Group B streptococcal infection overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [5]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [6]
Overview
Despite substantial progress in prevention of perinatal group B streptococcal (GBS) disease since the 1990s, GBS remains the leading cause of early-onset neonatal sepsis in the United States. Universal screening at 35--37 weeks' gestation for maternal GBS colonization and use of intrapartum antibiotic prophylaxis has resulted in substantial reductions in the burden of early-onset GBS disease among newborns. Although early-onset GBS disease has become relatively uncommon in recent years, the rates of maternal GBS colonization (and therefore the risk for early-onset GBS disease in the absence of intrapartum antibiotic prophylaxis) remain unchanged since the 1970s. Continued efforts are needed to sustain and improve on the progress achieved in the prevention of GBS disease. There also is a need to monitor for potential adverse consequences of intrapartum antibiotic prophylaxis (e.g., emergence of bacterial antimicrobial resistance or increased incidence or severity of non-GBS neonatal pathogens). In the absence of a licensed GBS vaccine, universal screening and intrapartum antibiotic prophylaxis continue to be the cornerstones of early-onset GBS disease prevention.
Historical Perspective
In the 1970s, the bacterium group B Streptococcus (GBS) emerged as the leading infectious cause of early neonatal morbidity and mortality in the United States.[1][2][3][4] Beginning in the mid 1980s, clinical trials and well-designed observational studies demonstrated that administering intravenous antibiotics during labor to women at risk for transmitting GBS to their newborns could prevent invasive disease in the first week of life (i.e., early-onset disease).[5][6][7][8][9] As a result of the collaborative efforts of clinicians, researchers, professional organizations, parent advocacy groups, and the public health community in the 1990s, recommendations for intrapartum prophylaxis to prevent perinatal GBS disease were issued in 1996 by the American College of Obstetricians and Gynecologists (ACOG)[10] and CDC[11] and in 1997 by the American Academy of Pediatrics (AAP).[12] Revised guidelines for the prevention of early-onset GBS disease issued in 2002 recommended universal culture-based screening of all pregnant women at 35-37 weeks gestation to optimize the identification of women who should receive intrapartum antibiotic prophylaxis.[13] The most recent CDC guidelines were published in 2010.[14]
Classification
Group B streptococcal (GBS) infection can be classified into three main categories depending on the type of affected subjects. GBS infection can occur in pregnant women, neonates, or non-pregnant adults mainly the elderly.[15] Neonatal GBS infection can be further classified into early-onset or late-onset depending on the timing of the onset of the symptoms. Infections in newborns occurring within the first week of life are designated as early-onset disease, whereas late-onset infections occur in infants aged >1 week, with most infections evident during the first 3 months of life. [14]
Pathophysiology
The gastrointestinal tract serves as the primary reservoir for Group B Streptococcus (GBS) and is the likely source of vaginal colonization. Early-onset neonatal infections are acquired vertically through exposure to GBS from the vagina of a colonized woman. GBS is characterized by its ability to adhere to epithelial surfaces, such as the vagina, placental membranes, blood brain barrier, and respiratory tract. GBS can penetrate the host cell barriers and evade the host's immune response. The polysaccharide antiphagocytic capsule is this bacterium's main virulence factor.
Causes
Group B Streptococcus (GBS) disease is caused by the infection with the bacterium GBS which is a beta hemolytic gram-positive streptococcus characterized by the presence of group B Lancefield antigen. GBS displays beta-hemolysis when cultured on a blood agar plate and produces zones of hemolysis that are only slightly larger than the colonies themselves. The species other name S. agalactiae, where "agalactiae" means "no milk", alludes to this. GBS hydrolyzes sodium hippurate and gives a positive response in the CAMP test. GBS is also sensitive to bile and will lyse in its presence. GBS is a species of the normal flora of the gut and female urogenital tract. The polysaccharide antiphagocytic capsule is this bacterium's main virulence factor.
Differential Diagnosis
Group B Streptococcus (GBS) infection causes a wide variety of clinical presentations depending on the type of the affected subjects; therefore, the differential diagnosis of GBS infection varies based on the age of the patient and their health condition. Early-onset GBS infection in neonates might lead to pneumonia, meningitis, or sepsis and it must be differentiated from other types of infectious agents in this category of patients.
