Candida glabrata intra-abdominal candidiasis is characterized by persistence within the peritoneal cavity and

Shaoji Cheng1, Cornelius J Clancy2, Douglas J Hartman3

  • 1Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Insights

This study reveals Candida glabrata

Area of Science:

  • Mycology
  • Infectious Diseases
  • Immunology

Background:

  • The pathogenesis of Candida glabrata infections remains poorly understood.
  • Candida glabrata is an opportunistic fungal pathogen causing significant morbidity and mortality.

Purpose of the Study:

  • To investigate the pathogenesis of intra-abdominal candidiasis (IAC) caused by Candida glabrata in a murine model.
  • To compare the virulence of different Candida glabrata strains and Candida albicans in IAC.
  • To elucidate the role of phospholipase B (PLB) in Candida glabrata pathogenesis.

Main Methods:

  • Intraperitoneal infection of mice with various strains of Candida glabrata and Candida albicans.
  • Assessment of mortality rates, abscess formation, fungal burdens, and neutrophil infiltration.
  • In vitro killing assays using human neutrophils.
  • Genetic manipulation of Candida glabrata, including disruption and reinsertion of PLB genes.

Main Results:

  • Candida glabrata strains exhibited variable virulence in IAC, with some causing high mortality.
  • A phospholipase B (PLB) deficient mutant showed reduced virulence, increased susceptibility to neutrophil killing, and faster abscess resolution.
  • Candida glabrata induced less severe acute disease but more persistent peritonitis and abscesses compared to Candida albicans in IAC.
  • Candida glabrata virulence was comparable to Candida albicans in hematogenously disseminated candidiasis.

Conclusions:

  • The developed mouse model of Candida glabrata IAC accurately mimics human disease and differentiates strain virulence.
  • Phospholipase B plays a role in Candida glabrata virulence and immune evasion.
  • Candida glabrata establishes persistent infections with dampened neutrophil responses, distinct from Candida albicans pathogenesis in IAC.

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