</i> for all isolates. Strong positive selection within patients targeted key virulence factors. Notably, convergent evolutionary trajectories were dominated by reduced acute virulence and recurrent changes in iron uptake regulation, capsule and lipopolysaccharide, and enhanced biofilm formation. These phenotypic changes likely represent clinical niche adaptations, with some resulting in trade-offs during gastrointestinal colonization. This study underscores the dynamic nature of within-host evolution and its role in shaping virulence in opportunistic pathogens, even on short time scales.</p>

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Parallel within-host evolution alters virulence factors in an opportunistic Klebsiella pneumoniae during a hospital outbreak

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月30日

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  • Greta Zaborskytė,
  • Karin Hjort,
  • Birgitta Lytsy,
  • Linus Sandegren

摘要

Bacterial pathogens adapt to host niches because of selective within-host pressures, an evolutionary process that offers invaluable insights into host-pathogen interactions. Here, we retrospectively track the evolution of a single multiresistant Klebsiella pneumoniae clone in 110 patients over a 5-year nosocomial outbreak. We combine comparative genomics with phenotypic characterization of mucoviscosity, serum survival, iron utilization, biofilm formation, and infection potential in Galleria mellonella for all isolates. Strong positive selection within patients targeted key virulence factors. Notably, convergent evolutionary trajectories were dominated by reduced acute virulence and recurrent changes in iron uptake regulation, capsule and lipopolysaccharide, and enhanced biofilm formation. These phenotypic changes likely represent clinical niche adaptations, with some resulting in trade-offs during gastrointestinal colonization. This study underscores the dynamic nature of within-host evolution and its role in shaping virulence in opportunistic pathogens, even on short time scales.