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Review
. 2025 Mar 13;38(1):e0015422.
doi: 10.1128/cmr.00154-22. Epub 2024 Nov 25.

Group B streptococcal infections in pregnancy and early life

Affiliations
Review

Group B streptococcal infections in pregnancy and early life

Gygeria Manuel et al. Clin Microbiol Rev. .

Abstract

SUMMARYBacterial infections with Group B Streptococcus (GBS) are an important cause of adverse outcomes in pregnant individuals, neonates, and infants. GBS is a common commensal in the genitourinary and gastrointestinal tracts and can be detected in the vagina of approximately 20% of women globally. GBS can infect the fetus either during pregnancy or vaginal delivery resulting in preterm birth, stillbirth, or early-onset neonatal disease (EOD) in the first week of life. The mother can also become infected with GBS leading to postpartum endometritis, and rarely, maternal sepsis. An invasive GBS infection of the neonate may present after the first week of life (late-onset disease, LOD) through transmission from caregivers, breast milk, and other sources. Invasive GBS infections in neonates can result in sepsis, pneumonia, meningitis, neurodevelopmental impairment, death, and lifelong disability. A policy of routine screening for GBS rectovaginal colonization in well-resourced countries can trigger the administration of intrapartum antibiotic prophylaxis (IAP) when prenatal testing is positive, which drastically reduces rates of EOD. However, many countries do not routinely screen pregnant women for GBS colonization but may administer IAP in cases with a high risk of EOD. IAP does not reduce rates of LOD. A global vaccination campaign is needed to reduce the significant burden of invasive GBS disease that remains among infants and pregnant individuals. In this narrative review, we provide a comprehensive overview of the global impact of GBS colonization and infection, virulence factors and pathogenesis, and current and future prophylactics and therapeutics.

Keywords: Group B Streptococcus; bacteria; colonization; covR; covS; early-onset disease; fetus; hemolysin; late-onset disease; meningitis; placenta; pneumonia; pregnancy; preterm birth; sepsis; stillbirth.

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Conflict of interest statement

K.N. has been a paid consultant for Pfizer related to a cost analysis project for neonatal invasive GBS unrelated to this review. All other authors declare no competing interests.

Figures

Fig 1
Fig 1
GBS infections can present as non-asymptomatic colonization (top panel) in mothers and invasive disease in mothers and neonates (bottom panel). GBS invasive disease spans a spectrum of clinical manifestations, time of presentation, and clinical outcomes. Neonatal invasive disease is characterized as Early-on-set GBS and Late-on-set GBS disease. GBS colonization of mothers is a leading risk factor for the development of neonatal disease with other potential GBS exposure.
Fig 2
Fig 2
GBS isolates are commonly grouped by four main classifications: serotypes, multilocus sequence typing (MLST), clonal complex, and virulence factors. Researchers and medical providers refer to GBS by categories to elicit those responsible for invasion and disease.
Fig 3
Fig 3
GBS contains diverse virulence factors that contribute to pathogenicity and colonization. This figure was modified from Fig. 1 in reference (239), published under a Creative Commons license. HvgA and FbsB2b, are specific to ST17, while Sbp1 and Srr2 are partially exclusive (38). The ST452 strain, a hybrid between ST17 and ST23, also expresses the surface proteins, Srr2 and FbsB2b (39).
Fig 4
Fig 4
Varied models are employed to understand GBS colonization, infection, and pathophysiology between mothers and neonates.

References

    1. Nocard N, Mollereau R. 1887. Sur une mammite contagieuse des vaches laitieres. Ann Inst Pasteur 1:109–126.
    1. Eickhoff TC, Klein JO, Daly AK, Ingall D, Finland M. 1964. Neonatal sepsis and other infections due to group B beta-hemolytic streptococci. N Engl J Med 271:1221–1228. doi: 10.1056/NEJM196412102712401 - DOI - PubMed
    1. Anne Schuchat SS. 2000. Group B streptococci: from emerging infection to prevention success story
    1. Lancefield RC, Hare R. 1935. The serological differentiation of pathogenic and non-pathogenic strains of hemolytic streptococci from parturient women. J Exp Med 61:335–349. doi: 10.1084/jem.61.3.335 - DOI - PMC - PubMed
    1. Fry R. 1938. Fatal infections by hemolytic Streptococcus group B. Lancet 231:199–201. doi: 10.1016/S0140-6736(00)93202-1 - DOI

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