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Group B streptococcus: Virulence factors and pathogenic mechanisms

Lawrence C Madoff, MD
Section Editor
Daniel J Sexton, MD
Deputy Editor
Allyson Bloom, MD


Group B streptococcus (GBS; Streptococcus agalactiae) is a gram-positive coccus that frequently colonizes the human genital and gastrointestinal tracts [1,2]. It is an important cause of infection in three populations:

Neonates – GBS infection is acquired in utero by ascending infection or during passage through the vagina. Neonatal disease is categorized by the age at onset into early- and late-onset infection. Early-onset most commonly presents at or within 12 hours of birth but, by definition, can occur through day six of life. The most common manifestations are bacteremia without a focus, sepsis, pneumonia, and/or meningitis. Late-onset infection occurs after day six and up to 90 days of life. It most often presents as bacteremia without a focus (65 percent of cases) but meningitis (32 percent) and focal infections also occur. Late-onset infections most frequently are caused by serotype III GBS. (See "Group B streptococcal infection in neonates and young infants".)

Pregnant women – GBS is a frequent cause of urinary tract infection (usually asymptomatic bacteriuria), chorioamnionitis, postpartum endometritis, and peripartum bacteremia. (See "Group B streptococcal infection in pregnant women".)

Nonpregnant adults – GBS is increasingly recognized as a cause of sepsis, soft tissue infections, and other focal infections in nonpregnant adults. These infections occur predominantly in those with chronic underlying medical conditions, such as diabetes mellitus, malignancy especially breast cancer, and liver disease. However, GBS also can cause infection in healthy patients over the age of 65 years. (See "Group B streptococcal infections in nonpregnant adults".)

The microbiology of GBS will be reviewed here. GBS infection and treatment in neonates and young infants, pregnant women, and nonpregnant adults and prevention strategies through chemoprophylaxis and vaccination are discussed separately. (See "Group B streptococcal infections in nonpregnant adults" and "Group B streptococcal infection in neonates and young infants" and "Group B streptococcal infection in pregnant women" and "Neonatal group B streptococcal disease: Prevention" and "Vaccines for the prevention of group B streptococcal disease".)

