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I. PROBLEM

Two infants were born within the past hour. One infant’s mother had premature rupture of membranes (PROM) but no antibiotics. The other infant’s mother was pretreated with antibiotics for a positive group B Streptococcus (GBS) culture taken at 36 weeks. Who should be evaluated, and who should receive empiric antibiotics? It is necessary to review some of the basic concepts of early-onset sepsis (EOS), such as definition, pathogenesis, incidence morbidity, and mortality, before treatment plans are discussed. Major organizations have varying recommendations on EOS. This on-call problem focuses on postdelivery antibiotics for suspected EOS. Late-onset sepsis is discussed in Chapter 146, and infections of premature infants with prolonged hospital stays may require a different workup and antibiotic choice.

  1. Definition of early-onset sepsis. There are multiple definitions:

    1. The National Institute of Child Health and Human Development and Vermont Oxford Network: The onset of sepsis at ≤72 hours of life. In term infants, it can be extended to <7 days of life.

    2. The Centers for Disease Control and Prevention: Blood culture– and/or cerebrospinal fluid (CSF) culture–proven infection occurring in the newborn at <7 days.

    3. The American Academy of Pediatrics (2018): Blood or CSF culture obtained within 72 hours after birth that is growing a pathogenic bacterial species.

    4. AAP definition of GBS EOS (2019). Isolation of group B Streptococcus organisms from the blood, cerebrospinal fluid, or another normally sterile site from birth through 6 days of age.

  2. Pathogenesis of early-onset sepsis differs in the term/late preterm infant and the preterm infant.

    1. Early-onset sepsis in the term/late term infants occurs most commonly during labor.

      1. Vertically transmitted (ascending infection). Ascending colonization with amniotic membrane rupture/leak before or during labor resulting in infection of the uterine compartment (amniotic fluid, placenta, umbilical cord, or fetus) with maternal gastrointestinal/genitourinary flora. The fetus can become infected by being colonized on the skin/mucous membranes (sepsis develops hours or days after birth), or the fetus aspirates or swallows infected amniotic fluid (sepsis begins in utero). GBS can also enter amniotic fluid through an occult tear. This is the most common cause of GBS early-onset disease (GBS EOD).

      2. Direct contact in the birth canal. The neonate can acquire the pathogen as it passes through the colonized birth canal during delivery.

      3. Transplacentally by hematogenous spread. Rarely, EOS develops before the onset of labor (eg, Listeria monocytogenes is typically transmitted from the mother to the fetus by hematogenous spread across the placenta).

    2. Early-onset sepsis in the preterm infant occurs most commonly before the onset of labor.

      1. Intra-amniotic infection from either microbial induced maternal inflammation (vaginal organisms) or the transplacental pathway (maternal oral flora or Listeria monocytogenes).

      2. Inflammation secondary to immune-mediated rejection of the fetus or placenta from a maternal extrauterine infection or reproductive/nonreproductive microbiota.

  3. Incidence of early-onset sepsis is highest among preterm and very low birthweight (VLBW) infants, and cases are inversely proportional to gestational age. EOS incidence is also higher among late preterm infants than term infants. The incidence of culture-proven EOS is approximately 0.8 ...

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