Early-Onset Sepsis

Early-onset sepsis (EOS) is invasive bacterial infection of the newborn that presents very soon after birth, conventionally within the first few days of life, and that is generally acquired from the mother around the time of labour and delivery. It is a central topic in neonatology because of its rapid course, its link to the maternal genital flora, and the way prevention at the time of birth has reshaped which babies get sick.

Definition

Early-onset sepsis is invasive infection of the neonate with onset in the first days of life — most definitions use a cutoff of 72 hours, some up to 7 days — typically reflecting vertical acquisition of organisms from the maternal genital tract around the time of birth.

Scope

This entry covers what defines early-onset sepsis, how it is acquired through vertical transmission, the pathogens that predominate, the risk factors that mark higher-probability infants, and how intrapartum prevention has changed its epidemiology. It is reference content on the concept and is not a protocol for evaluating or treating a particular newborn.

Core questions

• What timing cutoff distinguishes early-onset from late-onset sepsis, and why is it imperfect?
• How do organisms reach the infant before or during delivery?
• Which pathogens dominate early-onset disease, and how has prevention shifted them?
• Which maternal and perinatal factors raise the probability of early-onset infection?

Key concepts

• Onset within the first days of life
• Vertical (intrapartum) transmission
• Ascending infection from the genital tract
• Group B Streptococcus and Escherichia coli as leading organisms
• Maternal risk factors (e.g., prolonged rupture of membranes, intrapartum fever, preterm birth)
• Intrapartum antibiotic prophylaxis and its epidemiologic effect

Mechanisms

Early-onset sepsis generally begins with the organisms that colonise the maternal genital and gastrointestinal tract. These can ascend into the amniotic cavity, especially when the membranes rupture before or during labour, or can be acquired by the infant during passage through the birth canal. Group B Streptococcus and Escherichia coli are the organisms most often responsible. Because the exposure occurs around birth and the newborn's defences are immature, infection can progress quickly to a systemic inflammatory response. Widespread intrapartum antibiotic prophylaxis aimed at group B Streptococcus has reduced early-onset disease from that organism, shifting the relative contribution of other pathogens, particularly among preterm and very-low-birth-weight infants.

Clinical relevance

Early-onset sepsis is a major reason newborns are evaluated for infection in the hours after birth, and understanding its risk factors and changing epidemiology informs surveillance and prevention programmes. This entry describes the concept and the evidence around it; decisions about evaluating or managing an individual infant rest with the responsible clinicians and applicable guidelines.

Epidemiology

Surveillance from large neonatal networks shows that intrapartum prophylaxis has lowered the incidence of early-onset group B streptococcal disease, while Escherichia coli has become a relatively more prominent cause, particularly in preterm and very-low-birth-weight infants, in whom the burden and case-fatality of early-onset sepsis remain higher than in term infants.

History

The separation of neonatal sepsis by timing of onset, and the recognition of group B Streptococcus and Escherichia coli as the dominant early-onset pathogens, were established through twentieth-century perinatal research. The adoption of intrapartum antibiotic prophylaxis from the 1990s onward, and subsequent surveillance, documented a marked decline in early-onset group B streptococcal disease and prompted ongoing reassessment of the remaining burden.

Debates

How should well-appearing newborns at risk for early-onset sepsis be approached?

Because most infants exposed to risk factors are not infected, approaches to evaluating and observing well-appearing newborns are debated and have moved toward individualised, probability-based assessment rather than uniform testing; this is a methodological discussion, not a treatment recommendation here.

Seminal works

• shane-2017
• stoll-2016
• polin-2012

Frequently asked questions

What separates early-onset from late-onset sepsis?

Timing and usual route: early-onset disease appears within the first days of life and is generally acquired from the mother around birth, whereas late-onset disease appears later and is more often acquired from the environment.

Which organisms most commonly cause early-onset sepsis?

Group B Streptococcus and Escherichia coli are the leading causes; intrapartum prophylaxis has reduced early-onset group B streptococcal disease, making Escherichia coli relatively more prominent, especially in preterm infants.