What Causes Bacterial Vaginosis?
Bacterial vaginosis results from an ecological shift in the vaginal microbiome, where normal hydrogen peroxide-producing Lactobacillus species are replaced by high concentrations of anaerobic bacteria—primarily Prevotella, Mobiluncus, Gardnerella vaginalis, and Mycoplasma hominis. 1
The Fundamental Pathophysiology
The core mechanism is a disruption of the protective Lactobacillus-dominant vaginal ecosystem, allowing overgrowth of facultative and strict anaerobic bacteria that form polymicrobial biofilms on vaginal epithelial cells. 2, 3
This is not a single-pathogen infection but rather a polymicrobial dysbiosis—the organisms involved (Prevotella bivia, Prevotella disiens, Porphyromonas spp., Peptostreptococcus spp., and Mobiluncus spp.) are actually part of the normal endogenous vaginal flora that become pathogenic when they overgrow. 2
The loss of H₂O₂-producing Lactobacillus species removes the primary defense mechanism against colonization by catalase-negative anaerobic bacteria, creating a permissive environment for dysbiosis. 2
Is BV Sexually Transmitted?
Evidence from treatment trials does not support bacterial vaginosis as a classic sexually transmitted infection, yet multiple sexual partners and new sexual partners significantly increase risk. 2, 4
Women who have never been sexually active rarely develop BV, indicating that sexual activity plays a role in pathogenesis, though the exact mechanism remains unclear. 4
Treating male sexual partners does not prevent recurrence or alter clinical outcomes in women, which further argues against simple sexual transmission. 5, 4
Additional Risk Factors Beyond Sexual Activity
African-American ethnicity, low socioeconomic status, and a history of preterm birth are all independently associated with higher BV prevalence. 4
The rectum may serve as a reservoir for BV-associated flora, suggesting a pathogenesis similar to urinary tract infections where organisms migrate from the gastrointestinal tract. 2
Menstrual cycles and hormonal fluctuations contribute to recurrence, as the vaginal microbiome undergoes dynamic changes throughout the reproductive cycle. 4, 6
Why the Exact Etiology Remains Unknown
Despite decades of research, the precise trigger that initiates the shift from Lactobacillus dominance to anaerobic overgrowth is still not fully understood. 7, 6
The polymicrobial biofilm formed by BV-associated bacteria on vaginal epithelium is a key feature that complicates both understanding and treatment, as it shelters organisms from host defenses and antimicrobial agents. 3, 6
Critical Clinical Implications
Up to 50% of women meeting diagnostic criteria for BV are completely asymptomatic, meaning the dysbiosis can exist without triggering symptoms. 1, 5
BV increases risk for upper genital tract infections (pelvic inflammatory disease, endometritis), adverse pregnancy outcomes (preterm delivery, premature rupture of membranes), and acquisition of sexually transmitted infections including HIV. 2, 6
The high recurrence rate after treatment (often >60%) is attributed to the persistent biofilm, antimicrobial resistance in BV-associated bacteria, and possible recolonization from rectal flora—not reinfection from partners. 8