What is the pathophysiology of neonatal sepsis?

Updated: Jun 13, 2019
  • Author: Nathan S Gollehon, MD, FAAP; Chief Editor: Muhammad Aslam, MD  more...
  • Print
Answer

The infectious agents associated with neonatal sepsis have changed since the mid-20th century. During the 1950s, S aureus and E coli were the most common bacterial pathogens among neonates in the United States. Over the ensuing decades, Group B Streptococcus (GBS) replaced S aureus as the most common gram-positive organism causing early-onset sepsis.

Currently, GBS and E coli continue to be the most commonly identified microorganisms associated with neonatal infection. Additional organisms, such as coagulase-negative Staphylococcus epidermidis, L monocytogenes, Chlamydia pneumoniae, H influenzae, Enterobacter aerogenes, and species of Bacteroides and Clostridium have also been identified in neonatal sepsis.

Meningoencephalitis and neonatal sepsis can also be caused by infection with adenovirus, enterovirus, or coxsackievirus. Additionally, sexually transmitted diseases (eg, gonorrheasyphilis, herpes simplex virus [HSV] infection, cytomegalovirus [CMV] infection, hepatitis, human immunodeficiency virus [HIV] infection, rubellatoxoplasmosis, trichomoniasis, and candidiasis) have all been implicated in neonatal infection.

Bacterial organisms with increased antibiotic resistance have emerged and have further complicated the management of neonatal sepsis. [7] The colonization patterns in nurseries and personnel are reflected in the organisms currently associated with nosocomial infection. In neonatal intensive care units (NICUs), infants with lower birth weight and younger gestational ages have an increased susceptibility to these organisms.

S epidermidis, a coagulase-negative Staphylococcus, is increasingly seen as a cause of nosocomial or late-onset sepsis, especially in the premature infant, in whom it is considered the leading cause of late-onset infections. Its prevalence is likely related to several intrinsic properties of the organism that allow it to readily adhere to the plastic mediums found in intravascular catheters commonly required for the care of these infants.

The bacterial capsule polysaccharide adheres well to the plastic polymers of the catheters. Also, proteins found in the organism (AtlE and SSP-1) enhance attachment to the surface of the catheter. The adherence creates a capsule between microbe and catheter, preventing C3 deposition and phagocytosis. [8, 9]

Biofilms are formed on indwelling catheters by the aggregation of organisms that have multiplied under the protection provided by the adherence to the catheter. Slimes are produced at the site from the extracellular material formed by the organism, which provides a barrier to host defense as well as to antibiotic action, making coagulase-negative staphylococcal bloodstream infection (BSI) more difficult to treat. The toxins formed by S epidermidis have also been associated with necrotizing enterocolitis.

In addition to being a cause of neonatal sepsis, coagulase-negative Staphylococcus is ubiquitous as part of the normal skin flora. Consequently, it is a frequent contaminant of blood and cerebrospinal fluid (CSF) cultures. When a culture grows this organism, the clinical presentation, colony counts, and the presence of polymorphonuclear neutrophils (PMNs) on Gram staining of the submitted specimen often help differentiate true infection from contaminated culture specimens.

In addition to the specific microbial factors mentioned above, numerous host factors predispose the newborn to sepsis. [10] These factors are especially prominent in the premature infant and involve all levels of host defense, including cellular immunity, humoral immunity, and barrier function. Immature immune defenses and environmental and maternal factors contribute to the risk for neonatal sepsis, morbidity, and mortality, particularly in preterm and/or very low birthweight (VLBW) infants. [10, 11]  There may also be a genetic association. [10]


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!