Evaluation of Candida albicans and anaerobic bacterial co-expansion in vulvovaginal candidiasis: a cross-sectional study.

Background: Vulvovaginal candidiasis (VVC) is a common mucosal infection predominantly attributed to Candida albicans (C. albicans). However, this yeast frequently colonizes the vaginal niche without causing symptoms, indicating that additional microbial and host factors might contribute to disease onset and/or pathology. This study investigated whether VVC is associated with a shift in the vaginal microbiota. Methods: Vaginal samples from 96 non-pregnant women were stratified into three study groups: healthy (NEG, n = 54), asymptomatic (ASYMP, n = 20), and symptomatic (SYMP, n = 22). Vaginal pH, PMN infiltration, and C. albicans morphology in vaginal samples were assessed microscopically, while fungal load was quantified by qPCR and isolates were tested for hyphal formation and biofilm production. Vaginal microbiota was analyzed by 16S rRNA amplicon sequencing on a subset of 43 representative vaginal samples. Results: Most SYMP women exhibited a characteristic inflammatory profile, with 75% showing a vaginal pH ≥ 4.5, 95.45% presenting marked PMN infiltration (score 2) and all displaying filamentous C. albicans forms in vivo. In contrast, 90.91% of ASYMP women had a vaginal pH 4.5, none showed PMN infiltration (score 0), and 65% displayed the fungus exclusively in the yeast form. The vaginal burden of C. albicans DNA was 4.9-fold higher in SYMP than in ASYMP women. Of interest, symptomatic disease was associated with the selective co-enrichment of the anaerobic bacteria Dialister micraerophilus and Aerococcus christensenii, which emerged as the main microbial features distinguishing SYMP from ASYMP women. Notably, the relative abundance of Dialister micraerophilus positively correlated with both PMN infiltration score and vaginal pH. Conclusion: These findings identify Dialister micraerophilus and Aerococcus christensenii as key anaerobic bacterial signatures associated with VVC. Further studies are needed to assess the possible role of these bacteria in VVC causation or modification.