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Updated: May 2, 2026
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A Murine Model of Group B Streptococcus Vaginal Colonization
Published on: November 16, 2016
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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.
Infection and Immunity
|April 30, 2026
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.
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.
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