Group B streptococcus (GBS) is a β-hemolytic gram-positive bacterium that colonizes the lower genital tract of approximately 18% of women globally as an asymptomatic member of the gastrointestinal and/or vaginal flora. If established in other host niches, however, GBS is highly pathogenic. During pregnancy, ascending GBS infection from the vagina to the intrauterine space is associated with preterm birth, stillbirth, and fetal injury. In addition, vertical transmission of GBS during or after birth results in life-threatening neonatal infections, including pneumonia, sepsis, and meningitis. Although the mechanisms by which GBS traffics from the lower genital tract to vulnerable host niches are not well understood, recent advances have revealed that many of the same bacterial factors that promote asymptomatic vaginal carriage also facilitate dissemination and virulence. Furthermore, highly pathogenic GBS strains have acquired unique factors that enhance survival in invasive niches. Several host factors also exist that either subdue GBS upon vaginal colonization or alternatively permit invasive infection. This review summarizes the GBS and host factors involved in GBS's state as both an asymptomatic colonizer and an invasive pathogen. Gaining a better understanding of these mechanisms is key to overcoming the challenges associated with vaccine development and identification of novel strategies to mitigate GBS virulence.
Keywords: colonization and virulence; group B streptococcus; host–pathogen interaction; immune response; signal transduction systems.
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