Group B streptococcal infection epidemiology and demographics
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [5]
Overview
Group B Streptococcus (GBS) causes invasive disease primarily in infants, pregnant or postpartum women, and older adults, with the highest incidence among young infants.[1] Before active prevention was initiated, an estimated 7,500 cases of neonatal GBS disease occurred annually in the United States.[2] Striking declines in disease incidence coincided with increased prevention activities in the 1990s,[3] and a further reduction occurred following the issuance of the recommendation for universal screening in 2002.[4] However, GBS disease remains the leading infectious cause of morbidity and mortality among newborns in the United States.[1][5] The continued burden of disease and newly available data relevant to early-onset GBS disease prevention from the fields of epidemiology, obstetrics, neonatology, microbiology, molecular biology, and pharmacology prompted revision of the guidelines for early-onset GBS disease prevention.[6]
Epidemiology and Demographics
GBS in Pregnancy
Approximately 10%-30% of pregnant women are colonized with GBS in the vagina or rectum.[7][8][9]
GBS in Neonates
Incidence
Before active prevention was initiated, an estimated 7,500 cases of neonatal GBS disease occurred annually in the United States.[2]
As a result of prevention efforts, incidence of GBS has declined dramatically over the past 15 years, from 1.7 cases per 1,000 live births in the early 1990s to 0.34--0.37 cases per 1,000 live births in recent years. On the basis of data from CDC's Active Bacterial Core surveillance (ABCs) system, a network of 10 sites across the United States that conduct active, population-based surveillance, CDC estimates that in recent years, GBS has caused approximately 1,200 cases of early-onset invasive disease per year;[10] approximately 70% of cases are among babies born at term (≥37 weeks' gestation).[1]
Shown below is an image depicting the incidence of early- and late-onset invasive GBS disease between 1990 and 2008.
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Abbreviations: ACOG = American College of Obstetricians and Gynecologists and AAP = American Academy of Pediatrics.
Source: CDC.gov Adapted from Jordan HT, Farley MM, Craig A, et al. Revisiting the need for vaccine prevention of late-onset neonatal group B streptococcal disease. Pediatr Infect Dis J 2008;27:1057--64.
Race
The incidence of GBS infection is higher among black neonates compared to white. The disparity in early-onset GBS disease incidence between black and white infants has persisted after the 2002 CDC guidelines and is evident among both term and preterm infants.[11][5] Preliminary surveillance data from 2008 suggest that the racial disparity was reduced somewhat in 2008.[12] Incidence among all black infants declined to 0.49 cases per 1,000 live births, showing progress towards the Healthy People 2010 objective of 0.5 cases per 1,000 live births for all racial and ethnic groups.[13]
Shown below is an image depicting the incidence per 1,000 live births of early-onset invasive group B streptococcal disease in the 10 Active Bacterial Core surveillance areas during 2000-2007. Data are displayed for four demographic subsets: term white infants, term black infants, preterm white infants, and preterm black infants.
Source: Adapted from CDC. Trends in perinatal group B streptococcal disease---United States, 2000--2006. MMWR 2009;58:109--12.
GBS in Non-Pregnant Adults
References
- ↑ 1.0 1.1 1.2 Phares CR, Lynfield R, Farley MM, Mohle-Boetani J, Harrison LH, Petit S; et al. (2008). "Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005". JAMA. 299 (17): 2056–65. doi:10.1001/jama.299.17.2056. PMID 18460666.
- ↑ 2.0 2.1 Zangwill KM, Schuchat A, Wenger JD (1992). "Group B streptococcal disease in the United States, 1990: report from a multistate active surveillance system". MMWR CDC Surveill Summ. 41 (6): 25–32. PMID 1470102.
- ↑ Schrag SJ, Zywicki S, Farley MM, Reingold AL, Harrison LH, Lefkowitz LB; et al. (2000). "Group B streptococcal disease in the era of intrapartum antibiotic prophylaxis". N Engl J Med. 342 (1): 15–20. doi:10.1056/NEJM200001063420103. PMID 10620644.
- ↑ CDC. Perinatal group B streptococcal disease after universal screening recommendations---United States, 2003--2005. MMWR 2007;56:701--5.[1]
- ↑ 5.0 5.1 CDC. Trends in perinatal group B streptococcal disease---United States, 2000--2006. MMWR 2009;58:109--12.[2]
- ↑ Verani J.R., McGee L, and Schrag S.J. Prevention of Perinatal Group B Streptococcal Disease. Revised Guidelines from CDC, 2010.CDC.gov
- ↑ Regan JA, Klebanoff MA, Nugent RP (1991). "The epidemiology of group B streptococcal colonization in pregnancy. Vaginal Infections and Prematurity Study Group". Obstet Gynecol. 77 (4): 604–10. PMID 2002986.
- ↑ Yancey MK, Schuchat A, Brown LK, Ventura VL, Markenson GR (1996). "The accuracy of late antenatal screening cultures in predicting genital group B streptococcal colonization at delivery". Obstet Gynecol. 88 (5): 811–5. doi:10.1016/0029-7844(96)00320-1. PMID 8885919.
- ↑ Campbell JR, Hillier SL, Krohn MA, Ferrieri P, Zaleznik DF, Baker CJ (2000). "Group B streptococcal colonization and serotype-specific immunity in pregnant women at delivery". Obstet Gynecol. 96 (4): 498–503. PMID 11004347.
- ↑ CDC. Active Bacterial Core Surveillance Report, Emerging Infections Program Network, Group B Streptococcus, 2008. Atlanta, GA: US Department of Health and Human Services, CDC; 2009. Available at cdc.gov.
- ↑ CDC. Perinatal group B streptococcal disease after universal screening recommendations---United States, 2003--2005. MMWR 2007;56:701--5.[3]
- ↑ CDC. Active Bacterial Core Surveillance Report, Emerging Infections Program Network, Group B Streptococcus, 2008. Atlanta, GA: US Department of Health and Human Services, CDC; 2009. Available at CDC.gov
- ↑ US Department of Health and Human Services. Healthy people 2010: understanding and improving health. 2nd ed. United States Government Printing Office; 2000.