Neonatal sepsis or sepsis neonatorum is an important cause of morbidity and mortality among newborns 28 days of life or younger. It presents with the systemic signs of infection or isolation of a bacterial pathogen from the bloodstream.1 According to the infant’s age at the onset of symptoms, sepsis is classified as early or late.
Early-onset sepsis (EOS), discussed in this chapter, has the onset of symptoms within the first days of the newborn’s life. Perinatally acquired bacterial neonatal sepsis is a low-incidence, high-risk disease that can be defined as a bloodstream infection at 72 hours of age or less2 or, in the case of early-onset group B streptococcal (GBS) disease, as infection with the onset of symptoms through day 6 of life.3 Presentation of EOS is within 24 hours of life in 85%, in 24–48 hours in 5%, and within 48–72 hours in the rest of the neonates. Infections present earlier in preterm neonates.
Neonatal sepsis incidence is 1–5 cases/1000 live births. In term neonates, incidence is lower than in preterm, with 1–2 cases/1000 live births.4
Risk factors for neonatal sepsis include chorioamnionitis, intrapartum maternal fever (temperature ≥ 38°C [100.4°F]); rupture of membranes for 18 hours or longer5; delivery at less than 37 weeks’ gestation; 5-minute Apgar score 6 or less; maternal GBS colonization; maternal GBS or gram-negative bacteriuria during the current pregnancy; and prior delivery of neonate with GBS disease. Additional risk factors are the use of instrumentation, such as forceps, or placement of electrodes for intrauterine monitoring during labor and delivery.6 Black race is a risk factor for both early- and late-onset GBS sepsis, and the reasons behind this are not fully understood.7
Sepsis is a clinical syndrome that complicates severe infection, characterized by systemic inflammation and widespread tissue injury. Tissues remote from the original insult display the signs of inflammation, including vasodilation, increased microvascular permeability, and leukocyte accumulation. “Dysregulation” of the normal inflammatory response, with a massive and uncontrolled release of proinflammatory mediators, initiates a chain of events leading to widespread tissue injury. This host response, not the primary disease, is typically responsible for multiple-organ failure.
In an EOS, the most common route of transmission is vertical transmission by ascending contaminated amniotic fluid or bacteria colonizing or infecting the mother’s lower genitourinary tract.8
Clinical picture and outcome of neonatal sepsis depend on time of onset, maturity of the host defense mechanisms, associated complications, timing of initiation of appropriate antibiotics, and supportive therapy.
Factors contributing to neonatal susceptibility to bacterial infections are the following:
Anatomic and biochemical immaturity of skin and mucosal barriers (eg, lung, gut epithelia),
Reduced numbers or function of macrophages and dendritic cells in peripheral tissues (eg, lung),
Lower numbers ...