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Bacterial vaginosis (BV)-associated vaginal biofilms are complex, polymicrobial structures that play a central role in the pathogenesis and recurrence of bacterial vaginosis. These biofilms are typically initiated by Gardnerella vaginalis, which acts as a primary scaffold for the attachment of other anaerobic bacteria, including Atopobium vaginae, Prevotella, and Fannyhessea vaginae (Swidsinski et al., 2005). The bacteria within the biofilm are encased in a self-produced extracellular polymeric substance (EPS) matrix that provides a physical barrier against the host's immune system and significantly increases tolerance to standard antibiotic treatments like metronidazole (Alves et al., 2014). This protective environment allows the pathogens to persist even after clinical symptoms have resolved, leading to the high recurrence rates characteristic of BV. Therapeutic strategies are increasingly focusing on biofilm-disrupting agents, such as boric acid or enzymatic treatments, in combination with traditional antibiotics to achieve complete eradication (Muzny et al., 2019). Understanding the structural and functional dynamics of these biofilms is essential for developing more effective treatments to prevent complications such as preterm birth and the transmission of sexually transmitted infections (Cerca et al., 2022).
Drugs targeting the BV-associated biofilm work through several mechanisms: direct bactericidal action against anaerobic species (e.g., metronidazole), disruption of the extracellular polymeric matrix (e.g., DNase or boric acid), inhibition of bacterial attachment to the vaginal epithelium, and competitive exclusion by restoring commensal Lactobacillus species (Cerca et al., 2022; Machado et al., 2015).
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