A Nurse Practitioner's Guide to the Management of Herpes Simplex Virus-1 in Children

Janel M. Drugge, MSM, RN, PNP; Patricia Jackson Allen, MS, RN, PNP, FAAN


Dermatology Nursing. 2008;20(6):455-466. 

In This Article

Clinical Manifestations of HSV-1

Gingivostomatitis and orolabial HSV-1 infections. Gin gi vostomatitis, or herpes labialis, is the clinical consequence of HSV-1 infections that is most commonly seen in children and young adults (Waggoner-Fountain & Grossman, 2004). Gingivostomatitis appears as vesicles and open lesions inside and around the mouth, including the lips, tongue, hard and soft palate, and gums (Brady & Bernstein, 2004; Raborn & Grace, 1999). During classic primary HSV-1 infections, "a prodrome characterized by localized pain, tingling, burning, tenderness, parasthesia, lymphadenopathy, headache, fever, anorexia, or malaise precedes lesion formation" (Yeung-Yue et al., 2002, p. 251). Primary lesions are more severe and painful than recurrent lesions (see Figure 1).

Figure 1.

Primary HSV-1 infection. Source: Centers for Disease Control and Prevention (CDC), Public Health Image Library, 2008.

Secondary or recurrent herpes labialis appears at the outer edge of the lips (Brady & Bernstein, 2004). These lesions are commonly referred to as cold sores or fever blisters (Waggoner-Fountain & Grossman, 2004). Recurrent HSV-1 outbreaks are often milder than primary infections and usually occur in the same location as the primary infections. Recurrent infections are preceded by a prodrome of burning, itching, and tingling before lesion formation. The HSV-1 will continue to self-replicate within the first 2 days, producing an area of redness around the edge of the lips (Yeung-Yue et al., 2002). Within 3 to 4 days, multiple vesicles causing pain and discomfort appear on the erythematous base that fill with pus and eventually crust over (see Figure 2); the discomfort will usually resolve quickly after the crusting period has begun (Yeung-Yue et al., 2002). Most individuals with recurrent infections will have an estimated two herpes labialis outbreaks per year, but 5% to 10% have outbreaks of greater than six times per year (Rooney et al., 1993; Yeung-Yue et al., 2002). The number of lesions per outbreak varies based on the individual and the status of his/her immune system at the time of the outbreak.

Figure 2.

Orolabial HSV-1 infection. Source: CDC, Public Health Image Library, 2008.

According to Raborn and Grace (1999), children with active primary or secondary orolabial lesions may have a loss of energy, decreased appetite, and a fever. Eating or drinking may be difficult due to the discomfort of the lesions (Blevins, 2003; Yeung-Yue et al., 2002). Drinks with high acid content or salty foods may cause the lesions to be more painful. Consequently, children with the orolabial lesions may lose their appetites and may not want to drink, resulting in fluid and electrolyte imbalances and loss of caloric intake (Blevins, 2003; Waggoner-Fountain & Grossman, 2004). These children may need further medical care and intravenous hydration due to severe fluid and electrolyte loss (Brady & Bernstein, 2004).

Herpetic whitlow. Herpetic whitlow, also called digital herpes simplex, hand herpes, or finger herpes, is an HSV infection that is located on the fingers, hands, toes, or knees and is transmitted directly from an oral or genital lesion or vesicle on the body or from another infected person's body (Corey & Spear, 1986; Raborn & Grace, 1999). Typically, there is a break in the skin that allows the HSV to infect the tissue. Herpetic whitlow infections begin with pain and tingling on the cutaneous site and develop into single or multiple vesicles on an erythematous base (Waggoner-Fountain & Grossman, 2004; Yeung-Yue et al., 2002) (see Figure 3). Herpetic whitlow is more likely to be caused by oral HSV-1 lesions in children; however, the incidence of HSV-2 is increasing in sexually active teenagers and adults (Yeung-Yue et al., 2002). Herpetic whitlow develops in young children, with active oral lesions often as a result of chewing or sucking on fingers and thumbs (Brady & Bernstein, 2004). Health care professionals who may contact oral or genital secretions should wear gloves to prevent exposure to HSV, and if they do develop herpetic whitlow, they are required to use gloves to decrease the risk of transmission (Avitzur & Amir, 2002; Yeung-Yue et al., 2002).

