Herpes Simplex Virus (HSV) Infection in Neonates

Neonatal herpes simplex virus infection is usually transmitted during labor and/or delivery. Signs are typically a vesicular eruption and subsequent disseminated disease. Diagnosis is by viral culture, histology, serology, or molecular biology. Treatment is with high-dose parenteral acyclovir and supportive care.

Neonatal herpes simplex virus (HSV) infection has high mortality and significant morbidity. Incidence estimates range from 1/3,000 to 1/20,000 births. HSV type 2 causes about 80% of cases; 20% are caused by HSV type 1.

HSV is usually transmitted during delivery through an infected maternal genital tract. Transplacental transmission of virus and hospital-acquired spread from one neonate to another by hospital personnel or family may account for about 15% of cases. Mothers of neonates with HSV infection tend to have no history or symptoms of genital infection at the time of delivery.

Symptoms and Signs

Manifestations generally occur between the 1st and 2nd wk of life but may not appear until as late as the 4th wk. Patients may present with local or disseminated disease. Skin vesicles are common in either form, occurring in about 55% overall. Those with no skin vesicles usually present with localized CNS disease. In patients with isolated skin or mucosal disease, progressive or more serious forms of disease frequently follow within 7 to 10 days if left untreated.

Neonates with localized disease can be divided into 2 groups. One group has encephalitis manifested by neurologic findings, CSF pleocytosis, and elevated protein concentration, with or without concomitant involvement of the skin, eyes, and mouth. The other group has only skin, eye, and mouth involvement and no evidence of CNS or organ disease.

Neonates with disseminated disease and visceral organ involvement have hepatitis, pneumonitis, and/or disseminated intravascular coagulation with or without encephalitis or skin disease.

Other signs, which can occur singly or in combination, include temperature instability, lethargy, hypotonia, respiratory distress, apnea, and seizures.


Rapid diagnosis by viral culture or HSV PCR is essential. The most common site of retrieval is skin vesicles. The mouth, eyes, and CSF are also high-yield sites. In some with encephalitis, virus is found only in the brain. Diagnosis also can be made by neutralization with appropriate high-titer antiserum; immunofluorescence of lesion scrapings, particularly with use of monoclonal antibodies; and electron microscopy. If no diagnostic virology facilities are available, a Papanicolaou test of the lesion base may show characteristic multinucleated giant cells and intranuclear inclusions, but this procedure is less sensitive than culture, and false-positives also occur.


The mortality rate of untreated disseminated disease is 85%; among those with untreated local disease and encephalitis, it is about 50%. At least 95% of survivors have severe neurologic sequelae. Death is uncommon in those with local disease but without CNS or organ disease, except as the result of concomitant medical problems, but about 30% develop neurologic impairment, which may not manifest until 2 to 3 yr of age.


Acyclovir decreases the mortality rate by 50% and increases the percentage of children who develop normally from 10 to 50%; dose is 20 mg/kg IV q 8 h for 14 to 21 days. Vigorous supportive therapy is required, including appropriate IV fluids, alimentation, respiratory support, correction of clotting abnormalities, and control of seizure disorders. Herpetic keratoconjunctivitis requires concomitant systemic acyclovir and topical therapy with a drug such as trifluridine.

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