How does bacterial vaginosis (BV) increase the risk of preterm labor?

Mechanism of Bacterial Vaginosis in Preterm Labor

Bacterial vaginosis (BV) increases the risk of preterm labor primarily through inflammatory pathways triggered by altered vaginal microbiota, leading to cytokine release and weakening of fetal membranes. 1, 2

Pathophysiological Mechanisms

Microbial Dysbiosis

• BV represents a significant disruption of normal vaginal flora characterized by:
  • Decrease in protective hydrogen peroxide-producing Lactobacilli
  • Overgrowth of anaerobic bacteria, Gardnerella vaginalis, and Mycoplasma hominis 2
  • Shift from normal acidic pH (≤4.5) to elevated pH (>4.5) 2

Inflammatory Response

• The altered microbiota in BV triggers several inflammatory processes:
  1. Activation of pattern recognition receptors on vaginal epithelial cells 3
  2. Release of pro-inflammatory cytokines, particularly TNF-α and IL-1β 4
  3. Inhibition of normal chemotaxis and immune regulation 3

Membrane Weakening and Cervical Changes

• The inflammatory cascade leads to:
  • Production of proteolytic enzymes that weaken fetal membranes
  • Increased prostaglandin production that can trigger uterine contractions
  • Cervical ripening and effacement 1, 2

Genetic Susceptibility

• Research indicates genetic factors may play a role:
  • Women with certain TNF-α promoter polymorphisms (-G238A) and BV have significantly higher risk of preterm delivery (OR 2.6,95% CI 1.2-5.8) 4
  • This suggests an important gene-environment interaction in the preterm delivery pathway

Epidemiological Evidence

• Multiple studies demonstrate a clear association between BV and preterm labor:
  • BV is associated with preterm delivery with relative risk ranging from 1.4 to 6.9 2
  • Higher prevalence of BV in women with threatened preterm labor (25%) compared to term labor (11.3%) 5, 6
  • BV increases risk for premature rupture of membranes, spontaneous abortion, and preterm labor 2

Risk Factors and Vulnerable Populations

• BV in pregnancy is more common among:
  • African-American women
  • Women of low socioeconomic status
  • Women with previous preterm or low-birthweight deliveries 1
  • Women with other risk factors such as BMI <20 kg/m², vaginal bleeding, or short cervix (<2.5 cm) 1

Clinical Implications

• Screening considerations:

  • Current evidence does not support universal screening of asymptomatic pregnant women 1
  • Screening may be beneficial for high-risk women with previous preterm delivery, though evidence remains conflicting 1

• Treatment considerations:

  • Treatment options include oral metronidazole, metronidazole gel, or clindamycin cream 1, 2
  • First trimester: clindamycin cream preferred
  • Second and third trimesters: oral metronidazole, metronidazole gel, or clindamycin cream 2

Important Caveats

• Natural history shows that up to 50% of BV cases resolve spontaneously during pregnancy 1
• Treatment of asymptomatic BV in average-risk women has not shown benefit in preventing preterm delivery 1
• Some studies suggest potential harm from treatment in women without confirmed BV, with increased risk of very preterm delivery (<34 weeks) 1
• The relationship between BV and preterm birth appears to be associative rather than definitively causal, as treatment doesn't consistently prevent preterm birth 7

The complex interplay between vaginal microbiota, host immune response, and genetic factors in BV-associated preterm labor highlights the need for continued research into optimal screening and treatment strategies for high-risk pregnant women.