Pathogenesis of Bacterial Vaginosis: Discussion of Current Hypotheses Original paper

What Was Reviewed?

This review examines the competing hypotheses on bacterial vaginosis (BV) pathogenesis. BV is a prevalent vaginal condition linked to adverse health outcomes such as preterm labor, pelvic inflammatory disease, and increased susceptibility to sexually transmitted infections (STIs). Despite its clinical significance, BV’s underlying cause remains controversial. Researchers debate whether BV results from a single pathogen, microbial imbalance, sexual transmission, genetics, or hygiene practices. The review evaluates each hypothesis and identifies research gaps that must be addressed to improve prevention and treatment strategies.

Who Was Reviewed?

The review synthesizes findings from multiple studies, including epidemiological research, microbiome sequencing, and clinical trials. It assesses the variations in vaginal microbial communities and risk factors across different populations. It includes data comparing African American and European ancestry women, evaluating whether BV prevalence differences are due to genetic predisposition, sexual networks, or socioeconomic factors. In addition, it also examines studies on sexual behavior, hygiene, and microbial interactions to understand BV development and persistence.

What Were the Most Important Findings?

BV occurs when Lactobacillus-dominant vaginal microbiota shifts to an overgrowth of anaerobes like Gardnerella vaginalis, Atopobium, and Prevotella. A major debate centers on whether this microbial shift is the result of an exogenous infection or an imbalance within the vaginal ecosystem. One hypothesis suggests BV is a sexually transmitted condition, as studies consistently link new sexual partners and unprotected intercourse to increased BV risk. Condom use has been shown to reduce recurrence, and BV-associated bacteria, including G. vaginalis, have been detected in both male and female partners. However, conflicting data exist, particularly in cases of BV occurring in virginal individuals.

Another hypothesis proposes that G. vaginalis acts as a keystone pathogen, initiating biofilm formation that facilitates the overgrowth of anaerobic bacteria. These biofilms make BV highly resistant to antibiotic treatment, leading to frequent recurrence. This aligns with studies showing that biofilm persistence, rather than reinfection, is responsible for many recurrent BV cases.

Racial disparities in BV prevalence have also been noted, with African American women more likely to have diverse anaerobic vaginal microbiota compared to women of European ancestry. Some studies suggest genetic or environmental factors, such as diet and socioeconomic status, play a role. However, the evidence remains inconclusive.

What Are the Implications of This Review?

A deeper understanding of BV pathogenesis is essential for developing more effective treatment and prevention strategies. If BV is sexually transmitted, partner treatment may be necessary to reduce recurrence. Addressing biofilm resilience could improve antibiotic efficacy, potentially through biofilm-disrupting agents or microbiome restoration therapies. Additionally, racial disparities highlight the need for research into genetic, environmental, and behavioral influences on vaginal microbiota. Future studies should focus on controlled clinical trials and microbiome-based interventions to prevent and manage BV more effectively.