Vulvovaginal Candidiasis: A Current Understanding and Burning Questions. Original paper

What was reviewed?

This review article provided an extensive overview of vulvovaginal candidiasis (VVC), focusing on epidemiology, host immune response, fungal pathogenicity, microbiome interactions, and innovative therapeutic strategies. Specifically, it examined current knowledge surrounding Candida albicans and other Candida species as major pathogens in VVC, emphasizing the complexity of host-pathogen interactions and the multifactorial nature of this prevalent infection.

Who was reviewed?

The article synthesized information from various studies and clinical trials involving women who experience acute or recurrent VVC. It also included insights gained from animal models and cell-based studies designed to investigate underlying pathogenic mechanisms and host immune responses associated with VVC.

What were the most important findings?

The review highlighted several crucial findings regarding VVC pathogenesis. Candida albicans emerged as the primary causative agent, accounting for over 90% of cases, although non-albicans Candida (NAC) species, notably Candida glabrata, also significantly contributed to disease incidence. Key host-pathogen interactions were identified, including the yeast-to-hypha morphological transition as a critical event driving disease, accompanied by secretion of virulence factors such as candidalysin, a peptide essential for triggering inflammation. The NLRP3 inflammasome pathway was shown to be activated by candidalysin and other virulence factors, leading to neutrophil recruitment and inflammatory cytokine production, thus causing symptomatic inflammation rather than fungal clearance.

The microbiome was recognized as a potential factor influencing VVC development. Although Lactobacillus species generally maintain vaginal health through acid production, studies offered mixed findings regarding their protective role against Candida colonization. Some Lactobacillus strains provided antifungal effects, while others showed limited inhibitory activity, suggesting strain-specific differences in microbiome composition could influence susceptibility to infection.

What are the greatest implications of this review?

The implications of this review are significant for clinical management and research directions. Recognizing VVC as an immunopathology rather than purely an infection emphasizes the need for treatments targeting inflammatory pathways, such as NLRP3 inflammasome inhibitors, alongside traditional antifungal therapies. The variability in microbial interactions points to personalized therapeutic approaches involving probiotics and microbiome modulation. Additionally, insights into fungal pathogenicity mechanisms, especially candidalysin’s role, could guide the development of novel antifungal agents or vaccines, potentially reducing the global burden of VVC and recurrent episodes.