Herpes zoster (shingles) is reactivation of a latent infection with the varicella-zoster virus (VZV). After primary infection (chickenpox), the virus lays dormant in dorsal root ganglia for life. Reactivation may be triggered by immunosuppression, certain medications (eg, JAK inhibitors), other infections, or physical or emotional stress. The individual lifetime risk of developing herpes zoster is 1 in 3.

Cutaneous herpes zoster usually begins with a 1- to 3-day prodrome of burning pain or paresthesias in the affected dermatome, followed by eruption of erythematous papules and vesicles in the same distribution.

Involvement of a thoracic dermatome may simulate acute myocardial infarction. Involvement of the ophthalmic branch of the trigeminal nerve may lead to herpes zoster ophthalmicus. Herpes zoster oticus (Ramsay-Hunt syndrome) occurs with involvement of the vestibulocochlear nerve. Herpes zoster duplex is the simultaneous occurrence of zoster in 2 noncontiguous dermatomes, and herpes zoster multiplex refers to this phenomenon occurring in more than 2 dermatomes. Disseminated zoster, defined as more than 20 vesicles outside of the primary and adjacent dermatomes, is chiefly a problem of immunocompromised patients (patients with HIV, patients with cancer, and those on immunosuppressive drugs). Some patients may suffer acute segmental neuralgia, known as zoster sine herpete, without ever developing a visible skin eruption. Regional adenopathy may be seen.

Zoster may be accompanied by pain acutely. Additionally, a major concern after a zoster outbreak is postherpetic neuralgia, defined as pain and neuropathic symptoms that persist in a dermatome 1 month beyond resolution of the rash. Risk factors for postherpetic neuralgia include older age, female sex, presence of a prodrome, greater rash severity, and acute pain. Postherpetic neuralgia can be intractable and debilitating, and prevention is an important goal. Other less frequently encountered post-zoster sequelae include herpes zoster granulomatous dermatitis (where a granulomatous eruption develops weeks to months after zoster resolution) and skin infiltration of the site of healed zoster by cells from an underlying hematologic malignancy (so-called isotopic response).

Cerebrovascular accidents, peripheral motor neuropathies, neurogenic bladder, and diaphragmatic paralysis have been associated with zoster. Postherpetic abdominal pseudohernia refers to the abdominal asymmetry that is secondary to a motor neuropathy following zoster of a lower thoracic or lumbar dermatome. Herpes zoster encephalitis usually appears in the first 2 weeks after the onset of lesions, and it has a 10%-20% mortality rate. Lesions may also be at risk for bacterial superinfection. In extreme cases, necrotizing fasciitis may occur.

Immunocompromised patient considerations: Immunocompromised patients have a higher risk of disseminated zoster. In patients with HIV and AIDS, multidermatomal, necrotic, or recurrent zoster may occur. Persistent ulcers and chronic hyperkeratotic zoster are further manifestations. A strong association of herpes zoster multiplex with underlying malignancy (especially lymphoma) was reported in one retrospective study.