Herpes zoster (“shingles”) is caused by the same herpesvirus that causes varicella, the varicella-zoster virus (VZV). Primary infection with VZV manifests as varicella, commonly referred to as “chickenpox” (discussed in Chapter 7: Viral and Bacterial Exanthems), an illness that has dramatically decreased in incidence since the introduction of the VZV vaccine. After the initial infection, the virus remains latent in the sensory ganglia. Reactivation of the latent VZV results in herpes zoster.

The VZV vaccine is a live attenuated vaccine, thus herpes zoster can still result after vaccination.

Reactivation—into dermatomal “shingles”—may be caused by severe illness or infection with HIV, but most often it occurs spontaneously, without an obvious precipitating cause and is most likely a sign that immunity to VZV, which most people acquire in childhood, has decreased.

Reactivated VZV results in the anterograde migration of virions from the dorsal root ganglia to the skin resulting in a local vesicobullous eruption in a single, or less often multiple adjacent, sensory dermatomes.

The risk of herpes zoster increases with age and is 8 to 10 times more likely to develop in people 60 years of age or older. The disease also frequently develops in immunocompromised patients, such as transplant recipients and those with HIV infection or malignancy, particularly lymphoproliferative malignancies (e.g., Hodgkin disease).

The infectious course of herpes zoster infection, or VZV infection, is similar to that of HSV infection (see above).

Several days to weeks before the cutaneous eruption, patients may experience the following focal (dermatomal) symptoms: pain, numbness, pruritus, paresthesia, and skin tenderness or sensitivity (tactile allodynia).

The pain associated with herpes zoster is neuropathic in origin and has been described as “burning,” “crushing,” or “stabbing.” Occasionally, patients presenting with such pain have been thought to have a myocardial infarction or pleurisy, until the characteristic eruption of herpes zoster establishes the diagnosis.

Pain may be severe and debilitating in patients older than 50 but in children, herpes zoster is often asymptomatic.

The following sequence of events describes the evolution of herpes zoster:

Lesions begin as edematous, erythematous, urticaria-like papules that rapidly mature into clustered vesicles (blisters) or bullae overlying the erythematous base. Lesions tend to vary more in size than do the lesions of HSV (Figs. 17.31 and 17.32).

Successive crops continue to appear for 6 to 8 days. The blisters sometimes umbilicate (sag in the middle); and occasionally become pustular and/or hemorrhagic (Fig. 17.33).

In time, the vesicles dry into crusts or erosions that may heal and disappear completely; or resolve with postinflammatory hyperpigmentation or hypopigmentation and, possibly, scarring.

Lesions of herpes zoster in HIV-infected or other immunocompromised patients tend to be more verrucous and ulcerative, and often heal with scars.

Infrequently, zoster may present with dermatomal pain that is accompanied or followed by nonbullous or urticaria-like lesions. Rarely, skin lesions are absent (“zoster sine herpete”). Such cases can be difficult to identify because of the absence of a characteristic eruption.

Most straightforward cases of herpes zoster are diagnosed on the basis of clinical appearance of the lesions accompanied by pain, in a dermatomal distribution.

If necessary, in atypical presentations, a Tzanck smear should be obtained from the base of a fresh lesion (see the discussion of Tzanck preparation earlier in this chapter). A positive result suggests either HSV or VZV infection.

A viral culture, or direct fluorescence antibody (DFA) testing, may be necessary to establish the diagnosis. DFA testing is more sensitive than conventional viral cultures because of the lability of varicella-zoster virus (VZV).

A skin biopsy is generally unnecessary, but it can help to confirm the diagnosis.

Lesions of herpes zoster occur in a characteristic unilateral dermatomal (“zosteriform”) distribution.

Occasionally, lesions can involve contiguous dermatomes, extend beyond the midline, or occur bilaterally.

Although it can affect any dermatome, herpes zoster is most commonly found on the thoracic, trigeminal, lumbosacral, or cervical dermatomes.

Immunocompromised patients have a greater risk of multidermatomal zoster, recurrent zoster, and dissemination beyond the skin (e.g., into the eyes or the lungs).

Elderly persons and immunocompromised patients also tend to have more severe disease, with complications such as postherpetic neuralgia (PHN), disseminated zoster, and chronic herpes zoster.

PHN is defined as pain persisting for more than 1 month after the initial eruption of herpes zoster. The pain may also develop after a pain-free interval. The incidence of PHN increases with increasing age and lowered immune status.

In many elderly patients, PHN can cause chronic depression, anxiety, and social isolation.

Zoster that occurs in the ophthalmic division of the trigeminal nerve (V1 of cranial nerve V) is called herpes zoster ophthalmicus (Fig. 17.34). Eye involvement can present as conjunctivitis, acute retinal necrosis, uveitis, and/or retinal arteritis and can lead to blindness. Ophthalmic zoster warrants an immediate ophthalmologic consultation.

Zoster involvement of the geniculate ganglion of the facial nerve (cranial nerve VII) is referred to as the Ramsay Hunt syndrome and can result in facial nerve paralysis, loss of taste in the anterior two-thirds of the tongue, and dryness of the eyes and mouth. If the eighth cranial nerve is also involved tinnitus, hearing loss and/or vertigo can occur.

Disseminated Herpes Zoster (Fig. 17.35) is the occurrence of >20 lesions outside the primary dermatome and usually occurs in immunocompromised patients. This condition can become chronic and indistinguishable from varicella.

VZV infection occasionally occurs in pregnant women. A primary VZV infection (varicella) may result in severe fetal abnormalities; however, the development of herpes zoster during pregnancy does not appear to harm the developing fetus.