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Group BStreptococcus (GBS) is a leading cause of neonatal sepsis, pneumonia, and meningitis worldwide. In the majority of cases, GBS is transmitted vertically from mother to neonate, making maternal vaginal colonization a key risk factor for neonatal disease. The fungusCandida albicans is an opportunistic pathogen of the female genitourinary tract and the causative agent of vaginal thrush. Carriage ofC. albicans has been shown to be an independent risk factor for vaginal colonization by GBS. However, the nature of interactions between these two microbes is poorly understood. This study provides evidence of a reciprocal, synergistic interplay between GBS andC. albicans that may serve to promote their cocolonization of the vaginal mucosa. GBS strains NEM316 (serotype III) and 515 (serotype Ia) are shown to physically interact withC. albicans , with the bacteria exhibiting tropism for candidal hyphal filaments. This interaction enhances association levels of both microbes with the vaginal epithelial cell line VK2/E6E7. The ability of GBS to coassociate withC. albicans is dependent upon expression of the hypha-specific adhesin Als3. In turn, expression of GBS antigen I/II family adhesins (Bsp polypeptides) facilitates this coassociation and confers upon surrogateLactococcus lactis the capacity to exhibit enhanced interactions withC. albicans on vaginal epithelium. As genitourinary tract colonization is an essential first step in the pathogenesis of GBS andC. albicans , the coassociation mechanism reported here may have important implications for the risk of disease involving both of these pathogens.

Coassociation between Group B Streptococcus and Candida albicans Promotes Interactions with Vaginal Epithelium