Epidemiology and Demographics
Group B Streptococcus (GBS) causes invasive disease primarily in infants, pregnant or postpartum women, and older adults, with the highest incidence among young infants.[16] Before active prevention was initiated, an estimated 7,500 cases of neonatal GBS disease occurred annually in the United States.[17] Striking declines in disease incidence coincided with increased prevention activities in the 1990s,[18] and a further reduction occurred following the issuance of the recommendation for universal screening in 2002.[19] However, GBS disease remains the leading infectious cause of morbidity and mortality among newborns in the United States.[16][20] 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.[14]
Risk Factors
Maternal intrapartum GBS colonization is the primary risk factor for early-onset disease in infants. Additional risk factors for early-onset disease in infants include gestational age < 37 completed weeks, longer duration of membrane rupture, intra-amniotic infection, young maternal age, and black race.[14]
Screening
The Center of Disease Control and Prevention (CDC)'s screening guidelines for Group B streptococcal (GBS) infection recommend universal culture-based screening for all pregnant women for vaginal and rectal GBS colonization in order to determine which women should receive intrapartum GBS chemoprophylaxis. CDC recommended that women with unknown GBS colonization status at the time of delivery be managed according to the presence of intrapartum risk factors. CDC's guidelines recommend screening for vaginal and rectal GBS colonization at 35-37 weeks' gestation. Swabbing both the lower vagina and rectum (through the anal sphincter) increases the culture yield substantially compared with sampling the cervix or the vagina without also swabbing the rectum.[14] Routine screening for asymptomatic bacteriuria is recommended in pregnant women, and laboratories should screen urine culture specimens for the presence of GBS in concentrations of 104 colony-forming units (cfu)/ml or greater.[14]
Natural History, Complications and Prognosis
Group B Streptococcus (GBS) is the leading infectious cause of morbidity and mortality among infants in the United States, particularly among preterm neonates.[21][16][18] Most newborns with early-onset disease have symptoms on the day of birth. Babies who develop late-onset disease may appear healthy at birth and develop symptoms of GBS disease after the first week of life.
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Treatment
Medical Therapy
Primary Prevention
Secondary Prevention
Future or Investigational Therapies
References
- ↑ Chattopadhyay B (1975). "Fatal neonatal meningitis due to group B streptococci". Postgrad Med J. 51 (594): 240–3. PMC 2495958. PMID 1105496.
- ↑ McCracken GH (1973). "Group B streptococci: the new challenge in neonatal infections". J Pediatr. 82 (4): 703–6. PMID 4572746.
- ↑ Franciosi RA, Knostman JD, Zimmerman RA (1973). "Group B streptococcal neonatal and infant infections". J Pediatr. 82 (4): 707–18. PMID 4572747.
- ↑ Barton LL, Feigin RD, Lins R (1973). "Group B beta hemolytic streptococcal meningitis in infants". J Pediatr. 82 (4): 719–23. PMID 4572748.
- ↑ Allardice JG, Baskett TF, Seshia MM, Bowman N, Malazdrewicz R (1982). "Perinatal group B streptococcal colonization and infection". Am J Obstet Gynecol. 142 (6 Pt 1): 617–20. PMID 7039316.
- ↑ Boyer KM, Gotoff SP (1986). "Prevention of early-onset neonatal group B streptococcal disease with selective intrapartum chemoprophylaxis". N Engl J Med. 314 (26): 1665–9. doi:10.1056/NEJM198606263142603. PMID 3520319.
- ↑ Lim DV, Morales WJ, Walsh AF, Kazanis D (1986). "Reduction of morbidity and mortality rates for neonatal group B streptococcal disease through early diagnosis and chemoprophylaxis". J Clin Microbiol. 23 (3): 489–92. PMC 268680. PMID 3514659.
- ↑ Tuppurainen N, Hallman M (1989). "Prevention of neonatal group B streptococcal disease: intrapartum detection and chemoprophylaxis of heavily colonized parturients". Obstet Gynecol. 73 (4): 583–7. PMID 2494620.
- ↑ Garland SM, Fliegner JR (1991). "Group B streptococcus (GBS) and neonatal infections: the case for intrapartum chemoprophylaxis". Aust N Z J Obstet Gynaecol. 31 (2): 119–22. PMID 1930031.
- ↑ American College of Obstetricians and Gynecologists. ACOG committee opinion. Prevention of early-onset group B streptococcal disease in newborns. Number 173,June 1996. Committee on Obstetric Practice. American College of Obstetrics and Gynecologists. Int J Gynaecol Obstet 1996;54:197--205.
- ↑ CDC. Prevention of perinatal group B streptococcal disease: a public health perspective. MMWR 1996;45(No. RR-7).[1]
- ↑ American Academy of Pediatrics. Revised guidelines for prevention of early-onset group B streptococcal (GBS) infection. American Academy of Pediatrics Committee on Infectious Diseases and Committee on Fetus and Newborn. Pediatrics 1997;99:489--96.
- ↑ CDC. Prevention of perinatal group B streptococcal disease: revised guidelines from CDC. MMWR 2002;51(No. RR-11).[2]
- ↑ 14.0 14.1 14.2 14.3 14.4 14.5 Verani J.R., McGee L, and Schrag S.J. Prevention of Perinatal Group B Streptococcal Disease. Revised Guidelines from CDC, 2010.CDC.gov
- ↑ Edwards MS, Baker CJ (2005). "Group B streptococcal infections in elderly adults". Clin Infect Dis. 41 (6): 839–47. doi:10.1086/432804. PMID 16107984.
- ↑ 16.0 16.1 16.2 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.
- ↑ 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.
- ↑ 18.0 18.1 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.[3]
- ↑ CDC. Trends in perinatal group B streptococcal disease---United States, 2000--2006. MMWR 2009;58:109--12.[4]
- ↑ Baker CJ, Barrett FF (1974). "Group B streptococcal infections in infants. The importance of the various serotypes". JAMA. 230 (8): 1158–60. PMID 4608888.