Vaginal candidiasis is a common disorder in women of childbearing age, caused primarily by Candida albicans. Since C. albicans is a commensal fungus of the vaginal mucosa, a long-standing question is how the fungus switches from being a harmless commensal to a virulent pathogen. Clinical studies and murine vaginitis models suggest that host inflammatory processes drive the onset of symptomatic infection. In previous work with fresh clinical samples, we found that the pro-inflammatory cell wall polysaccharide β-glucan is largely masked from immune recognition during vulvovaginal infection. Enhanced β-glucan availability was only found in hyphae from symptomatic patients with strong neutrophil infiltration. There was high variability in levels of β-glucan exposure and hyphal morphology among colonizing and infection-associated isolates, and we reasoned that this could be explained by fungal-intrinsic factors and/or host-associated traits. We assayed several aspects of C. albicans isolated from symptomatic and asymptomatic individuals to determine any associations between fungal-intrinsic traits and virulence: MLST analysis, sequencing of the gene encoding the candidalysin toxin, and propensity to form hyphal cells. Preliminary results suggest that none of these indicators correlates with isolates causing symptomatic infection, indicating that host-intrinsic mechanisms may play the most important role in the occurrence of symptomatic infections
