Herpes Simplex Virus
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Herpes simplex virus (HSV) is an enveloped double-stranded DNA virus. It exists as two distinct subtypes, HSV-1 and HSV-2, and is responsible for a wide spectrum of illness ranging from fever blisters to genital ulcers and fatal encephalitis. It establishes lifelong latency and can lead to interval episodes of asymptomatic shedding and disease recurrence.
- HSV-1 infects 40–80% of the U.S. population by young adulthood.
- HSV-2 incidence increases during adolescence and adulthood, infecting 20–35% of U.S. adults by age 40 years.
- In the United States, approximately 1,500 cases of neonatal HSV (1:3,200 live births) occur every year, primarily due to HSV-2.
- Following the neonatal period, HSV-1 infections predominate among children.
- Perinatal infection
- The majority of neonatal HSV infections (85%) occur through contact with maternal HSV shed within the birth canal. A smaller proportion (5%) of infections occur in utero.
- The majority (60–80%) of mothers of infected infants have no symptoms of HSV infection at the time of delivery.
- Children born to mothers with primary genital HSV infection at time of delivery are at highest risk (up to 60%). In contrast, the risk of neonatal infection with recurrent maternal genital herpes is significantly lower (2–5%).
- In the setting of active genital herpes (lesions or pain), cesarean delivery is recommended, preferably within 4 hours of rupture of membranes. However, infections may still occur despite cesarean delivery and intact amniotic membranes.
- Cesarean delivery is not recommended for mothers with a history of genital HSV in the absence of lesions or symptoms.
- Fetal scalp monitors should be avoided in women with suspected genital HSV.
- The use of antiviral therapy (acyclovir or valacyclovir) after 36 weeks’ gestation decreases viral shedding and reactivation of genital lesions in mothers with a history of genital HSV, although breakthrough infections may still occur.
- Postnatal infection (neonates and children)
- Secretions of active HSV lesions are highly infectious, and asymptomatic viral shedding is common. 10% of neonatal HSV infections are contracted postpartum through direct contact with infectious fluids.
- Standard universal precautions are appropriate in caring for recurrent/localized lesions in immunocompetent persons.
- Contact precautions should be considered in neonates, immunocompromised persons with active lesions, and in severe primary mucocutaneous HSV.
- Contact with genital/cutaneous HSV lesions (e.g., sexual intercourse, wrestling) should be avoided until lesions resolve.
- Spread occurs typically via contact with abraded skin or mucous membranes.
- The incubation period for primary infection is approximately 2 to 12 days.
- Viral replication begins at the portal of entry (epithelia) and commences within sensory ganglia. Migration occurs back to the site of inoculation, with subsequent destruction of epithelial cells.
- Following initial infection, the virus remains latent in sensory neural ganglia and can be reactivated by UV exposure, trauma, stress, hormonal changes, or immunosuppression.
- Viral dissemination occurs most often in neonates, pregnant women, or immunosuppressed patients.
- HSV antibodies provide a degree of cross protection across serotypes; previous infection with one HSV serotype (e.g., HSV-1) can decrease the severity of infection with the alternate serotype (e.g., HSV-2).
- HSV antiviral resistance is rare among healthy individuals but can develop in immunocompromised hosts and in the setting of herpetic keratitis.
- Risk factors for HSV-1 and HSV-2 infection include older age and lower socioeconomic status.
- Additional risk factors for HSV-2 include number of lifetime sexual partners and female gender.
Commonly Associated Conditions
- Herpes gladiatorum
- Herpetic whitlow
- Eczema herpeticum
- Erythema multiforme