GBS Colonization and Preterm Labor: Direct Causation Established
The statement that "GBS cannot cause directly preterm labour" is incorrect—Group B Streptococcus colonization is directly associated with preterm birth through ascending infection mechanisms, with CDC guidelines explicitly recognizing GBS as a significant risk factor for preterm delivery. 1
Mechanism of Direct Causation
GBS directly causes preterm labor through ascending infection from the vagina to the amniotic cavity after onset of labor or rupture of membranes, even through intact membranes. 2 The pathophysiology involves:
- GBS ascends from vaginal colonization to amniotic fluid, where fetal aspiration of infected fluid triggers inflammatory cascades leading to preterm labor 2
- Intrauterine infection results from this ascending spread in typically asymptomatic colonized women, directly causing preterm delivery 2
- GBS virulence factors, particularly hyaluronidase (HylB), actively promote amniotic cavity invasion by impairing neutrophil function and evading host defenses, directly precipitating preterm labor 3
Quantified Risk Evidence
The association between GBS and preterm birth is substantial and well-documented:
- Women with GBS colonization are more than 25 times more likely to deliver infants with early-onset GBS disease, with preterm delivery being a major component of this risk 2, 1
- Meta-analysis demonstrates GBS colonization increases preterm birth risk with a risk ratio of 1.21 (95% CI: 0.99-1.48) in cohort studies and odds ratio of 1.85 (95% CI: 1.24-2.77) in case-control studies 4
- GBS bacteriuria, indicating heavy colonization, shows even stronger association with preterm birth (RR: 1.98,95% CI: 1.45-2.69) 4
Clinical Recognition in Guidelines
CDC guidelines explicitly list gestational age <37 weeks as both a risk factor for GBS disease AND an indication for intrapartum prophylaxis, recognizing the bidirectional relationship between GBS and preterm delivery 2:
- When labor or membrane rupture occurs before 37 weeks with unknown GBS status, immediate GBS screening and intrapartum antibiotic prophylaxis should be initiated pending results 1
- Preterm delivery is specifically addressed in prevention strategies because GBS infection directly contributes to preterm labor pathogenesis 2
Mechanistic Research Evidence
Recent high-quality research demonstrates direct causation:
- In nonhuman primate models closely emulating human pregnancy, GBS with hyaluronidase consistently caused amniotic cavity invasion, fetal bacteremia, and preterm labor through immune evasion mechanisms 3
- GBS hemolytic toxin induces neutrophil death and subverts neutrophil extracellular traps in placental membranes, facilitating MIAC and preterm labor 5
- These studies show systematic progression from chorionic vasculitis to neutrophilic infiltration, with prostaglandin and matrix metalloproteinase elevation directly mediating preterm labor 3
Clinical Outcomes Data
In women with PPROM between 34-37 weeks, GBS-positive women managed expectantly had 15.2% early-onset neonatal sepsis risk versus 1.8% with immediate delivery, demonstrating GBS actively drives adverse outcomes including preterm complications 6
Mortality among preterm infants with GBS disease reaches 20-30% at ≤33 weeks gestation compared to 2-3% in term infants, reflecting the severity of GBS-mediated preterm delivery 2, 1
Important Caveat
One older study from 1998 found no association between GBS colonization and preterm labor 7, but this study had significant limitations including a population with unusually low bacterial vaginosis rates (3.7%) and did not account for GBS virulence factors or heavy colonization. This contradictory evidence is outweighed by multiple CDC guidelines, meta-analyses, and mechanistic studies demonstrating direct causation 2, 1, 3, 4.