Asmita Shukla1, J D Sobel2. 1. Department of Internal Medicine, Wayne State University School of Medicine, 540 E. Canfield St., 1241 Scott Hall, Detroit, MI, 48021, USA. 2. Department of Internal Medicine, Wayne State University School of Medicine, 540 E. Canfield St., 1241 Scott Hall, Detroit, MI, 48021, USA. Jsobel@med.wayne.edu.
Abstract
PURPOSE OF REVIEW: Goal was to review epidemiology, pathophysiology, and prevention of post-antibiotic Candida vulvovaginitis (VVC). RECENT FINDINGS: Antibacterial therapy, whether systemic or locally applied to the vagina, represents the single most frequent and predictable cause or triggering mechanism of symptomatic vulvovaginal candidiasis (VVC). Such initiating mechanisms may precipitate sporadic or recurrent episodes of VVC. In spite of this widely recognized association, the exact mechanism whereby antibiotics of all classes cause acute exacerbation of symptomatic vaginal disease remains largely unstudied and therefore largely unknown. Pathophysiology is hypothesized to be reduction or alteration of vaginal microbiome restraints of yeast colonization, proliferation, and expression of virulence characteristics. The predictable link between antibiotic use and post-antibiotic VVC affords practitioners an opportunity for timely intervention using selective, convenient antimycotics usually drugs but possibly probiotic measures. Indications and limitation of these steps are discussed.
PURPOSE OF REVIEW: Goal was to review epidemiology, pathophysiology, and prevention of post-antibiotic Candida vulvovaginitis (VVC). RECENT FINDINGS: Antibacterial therapy, whether systemic or locally applied to the vagina, represents the single most frequent and predictable cause or triggering mechanism of symptomatic vulvovaginal candidiasis (VVC). Such initiating mechanisms may precipitate sporadic or recurrent episodes of VVC. In spite of this widely recognized association, the exact mechanism whereby antibiotics of all classes cause acute exacerbation of symptomatic vaginal disease remains largely unstudied and therefore largely unknown. Pathophysiology is hypothesized to be reduction or alteration of vaginal microbiome restraints of yeast colonization, proliferation, and expression of virulence characteristics. The predictable link between antibiotic use and post-antibiotic VVC affords practitioners an opportunity for timely intervention using selective, convenient antimycotics usually drugs but possibly probiotic measures. Indications and limitation of these steps are discussed.
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