Group B Streptococcus (GBS) is a leading cause of neonatal sepsis and meningitis. In most cases, GBS is transmitted vertically from mother to baby during or just preceding birth. Maternal genitourinary tract colonisation is thus a significant risk factor for neonatal GBS disease. Candida albicans is the predominant fungal pathogen affecting humans, causing a range of infections from systemic candidiasis to oral or vaginal thrush. Most women (75%) will experience vaginal thrush, with pregnancy increasing the likelihood of disease.
We have shown previously that a synergistic relationship exists between oral Streptococcus bacteria and C. albicans within the oral cavity. This study aims to investigate if a similar interkingdom association exists between C. albicans and GBS, and how this may influence the colonisation or pathogenic capabilities of these two microorganisms within the genitourinary tract.
In vitro assays show that C. albicans promotes association of GBS with vaginal epithelial cells, and vice versa. Furthermore, utilising knockout, complemented and heterologous expression strains, GBS antigen I/II family adhesins (BspA/BspC) and candidal hypha-specific adhesin Als3 are identified as critical molecular determinants of this process. Modulation of host responses by this association has also been explored.
This work shows for the first time that C. albicans and GBS may interact synergistically to enhance colonisation of vaginal epithelium, and that surface proteins belonging to two major adhesin families play a critical role in this association. Such interkingdom interactions may serve as novel targets to combat risk of both maternal and neonatal disease by these pathogenic microbes.