eMedicine Specialties > Emergency Medicine > Infectious Diseases

Herpes Zoster

Author: Richard S Krause, MD, Senior Faculty, Department of Emergency Medicine, State University of New York at Buffalo School of Medicine
Contributor Information and Disclosures

Updated: Nov 23, 2009

Introduction

Background

Varicella-zoster virus (VZV) is the agent causing chickenpox, the common childhood infection. Following resolution of chickenpox, VZV lies dormant in the spinal dorsal root ganglia until reactivation results in herpes zoster (shingles). "Shingles" is a syndrome characterized by a painful, unilateral vesicular rash, as in the image below, usually restricted to a dermatomal distribution. At times, especially in the immunosuppressed patient, the infection may spread and produce severe systemic illness with involvement of multiple visceral organs and multiple dermatomes (disseminated zoster).

Pathophysiology

Exactly why VZV reactives from latency is not fully understood. However, VZV-specific cell-mediated immunity has been shown to be a major factor in determining reactivation of VZV. Cell-mediated VZV-specific immunity decreases with age and in patients with certain malignancies. These groups have much higher rates of herpes zoster. Patients with hypogammaglobulinemia (a defect of humoral but not cellular immunity) do not have a higher rate of zoster. This supports the concept of an important role for cell-mediated immunity in the pathogenesis of VZV infection.
 
VZV reactivation causes inflammation in the dorsal root ganglion accompanied by hemorrhagic necrosis of nerve cells. The result is neuronal loss and fibrosis. The distribution of the rash corresponds to the sensory fields of the infected neurons within a specific ganglion. The anatomic location of the involved dermatome often determines the specific manifestations (eg, herpes zoster ophthalmicus causing ocular complications when the trigeminal ganglion is involved).

Frequency

United States

Approximately 95% of adults in the United States have antibodies to the varicella-zoster virus and are vulnerable to reactivation infection. A person of any age with a prior varicella infection may develop zoster, but incidence increases with advancing age due to declining immunity. Approximately 4% of patients with zoster will develop a recurrent episode later in life.  

A study of patients in a large health maintenance organization (HMO) in the United States revealed 1075 cases from 1990-1992.¹ The following characteristics were noted:

• Incidence was 215 cases per 100,000 people per year.
• Older patients were more at risk (1424 cases per 100,000 people per year for age >75 y).
• Fewer than 5% of cases were in children and younger adolescents.
• Three of 4 patients with recurrent zoster were HIV positive.

Mortality/Morbidity

• A common complication of herpes zoster is postherpetic neuralgia, pain that persists for longer than 1 month following resolution of the vesicular rash. This complication is more common in patients older than 50 years. Postherpetic neuralgia may develop as a continuation of pain that accompanies acute zoster, or it may develop following apparent resolution of the initial zoster reactivation. The pain of postherpetic neuralgia usually resolves within 6 months. However, 1% of patients continue to have pain for 1 year or longer.
• Herpes zoster may be associated with a secondary bacterial infection at the site of the rash (typically streptococcal or staphylococcal).
• Herpes zoster involving the ophthalmic branch of the trigeminal nerve may be associated with conjunctivitis, keratitis, corneal ulceration, iridocyclitis, glaucoma, and blindness.
• Complications of the Ramsay Hunt syndrome (zoster involving cranial nerves V, IX, and X) may include peripheral facial nerve weakness and deafness.
• Meningoencephalitis secondary to herpes zoster is more likely to be seen in immunocompromised patients than in immunocompetent patients. Other CNS complications may include myelitis, cranial nerve palsies, and granulomatous angiitis. Granulomatous angiitis may result in the development of a cerebrovascular accident.
• Disseminated zoster may be seen in immunocompromised patients. In such cases, hematogenous spread may result in the involvement of multiple dermatomes. Visceral involvement can also occur. Such systemic involvement can lead to death due to encephalitis, hepatitis, or pneumonitis.

Race

Blacks are one-fourth as likely as whites to develop herpes zoster.

Sex

Incidence is equal in males and females.

Age

Incidence of herpes zoster increases with age. Approximately 80% of cases occur in persons older than 20 years. Fewer than 5% of cases are in those younger than 14 years.

Clinical

History

Prodromal pain precedes the rash in approximately 75% of patients, typically confined to the same dermatomal distribution. Initially vesicular, the rash gradually becomes pustular and then crusts over a period of 7-10 days. As with chickenpox, once crusting occurs, the lesion is no longer infectious. Scarring and hypopigmentation or hyperpigmentation may persist for a long period. 

• Most patients describe the pain as burning, throbbing, or stabbing.
• The involved area may be tender to palpation.
• The rash may be pruritic.
• Depending on the involved dermatome, the pain may be attributed to other etiologies such as renal colic, biliary pain, or acute coronary syndrome. 
• Zoster is generally limited to 1 dermatome or at most 2 or 3 adjacent dermatomes in normal hosts.
• The thoracic dermatomes are the most commonly involved sites, followed by the lumbar dermatomes.
• Fewer than 20% of patients have systemic symptoms, such as headache, fever, malaise, or fatigue.
• Pain duration is variable but usually less than 1 month. 
  • Pain lasting longer than 1 month is referred to, by definition, as postherpetic neuralgia.
  • Of patients, 10-15% will have pain for more than 1 month.
  • Zoster sine herpete is defined as pain and paresthesias along the dermatome without the development of visible cutaneous involvement.

Physical

• The primary physical finding is a rash in a unilateral dermatomal distribution; the rash may be erythematous, vesicular, pustular (as depicted in the image below), or crusting, depending on the stage of disease. 
• 
  

  

  Herpes zoster on the neck.

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  Herpes zoster on the neck.

  
  
  • The initial rash is typically "herpetic" in appearance: small vesicles grouped on an erythematous base. It has been described as "dew drops on a rose petal."
  • Bilateral rash is rare.
  • Zoster lesions occur simultaneously and remain in congruent stages of healing.
  • Lesions on the tip of the nose signify involvement of the nasociliary nerve; this finding mandates slit-lamp examination with fluorescein stain to look for the dendritic corneal lesions of herpetic keratitis.
• Depending on the dermatome involved, physical examination findings may include the following: 
  • Corneal ulcers, conjunctivitis
  • Regional lymphadenopathy
  • Cranial nerve palsies
  • Peripheral facial nerve palsy
  • Delirium, confusion, coma (in patients with meningoencephalitis)

Causes

Herpes zoster is caused by reactivation of VZV as described in Pathophysiology.

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