Group B streptococcal infection risk factors
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]
Overview
Maternal intrapartum Group B streptococcus (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.[1]
Risk Factors
GBS Infection in Neonates
Risk factors for GBS infection in neonates include:[2][3][1]
- Maternal colonization
- Gestational age <37 completed weeks
- Longer duration of membrane rupture
- Intra-amniotic infection
- Young maternal age
- Black race
- Low maternal levels of GBS-specific anticapsular antibody
- Previous delivery of an infant with invasive GBS disease
- Obstetric procedures
- Internal fetal monitoring devices
- More than five or six digital vaginal examinations after onset of labor
- Rupture of membranes
Maternal intrapartum GBS colonization is the primary risk factor for early-onset disease in infants. A classic prospective cohort study conducted during the 1980s revealed that pregnant women with GBS colonization were >25 times more likely than pregnant women with negative prenatal cultures to deliver infants with early-onset GBS disease.[2][1]
Heavy colonization, defined as culture of GBS from direct plating rather than from selective broth only, is associated with higher risk for early-onset disease.[4][5][1]
GBS identified in clean-catch urine specimens during any trimester is considered a surrogate for heavy maternal colonization and also is associated with a higher risk for early-onset GBS disease.[6][7][1]
In a 1985 report of factors associated with early-onset disease, women with gestation <37 weeks, membrane rupture of >12 hours, or intrapartum temperature >99.5ºF (>37.5ºC) had 6.5 times the risk for having an infant with early-onset GBS disease compared with women who had none of these risk factors.[2] Of note, women who had one of these risk factors but who had negative prenatal screening cultures were at relatively low risk for early-onset GBS disease (incidence: 0.9 cases per 1,000 births) compared with women who were colonized prenatally but had none of the risk factors (incidence: 5.1 cases per 1,000 births).[2][1]
Some observational studies have reported an association between early-onset GBS disease and certain obstetric procedures, such as the use of internal fetal monitoring devices[3][8] and more than five or six digital vaginal examinations after onset of labor or rupture of membranes.[8] However, lack of randomization in observational studies can result in confounding, because certain procedures might be used more frequently in high-risk settings.[9] Although concern has been raised about performing other obstetric procedures (e.g., membrane stripping and mechanical and/or pharmacologic cervical ripening) on GBS-colonized women, available data are not sufficient to determine whether these procedures are associated with an increased risk for early-onset disease.[10][11][1]
GBS Infection in Non-Pregnant Adults
Shown below is a list of conditions associated with a higher rate of GBS infection in non-pregnant adults:[12]
- Advanced age
- Bedridden state
- Diabetes mellitus
- Cirrhosis
- Malignancy
- Seevre peripheral vascular disease
- Corticosteroid treatment
- Chronic renal failure
- Stroke
- Decubitus ulcer
- Neurogenic bladder
- Joint prosthesis
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Verani J.R., McGee L, and Schrag S.J. Prevention of Perinatal Group B Streptococcal Disease. Revised Guidelines from CDC, 2010.CDC.gov
- ↑ 2.0 2.1 2.2 2.3 Boyer KM, Gotoff SP (1985). "Strategies for chemoprophylaxis of GBS early-onset infections". Antibiot Chemother (1971). 35: 267–80. PMID 3931544.
- ↑ 3.0 3.1 Adair CE, Kowalsky L, Quon H, Ma D, Stoffman J, McGeer A; et al. (2003). "Risk factors for early-onset group B streptococcal disease in neonates: a population-based case-control study". CMAJ. 169 (3): 198–203. PMC 167120. PMID 12900477.
- ↑ Regan JA, Klebanoff MA, Nugent RP, Eschenbach DA, Blackwelder WC, Lou Y; et al. (1996). "Colonization with group B streptococci in pregnancy and adverse outcome. VIP Study Group". Am J Obstet Gynecol. 174 (4): 1354–60. PMID 8623869.
- ↑ Yancey MK, Duff P, Kubilis P, Clark P, Frentzen BH (1996). "Risk factors for neonatal sepsis". Obstet Gynecol. 87 (2): 188–94. doi:10.1016/0029-7844(95)00402-5. PMID 8559521.
- ↑ Liston TE, Harris RE, Foshee S, Null DM (1979). "Relationship of neonatal pneumonia to maternal urinary and neonatal isolates of group B streptococci". South Med J. 72 (11): 1410–2. PMID 388649.
- ↑ Heath PT, Balfour GF, Tighe H, Verlander NQ, Lamagni TL, Efstratiou A; et al. (2009). "Group B streptococcal disease in infants: a case control study". Arch Dis Child. 94 (9): 674–80. doi:10.1136/adc.2008.148874. PMID 19457879.
- ↑ 8.0 8.1 Adams WG, Kinney JS, Schuchat A, Collier CL, Papasian CJ, Kilbride HW; et al. (1993). "Outbreak of early onset group B streptococcal sepsis". Pediatr Infect Dis J. 12 (7): 565–70. PMID 8345997.
- ↑ Gibbs RS, Schrag S, Schuchat A (2004). "Perinatal infections due to group B streptococci". Obstet Gynecol. 104 (5 Pt 1): 1062–76. doi:10.1097/01.AOG.0000144128.03913.c2. PMID 15516403.
- ↑ Boulvain M, Stan C, Irion O (2001). "Membrane sweeping for induction of labour". Cochrane Database Syst Rev (2): CD000451. doi:10.1002/14651858.CD000451. PMID 11405964.
- ↑ Heinemann J, Gillen G, Sanchez-Ramos L, Kaunitz AM (2008). "Do mechanical methods of cervical ripening increase infectious morbidity? A systematic review". Am J Obstet Gynecol. 199 (2): 177–87, discussion 187-8. doi:10.1016/j.ajog.2008.05.005. PMID 18674661.
- ↑ 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.