A review of group B streptococcus (Gbs) vaginal colonization and ascending intrauterine infection: interaction between host immune responses and gbs virulence factors

Vaginal colonization with Group B streptococcus (GBS) or Streptococcus agalactiae can potentially cause ascending intrauterine infection among pregnant women, and hence it is known as one of the risk factors for preterm delivery. Ascending intrauterine infection may also cause the transmission of GBS to the fetus in utero and the newborn during delivery, leading to the development of early onset of neonatal infection. GBS are βhemolytic, gram-positive bacteria that are opportunistic commensal of the gastrointestinal and urogenital tract of approximately 18% of pregnant women globally. Intrapartum antibiotic prophylaxis (IAP) only reduces the rate of early onset neonatal infection, but not the late onset neonatal infection. Thus, the development of GBS vaccine is thought to be important to decrease the rate of preterm delivery and neonatal infections particularly in low-and-middle income countries where IAP program is not feasible. Vaccination can also be cost-effective for the healthcare system when executed together with IAP program. The aim of the current review is to summarize the mechanisms on how the GBS virulence factors interact with host immune components in the gestational tissues, leading to cervicovaginal colonization and ascending intrauterine infection. The elucidation of these mechanisms is essential for expediting the development of vaccines and novel therapeutic measures targeting these GBS virulence factors that will hamper the vaginal colonization, ascending intrauterine infection and conceptus tissue invasion by GBS. These strategies are crucial to potentially reduce the rate of preterm delivery and subsequent serious complications in the newborn

Expression of virulence genes in group B streptococcus isolated from symptomatic pregnant women with term and preterm delivery

Aims: Maternal vaginal Group B Streptococcus (GBS) colonization is considered a risk factor for preterm delivery and, consequently, neonatal infections. Previous studies have portrayed the important roles of these virulence factors, including hemolytic pigment, hyaluronidase (HylB), serine-rich protein (Srr) and bacterial surface adhesion of GBS (BsaB) in mediating GBS colonization and intrauterine ascending infection, causing preterm delivery. This study aimed to investigate the association between mRNA expression of virulence genes in GBS isolates obtained from symptomatic pregnant women and preterm delivery. Methodology and results: GBS isolates were obtained from high vaginal swabs of 40 symptomatic pregnant women of gestational age of less than 37 weeks. RNA was extracted from these GBS isolates and RT-qPCR was performed to determine the relative mRNA expression of GBS virulence genes, including CylE (encode enzyme required for the biosynthesis of the hemolytic pigment), HylB, Srr-1 and BsaB. Socio-demographic details and obstetric history were not found to be associated with the delivery outcomes of these women. The GBS isolates from symptomatic pregnant women who delivered prematurely showed a higher expression of CylE gene and a trend towards an elevated expression of HylB gene compared to women with term delivery. While the expression of both Srr-1 and BsaB genes was similar between symptomatic pregnant women who had term or preterm delivery. Conclusion, significance and impact of study: The results suggest that following vaginal colonization, both CylE and HylB genes are likely to contribute to intrauterine ascending infection and inflammation, leading to preterm delivery in humans. These virulence factors may be targeted for the pre-clinical stages of vaccine development or therapeutic intervention