Dr. Kim Capone, Lead educator of IVH and Chief Science Officer for Vaginal Biome Science.
The vaginal microbiome, after so many years in the background, is now recognized as a key determinant of women’s health. In a 2025 JCI review Gilbert et al. present compelling evidence that bacterial vaginosis (BV), characterized by a shift from a Lactobacillus-dominant to diverse anaerobic microbial communities, is not just a benign imbalance, but a risk amplifier for infections, inflammation, and chronic vulvar conditions. For clinicians, this reframes BV as a critical point of intervention.
BV as a Gateway to Other Infections
BV is consistently associated with increased risk of sexually transmitted infections (STIs), including chlamydia, gonorrhea, trichomoniasis, HSV, HPV, and HIV. These risks persist even in asymptomatic women. BV-associated species such as Gardnerella, Prevotella, and Fannyhessea (formerly Atopobium) disrupt epithelial barriers, form biofilms, and modulate immune responses, facilitating pathogen persistence and synergy.
For example, Gardnerella has been shown in mouse models to promote upper genital tract infection by Group B Streptococcus and to trigger recurrent E. coli-driven UTIs. These conditions are biologically enabled by dysbiosis.
Vaginal Immunity and Inflammation
BV is also immunologically disruptive. It increases proinflammatory cytokines like IL-1β and TNF-α while lowering protective immune mediators such as secretory leukocyte protease inhibitor (SLPI). These shifts can promote HIV acquisition and support HPV persistence and progression to cervical dysplasia, underscoring the systemic consequences of microbial imbalance.
Vulvar Health and Microbiome Disruption
The mechanisms that underlie BV, such as chronic inflammation, mucosal disruption, and biofilm formation, are also relevant to chronic vulvar conditions. These include inflammatory dermatoses like lichen sclerosus and chronic pain conditions like vulvodynia, which may be exacerbated by microbial shifts and barrier breakdown. BV-associated sialidase activity and glycan degradation may further sensitize tissues to irritation or immune dysregulation. While causality remains under study, microbiome restoration offers a promising adjunct strategy for managing chronic vulvar symptoms.
BV Recurrence: More Than Microbes
BV is notoriously recurrent, in part because its drivers extend beyond bacterial overgrowth. Systemic factors including stress, poor nutrition, smoking, douching, vitamin D deficiency, and socioeconomic hardship are all linked to recurrence. Partner treatment, especially in heterosexual couples, can reduce recurrence and supports the view of BV as sexually transmissible in some cases. Still, many women experience persistent BV without new partners, highlighting its multifactorial nature and the need for personalized, multifaceted care.
Clinical Insights: Managing BV Through a Microbiome-Informed Lens
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Think beyond symptoms: Consider microbiome assessment in women with recurrent BV, UTIs, STIs, or vulvovaginal discomfort, even if asymptomatic for BV. High-diversity CST-IV microbiome profiles still confer risk.
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Understand recurrence: BV may behave as an STI in some cases, but many women relapse without sexual exposure. It’s not purely transmissible.
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Address root causes: Stress, poor diet, smoking, and douching all destabilize the vaginal ecosystem and must be addressed for sustained remission.
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Support protective flora: Use lactic acid–based gels to maintain low vaginal pH, vaginal probiotics to replenish lactobacilli, and vulvar washes that are pH-balanced and microbiome-safe to minimize pathogen transfer and support barrier health.
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Personalize the plan: Effective management requires layered care such a microbiome restoration, behavioral support, and sometimes partner treatment.
Bottom Line: BV is a signal of systemic vulnerability, not simply a local imbalance. By addressing upstream drivers and using microbiome-supportive tools, clinicians can move beyond symptom control and advance long-term vaginal health.
