RodA Promotes Intestinal Colonization by Group B Streptococcus.

Area of Science:

• Microbiology
• Bacterial Pathogenesis
• Molecular Biology

Background:

• Group B Streptococcus (GBS) intestinal colonization is a key factor in infant late-onset disease.
• The gene rodA encodes a peptidoglycan polymerase involved in bacterial cell wall synthesis and integrity.

Purpose of the Study:

• To investigate the role of rodA in GBS gastrointestinal colonization.
• To understand the impact of rodA deletion on GBS morphology, growth, and host cell interactions.

Main Methods:

• Comparison of wild-type GBS (A909 WT) and a rodA deletion mutant (A909ΔrodA) in a murine model.
• Transmission electron microscopy (TEM) for morphological analysis.
• In vitro assessment of growth under stress and host cell adhesion.

Main Results:

• The A909ΔrodA mutant exhibited altered morphology (chaining/aggregation) and confirmed capsule presence.
• In competitive colonization, A909 WT outcompeted A909ΔrodA, though monocolonization showed similar bacterial burdens.
• The mutant showed impaired growth in bile and increased adhesion to intestinal epithelial cells in vitro.

Conclusions:

• rodA is crucial for GBS intestinal colonization fitness.
• Deletion of rodA increases GBS susceptibility to GI stressors and reduces its competitive ability in vivo.