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Literature review current through: Nov 2017. | This topic last updated: Jun 22, 2017.
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  1. Edwards MS, Nizet V, Baker CJ. Group B Streptococcal Infections. In: Infectious Diseases of the Fetus and Newborn Infant, 7th ed, Remington JS, Klein JO, Wilson CB, et al (Eds), Elsevier Saunders, Philadelphia 2011. p.419.
  2. Wessels MR, Kasper DL. Group B streptococcus. In: Infectious Diseases, Gorbach SL, Bartlett JG, Blacklow NR (Eds), WB Saunders, Philadelphia 1997.
  3. Madoff, LC, Kasper, DL. Group B streptococcal infection. In: Obstetric and Perinatal Infections, Charles, D (Ed), Mosby Year Book, Boston, 1993, p. 210.
  5. Meehan M, Cafferkey M, Corcoran S, et al. Real-time polymerase chain reaction and culture in the diagnosis of invasive group B streptococcal disease in infants: a retrospective study. Eur J Clin Microbiol Infect Dis 2015; 34:2413.
  6. Metcalf BJ, Chochua S, Gertz RE Jr, et al. Short-read whole genome sequencing for determination of antimicrobial resistance mechanisms and capsular serotypes of current invasive Streptococcus agalactiae recovered in the USA. Clin Microbiol Infect 2017; 23:574.e7.
  7. Jennings HJ, Katzenellenbogen E, Lugowski C, Kasper DL. Structure of native polysaccharide antigens of type Ia and type Ib group B Streptococcus. Biochemistry 1983; 22:1258.
  8. Jennings HJ, Rosell KG, Katzenellenbogen E, Kasper DL. Structural determination of the capsular polysaccharide antigen of type II group B Streptococcus. J Biol Chem 1983; 258:1793.
  9. Wessels MR, Benedí WJ, Jennings HJ, et al. Isolation and characterization of type IV group B Streptococcus capsular polysaccharide. Infect Immun 1989; 57:1089.
  10. Rubens CE, Wessels MR, Heggen LM, Kasper DL. Transposon mutagenesis of type III group B Streptococcus: correlation of capsule expression with virulence. Proc Natl Acad Sci U S A 1987; 84:7208.
  11. Wessels MR, Benedi VJ, Kasper DL, et al. Type III capsule and virulence of group B streptococci. In: Genetics and Molecular Biology of Streptococci, Lactococci, and Enterococci, Dunny GM, Cleary PP, McKay LL (Eds), American Society for Microbiology, Washington, DC 1991. p.219.
  12. Kasper DL. Bacterial capsule--old dogmas and new tricks. J Infect Dis 1986; 153:407.
  13. Berti F, Campisi E, Toniolo C, et al. Structure of the type IX group B Streptococcus capsular polysaccharide and its evolutionary relationship with types V and VII. J Biol Chem 2014; 289:23437.
  14. Baker CJ, Kasper DL. Correlation of maternal antibody deficiency with susceptibility to neonatal group B streptococcal infection. N Engl J Med 1976; 294:753.
  15. Carlin AF, Uchiyama S, Chang YC, et al. Molecular mimicry of host sialylated glycans allows a bacterial pathogen to engage neutrophil Siglec-9 and dampen the innate immune response. Blood 2009; 113:3333.
  16. Doran KS, Engelson EJ, Khosravi A, et al. Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid. J Clin Invest 2005; 115:2499.
  17. Tazi A, Disson O, Bellais S, et al. The surface protein HvgA mediates group B streptococcus hypervirulence and meningeal tropism in neonates. J Exp Med 2010; 207:2313.
  18. Lamy MC, Zouine M, Fert J, et al. CovS/CovR of group B streptococcus: a two-component global regulatory system involved in virulence. Mol Microbiol 2004; 54:1250.
  19. Liu GY, Doran KS, Lawrence T, et al. Sword and shield: linked group B streptococcal beta-hemolysin/cytolysin and carotenoid pigment function to subvert host phagocyte defense. Proc Natl Acad Sci U S A 2004; 101:14491.
  20. Whidbey C, Harrell MI, Burnside K, et al. A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta. J Exp Med 2013; 210:1265.
  21. Johnson DR, Ferrieri P. Group B streptococcal Ibc protein antigen: distribution of two determinants in wild-type strains of common serotypes. J Clin Microbiol 1984; 19:506.
  22. Madoff LC, Michel JL, Gong EW, et al. Protection of neonatal mice from group B streptococcal infection by maternal immunization with beta C protein. Infect Immun 1992; 60:4989.
  23. Madoff LC, Michel JL, Gong EW, et al. Group B streptococci escape host immunity by deletion of tandem repeat elements of the alpha C protein. Proc Natl Acad Sci U S A 1996; 93:4131.
  24. Gravekamp C, Kasper DL, Michel JL, et al. Immunogenicity and protective efficacy of the alpha C protein of group B streptococci are inversely related to the number of repeats. Infect Immun 1997; 65:5216.
  25. Baron MJ, Filman DJ, Prophete GA, et al. Identification of a glycosaminoglycan binding region of the alpha C protein that mediates entry of group B Streptococci into host cells. J Biol Chem 2007; 282:10526.
  26. Konto-Ghiorghi Y, Mairey E, Mallet A, et al. Dual role for pilus in adherence to epithelial cells and biofilm formation in Streptococcus agalactiae. PLoS Pathog 2009; 5:e1000422.
  27. Margarit I, Rinaudo CD, Galeotti CL, et al. Preventing bacterial infections with pilus-based vaccines: the group B streptococcus paradigm. J Infect Dis 2009; 199:108.
  28. Morello E, Mallet A, Konto-Ghiorghi Y, et al. Evidence for the Sialylation of PilA, the PI-2a Pilus-Associated Adhesin of Streptococcus agalactiae Strain NEM316. PLoS One 2015; 10:e0138103.
  29. Nizet V, Gibson RL, Chi EY, et al. Group B streptococcal beta-hemolysin expression is associated with injury of lung epithelial cells. Infect Immun 1996; 64:3818.
  30. Glaser P, Rusniok C, Buchrieser C, et al. Genome sequence of Streptococcus agalactiae, a pathogen causing invasive neonatal disease. Mol Microbiol 2002; 45:1499.
  31. Tettelin H, Masignani V, Cieslewicz MJ, et al. Complete genome sequence and comparative genomic analysis of an emerging human pathogen, serotype V Streptococcus agalactiae. Proc Natl Acad Sci U S A 2002; 99:12391.
  32. Flores AR, Galloway-Peña J, Sahasrabhojane P, et al. Sequence type 1 group B Streptococcus, an emerging cause of invasive disease in adults, evolves by small genetic changes. Proc Natl Acad Sci U S A 2015; 112:6431.