Group B streptococcal infection risk factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Overview[edit | edit source]

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[edit | edit source]

GBS Infection in Neonates[edit | edit source]

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[edit | edit source]

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[edit | edit source]

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