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RodA promotes intestinal colonization by group B Streptococcus.

Michelle J Vaz1, Sanjana Sankaran1, Molly E Sharp2

  • 1Department of Pediatrics, NYU Grossman School of Medicine, New York, New York, USA.

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Summary

Group B Streptococcus (GBS) rodA is essential for gut colonization fitness. Deleting rodA impairs GBS competition in mice and increases susceptibility to bile, highlighting its role in intestinal survival.

Keywords:
Streptococcus agalactiae (Group B Streptococcus)gastrointestinal colonizationmurine modelrodA

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Pathogenesis

Background:

  • Group B Streptococcus (GBS) intestinal colonization is a key factor in infant late-onset disease.
  • The shape, elongation, division, and sporulation (SEDS) family protein RodA is involved in bacterial cell wall synthesis and integrity.

Purpose of the Study:

  • To investigate the role of the peptidoglycan polymerase gene rodA in GBS gastrointestinal colonization.
  • To assess the impact of rodA deletion on GBS morphology, growth under stress, host cell interaction, and colonization competitiveness.

Main Methods:

  • Comparison of wild-type (A909 WT) and isogenic rodA deletion mutant (A909ΔrodA) GBS strains.
  • Transmission electron microscopy (TEM) for morphological analysis.
  • Murine monocolonization and cocolonization models to assess GI tract colonization.
  • In vitro growth assays under intestinal stress conditions (e.g., bile) and adhesion assays with intestinal epithelial cells.

Main Results:

  • A909ΔrodA exhibited a unique chaining/aggregation phenotype and confirmed capsule presence.
  • In cocolonization, A909 WT outcompeted A909ΔrodA, but monocolonization showed comparable bacterial burdens.
  • The ΔrodA mutant displayed impaired growth in bile and increased adhesion to intestinal epithelial cells in vitro.

Conclusions:

  • RodA is crucial for GBS fitness and competitive colonization in the murine gut.
  • Deletion of rodA increases GBS sensitivity to gastrointestinal stressors and impairs in vivo competitive ability.