Antifungal Resistance in Vaginal Candidiasis Among Reproductive-age Women: A Review.

Abstract

Candida is a type of fungus that can cause infections in humans. Sometimes, these infections become tough to treat because the Candida fungus resists antifungal drugs. This resistance depends on both the specific type of Candida and how it interacts with the human body. For instance, Candida can change its genetic makeup or produce proteins that pump out the drugs, making them less effective. Additionally, Candida can form a protective layer called a biofilm, which shields it from the drugs. Candida can cause a variety of diseases, and vaginal candidiasis is among the most troublesome. Nearly every woman experiences this infection at least once in her lifetime. Higher rates of treatment failures and recurrent infections result from the developing issue of antifungal resistance, underscoring the need for a more thorough understanding of resistance mechanisms. Changes in hormonal levels and immune responses can significantly influence the effectiveness of antifungal treatments. Hormonal fluctuations can alter vaginal pH and immune functions, which in turn affects Candida colonization and persistence. Moreover, an imbalance in the vaginal microbiome can lead to an overgrowth of Candida and lead to the drug resistance candidiasis. This review delves into the molecular pathways that contribute to the resistance of vaginal candidiasis to antifungal treatments, focusing on both acquired and intrinsic resistance mechanisms. Acquired resistance develops due to genetic alterations following antifungal exposure, including mutations in genes encoding drug targets, overexpression of efflux pumps, and increased biofilm formation. In contrast, intrinsic resistance refers to the innate traits of the Candida species that inherently reduce the efficacy of antifungal agents. These characteristics include changes in membrane sterols, genetic mutations in target enzymes, and the presence of efflux pumps that remove antifungal medications. Understanding these complex mechanisms can inform future therapeutic strategies and improve clinical outcomes.