Clinical overview
Vulvovaginal candidiasis (VVC) is one of the most common reasons women self-medicate, present to pharmacists, and arrive at gynaecology clinics. Up to 75% of women will experience at least one episode in their lifetime; ~10% develop recurrent (≥4 episodes per year) disease, the management of which is more nuanced than acute single episodes. The pathology — fungal colonisation transitioning to symptomatic infection in the right immunological and microbial milieu — explains why it is so common and why it recurs.
Core knowledge
Aetiology
- Candida albicans — 80–90% of clinically symptomatic episodes.
- Non-albicans Candida species: C. glabrata, C. krusei, C. parapsilosis, C. tropicalis — more common in recurrent disease, immunocompromise, postmenopausal women, and after antifungal exposure; often more resistant to azoles.
Candida is part of normal gut and sometimes vaginal flora. Symptomatic infection arises when:
- Local immune environment changes (high oestrogen, pregnancy, COC, glucocorticoids, immunosuppression).
- Antibiotic use disrupts protective lactobacilli.
- Glycaemic control deteriorates (diabetes).
- Local barrier disruption (irritants, tight clothing).
- HIV infection with low CD4 — recurrent candidiasis is one of the WHO clinical staging signs.
Pathology
Candida yeast and pseudohyphae adhere to damaged vaginal epithelium while PMNs drive itch, erythema and oedema.
- Yeast-to-hyphal phenotype switch is associated with virulence; hyphal forms invade epithelium.
- Adhesion via candidal adhesins (Als family proteins) to vaginal epithelial cells.
- Epithelial damage, breakdown of barrier, exposure of nerves → itch and burning.
- Inflammatory response with PMN infiltration, oedema, erythema.
- Biofilm formation in chronic/recurrent disease; biofilm enhances antifungal resistance.
Clinical features (correlating pathology to presentation)
