What Causes Bacterial Vaginosis
Bacterial vaginosis results from the replacement of normal hydrogen peroxide-producing Lactobacillus species in the vagina with high concentrations of anaerobic bacteria (such as Prevotella and Mobiluncus species), Gardnerella vaginalis, and Mycoplasma hominis. 1, 2
The Microbial Disruption
The fundamental pathophysiology involves a shift from a healthy, Lactobacillus-dominated vaginal ecosystem to a polymicrobial state:
Normal vaginal flora is dominated by Lactobacillus species that produce lactic acid, hydrogen peroxide (H₂O₂), and bacteriocins, which maintain an acidic environment (pH <4.5) that protects against pathogenic overgrowth 3
In BV, this protective Lactobacillus population is depleted or absent, allowing anaerobic bacteria to proliferate unchecked 1, 4
The specific bacteria that overgrow include Gardnerella vaginalis (the most commonly identified organism), Prevotella species, Mobiluncus species, Atopobium vaginae, and Mycoplasma hominis 1, 5, 3
These organisms form a polymicrobial biofilm on the vaginal mucosal surface, which helps shelter the bacteria from the host immune response and contributes to treatment resistance 6, 3
What Triggers This Microbial Shift
The exact cause of the microbial alteration is not fully understood, but several factors are associated with BV development 1:
Multiple sexual partners are strongly associated with BV, though it remains unclear whether BV results from acquisition of a sexually transmitted pathogen 1, 2
Women who have never been sexually active are rarely affected, suggesting some relationship to sexual activity, though BV is not classified as a sexually transmitted infection 1, 2
Importantly, treating male sexual partners has not been shown to prevent BV recurrence, which further supports that BV is not simply a sexually transmitted infection 1, 2, 7
Key Clinical Pitfall
The most common misconception is treating BV as a sexually transmitted infection requiring partner treatment. The evidence clearly shows this approach is ineffective 1, 2. Instead, focus on restoring the patient's vaginal Lactobacillus population, as the failure of beneficial Lactobacillus strains (particularly L. crispatus) to recolonize after antibiotic treatment explains the 50-80% recurrence rate within one year 8, 6.