Abstract
Vulvovaginal candidiasis (VVC) is a widespread vaginal infection primarily caused by Candida albicans. VVC affects up to 75% of women of childbearing age once in their life, and up to 9% of women in different populations experience more than three episodes per year, which is defined as recurrent vulvovaginal candidiasis (RVVC). RVVC results in diminished quality of life as well as increased associated healthcare costs. For a long time, VVC has been considered the outcome of inadequate host defenses against Candida colonization, as in the case of primary immunodeficiencies associated with persistent fungal infections and insufficient clearance. Intensive research in recent decades has led to a new hypothesis that points toward a local mucosal overreaction of the immune system rather than a defective host response to Candida colonization. This review provides an overview of the current understanding of the host immune response in VVC pathogenesis and suggests that a tightly regulated fungus–host–microbiota interplay might exert a protective role against recurrent Candida infections.
Highlights
Vulvovaginal candidiasis (VVC) is a debilitating pathological condition caused by Candida species, commonly characterized by vulvar itching, burning, pain while urinating, and vaginal discharge [1]
Up to 9% of women in various populations experience more than three or four episodes within one year, which is regarded as recurrent vulvovaginal candidiasis (RVVC) [6]
Several factors can alter the vaginal microbiota in patients with RVVC: firstly, changes in the H2O2-producing Lactobacillus community (e.g., L. acidophilus, L. gasseri and L. vaginalis), and secondly, a high estrogen condition as well as diversity in carbon sources, short-chain fatty acids or eicosanoids composition (Table 1) [19,20,21,22,23,24,25]
Summary
Vulvovaginal candidiasis (VVC) is a debilitating pathological condition caused by Candida species, commonly characterized by vulvar itching, burning, pain while urinating, and vaginal discharge [1]. Up to 9% of women in various populations experience more than three or four episodes within one year, which is regarded as recurrent vulvovaginal candidiasis (RVVC) [6]. Worldwide prevalence and epidemiological data are rare and inaccurate because they are mostly carried out from self-reports and local general practitioner diagnosis. In this regard, Denning et al systematically assessed epidemiological studies from 1985 to 2016 and, basing their study on the 6000 online surveys from five Western European countries and the United States by Foxman et al, documented a global annual prevalence of 3871 RVVC cases per 100,000 women, with the highest frequency (9%) in patients aged between 25 and 34 years old [6,7]. We hypothesize that RVVC might be due to a dysregulated immune system in response to Candida colonization rather than a defective host defense
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