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Determination of Biofilm Initiation on Virus-infected Cells by Bacteria and Fungi
Published on: July 6, 2016
Bacterial Vaginosis and Vulvovaginal Candidiasis Pathophysiologic Interrelationship
Jack D Sobel1, Yogitha Sai Vempati2
1C.S. Mott Center for Growth and Human Development, 275 E. Hancock St, Detroit, MI 48201, USA.
Recurrent bacterial vaginosis (BV) may trigger recurrent vulvovaginal candidiasis (VVC) by compromising immune defenses. This link explains why some women experience persistent BV and VVC, impacting treatment outcomes.
Area of Science:
- Gynecology
- Infectious Diseases
- Immunology
Background:
- Bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC) are common causes of vaginal symptoms.
- These infections are typically considered independent, with distinct pathogenic mechanisms.
- Clinical observations suggest a potential link between recurrent BV (RBV) and recurrent VVC (RVVC).
Purpose of the Study:
- To discuss the biological basis for the interrelationship between RBV and RVVC.
- To explore how BV dysbiosis may compromise immune defenses, leading to VVC.
- To examine the contribution of BV to antifungal resistance and refractory VVC.
Main Methods:
- Review of existing literature and clinical experience.
- Discussion of pathogenic mechanisms underlying BV and VVC.
- Analysis of immune system interactions in the vaginal environment.
Main Results:
- BV dysbiosis compromises local immune defenses, reducing vaginal yeast tolerance.
- A pro-inflammatory environment induced by BV can lead to mixed infections or post-treatment VVC.
- Repeated antimicrobial use and RBV can promote fluconazole resistance in Candida albicans.
Conclusions:
- RBV is a significant trigger for RVVC, independent of antibiotic use.
- BV-induced immune compromise and inflammation are key factors in RVVC development.
- Understanding this link is crucial for managing refractory VVC and improving therapeutic outcomes.
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