Approximately 25-65% of pregnant women have genital infection with herpes simplex virus type 1 (HSV-1) or herpes simplex virus type 2(HSV-2).
Approximately 20-30% of pregnant women are infected with HSV-2.
Neonatal HSV infection defined as infection with presentation within 28 days of birth.
Neonatal HSV associated with devastating results.
Untreated neonatal HSV associated with a 40% survival rate.
Neonatal HSV infection rate ranges from 1 case per 3200 to 1 in 10,000 live births.
Approximately 1500 cases annually.
Incidence higher than congenital syphilis, Toxoplasmosis, congenital rubella in years when the virus was not epidemic.
Most neonatal infections result from exposure to HSV in the genital tract during delivery.
Most cases HSV-2.
Neonatal HSV usually occurs in babies who are born to women with primary, asymptomatic HSV.
Three periods for neonatal transmission: antenatal, intrapartum, and postnatal.
Approximately 85% of neonatal HSV infections transmitted perinatally, during the delivery when the neonate is in contact with infected genital secretions.
5% of infections acquired congenitally, being transmitted in utero.
10-15% of cases after delivery from nonmaterial sources.
Highest risk occurs from new primary infections in the mother during the third trimester.
In utero and postnatal infections can occur occasionally.
The risk of transmission is significantly higher when women acquire genital HSV-1 or 2 during pregnancy compared to women that have long-standing HSV-2 infection in whom the virus is reactivated in the genital tract at term: 25-50% vs. less than 1%.
Rarely this virus can cause life-threatening hepatitis in pregnant women, usually in the third trimester, and in the absence of mucocutaneous lesions.
Neonatal HSV classified into three disease categories: localized skin, eye and mouth disease, occurring in 45% patients, CNS disease with or without skin, eye,, or mouth lesions, accounting for 33% of patients, and disseminated disease with multiorgan involvement accounting for 25% of patients.
Neonatal HSV outcome depends on extent of disease, with approximately 30% of infants with disseminated disease dying and 20% have neurologic sequelae (Kimberlin DW et al).
Only 6% of neonates with HSV CNS disease die, while 70% have permanent neurological damage.
Neonatal HSV with skin, eye and mouth disease is usually only rarely associated with neurologic impairment or with death.
HSV in sensory ganglia have latent periodic reactivation of localized disease.
Whether CNS HSV subclinically reactivates is not known.
Infants with neonatal HSV and surviving with CNS involvement have improved neurodevelopment outcomes with oral acyclovir therapy for 6 months (Kimberlin DW et al).
Electroencephalogram should be for performed early in those infants with suspected CNS disease, and it will reveal abnormalities prior to CSF or imaging analyses.
Localized disease typically manifests with clustered vesicles on an erythematous base.
Intrauterine HSV presents, with a more severe systemic complication rate and consists of cutaneous vesicles, CNS, and ophthalmologic findings.
40% of patients with neonatal HSV present with skin manifestations other than vesicles or bullae.
Untreated neonatal HSV infection is associated mortality rate of 80%.
In patients with early intervention there may still be severe physical and developmental disabilities.
Recommended treatment for neonatal HSV is supportive care and antiviral therapy with intravenous acyclovir 60 mg per kilogram per day for 3-4 weeks.