Herpes Simplex Virus

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HSV infection is a member of the herpesviridae family. Two serotypes of HSV have been identified: HSV-1 and HSV-2. HSV-1 most often affects the mouth and is usually transmitted in childhood by contact with infected saliva. HSV-2 is generally

Table 1 Varicella Zoster Virus Infections









Pruritus, pain,

Vesicular lesion


If immunosup-


fever, malaise

with erythe-


pressed: varicella


matous base

herpes simplex; hand, foot, and mouth disease; rickettsialpox; impetigo

zoster immuno-globulin within 96 hr of exposure for naive patient; otherwise, acyclovir, valacyclovir, famciclovir within 48-72 hr of rash

Herpes zoster

Pink, urticarial


Supportive and


plaques in

herpes simplex,

local care;

of latent



analgesics, cool/




wet compresses,



colloidal oatmeal

with central

insect bites,



candida, drug

Oral antiviral





within 48-72 hr

associated with anogenital infection, and it usually is transmitted from anogenital or oral-genital sexual contact or transmission from a mother to her newborn. However, 14% to 47% of genital herpes results from HSV-1 (7). Thirty to fifty percent of pregnant women with a primary HSV outbreak transmit the disease to their newborn (8).

Transmission generally occurs from skin-to-skin contact and introduction of the virus into the basal cell layers of susceptible mucosal surfaces. Following the primary infection, the virus is not eliminated, but exists in a latent form in nerve cell ganglia. The trigeminal ganglia are usually involved following oral HSV infection, and the virus is harbored in the sacral nerve root ganglia, S2-S5, following genital infection.

Often, the initial infection with HSV is subclinical and asymptomatic. However, when present, this primary outbreak in the genital area is characterized by local pain, itching, and vaginal or urethral discharge. This is followed by the development of scattered painful vesicles on an erythematous base with shallow, round erosions (Fig. 3). On keratinized skin, these may be somewhat more long lived and progress to crusts. Fever, painful lymphadenopathy, headache, myalgia, herpetic urethritis, or cervicitis may also develop. Lesions generally heal in 8 to 10 days. The primary outbreak is usually eventually followed by recurrent episodes when the latent virus reactivates and affects overlying skin. These recurrences occur with variable frequency, duration, and severity. Generally, recurrent episodes exhibit clusters of vesicles or coalescing erosions, with mild or no pain and shorter duration (Fig. 4). Constitutional symptoms are mild or absent. Because the initial infection is often subclinical, the first recognized episode of HSV infection frequently exhibits the pattern of a recurrent outbreak and may occur long after the original exposure to the virus.

Genital Herpes Black Women

Figure 3 This photograph shows the scattered vesicles and round erosions that are classic for a primary herpes simplex infection.

Acute herpetic gingivostomatitis represents the primary HSV infection of the mouth. This occurs almost exclusively in children six months to five years old, and present with the abrupt onset of vesicular lesions on the oral mucosa, tongue, perioral skin, and lips. The vesicles quickly erode and develop coalescing erosions

Mucous Membrane With Herpes
Figure 4 Recurrent herpes simplex virus infection exhibits grouped, coalescing vesicles that often falsely appear pustular on dry, keratinized skin after several days; these become almost immediately erosive on modified mucous membranes.

on mucous membrane and crusts on keratinized skin. The gingivae are swollen, erythematous, and friable. These children have high fevers 102° F to 104° F, anorexia, dysphagia, and listlessness.

Reactivation and replication of latent virus can be induced by many factors including fever, trauma, stress, sunlight, and menses. Reactivation is most severe in immunocompromised patients. Recurrent genital outbreaks from HSV-2 are more frequent than from HSV-1.

Even in the absence of clinical recurrences, patients shed the virus asymptoma-tically and intermittently into the genital tract. Most HSV infections are transmitted during asymptomatic shedding. The HSV shedding rate has been reported as 15.4% of days by culture and 40.2% of days by polymerase chain reaction (PCR), with the subclinical shedding rate being 6.6% of days by culture and 27.1% of days by PCR (9). Shedding was decreased but not eliminated by chronic suppression with oral acyclo-vir and valacyclovir therapy (9).

The transmission of HSV from an infected mother to the neonate occurs primarily when the mother is experiencing the uncommon event of an active primary HSV infection during labor. The risk in women with recurrent disease or asymptomatic shedding is very low. However, neonatal HSV infection is very often devastating, producing severe brain damage, eye disease, skin lesions, and, often, death. Fortunately, in the past few years, the morbidity and mortality have improved substantially, although neonatal HSV remains a serious disease. The mortality has decreased from 85% to 29% in the past 30 years, and the proportion of patients with disseminated disease who are developing normally at one year has increased to 83% from 50% (10).

HSV infection of anogenital skin is sometimes confused with candidiasis, folliculitis, impetigo, and allergic contact dermatitis. The diagnosis of HSV is generally made by the onset and morphology, and confirmed by laboratory testing because this diagnosis frequently produces denial and depression. Cultures are widely available but notoriously yield false-negative results. A viral culture is performed by a vigorous swab of a vesicle that has been unroofed. The PCR evaluation is extremely sensitive but is less widely available. Swabs frequently must be mailed to an academic medical center or large commercial laboratory. A biopsy from the edge of an erosion or a sample of an intact vesicle is very sensitive test for the herpes virus but does not differentiate HSV from the VZV; that differentiation is made upon the setting. Serologic assays are often used for diagnosing recurrent disease or past exposure but do not indicate whether the current eruption is because of HSV infection.

The treatment of a genital HSV infection requires careful and caring patient education and support. Pain control and local care to include soaks and treatment of secondary infection is especially important for a primary herpetic outbreak. Occasionally, edema and dysuria require insertion of a urinary catheter. Otherwise, the use of any of the antiviral therapies for HSV infection can shorten outbreaks if given early in the course. A 10-day course of acyclovir 200 mg five times a day, valacyclovir 1 g b.i.d., or famciclovir 125 mg b.i.d. is indicated for a primary infection, and five day course of acyclovir 200 mg five times a day, valacyclovir 500 mg b.i.d., or famciclovir 125 mg b.i.d. for recurrent disease. Immunosuppressed patients sometimes require higher and/or longer dosing, or occasionally intravenous therapy. Vaccines are being investigated.

Patients who experience frequent recurrences, very severe recurrences, or who have seronegative partners may benefit from daily suppressive therapy both to avoid recurrences and to minimize (but not eliminate) transmission risk. These doses are

Table 2 Herpes Simplex Virus



Clinical appearance

Differential diagnosis


Herpes simplex virus (HSV), primary infection

HSV, recurrent infection

Fever, lympha-denopathy, malaise, headache (may be asymptomatic)

Itching or pain followed by skin lesions, constitutional symptoms mild or absent

Painful scattered vesicles and round erosions often affecting both mucous membrane and keratinized skin of the genitalia. (May be subclinical) One or two areas of clusters of vesicles or round, coalescing

Herpes zoster; Acyclovir, valacyclovir, famciclovir candidiasis; folliculitis; allergic contact dermatitis; hand, foot, and mouth disease

Herpes zoster, If mild or late, candidiasis, folliculitis, allergic contact dermatitis, fixed drug eruption no therapy;

otherwise, acyclovir, valacyclovir, famciclovir acyclovir 400 mg twice a day, valacyclovir 500 or 1000 mg each day, or famciclovir 250 mg twice daily (Table 2).

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