Neonatal Herpes Infection: A Review

Leslie A. Parker, MSN, RNC, NNP; Sheryl J. Montrowl, MSN, RNC, NNP

Disclosures

NAINR. 2004;4(1) 

In This Article

Background

Herpes infections have been referenced in medical literature for centuries. Ancient Greeks and Romans coined the term "herpes" meaning to creep or crawl.[4] In the 1700s a French physician, Astru, made the association between herpectic lesions and genital ulcers, but the distinction between the epidemiology and clinical differences of HSV-1 and HSV-2 were not apparent until the 1960s.[5]

HSV is a double-stranded DNA-enveloped virus belonging to the Herpesviridae family, which is further divided into alpha, beta, and gamma. HSV-1 and HSV-2 both belong to the alpha-herpesvirinae subfamily, genus Simplexvirus.[6] Viruses of the genus Simplexvirus are characterized by a variable host range, short replication cycle, and the ability to destroy infected cells and establish latent infections.[6] The basic structure of HSV consists of a central core and an inner core. The central core is comprised of viral DNA surrounded by a coating composed of tubular proteins. An envelope derived from cellular membranes containing viral proteins surrounds the inner core. Embedded in this layer are several viral-encoded glycoproteins (gB, gC, gD, and gE) that are important for attachment to the host cell receptors, cell penetration, and viral immune escape mechanisms.[7]

Herpes virus infection can affect a wide range of cells including both neural and epithelial tissues.[8] Neural tissue infections result in either latency or destruction of neurons and glial cells. Epithelial infection causes destruction of epithelial cells with the formation of a vesicle, which contains a high titer of virus. After primary infection in the epithelial cells, the virus enters the sensory neurons and is transported to sensory ganglia, where it becomes latent and lies dormant. Viral reactivation can occur after stimuli [such as ultraviolet (UV) light, fever, or trauma], facilitating asymptomatic shedding or epithelial infection usually of a less severe nature. Herpes viruses are unique in that they can establish latency following symptomatic or asymptomatic primary infection and subsequent reactivation can occur with or without symptoms despite the presence of humoral and cellular immunity.[9,10] Thus, an individual infected with HSV is always a potential reservoir of infectious virus.[11]

Genital HSV infections are among the most common sexually transmitted infections in the United States, with 600,000 new cases diagnosed each year.[1,6] Although HSV-2 is the most common cause of genital HSV infections, changes in sexual practices have increased the incidence of genital HSV-1 infections. Epidemiologic studies of HSV show humans are the primary hosts and close interpersonal contact is required for transmission. Factors most highly associated with infection are race, age, and years of sexual experience.[6,12] Several studies showed seroconversion during pregnancy to be about 2 to 3% and often the women are not aware of this conversion as their partners were asymptomatic.[13] Even women in long-term monogamous relationships can become infected because they may not convert for years.[14]

Genital HSV infection in the adult population is classified into three clinical designations, primary genital HSV, nonprimary first episode genital HSV, and recurrent genital HSV. Primary genital HSV is defined as acquiring HSV when antibodies to HSV-1 and HSV-2 are absent. This usually presents with painful vesicles in clusters on the inflammed area. Primary genital HSV may be accompanied by pruritis, dysuria, vaginal discharge, and tender adenopathy. In addition the individual may have fever, malaise, and myalgia for one to two days before lesions appear. Viral shedding begins two days after onset and continues until reepithelialization of lesions. Nonprimary first episode genital HSV is defined as acquisition of HSV-1 or -2 with antibodies to the other type, whereas recurrent genital HSV is reactivation of genital HSV where the lesion is the same type as the sera.[6]

Primary HSV infection in the last trimester of pregnancy carries a transmission rate of 30 to 50% whereas in recurrent infection the transmission rate is decreased to 0 to 5%.[13,15,16] This lower transmission rate is due to the lower viral titer, transplacentally protective antibodies, and lower frequency of cervical viral shedding during recurrent infection.[17]

Neonatal HSV can be acquired intrauterine, intrapartum, or postpartum. It is most commonly caused by HSV-2, but 15 to 30% of cases can be attributed to HSV-1.[18,19,20] Transplacentally acquired infection accounts for 5% of neonatal HSV infections and is defined as presence of skin vesicles or scarring, chorioretinitis, hydroencephaly, microophthalmia, microcephaly, or an abnormal computerized tomogram (CT) scan of the head within the first week of life.[21,22] These infants frequently present with low birth weight due to prematurity or intrauterine growth restriction and may be extremely ill immediately following delivery with multiorgan system involvement.

Transmission during delivery is the most common route of infection accounting for 86 to 90% of neonatal HSV cases.[6,23] Transmission can be 10 times higher in women who acquire primary HSV late in pregnancy as opposed to recurrent disease.[19,24,25,26] Predictors of transmission include location, number, and duration of lesions. Cervical shedding as opposed to vulvar shedding and multiple lesions that last longer all increase risk of infection. Unfortunately, identifying who is at risk is difficult, as 60 to 80% of mothers with infected newborns are asymptomatic at delivery and have no history of HSV.[27,28]

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