Comparative analysis of commensal and pathogenic vulvovaginal clinical isolates of Candida albicans: hyphal morphology, molecular genetics and phylogenetic relationships

Introduction. Vulvovaginal candidiasis (VVC) is a common disorder affecting approximately 75% of women of childbearing age at least once during their life and it is caused primarily by Candida albicans. However, C. albicans is also a normal harmless commensal of the vaginal mucosa, hence a long-standing question is how the fungus switches from commensal state to a virulent pathogen. Studies performed in a murine vaginitis model suggest that host inflammatory processes drive the onset of symptomatic infection. Accordingly, our recent work on clinical samples from colonized and symptomatic women revealed different propensity to form hyphae. In addition, β-glucan, a fungal cell wall pro-inflammatory polysaccharide, was largely masked from immune recognition during vaginitis and enhanced β-glucan availability was only found in hyphae from symptomatic patients with a concomitant massive neutrophil infiltration. Materials and Methods. To further investigate any association between fungal virulence traits and VVC outcome, the following parameters were analyzed on commensal and clinically relevant isolates: MLST analysis, sequencing of the gene encoding the candidalysin toxin and percentage of hyphal fragments. Results. The results obtained so far suggest that none of these fungus-related parameters allow to discriminate between commensal and clinically relevant isolates. Discussion and Conclusions. Taken together, our preliminary data indicate that host-intrinsic mechanisms, rather than the fungus’ intrinsic virulence traits, may play a key role in the occurrence of VVC.