Neonatal sepsis may be categorized as early-onset or late-onset. Of newborns with early-onset sepsis, 85% present within 24 hours, 5% present at 24-48 hours, and a smaller percentage present within 48-72 hours. Onset is most rapid in premature neonates.

Early-onset sepsis is associated with acquisition of microorganisms from the mother. Transplacental infection or an ascending infection from the cervix may be caused by organisms that colonize the mother’s genitourinary (GU) tract; the neonate acquires the microorganisms as it passes through the colonized birth canal at delivery. The microorganisms most commonly associated with early-onset infection include the following [1] :

te-onset sepsis occurs at 4-90 days of life and is acquired from the caregiving environment. Organisms that have been implicated in causing late-onset sepsis include the following:

Trends in late-onset sepsis show an increase in coagulase-negative streptococcal sepsis; most of these isolates are susceptible to first-generation cephalosporins. [2]The infant’s skin, respiratory tract, conjunctivae, gastrointestinal (GI) tract, and umbilicus may become colonized from the environment, and such colonization to the possibility of late-onset sepsis from invasive microorganisms. Vectors for such colonization may include vascular or urinary catheters, other indwelling lines, or contact with caregivers who have bacterial colonization.

Pneumonia is more common in early-onset sepsis, whereas meningitis and bacteremia are more common in late-onset sepsis. Premature and ill infants are more susceptible to sepsis and subtle nonspecific initial presentations; considerable vigilance is therefore required in these patients so that sepsis can be effectively identified and treated.

When neonatal sepsis is suspected, treatment should be initiated immediately because of the neonate’s relative immunosuppression. Begin antibiotics as soon as diagnostic tests are performed (see Treatment).

For patient education information, see Sepsis (Blood Infection).

 

 

 

 

Trends in the epidemiology of early-onset sepsis show a decreasing incidence of GBS disease. This can be attributed to the implementation of a prenatal screening and treatment protocol for GBS.


In a 2009 study involving 4696 women, prenatal cultures showed a GBS colonization rate of 24.5%, with a positive culture rate of 18.8% at the time of labor. As many as 10% of prenatally culture-negative women were found to have positive cultures at the time of labor. With intrapartum antibiotic prophylaxis rates of 93.3%, 0.36 of 1000 infants developed early-onset GBS disease. [2, 3]

 

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