A Man With Skin Plaques Has Severe Pain After Eating

Herpes zoster develops when viral elements that have remained dormant within any neuronal dorsal root ganglion are activated, resulting in a transient viremia that usually leads to a unilateral, "zosteriform" eruption of grouped, herpetiform vesicles conforming to a specific dermatome. This is typically preceded by a prodrome of intense neuropathic pain or pruritus that can mimic other causes of pain, depending on where the eruption appears. VZV reactivation leading to the development of herpes zoster can occur at any time after primary infection and may be due to lowered immunity, stress, radiation, or trauma. It can also spontaneously occur.^[8]

The incidence of herpes zoster has significantly decreased owing to the development two zoster vaccines. The newest, Shingrix, uses a lyophilized recombinant VZV surface glycoprotein E (gE) antigen component.^[5] It is more effective than Zostavax, a live-attenuated VZV vaccine, which was the first available. Zostavax could not be administered to immunocompromised individuals.^[9] Shingrix is indicated in adults aged 50 years or older.^[5]The differential diagnosis of herpes zoster includes any inflammatory or infectious eruption presenting with localized vesicles and crusted papules and plaques; it includes herpes simplex infection, bullous arthropod bites, bullous impetigo, contact dermatitis, and phytophotodermatitis.^[2]

Herpes zoster can be diagnosed on the basis of history and physical examination alone. Tzanck smear and direct immunofluorescence can provide confirmation, although Tzanck smear does not allow differentiation among herpesviruses.^[1] Additional potential laboratory tests include VZV immunoglobulin M (IgM) and immunoglobulin G (IgG), polymerase chain reaction (PCR), and viral culture. Of these options, PCR produces fast results with high sensitivity; viral culture, although specific, lacks sensitivity and takes longer than 1 week to produce results.

Serologic assays are only helpful after the illness, because they must be obtained twice: once during the acute phase and again 2-3 weeks later, during the convalescent phase. They must reveal a fourfold increase in VZV IgG titers to confirm the diagnosis.^[2] VZV IgM antibodies lack sensitivity and specificity; furthermore, VZV IgM positivity does not differentiate between primary infection and reactivation.^[1]

The treatment of herpes zoster is similar to that of primary VZV infection. In addition to acyclovir and valacyclovir, alternative antiviral agents include penciclovir, famciclovir, foscarnet (useful for acyclovir-resistant VZV isolates), cidofovir (for acyclovir- and foscarnet-resistant strains), interferon (which has been shown to reduce the risk for viral dissemination in immunocompromised patients), and vidarabine (largely obsolete now, owing to its replacement by less toxic and more effective agents).^[7] Systemic corticosteroids have shown benefit as an adjunctive therapy to reduce pain but do not decrease the likelihood of postherpetic neuralgia and are associated with several side effects; thus, they should not be routinely administered to all patients.^[8]

Additional supportive and symptomatic measures to treat zoster and prevent complications include nonocclusive and nonadherent dressings; astringent soaks (eg, Domeboro solution); neuromodulators (eg, gabapentin, tricyclic antidepressants, pregabalin, lidocaine patches); short-acting narcotics; and, for severe pain, sympathetic nerve blocks.^[7]

The complications of herpes zoster are many and varied, often depending on the area of the body affected. Sequelae may include postherpetic neuralgia (the most common, affecting nearly one half of all patients), secondary cutaneous bacterial infection, colitis, pneumonia/pneumonitis, meningoencephalitis, vasculopathy, otic and ocular complications, and the Wolf isotopic response (the development of other skin lesions or eruptions in an area of prior zoster).^[10]

Presentations of zoster are significantly more severe and varied in immunocompromised individuals. The cutaneous morphology can vary from typical to persistent, crusted, verrucous papules, nodules, and plaques.^[2] The cutaneous distribution may be bilateral, multidermatomal, or disseminated (defined as > 20 lesions outside of the adjacent dermatomes), and may even present with visceral involvement, as in the patient in this case.^[6,10]

A review of the literature suggests that decreased cell-mediated immunity may predispose patients to disseminated cutaneous disease and visceral involvement; such patients include those receiving immunosuppressive therapies, HIV-positive patients, transplant recipients, and patients with a history of hematologic cancer, as in this case.^[11] Specifically, T-cell–mediated mechanisms are vital to the immune response to VZV infection; low CD4+ T-cell counts in long-term allotransplant survivors have a known association with infectious morbidity.^[12]

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