Introduction to Herpes zoster

Introduction

Also called shingles, herpes zoster is an acute unilateral and segmental inflammation of the dorsal root ganglia caused by infection with the herpesvirus varicella-zoster, which also causes chickenpox. 

This infection usually occurs in adults. It produces localized vesicular skin lesions confined to a dermatome and severe neuralgic pain in peripheral areas innervated by the nerves arising in the inflamed root ganglia.

The prognosis is good unless the infection spreads to the brain. Eventually, most patients recover completely, except for possible scarring and, in corneal damage, visual impairment. Occasionally, neuralgia may persist for months or years.
Herpes zoster is found primarily in adults, especially those older than age 50. It seldom recurs.

Pathophysiology
Herpes zoster results from reactivation of varicella virus that has lain dormant in the cerebral ganglia (extramedullary ganglia of the cranial nerves) or the ganglia of posterior nerve roots since a previous episode of chickenpox.
Exactly how or why this reactivation occurs isn’t clear. Some believe that the virus multiplies as it’s reactivated and that it’s neutralized by antibodies remaining from the initial infection. However, if effective antibodies aren’t present, the virus continues to multiply in the ganglia, destroy the host neuron, and spread down the sensory nerves to the skin.

Clinical features
Herpes zoster usually runs a typical course with classic signs and symptoms. Serious complications sometimes occur.

Onset of disease
Herpes zoster begins with fever and malaise. Within 2 to 4 days, severe deep pain, pruritus, and paresthesia or hyperesthesia develop, usually on the trunk and occasionally on the arms and legs in a dermatomal distribution. Pain may be continuous or intermittent and usually lasts from 1 to 4 weeks.

Skin lesions
Up to 2 weeks after the first symptoms, small, red, nodular skin lesions erupt on the painful areas. These lesions commonly spread unilaterally around the thorax or vertically over the arms or legs. Sometimes nodules don’t appear, but when they do, they quickly become vesicles filled with clear fluid or pus.
About 10 days after they appear, the vesicles dry and form scabs. (See Skin lesions in herpes zoster.) When they rupture, such lesions commonly become infected and, in severe cases, may lead to the enlargement of regional lymph nodes; they may even become gangrenous. Intense pain may occur before the rash appears and after the scabs form.

Cranial nerve involvement
Occasionally, herpes zoster involves the cranial nerves, especially the trigeminal and geniculate ganglia or the oculomotor nerve. Geniculate zoster may cause vesicle formation in the external auditory canal, ipsilateral facial palsy, hearing loss, dizziness, and loss of taste.
Trigeminal ganglion involvement causes eye pain and, possibly, corneal and scleral damage and impaired vision. Rarely, oculomotor involvement causes conjunctivitis, extraocular weakness, ptosis, and paralytic mydriasis.

Rare complications
In rare cases, herpes zoster leads to generalized central nervous system infection, muscle atrophy, motor paralysis (usually transient), acute transverse myelitis, and ascending myelitis. More commonly, generalized infection causes acute retention of urine and unilateral paralysis of the diaphragm. In postherpetic neuralgia, a complication most common in elderly patients, intractable neuralgic pain may persist for years. Scars may be permanent.

Diagnosis
A positive diagnosis of herpes zoster usually isn’t possible until the characteristic skin lesions develop. Before then, the pain may mimic that of appendicitis, pleurisy, or other conditions. Diagnostic test results include the following:

• Examination of vesicular fluid and infected tissue shows eosinophilic intranuclear inclusions and varicella virus.
• Lumbar puncture shows increased cerebrospinal fluid (CSF) pressure; examination of CSF shows increased protein levels and, possibly, pleocytosis.
• Staining antibodies from vesicular fluid and identification under fluorescent light differentiate herpes zoster from localized herpes simplex.

Treatment

• No specific treatment exists. 
• The primary goal of supportive treatment is to relieve itching and neuralgic pain with calamine lotion or another antipruritic; aspirin, possibly with codeine or another analgesic; and, occasionally, collodion or compound benzoin tincture applied to unbroken lesions.
• If bacteria have infected ruptured vesicles, treatment usually includes an appropriate systemic antibiotic.
• Trigeminal zoster with corneal involvement necessitates instillation of idoxuridine ointment or another antiviral agent.
• To help a patient cope with the intractable pain of postherpetic neuralgia, administer a systemic corticosteroid, such as cortisone or, possibly, corticotropin, to reduce inflammation as well as tranquilizers, sedatives, or tricyclic antidepressants with phenothiazines.
• Acyclovir seems to stop progression of the rash and prevent visceral complications. 
• In immunocompromised patients—both children and adults—acyclovir therapy may be administered I.V. The drug appears to prevent disseminated, life-threatening disease in some patients.