Abstract

Introduction: CVV is the most common fungal infection in women of childbearing age. Fluconazole is the main antifungal drug used for the treatment of candidiasis; however, resistance to this pharmacological agent is known to be increasing.
Objective: To describe the main molecular mechanisms involved in fluconazole resistance in Candida albicans species and to determine its role as the main causative agent of CVV.
Methods: An integrative review was performed under the PRISMA methodology and categories of analysis were established to describe the mechanisms of resistance: Ergosterol biosynthesis and efflux pumps. The other category was Candida as a causal agent of CVV.
Results: The molecular resistance mechanisms expressed by C. albicans are mainly overexpression and point mutation of the ERG11 gene, followed by overexpression of the ERG3, CDR1, CDR2 and MDR1 genes. The morphological modification of yeasts to hyphae is the main mechanism responsible for the change from commensal germ to the pathogen in the vulvovaginal mucosa.
Conclusion: Candida albicans is currently the most important pathogen in humans, due to its high rate of colonization and mortality. The literature has focused on describing gene expression and highlights the need for other techniques to evaluate mutations, which may provide greater specificity and relevance in the phenomenon of fluconazole resistance.

Keywords:Candida albicans; Vulvovaginal candidiasis (CVV); Fluconazole; Fungal drug resistance