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Neonatal early-onset sepsis (EOS).


Review EOS epidemiology and microbiology; approach for prevention of group B Streptococcus (GBS)-specific EOS; identification and management of infants at increased risk for EOS.



Neonatal EOS is defined as blood and/or cerebrospinal fluid (CSF) culture-proven infection occurring in the newborn at less than 7 days of age. Among preterm infants, time frame is limited to infection occurring <72 hours of age.


Current EOS incidence is ∼0.8 cases per 1000 live births in United States. Incidence and case fatality rate are strongly influenced by preterm birth. Among preterm, very-low birth weight (VLBW) infants (birth weight <1500 g) EOS incidence is ∼11 cases per 1000 live births; for infants born 22−24 weeks’ gestation, the incidence is as high as 30−35 cases per 1000 live births. Case-fatality rates also track with prematurity; 1−2% among term infants but ∼50% among those born ≤24 weeks’ gestation.


GBS is the leading cause of EOS in the term population, accounting for ∼40% of EOS cases. Escherichia coli accounts for ∼15% of term cases. In contrast, among infants born <34 weeks’ gestation, E. coli accounts for ∼50% of EOS cases among preterm infants and GBS ∼20%. Enterococcus, viridans streptococcus, and gram-negative organisms account for most other cases. Fungal species, staphylococcus, and Listeria are all uncommon causes of EOS, each accounting for <1−3% of reported cases. Centers where anaerobic cultures are obtained have reported ∼15% of EOS cases occurring among VLBW infants to be caused by strict anaerobic bacteria, primarily Bacteroides species.

Pathogenesis and Prevention

EOS pathogenesis predominantly occurs by ascending colonization and infection of the uterine compartment and fetus with microbial species from the maternal genitourinary flora during labor and/or during vaginal delivery. Clinical risk factors for EOS include those factors that provide opportunity for this pathogenesis (such as preterm and/or prolonged rupture of membranes [ROM]) or reflect progressive maternal inflammation and infection (such as maternal fever). Although the pathogenesis of EOS primarily occurs during labor and delivery for term infants, rarely intraamniotic infection may occur prior to the onset of labor and may even cause stillbirth. In contrast, onset of infection is often uncertain among preterm infants. Intraamniotic infection may precede and cause preterm labor or premature ROM (PROM) and prolonged periods of premature cervical dilatation and/or PROM may facilitate ascending infection. Occasionally, preterm EOS may be caused by bloodborne spread of infection across the placenta, as is the case with Listeria monocytogenes infection. Primary prevention of GBS-specific EOS can be achieved via the administration of intrapartum antibiotic prophylaxis (IAP) to mothers colonized with GBS, to reduce the burden of maternal and fetal colonization with this organism. Although IAP has reduced incidence, EOS-associated mortality and morbidity remain substantial. Thus assessing a newborn infant for risk of EOS, appropriate determination of infection and timely institution of treatment constitute critical parts of early newborn care.



Primary Prevention of EOS

Multiple obstetric management strategies aim to protect both mother and fetus from infection and are not within the scope of this chapter. Current national recommendations from the American Academy of Pediatrics ...

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