Overview of Neonatal Infections
Neonatal infection can be acquired
Common viral agents include herpes simplex viruses, HIV, cytomegalovirus (CMV), and hepatitis B. Intrapartum infection with HIV or hepatitis B occurs from passage through an infected birth canal or by ascending infection if delivery is delayed after rupture of membranes; these viruses can less commonly be transmitted transplacentally. CMV is commonly transmitted transplacentally.
In utero infection, which can occur any time before birth, results from overt or subclinical maternal infection. Consequences depend on the agent and timing of infection in gestation and include spontaneous abortion, intrauterine growth restriction, premature birth, stillbirth, congenital malformation (eg, rubella), and symptomatic (eg, CMV, toxoplasmosis, syphilis) or asymptomatic (eg, CMV) neonatal infection.
Neonatal infections with herpes simplex viruses, HIV, hepatitis B, group B streptococci, enteric gram-negative organisms (primarily Escherichia coli), Listeria monocytogenes, gonococci, and chlamydiae usually occur from passage through an infected birth canal. Sometimes ascending infection can occur if delivery is delayed after rupture of membranes.
Postpartum infections are acquired from contact with an infected mother directly (eg, tuberculosis, which also is sometimes transmitted in utero) or through breastfeeding (eg, HIV, CMV) or from contact with family or visitors, health care practitioners, or the hospital environment (numerous organisms—see Neonatal Hospital-Acquired Infection).
Risk of contracting intrapartum and postpartum infection is inversely proportional to gestational age. Neonates are immunologically immature, with decreased polymorphonuclear leukocyte, monocyte, and cell-mediated immune function; premature infants are particularly so (see also Perinatal Physiology : Neonatal immunologic function).
Maternal IgG antibodies are actively transported across the placenta, but effective levels for all organisms are not achieved until near term. IgM antibodies do not cross the placenta. Premature infants have decreased intrinsic antibody production and reduced complement activity. Premature infants are also more likely to require invasive procedures (eg, endotracheal intubation, prolonged IV access) that predispose to infection.
Symptoms and signs of infection in neonates tend to be nonspecific (eg, vomiting or poor feeding, increased sleepiness or lethargy, fever or hypothermia, tachypnea, rashes, diarrhea, abdominal distention). Many congenital infections acquired before birth can cause or be accompanied by various symptoms or abnormalities (eg, growth restriction, deafness, microcephaly, anomalies, failure to thrive, hepatosplenomegaly, neurologic abnormalities).
A wide variety of infections, including sepsis, should be considered in neonates who are ill at or shortly after birth, particularly those with risk factors. Infections such as congenital rubella, syphilis, toxoplasmosis, and CMV should be pursued in neonates with abnormalities such as growth restriction, deafness, microcephaly or other physical anomalies, hepatosplenomegaly, or neurologic abnormalities.
The primary treatment for presumed bacterial infection in the neonate is prompt empiric antimicrobial therapy with drugs such as ampicillin and gentamicin or ampicillin and cefotaxime. Final drug selection is based on culture results similar to the practice in adults, because infecting organisms and their sensitivities are not specific to neonates. However, drug dose and frequency are affected by numerous factors, including age and weight (see tables in Antibiotics in Neonates).
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