Pathogenesis of Bacterial Vaginosis
Bacterial vaginosis results from the replacement of normal hydrogen peroxide (H₂O₂)-producing Lactobacillus species in the vagina with high concentrations of anaerobic bacteria (including Prevotella species, Mobiluncus species, and Peptostreptococcus species), Gardnerella vaginalis, and Mycoplasma hominis. 1, 2
Microbial Shift Mechanism
The pathogenesis centers on a fundamental disruption of the vaginal ecosystem:
Loss of protective lactobacilli: The normal vaginal flora, dominated by H₂O₂-producing Lactobacillus species, becomes depleted or absent 1, 3
Overgrowth of anaerobic organisms: This creates a vacuum that allows massive proliferation of anaerobic bacteria including Prevotella bivia, Prevotella disiens, Porphyromonas species, Mobiluncus species, and Peptostreptococcus species 3
Facultative anaerobes join the mix: Gardnerella vaginalis and Mycoplasma hominis become prominent members of this altered flora 1
Protective Role of Lactobacilli
The mechanism by which normal lactobacilli prevent BV involves multiple protective factors:
Hydrogen peroxide production: H₂O₂-producing Lactobacillus species protect against colonization by catalase-negative anaerobic bacteria 3
Lactic acid production: Lactobacilli maintain the acidic vaginal environment (pH <4.5) through lactic acid production, which inhibits pathogenic bacterial growth 4
Bacteriocin production: Additional antimicrobial compounds produced by lactobacilli help maintain vaginal health 4
Unknown Etiologic Factors
The fundamental cause of this microbial alteration remains poorly understood despite decades of research. 1, 5
Key observations about etiology include:
Sexual activity association: BV is associated with having multiple sex partners, and women who have never been sexually active are rarely affected 1
Not definitively sexually transmitted: Despite the sexual association, it remains unclear whether BV results from acquisition of a sexually transmitted pathogen 1, 5
Partner treatment ineffective: Treatment of male sex partners has not been beneficial in preventing recurrence of BV, arguing against simple sexual transmission 1, 6
Possible rectal reservoir: The pathogenesis may be similar to urinary tract infections, with the rectum potentially serving as a reservoir for some BV-associated flora 3
Clinical Manifestations of the Microbial Shift
The altered flora produces characteristic clinical findings:
Elevated vaginal pH: The loss of lactic acid-producing lactobacilli results in vaginal pH rising above 4.5 1
Amine production: The anaerobic bacteria produce amines that create the characteristic fishy odor, particularly when alkalinized with KOH (positive whiff test) 1
Clue cells: Vaginal epithelial cells become coated with the adherent bacteria, creating the pathognomonic "clue cells" seen on microscopy 1
Non-inflammatory discharge: Despite the massive bacterial overgrowth, BV characteristically produces minimal inflammatory response, resulting in a homogeneous white discharge without significant white blood cells 1, 7
Common Pitfalls in Understanding BV Pathogenesis
Do not confuse BV with a simple infection by a single pathogen—it is a complex polymicrobial syndrome involving multiple organisms 8. The presence of Gardnerella vaginalis alone does not indicate BV, as this organism can be isolated from vaginal cultures in approximately half of normal women 1. Culture for G. vaginalis is therefore not recommended as a diagnostic tool because it lacks specificity 1.