Causes of Bacterial Vaginosis
Bacterial vaginosis results from replacement of normal hydrogen peroxide-producing Lactobacillus species in the vagina with high concentrations of anaerobic bacteria, though the exact trigger for this microbial shift remains incompletely understood. 1
Primary Pathophysiologic Mechanism
The fundamental cause is loss of protective H₂O₂-producing Lactobacillus species (particularly L. crispatus), which allows overgrowth of anaerobic bacteria including Bacteroides species, Mobiluncus species, Gardnerella vaginalis, Prevotella bivia, Prevotella disiens, Porphyromonas species, Peptostreptococcus species, and Mycoplasma hominis 1, 2, 3
This represents an ecological disruption rather than infection with a single pathogen—it is a syndrome of vaginal dysbiosis, not a traditional infection 1, 2
Sexual and Behavioral Risk Factors
BV is strongly associated with sexual activity: women who have never been sexually active are rarely affected, and acquisition correlates with having multiple sex partners 1, 3
However, BV is not considered exclusively a sexually transmitted disease because treating male partners does not prevent recurrence in women 1
Behavioral factors that may contribute include smoking, lack of condom use, and certain contraceptive choices 4
Alternative Pathogenic Pathways
The rectum may serve as a reservoir for BV-associated flora, suggesting pathogenesis similar to urinary tract infections with fecal contamination 3
Many of the organisms associated with BV (except Mobiluncus) are actually members of normal endogenous vaginal flora that overgrow when Lactobacillus protection is lost 3
Environmental and Chemical Triggers
Chemical or mechanical irritation from products like regular soap, douches, and other vaginal products can disrupt the protective vaginal ecosystem, potentially triggering the microbial shift 5
Loss of the acidic vaginal pH (normally 3.8-4.2) to pH >4.5 both results from and perpetuates the loss of Lactobacillus dominance 6, 5
Key Clinical Caveat
- The exact trigger that initiates the replacement of Lactobacillus with anaerobic bacteria remains unknown despite decades of research—this is why recurrence rates after antibiotic treatment are 50-80% within one year, as antibiotics eliminate the overgrowth but do not restore protective Lactobacillus colonization 1, 4