Herpes Simplex Virus
Stuart P. Adler
Herpes simplex virus (HSV), a common cause of morbidity among humans, has two distinct serotypes: HSV-1 and HSV-2. HSV-1 primarily causes cold sores, with oral or labial lesions being the most common manifestation. HSV-1 is presumably transmitted by contact with infected saliva or cutaneous lesions. HSV-2 is found predominantly in the genital areas and causes vesicular lesions with red borders that often appear in crops or clusters with satellite lesions. Both oral and genital lesions are often swollen and painful but eventually crust over and heal. HSV-2 transmission can be reduced with the use of condoms.
Newborns under 1 month of age are especially susceptible, because infection of the skin and mucous membranes by herpes simplex leads to viremia with viral dissemination to multiple organs, including the central nervous system. Newborns usually become infected at birth via contact with maternal cervical—vaginal secretions infected with HSV-2, but occasionally become infected via contact with infected personnel or contaminated equipment in the nursery.
In adults, HSV usually causes an asymptomatic infection, but occasionally HSV-1, or less commonly HSV-2, invades the central nervous system, causing encephalitis. This occurs when virus in the upper respiratory tract migrates along the olfactory nerve through the cribriform plate, most typically into the frontal or temporal lobes. The most common manifestations of herpes infection, however, are cutaneous, mucocutaneous, or oculocutaneous lesions.
BIOLOGY OF HERPES SIMPLEX VIRUS
HSV particles contain a double-stranded DNA genome enclosed in a nucleocapsid surrounded by enveloped glycoprotein. HSV may survive in humans for decades in spite of circulating neutralizing antibodies. After a primary infection, the virus usually remains latent in neuroganglion cells. Reactivation from these cells, with or without symptoms, is the hallmark of HSV infection. Reactivation of HSV may occur frequently over time and can be induced by stimuli noxious to the skin, such as ultraviolet radiation.
EPIDEMIOLOGY OF HERPES SIMPLEX
The prevalence of HSV infections among humans has been determined by virologic and seroepidemiologic surveys. Based on serologic surveys of adults (antibodies to either HSV-1, HSV-2, or both), seroprevalence ranges from 15% to 100% (1, 2, 3, 4 and 5). Seroprevalence is associated with many variables including socioeconomic status, crowded living conditions, age, geographic location, and sexual practices. Surveys using viral isolation from healthy individuals without HSV disease, to determine prevalence of HSV infection, have found that between 1% and 20% of asymptomatic children and adults are shedding HSV-1 in saliva at any given time. However, in populations in which individuals are cared for or live together for a long time, the prevalence may increase to over 30% (6).
Immunocompromised patients, particularly those with acquired immunodeficiency syndrome or receiving a stem cell or solid organ transplant, will shed HSV either symptomatically or asymptomatically following infection. Estimates on the frequency of asymptomatic infection and seropositive patients after transplantation range up to 80%.
Between 0.1% and 7.3% of men attending sexually transmissible diseases clinics have HSV-2 infections (7). In pregnant women from lower socioeconomic groups, the cumulative incidence of asymptomatic shedding varies between 1% and 4% (8). The cumulative incidence is significantly higher in high-risk populations such as prostitutes, who may have a cumulative incidence up to 12% (9). Asymptomatic genital shedding of HSV-2 is intermittent, and serial studies have found that the virus is not persistently present and varies from individual to individual.
HSV TRANSMISSION IN HOSPITALS
Prevalence of Herpes Simplex Shedding Among Hospital Personnel and Adult and Pediatric Patients
No studies have addressed the prevalence of asymptomatic shedding of HSV among hospitalized adults or children. Among institutionalized children, however, one
6-year study that used serologic testing and viral isolation at a children’s home found that, of 70 initially seronegative children, 8 (11.4%) had a primary infection while at the home and 6 were symptomatic (6). In another study in Australia, in a home for children under age 3 years, 29 of 43 seronegative children developed HSV antibodies over 1 year (10). The prevalence of HSV infections among any hospitalized group will depend highly on whether the patients are immunocompromised and on socioeconomic background, the presence of risk factors for HSV, and the history of previous HSV infection. Hence, for practical purposes, hospital personnel should assume that all patients are potentially infectious for HSV.
6-year study that used serologic testing and viral isolation at a children’s home found that, of 70 initially seronegative children, 8 (11.4%) had a primary infection while at the home and 6 were symptomatic (6). In another study in Australia, in a home for children under age 3 years, 29 of 43 seronegative children developed HSV antibodies over 1 year (10). The prevalence of HSV infections among any hospitalized group will depend highly on whether the patients are immunocompromised and on socioeconomic background, the presence of risk factors for HSV, and the history of previous HSV infection. Hence, for practical purposes, hospital personnel should assume that all patients are potentially infectious for HSV.
In 1980, Hatherley and coworkers (11) studied the frequency of asymptomatic HSV excretion in the saliva of 384 asymptomatic members of the staff of an obstetric hospital. HSV was isolated from 10% of the employees.
Healthcare-Associated HSV Transmission
HSV transmission in the hospital is an infrequent but serious problem when it occurs. Documented hospital transmission of HSV has been confirmed in numerous studies, with the virus being transmitted from patient to patient, from personnel to patient, and from patient to personnel.
The patients at highest risk for healthcare-associated acquisition of HSV are infants <30 days of age (see Chapter 52). Several studies have documented acquisition of HSV by hospitalized infants, occasionally with fatal outcomes. The first cluster of cases was reported in 1975 by Francis and colleagues (12), who identified four fatal infections that occurred over a 2-month period in a pediatric intensive care unit. Each patient was infected with HSV-2.
In the late 1970s, DNA fingerprinting of HSV became possible. Halperin and associates (13) first determined that each epidemiologically unrelated strain had a different endonuclease pattern and thatepidemiologically related strains had identical DNA fingerprints. This technique has been applied to a number of outbreaks of HSV infection in the hospital and is a potent epidemiologic tool to confirm HSV transmission.
Infants who acquire HSV infection during the first month of life always do so postnatally. The usual source of acquisition is the maternal genital tract, although infants may acquire HSV-1 from labial lesions of either parent; occasionally, infections have been acquired by nursing infants from breast lesions. In 1978, Linnemann and coworkers (14) observed two infants in a nursery infected within 1 month with HSV-1. The two isolates had identical DNA fingerprints. The source of infection for one child was the father’s labial lesion, implying that the second child had acquired HSV virus via horizontal transmission in the nursery.
In 1983, Hammerberg and colleagues (15) described an HSV outbreak in a nursery in which four infants acquired HSV-1 infection over 10 days. DNA patterns of each of the four isolates were identical, indicating the strong possibility of horizontal transmission. In 1984, Van Dyke and Spector (16) reported a case of apparent transmission of HSV-1 from a physician with a labial lesion to an infant who had received endotracheal suctioning for meconium aspiration. This was the first reported case of transmission of HSV from hospital staff to a patient.
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