Figure 3.

Herpetic whitlow. Source: CDC, Public Health Image Library, 2008.

Herpes gladiatorum. Herpes gladiatorum is an HSV infection of the thorax, ear, face, and hands among athletes in contact sports, such as wrestling, water polo, or rugby (Waggoner-Fountain & Grossman, 2004) (see Figure 4). This infection is usually the result of HSV-1 transmission by direct skin-to-skin contact during practice or competition (Yeung-Yue et al., 2002). Herpes gladiatorum occurs in 2.6% of high school wrestlers and between 20% to 40% of National Collegiate Athletic Association (NCAA) Division I wrestlers (Anderson, 1999). The stresses of weight loss, competition, and school work may lead to reoccurring infections, and therefore, increased spread of the virus during sports seasons (Anderson, 1999). The average incubation period is 3 to 5 days before symptoms (such as sore throat, malaise, fever, neck lymphadenopathy, and raised erythematous rash) develop (Anderson, 1999). The NCAA and the National Federation of State High School Association mandate wrestlers to refrain from competition for 5 days to allow HSV infections to heal (Anderson, 2005). Infections usually clear entirely within 10 to 14 days.

Figure 4.

Herpes simplex rash over trunk. Source: CDC, Public Health Image Library, 2008.

Eczema herpeticum. Eczema herpeticum, also known as Kaposi's varicelliform eruption, is a disseminated herpes infection of severe vesicular lesions at the sites of pre-existing epidermal disruption and is typically caused by HSV-1 (Fivenson, Breneman, & Wander, 1990; Yeung-Yue et al., 2002). Young children with damaged skin due to atopic dermatitis (eczema) are the most frequently affected; however, children with various skin disorders and burns can also develop this condition (Khan, Shaw, Clark, & Afzal, 2005; Yeung-Yue et al., 2002). After exposure of the disrupted skin to the virus, multiple vesicles develop in crops over a period of 7 to 9 days eventually grouping together on previously disrupted and neighboring normal skin (Behrman et al., 2007). The severity of the infection can vary from mild, itchy, and uncomfortable (Behrman et al., 2007), or it may be fatal if severe infections are not treated effectively with antiviral medications (Khan et al., 2005; Yeung-Yue et al., 2002). In severe untreated infections, death may result from loss of fluid, electrolytes, and protein through the disrupted skin, dissemination of the virus into multiple organ systems, or from secondary bacterial involvement (Behrman et al., 2007).

Herpes genitalis. Herpes genitalis is typically caused by HSV-2; however, up to one-third of new cases are caused by HSV-1, usually resulting in a milder form of the infection appearing within 3 days to 2 weeks after initial exposure (Benedetti, Corey, & Ashley, 1994; Lafferty, Downey, Celum, & Wald, 2000; Langenberg, Corey, Ashley, Leong, & Straus, 1999; Yeung-Yue et al., 2002). Lesions are painful and appear on the vulva, vagina, urethral, perianal skin, buttocks, or thighs in women, and on the penis or perianal area in men (see Figures 5 and 6) (Yeung-Yue et al., 2002). Recurrent lesions are less painful and milder than primary lesions. Asymptomatic individuals have a high rate of viral shedding, and thus, can transmit the virus during sexual intercourse even if no lesions are present (Wald, Zeh, Selke, Ashley, & Corey, 1995; Yeung-Yue et al., 2002).

Figure 5.

Herpes genitalis. Source: CDC, Public Health Image Library, 2008.

Figure 6.

Herpes genitalis. Source: CDC, Public Health Image Library, 2008.


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