Infectious Disease · Neonatal Sepsis
The facts most likely to be tested
Streptococcus agalactiae is the most common cause of neonatal sepsis and meningitis in the United States.
Universal rectovaginal screening for GBS colonization is performed at 36 0/7 to 37 6/7 weeks gestation.
Intrapartum antibiotic prophylaxis (IAP) with penicillin G is the gold standard for preventing early-onset GBS disease.
Mothers with GBS bacteriuria during the current pregnancy or a previous infant with invasive GBS disease require IAP regardless of current screening results.
Early-onset GBS disease typically presents within the first 24 to 48 hours of life with respiratory distress, apnea, or sepsis.
Late-onset GBS disease occurs between 7 days and 3 months of age and is most frequently associated with meningitis.
Patients with a penicillin allergy who are at high risk for anaphylaxis require susceptibility testing to determine if clindamycin or vancomycin is appropriate for IAP.
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A 28-year-old G2P1 woman at 37 weeks gestation presents in active labor. Her prenatal records indicate a positive rectovaginal culture for Group B Streptococcus obtained at 36 weeks. She has no known drug allergies. She is currently afebrile and the fetal heart rate is reassuring. The patient has not yet received any medications during this admission.
What is the most appropriate management to prevent neonatal infection in this patient?
Intrapartum intravenous penicillin G
This tests the requirement for IAP in patients with a positive GBS screen; penicillin G is the drug of choice to prevent vertical transmission and early-onset neonatal sepsis.
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Etiology / Epidemiology
Caused by Streptococcus agalactiae; maternal colonization is the primary risk factor.
Clinical Manifestations
Presents as early-onset sepsis (respiratory distress, lethargy) or late-onset meningitis.
Diagnosis
Intrapartum NAAT/culture screening; definitive diagnosis via blood/CSF culture.
Treatment
Intravenous Penicillin G is the drug of choice for intrapartum prophylaxis.
Prognosis
High mortality if untreated; neurologic sequelae common in survivors of meningitis.
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Epidemiology & Etiology
GBS is a gram-positive coccus that colonizes the maternal genital and GI tracts. Vertical transmission occurs during labor or via ascending infection after membrane rupture. Major risk factors include prolonged rupture of membranes (>18 hours), maternal fever, and prematurity.
Pertinent Anatomy
The pathogen ascends from the vaginal canal into the amniotic fluid. In neonates, the primary portals of entry are the respiratory tract and the bloodstream, leading to systemic dissemination.
Pathophysiology
GBS produces a polysaccharide capsule that inhibits phagocytosis, facilitating rapid bacterial proliferation. Early-onset disease (<7 days) typically manifests as pneumonia or sepsis, while late-onset disease (7-90 days) frequently presents as meningitis. The inflammatory response leads to systemic cytokine release and potential multi-organ failure.
Clinical Manifestations
Early-onset disease presents within 24 hours with respiratory distress, apnea, and tachycardia. Late-onset disease is characterized by fever of unknown origin, irritability, and poor feeding. Red flags include bulging fontanelle, seizures, and signs of septic shock.
Diagnosis
Universal screening via rectovaginal culture at 36-37 weeks gestation is the standard of care. Definitive diagnosis in the neonate requires blood culture or CSF culture. A CSF profile showing pleocytosis and elevated protein is diagnostic for meningitis.
Treatment
Intravenous Penicillin G is the first-line agent for intrapartum prophylaxis. If the mother has a penicillin allergy, use cefazolin (if low risk of anaphylaxis) or clindamycin (if high risk). Do not use tetracyclines in neonates due to dental staining.
Prognosis
Early recognition is critical to prevent septic shock and death. Survivors of GBS meningitis are at high risk for long-term neurodevelopmental impairment, including hearing loss and cognitive deficits.
Differential Diagnosis
E. coli sepsis: often indistinguishable clinically from GBS
Listeria monocytogenes: associated with meconium-stained amniotic fluid
Herpes Simplex Virus: look for vesicular skin lesions
Respiratory Distress Syndrome: common in preterm infants without infection
Congenital Syphilis: look for hepatosplenomegaly and rash