Herpes zoster is infection that results when varicella-zoster virus reactivates from its latent state in a posterior dorsal root ganglion. Symptoms usually begin with pain along the affected dermatome, followed in 2 to 3 days by a vesicular eruption that is usually diagnostic. Treatment is antiviral drugs given within 72 h after skin lesions appear.
Chickenpox and herpes zoster are caused by the varicella-zoster virus (human herpesvirus type 3); chickenpox is the acute invasive phase of the virus (see Chickenpox), and herpes zoster (shingles) represents reactivation of the latent phase. Herpes zoster inflames the sensory root ganglia, the skin of the associated dermatome, and sometimes the posterior and anterior horns of the gray matter, meninges, and dorsal and ventral roots. Herpes zoster frequently occurs in elderly and HIV-infected patients and is more severe in immunocompromised patients. There are no clear-cut precipitants.
Symptoms and Signs
Lancinating, dysesthetic, or other pain develops in the involved site, followed in 2 to 3 days by a rash, usually crops of vesicles on an erythematous base. The site is usually one or more adjacent dermatomes in the thoracic or lumbar region. Lesions are typically unilateral. The site is usually hyperesthetic, and pain may be severe. Lesions usually continue to form for about 3 to 5 days. Herpes zoster may disseminate to other regions of the skin and to visceral organs, especially in immunocompromised patients.
Fewer than 4% of patients with herpes zoster experience another outbreak. However, many, particularly the elderly, have persistent or recurrent pain in the involved distribution (postherpetic neuralgia), which may persist for months, years, or permanently. Infection in the trigeminal nerve is particularly likely to lead to severe, persistent pain. The pain of postherpetic neuralgia may be sharp and intermittent or constant and may be debilitating.
Geniculate zoster (Ramsay Hunt syndrome) results from involvement of the geniculate ganglion. Ear pain, facial paralysis, and sometimes vertigo occur. Vesicles erupt in the external auditory canal, and taste may be lost in the anterior two thirds of the tongue (see Herpes Zoster Oticus).
Ophthalmic herpes zoster (see also Herpes Zoster Ophthalmicus) results from involvement of the gasserian ganglion, with pain and vesicular eruption in and around the eye, in the distribution of the ophthalmic division of the 5th cranial nerve. Vesicles on the tip of the nose (Hutchinson sign) indicate involvement of the nasociliary branch and a higher risk of severe ocular disease. However, the eye may be involved in the absence of lesions on the tip of the nose.
Intraoral zoster is uncommon but may produce a sharp unilateral distribution of lesions. No intraoral prodromal symptoms occur.
Herpes zoster is suspected in patients with the characteristic rash and sometimes in patients with typical pain in a dermatomal distribution. Diagnosis is usually based on the virtually pathognomonic rash. If the diagnosis is equivocal, detecting multinucleate giant cells with a Tzanck test can confirm infection, but the Tzanck test is positive with herpes zoster or herpes simplex. Herpes simplex virus (HSV) may cause nearly identical lesions, but unlike herpes zoster, HSV tends to recur and is not dermatomal. Viruses can be differentiated by culture or PCR. Antigen detection from a biopsy sample can be useful.
Wet compresses are soothing, but systemic analgesics are often necessary. Treatment with oral antivirals decreases the severity and duration of the acute eruption, the incidence of postherpetic neuralgia, and the rate of serious complications in immunocompromised patients. Treatment should start as soon as possible, ideally during the prodrome, and is likely to be ineffective if given > 72 h after skin lesions appear. Famciclovir 500 mg po tid for 7 days and valacyclovir 1 g po tid for 7 days have better bioavailability with oral dosing than acyclovir, and therefore for herpes zoster, they are generally preferred to oral acyclovir 800 mg 5 times/day for 7 to 10 days. Corticosteroids do not decrease the incidence of postherpetic neuralgia.
For less severely immunocompromised patients, oral famciclovir, valacyclovir, or acyclovir (see above) is a reasonable option; famciclovir and valacyclovir are preferred. For severely immunocompromised patients, acyclovir is recommended at a dosage of 10 mg/kg IV q 8 h for 7 days for adults and 20 mg/kg IV q 8 h for 7 days for children < 12 yr.
Although data concerning the safety of acyclovir and valacyclovir during pregnancy are reassuring, the safety of antiviral therapy during pregnancy is not firmly established. Because congenital varicella can result from maternal varicella but has not been documented to result from maternal zoster, the potential benefit of treatment of pregnant patients should outweigh possible risks to the fetus. Pregnant patients with severe rash, severe acute pain, or ophthalmic zoster can be treated with valacyclovir or acyclovir, especially in later stages of pregnancy.
Management of postherpetic neuralgia can be particularly difficult. Treatments include gabapentin, cyclic antidepressants, and topical capsaicin or lidocaine ointment. Opioid analgesics may be necessary. Intrathecal methylprednisolone may be of benefit. A recent study suggests that injecting the entire affected area with botulinum toxin A (40 injections in a chessboard pattern) can reduce pain.
For treatment of ophthalmic herpes zoster, an ophthalmologist should be consulted (see Treatment). For treatment of otic herpes zoster, an otolaryngologist should be consulted (see Treatment).
Adults ≥ 60 yr should have a single dose of zoster vaccine (a more potent preparation of varicella vaccine) whether they have had herpes zoster or not. This vaccine has been shown to decrease the incidence of zoster.
Last full review/revision April 2013 by Kenneth M. Kaye, MD
Content last modified May 2013