Neonatal Sepsis

Neonatal sepsis (from Greek nēos — new, Latin natus — birth and Greek sepsis — decay) is a life-threatening condition representing a systemic generalized inflammatory response of a newborn’s body in response to an infectious agent entering the bloodstream.

Etiology and pathophysiology

The disease is classified into early-onset sepsis (within the first 72 hours of life) and late-onset sepsis.

Early-onset sepsis is most commonly associated with vertical transmission: the infant becomes infected in utero or, more commonly, at the time of passing through the mother’s infected birth canal (typical pathogens include group B streptococcus and Escherichia coli).

The pathogenesis is due to the insufficiency of mucosal barrier mechanisms and the physiological immaturity of the newborn’s immune system. Vulnerability factors include:

• reduced phagocytic activity of leukocytes;
• a low number of T helper cells and their functional “naivety”;
• low levels of IgM and IgA.

As a result, the pathogen rapidly breaches local protective barriers and enters the bloodstream (bacteremia).

The body responds with a potent release of pro-inflammatory cytokines (“cytokine storm”), which may lead to shock due to the activation of the complement system and the intrinsic coagulation pathway.

Clinical significance

Neonatal sepsis is characterized by a rapid, sometimes fulminant, progression and high mortality. The clinical picture in neonates is often atypical.

Instead of classic fever, the following symptoms may be observed:

• hypothermia (decreased body temperature) or temperature fluctuations;
• marked lethargy;
• poor sucking or refusal;
• periods of apnea (cessation of breathing);
• bradycardia;
• mottling of the skin due to microcirculation disorders.

Upon the slightest suspicion of sepsis, doctors immediately commence empirical broad-spectrum intravenous antibiotic therapy, without waiting for blood culture results (which take several days).