Bacterial Vaginosis and Group B Streptococcal Colonization and Preterm Delivery in a Low-Risk Population

Abstract

Objective: To evaluate the relationship between bacterial vaginosis (BV) and group B streptococcal (GBS) colonization in the 2nd trimester of pregnancy and preterm delivery. Methods: 1,197 pregnant women between 22 and 25 weeks’ gestation had a high vaginal swab for assessment of BV and GBS. Exclusion criteria were: previous preterm delivery, or mid-trimester abortion or termination of pregnancy, multiple gestation, oligo- or polyhydramnios, placenta previa, fetal abnormalities, uterine malformations, cervical incompetence, cervical cerclage, or receipt of an antibiotic effective against BV or GBS following the screening. All women had no risk factors for preterm delivery. The primary outcome measure in this analysis was spontaneous preterm delivery before 37 weeks’ gestation. Results: The preterm delivery rate was 8.7%, while the maternal BV and GBS colonization rates were 7.9 and 12.5%, respectively. Following adjustment for potential confounders BV was associated with an increased risk of preterm delivery (RR 2.19; CI: 1.21–3.98) (p = 0.01). On the contrary, GBS colonization was found to have a negative correlation with preterm birth (RR 0.43; 95% CI: 0.19–1.00). Conclusions: Although BV is a risk factor for preterm delivery, GBS colonization in the 2nd trimester of pregnancy has an inverse correlation with preterm delivery.

Predictive value for preterm birth of abnormal vaginal flora, bacterial vaginosis and aerobic vaginitis during the first trimester of pregnancy

“…The observed PTB rate of 7% in this study is similar to the expected rate in Flanders during the same period (7.4%; singletons 6.3%) 11 . Numerous studies have consistently shown that bacterial vaginosis and AVF at 12–24 weeks are associated with increased risks of PTB, preterm rupture of the membranes, chorioamnionitis, fetal infection and cerebral palsy 12–22 . However, studies applying strict criteria for full bacterial vaginosis (a Nugent score above 7, overall granular flora, >20% clue cells and LBG III) did not find a significant correlation between BV and the risk of PTB 14,18,23 …”

“…11 Numerous studies have consistently shown that bacterial vaginosis and AVF at 12-24 weeks are associated with increased risks of PTB, preterm rupture of the membranes, chorioamnionitis, fetal infection and cerebral palsy. [12][13][14][15][16][17][18][19][20][21][22] However, studies applying strict criteria for full bacterial vaginosis (a Nugent score above 7, overall granular flora, >20% clue cells and LBG III) did not find a significant correlation between BV and the risk of PTB. 14,18,23 Helen McDonald pointed out in the early 1990s that women with an increased risk for PTB have two types of AVF, one consisting of predominantly BV flora, and the other of aerobic microorganisms, such as Klebsiella and Escherichia coli.…”

The influence of bacterial vaginosis on gestational week of the completion of delivery and biochemical markers of inflammation in the serum

“…Microorganisms that cause BV can ascendantly spread from lower parts of genital tract to upper parts and lead to chorioamnionitis, a preterm rupture of fetal membranes and preterm delivery 3,25,26 . Then, microorganisms can produce proteolytic enzymes that increase epithelium permeability in vagina, and allow passage of very pathogenic microorganisms 27,28 . Results of other researches indicate the role of local immunological factors, genetically predisposed and depending on their presentation to microorganisms causing BV, local inflammatory mediators such as cytokines, chemokines, and growth factors that determine what kind of consequences will appear.…”

Genitourinary pathogens and preterm birth

“…failed to reduce the risk of preterm birth (P ¼ 0.84). Studies of bacterial vaginosis in pregnancy and preterm birth published since 2003 continue to emphasize an inconsistency of existing evidence(Table 3)[16,23,[61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][77][78]. Two additional RCTs have been consequently published but failed to replicate the findings of the Cochrane review, though this may represent the use of different treatment approaches[61,62].…”