Abstract

Group B streptococcus (GBS) is a gram-positive bacteria that asymptomatically colonizes the vaginal tract. However, during pregnancy maternal GBS colonization greatly predisposes the mother and baby to a wide range of adverse outcomes, including preterm birth (PTB), stillbirth, and neonatal infection. Although many mechanisms involved in GBS pathogenesis are partially elucidated, there is currently no approved GBS vaccine. The development of a safe and effective vaccine that can be administered during or prior to pregnancy remains a principal objective in the field, because current antibiotic-based therapeutic strategies do not eliminate all cases of invasive GBS infections. Herein, we review our understanding of GBS disease pathogenesis at the maternal-fetal interface with a focus on the bacterial virulence factors and host defenses that modulate the outcome of infection. We follow GBS along its path from an asymptomatic colonizer of the vagina to an invasive pathogen at the maternal-fetal interface, noting factors critical for vaginal colonization, ascending infection, and vertical transmission to the fetus. Finally, at each stage of infection we emphasize important host-pathogen interactions, which, if targeted therapeutically, may help to reduce the global burden of GBS.

Highlights

  • Group B Streptococcus (GBS) is a gram-positive, b-hemolytic, and chain-forming bacterium that can asymptomatically colonize the human vaginal and gastrointestinal tracts

  • We summarize the seminal studies and recent advances that define our understanding of GBS disease pathogenesis at the maternalfetal interface, focusing on the interplay between bacterial virulence factors and host defenses that leads to GBS clearance or invasion

  • National and regionspecific discrepancies between screening guidelines and the use of intrapartum antibiotic prophylaxis (IAP) confounds the accurate detection of invasive GBS disease cases, limiting the ability to control the associated adverse outcomes through intervention

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Summary

INTRODUCTION

Group B Streptococcus (GBS) ( called Streptococcus agalactiae) is a gram-positive, b-hemolytic, and chain-forming bacterium that can asymptomatically colonize the human vaginal and gastrointestinal tracts. During pregnancy, GBS can become highly invasive and pathogenic to the fetus and mother, leading to adverse outcomes. The complex pathogenesis of maternal and infant GBS infection arises due to the large arsenal of the bacterium’s virulence factors, which can vary widely across strains and undergo altered expression depending on the host niche. Host-pathogen interactions that alter the balance between vaginal tract colonization and GBS invasive disease ascending into the uterus are beginning to be elucidated (Vornhagen et al, 2018a). We summarize the seminal studies and recent advances that define our understanding of GBS disease pathogenesis at the maternalfetal interface, focusing on the interplay between bacterial virulence factors and host defenses that leads to GBS clearance or invasion

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