Scottsdale, Arizona, U.S.A.
Southeast Vulvar Clinic, Charlotte, North Carolina, U.S.A.
Varicella zoster virus (VZV) is a member of the herpes virus group. It persists in the body as a latent infection after the primary infection. Primary infection with VZV results in chicken pox (varicella). Herpes zoster (shingles) represents a one-time reactivation. VZV enters through the respiratory tract and conjunctiva.
The initial infection results from transmission through the respiratory tract from inoculation through respiratory tract secretions, respiratory contact with airborne droplets, or by direct contact or inhalation of aerosols from vesicular fluid of skin lesions. By the time the rash appears, the virus has cleared from the respiratory tract and transmission to others is unlikely. The rash of varicella is generalized and pruritic, with individual lesions advancing from macules to papules to vesicular lesions before crusting (Fig. 1). The rash first appears on the scalp and progresses to the trunk and extremities. The majority of lesions remain on the trunk in a centripetal distribution. Lesions can also be seen on the mucous membranes of the oropharynx, respiratory tract, vagina, conjunctiva, and cornea. Although mucous membrane lesions also develop as vesicles, the fragile mucous membrane blister roof, lacking a stratum corneum, is shed almost as soon as it forms, leaving round erosions. Vaginal involvement is manifested as a vaginal discharge, often purulent.
Keratinized skin lesions begin as pink papules that develop a central vesicle approximately 2 to 4 mm in diameter. Classically, these become pustular and develop a central crust, leaving an annular blister. Lesions evolve over several days and exhibit all stages of development simultaneously. Systemic signs of varicella are generally self-limited and mild. These consist of malaise, itching, and fever up to 102°F for two to three days. Adults may experience a more severe clinical course. Recovery from primary varicella usually results in lifetime immunity from another generalized outbreak of varicella, but not necessarily from reactivation of latent infection.
Herpes zoster (shingles) occurs when latent VZV resurfaces. Factors associated with recurrent disease include aging, immunosuppression, intrauterine exposure, and varicella infection at an early age. The eruption occurs unilaterally in the distribution of a dermatome supplied by a dorsal root or extramedullary cranial nerve sensory ganglion. Clinically, this is often seen on the trunk or the area of the fifth cranial nerve, but herpes zoster can appear on the buttock, perineum, and vulva (Fig. 2). Typically, two to four days prior to visible eruptions, patients report pain and par-esthesia in the involved area. This is followed by discrete urticarial plaques scattered along a dermatome. Small, clustered blisters appear on the plaques, coalescing into larger bullae that may become hemorrhagic.
The differential diagnosis of varicella includes folliculitis, primary herpes simplex virus (HSV) infection or eczema herpeticum, and bullous impetigo. The diagnosis of VZV infection is generally easily made on the basis of the morphology of the skin findings. The virus can be cultured from mononuclear cells of an infected person from five days before to one to two days following the appearance of a rash. Specimens are collected from crusts or by unroofing a fluid-filled vesicle and rubbing the base with a polyester swab. A number of molecular assays for varicella antibody are available.
Complications of varicella infection include secondary bacterial infections, pneumonia, central nervous system manifestations including aseptic meningitis and encephalitis, and Reyes syndrome from VZV and aspirin exposure in young children.
In addition, complications from herpes zoster can include postherpetic neuralgia, herpes zoster ophthalmicus, and facial nerve involvement including Ramsey Hunt Syndrome. Maternal varicella may result in infection of the neonate with a fatality rate as high as 30% (1). Primary varicella infection in the first 20 weeks of gestation can be associated with a variety of abnormalities, collectively referred to as congenital varicella syndrome.
The treatment of varicella and herpes zoster with antiviral medication in immunocompetent patients is only beneficial when begun in the first two or three days. Varicella in an immunocompetent adult is treated orally with acyclovir 800 mg four times a day for five days (children receive 20 mg/kg up to the adult dose). The therapy of herpes zoster in an immunocompetent patient includes valacyclovir 1 g three times a day for one week, famciclovir 500 mg every eight hours, or acyclovir 800 mg every four hours. Immunosuppressed patients with varicella and those with complicated herpes zoster are generally admitted to the hospital for intravenous acyclovir. There are clinical trials that suggest a decrease in the likelihood or severity of postherpetic neuralgia when antiviral agents are used early in the course of herpes zoster, and other trials that suggest no benefit (2). In practice, most patients, especially the elderly who are at greatest risk for long-lasting pain, are treated with antiviral agents (3).
Immunization against varicella is now standard of care, and the efficacy is good but not perfect (4). There is concern that vaccination may be less effective than natural immunity, resulting in a higher risk of postherpetic neuralgia, but this has not been definitively proven (5). However, newer information has shown that immunization of adults decreases the incidence and severity of herpes zoster and postherpetic neuralgia (Table 1) (6).
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