RodA Promotes Intestinal Colonization by Group B Streptococcus

Background Group B Streptococcus (GBS) intestinal colonization is critical for the pathogenesis of late-onset (LO) disease in infants. Using a murine model, we explore the role of rodA , which encodes a peptidoglycan polymerase RodA, belonging to the Shape, Elongation, Division, and Sporulation (SEDS) family that participates in peptidoglycan synthesis and maintenance of cell wall integrity. Methods We investigated the contribution of rodA to GBS gastrointestinal (GI) colonization using a wild-type strain (A909 WT) and an isogenic in-frame deletion mutant of rodA (A909Δ rodA ). Morphological differences between the two strains were examined by transmission electron microscopy (TEM), and the contribution of rodA to GI colonization was assessed in a murine model through monocolonization and cocolonization experiments. We evaluated the growth of the mutant strain under intestinal physiological stress conditions and characterized its interactions with host epithelial cells in vitro. Results A909Δ rodA showed a unique chaining/aggregation phenotype compared to the A909 WT strain, with the presence of capsule confirmed via TEM and immunoblotting. In murine cocolonization experiments, A909 WT outcompeted A909Δ rodA ; however, monocolonization experiments exhibited comparable colonization and bacterial burden across the GI tract. In vitro experiments revealed impaired growth in bile and an increase in adhesion to intestinal epithelial cells by the Δ rodA mutant. Conclusion(s) rodA plays a role in GBS intestinal colonization. Deletion of rodA increases sensitivity to gastrointestinal stressors in vitro and causes a pronounced defect in competition in vivo, suggesting that the presence of rodA increases the fitness of GBS in the gut.