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<p>Aortitis due to hypervirulent <i>Klebsiella pneumoniae</i> (hvKp) in a Belarusian male from central New York is described. Isolates at the time of diagnosis (Kp031824-1, Kp031824-2) and after 12 weeks of antimicrobial therapy (Kp070124) were characterized. Kp070124 was genomically and phenotypically unchanged retaining its capsular polysaccharide and mucoviscosity. In vitro studies established that capsule minus derivatives of Kp031824-1 and Kp031824-2 can occur due to mutations in <i>wcaJ</i>. But this genotype/phenotype was not selected for in Kp070124 after ≥15 weeks in the systemic compartment. Compared to capsule minus derivatives, the capsule positive phenotype demonstrated resistance to phagocytosis, but not to complement mediated bactericidal activity, suggesting resistance to phagocytosis is a more important defense mechanism at this site of infection. These data also support that a capsule positive, mucoviscous phenotype is selected for during infections in the systemic compartment. The surprising result that capsule positive strains have increased sensitivity to complement mediated bactericidal activity compared to capsule minus strains requires further investigation. The duration of therapy for this syndrome remains unclear but should be prolonged; adjunctive therapies (e.g. phage therapy, passive immunization, augmentation of cell mediated bactericidal activity) may be needed to overcome the protection endowed by the mucoviscous capsule of hvKp.</p>

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Hypervirulent Klebsiella pneumoniae causing aortitis retains its capsule and mucoviscosity and remains genotypically and phenotypically stable over time

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月13日

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  • Thomas A. Russo,
  • Ulrike Carlino-MacDonald,
  • Zachary J. Drayer,
  • Connor J. Davies,
  • Alan Hutson,
  • Ting L. Luo,
  • Melissa J. Martin,
  • Patrick T. McGann,
  • Francois Lebreton,
  • Alan Sanders

摘要

Aortitis due to hypervirulent Klebsiella pneumoniae (hvKp) in a Belarusian male from central New York is described. Isolates at the time of diagnosis (Kp031824-1, Kp031824-2) and after 12 weeks of antimicrobial therapy (Kp070124) were characterized. Kp070124 was genomically and phenotypically unchanged retaining its capsular polysaccharide and mucoviscosity. In vitro studies established that capsule minus derivatives of Kp031824-1 and Kp031824-2 can occur due to mutations in wcaJ. But this genotype/phenotype was not selected for in Kp070124 after ≥15 weeks in the systemic compartment. Compared to capsule minus derivatives, the capsule positive phenotype demonstrated resistance to phagocytosis, but not to complement mediated bactericidal activity, suggesting resistance to phagocytosis is a more important defense mechanism at this site of infection. These data also support that a capsule positive, mucoviscous phenotype is selected for during infections in the systemic compartment. The surprising result that capsule positive strains have increased sensitivity to complement mediated bactericidal activity compared to capsule minus strains requires further investigation. The duration of therapy for this syndrome remains unclear but should be prolonged; adjunctive therapies (e.g. phage therapy, passive immunization, augmentation of cell mediated bactericidal activity) may be needed to overcome the protection endowed by the mucoviscous capsule of hvKp.