Description, Causes and Risk Factors:
Herpes simplex virus type 1 or 2 infection transmitted from the mother to the newborn infant, often during passage through an infected birth canal; severity varies from mild-to-fatal generalized infection, the latter especially with primary maternal genital herpes.
Neonatal herpes is acquired during one of three distinct periods: intrauterine (in utero), peripartum (perinatal), and postpartum (postnatal). Among infected infants, the time of transmission for the overwhelming majority (85%) of neonates is the peripartum period. An additional 10 percent of infected neonates acquire the virus postnatally, and the ?nal 5 percent are infected with HSV in utero. The ?ve factors known to in?uence transmission of HSV from mother to neonate are:
Maternal antibody status.
Duration of rupture of membranes.
Integrity of mucocutaneous barriers.
Mode of delivery (cesarean versus vaginal delivery).
Type of maternal infection (primary versus. recurrent).
Infants born to mothers who have a ?rst episode of genital HSV infection near term are at much greater risk of developing neonatal herpes than are those whose mothers have recurrent genital herpes. This increased risk is caused both by lower concentrations of transplacentally passaged HSV-speci?c antibodies (which also are less reactive to expressed polypeptides) in women with primary infection and by the higher quantities of HSV that are shed for a longer period of time in the maternal genital tract when compared with women who have recurrent genital HSV infection. The largest assessment of the in?uence of the type of maternal infection on the likelihood of neonatal transmission involved almost 40,000 women without clinical evidence of genital HSV infection who were cultured within 48 hours of delivery. Of these, 121 women were identi?ed who both were asymptomatically shedding HSV and for whom sera were available for serologic analysis. In this large trial, 57 percent of babies delivered to women with ?rst episode primary infection developed neonatal HSV disease compared with 25 percent of babies delivered to women with ?rst-episode, non-primary infection and 2 percent of babies delivered to women with recurrent HSV disease.
Neonates with higher neutralizing antibody titers are less likely to become infected with HSV after perinatal exposure during passage through an infected birth canal, illustrating the protective effects of preexisting antibody in preventing the acquisition of neonatal HSV disease. Among HSV-infected neonates, anti-HSV neutralizing antibody titers also correlate with the extent of the disease, with babies with higher neutralizing antibody titers being more likely to have localized disease (and less likely to have disseminated disease) once they are infected. Similarly, high maternal or neonatal anti-HSV ADCC antibody levels or high neonatal antiviral neutralizing levels each are associated independently with an absence of disseminated HSV infection.
HSV infections acquired either peripartum or postpartumcan be classi?ed as (1) disseminated disease involving multiple visceral organs, including lung, liver, adrenal glands,skin, eye, and the brain (disseminated disease); (2) CNS disease, with or without skin lesions (CNS disease); and (3)disease limited to the skin, eyes, and/or mouth. This classi?cation system is predictive of both morbidity and mortality.Patients with disseminated or SEM disease generally present to medical attention at 10 to 12 days oflife, whereas patients with CNS disease on average presentsomewhat later at 16 to 19 days of life.
The current estimated rate of occurrence of neonatal HSV disease in the United States is approximately one in 3200 deliveries. Thus, the United States, with approximately 4.0 million deliveries per year, has an estimated 1500 cases of neonatal HSV infection annually.
Signs and symptom include,
Disseminated intravascular coagulation (DIC).
The diagnosis of neonatal HSV infections has been revolutionized by the application of PCR technology to clinical specimens including CSF and blood. Direct comparisons of the results of these studies are complicated by differences in the methods used in different laboratories. In the largest series, CSF specimens from 77 neonates in the United States with culture-proven HSV disease were evaluated retrospectively by PCR. The results of this analysis both enhanced the understanding of the spectrum of the natural history of neonatal HSV disease and validated the utilization of PCR in the management of such infants.
In the pre-antiviral era, 85 percent of patients with disseminated neonatal HSV disease died by the time they were 1 year of age, as did 50 percent of patients with CNS neonatal HSV disease. Evaluations of two different doses of vidarabine (VIRA-A™) and of a lower dose of acyclovir (30 mg/kg/d for 10 days) documented that both of these antiviral drugs reduce the rate of mortality to comparable degrees, with mortality rates at 1 year from disseminated disease decreasing to 54 percent and from CNS disease decreasing to 14 percent. Despite its lack of therapeutic superiority, the lower dose of acyclovir quickly supplanted vidarabine as the treatment of choice for neonatal HSV disease because of its favorable safety pro?le and its ease of administration. Unlike acyclovir, vidarabine had to be administered during prolonged infusion times and in large volumes of ?uid.
Lethargy and severe hepatitis are associated with mortality among patients with disseminated disease, as are prematurity and seizures in patients with CNS disease.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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