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Neonatal infection can be acquired in utero transplacentally, through the birth canal during delivery (intrapartum), and from external sources after birth (postpartum).
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 neonatal infection (eg, toxoplasmosis, syphilis).
Intrapartum infection occurs from passage through an infected birth canal or by ascending infection if delivery is delayed after rupture of membranes. Common viral agents include herpes simplex, HIV, cytomegalovirus (CMV), and hepatitis B; these can less commonly be transmitted transplacentally. Bacterial agents include group B streptococci, enteric gram-negative organisms (primarily Escherichia coli), gonococci, and chlamydiae.
Postpartum infections are acquired from contact with an infected mother either directly (eg, TB, which also is sometimes transmitted in utero) or through breastfeeding (eg, HIV, CMV) or from contact with health care practitioners and the hospital environment (numerous organisms—see Infections in Neonates: Neonatal Hospital-Acquired Infection).
Risk
factors:
Risk of contracting intra- and postpartum infection is inversely proportional to gestational age. Neonates are immunologically immature, with decreased PMN and monocyte function; premature infants are particularly so (see also Perinatal Physiology: Immunologic). Maternal IgG antibodies are actively transported across the placenta, but effective levels 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.
Antibacterial
therapy:
Drug selection is similar to that in adults (see Bacteria and Antibacterial Drugs: Selection and Use of Antibacterial Drugs), because infecting organisms and their sensitivities are not specific to neonates. However, numerous factors, including age and weight, affect dose and frequency (see Table 1: Infections in Neonates: Recommended Dosages of Selected Parenteral Antibiotics for Neonates and Table 2: Infections in Neonates: Recommended Dosages of Selected Oral Antibiotics for Neonates
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Table 2
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Recommended Dosages of
Selected Oral Antibiotics for Neonates
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Antibiotic
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Dosage
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Interval
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Comments
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Amoxicillin
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15 mg/kg
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q 8 h
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Limited data
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Cefaclor
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15 mg/kg
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q 8 h
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Limited data
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Clindamycin *
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5 mg/kg
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q 6–8 h
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Limited data
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Colistin
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3–5 mg/kg
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q 8 h
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For gastroenteritis caused by enteropathogenic strains of Escherichia coli, and for prophylaxis of neonates at high risk for necrotizing enterocolitis, for 5 days. May be systemically absorbed in the presence of significant diarrhea. Unproven efficacy and safety
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Erythromycin estolate
Erythromycin ethylsuccinate
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10 mg/kg
12.5 mg/kg
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q 8 h
q 6 h
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For chlamydial infections or pertussis
For chlamydial infections or pertussis
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Fluconazole
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3–6 mg/kg
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q 24 h
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For candidal infections
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Flucytosine
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12.5–37.5 mg/kg
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q 6 h
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Limited data. Use only in combination with amphotericin B , to retard emergence of resistance
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Neomycin
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30–35 mg/kg
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q 8 h
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See Colistin
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Rifampin †
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10 mg/kg
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q 24 h
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For TB
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5 mg/kg
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q 12 h
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For meningococcus prophylaxis for 2 days
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10 mg/kg
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q 24 h
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For Haemophilus influenzae prophylaxis for 4 days
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*The dose for neonates < 7 days who are < 2000 g is 5 mg/kg q 12 h.
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†Serum levels in preterm infants should be monitored.
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In neonates, the ECF constitutes up to 45% of total body weight, requiring relatively larger doses of certain antibiotics (eg, aminoglycosides) compared to adults. Lower serum albumin concentrations in premature infants may reduce antibiotic protein binding. Drugs that displace bilirubin from albumin (eg, sulfonamides, ceftriaxone ) increase the risk of kernicterus.
Absence or deficiency of certain enzymes in neonates may prolong the half-life of certain antibiotics ( chloramphenicol ) and increase the risk of toxicity. Changes in GFR and renal tubular secretion during the 1st month of life necessitate dosing changes for other drugs (eg, penicillins, aminoglycosides, vancomycin ).
Last full review/revision November 2005
Content last modified November 2005
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