Vulvovaginal candidiasis: pathogenesis, virulence factors, diagnosis, and therapeutic approach

Vulvovaginal candidiasis (VVC) is one of the most prevalent fungal infections worldwide, affecting millions of women annually, particularly those of reproductive age. The infection is primarily caused by Candida albicans , although non- albicans Candida (NAC) species such as C. glabrata, C. tropicalis, C. parapsilosis, and C. krusei are increasingly implicated in clinical cases. Various factors, including hormonal fluctuations, antibiotic use, immunosuppression, diabetes mellitus, and changes in vaginal microbiota composition, contribute to fungal overgrowth and infection. The clinical presentation of VVC is characterized by vulvovaginal itching, irritation, dysuria, and thick, white, odorless discharge. The pathogenesis of Candida spp. involves multiple virulence factors, including morphological transition, adhesion to epithelial cells, biofilm formation, enzymatic secretion, and immune evasion strategies. While conventional diagnostic methods such as microscopy and culture remain widely used, molecular approaches have improved the sensitivity and specificity of species identification. Antifungal therapy primarily relies on azoles, although emerging resistance to fluconazole among Candida species, particularly NAC, poses significant treatment challenges. This review provides a comprehensive analysis of the pathogenesis, virulence mechanisms, diagnosis, and therapeutic strategies for VVC, emphasizing the impact of antifungal resistance and the need for novel treatment approaches.