It is uncertain what factors induce the varicella zoster virus to reactivate. Herpes zoster occurs infrequently in healthy children. Diminished cellular immunity, however, seems to increase risk of reactivation because incidence increases with age and in immunocompromised states.

Pathophysiology: Herpes zoster is a cutaneous viral infection that manifests as a vesicular rash generally involving the skin of a single, unilateral dermatome. Approximately 4-5 days before the eruption appears, the patient may experience preeruptive pain, itching, or burning along the effected dermatome.

Historically, herpes zoster was thought to be an indicator for an underlying malignancy. More recent studies have shown no increased incidence of malignancy in children with herpes zoster. Approximately 3% of pediatric zoster cases occur in children with malignancies. Given this evidence, a malignancy workup is not indicated in an otherwise healthy child who has herpes zoster.

Frequency:

• In the US: Herpes zoster is uncommon in childhood. More than 66% of affected patients are older than 50 years. Of all patients with zoster, fewer than 10% are younger than 20 years, and 5% are younger than 15 years. Although zoster is primarily a disease of adults, it has been noted as early as the first week of life. This occurs in infants born to mothers who had primary varicella zoster virus infection during pregnancy.

  Incidence of the disease increases with age throughout childhood and adult life. Lifetime incidence is 10-20%. Approximately 25% of human immunodeficiency virus (HIV)-positive patients and 7-9% of renal and cardiac transplant patients experience a bout of zoster. Recurrent herpes zoster occurs almost exclusively among the immunosuppressed.

  In the US, zoster occurs in 300,000-500,000 individuals annually. Nearly 100% of American adults are seropositive for VZV antibodies. Since routine use of the live, attenuated varicella vaccine began in 1994, preliminary observations have revealed zoster frequency is significantly higher among children who had natural exposure to varicella, compared to those who were vaccinated.

Race: African Americans are 25% less likely than whites to develop herpes zoster.

Sex: Men and women are equally affected.

History: Children commonly experience systemic symptoms before cutaneous manifestations erupt. Acute phase symptoms include the following:

• Pain (This occasionally may be so severe that it may mimic appendicitis, renal calculi, or biliary colic.)
• Pruritus
• Low-grade fever
• Malaise
• Headache
• Regional lymphadenopathy

Physical: A unilateral dermatomal eruption begins as grouped vesicles on an erythematous base. These round to oval red lesions with surmounting clear fluid filled blisters usually measure several centimeters in diameter and are oriented along the track of dermatomal innervation. Over the ensuing days, the fluid becomes cloudy and pustular and finally, with rupture of the blisters, grouped crusted erosions are left. Thoracic dermatomes are the most common site, and involvement of multiple contiguous dermatomes is common. Lesions erupt over 7 days and develop a crust by 14-21 days.

Approximately 17-35% of patients with herpes zoster also have a few scattered vesicles in sites remote from the primary dermatome. This is likely secondary to viremia and should not be confused with generalized herpes zoster. The generalized form occurs in 2-10% of herpes zoster patients.

Physical examination should include a slit lamp exam for corneal findings if lesions are found in the distribution of the V1 branch of the trigeminal nerve.

Causes: Although VZV reactivates for unknown reasons, childhood herpes zoster has several recognized risk factors. These include the following:

• Acute lymphocytic leukemia and other malignancies
• Immunocompromised patients as a result of treatments or HIV
• In utero varicella exposure
• Primary varicella zoster infection in infants younger than 1 year.

Lab Studies:

• Patient history and clinical findings are the primary bases for a herpes zoster diagnosis. Although varicella zoster virus can be cultured, its growth rate usually is too slow to make a timely contribution to diagnosis.

• A Tzanck smear, prepared from fluid contained in vesicular lesions, confirms the lesion is herpetic. The test does not differentiate among herpes zoster, varicella zoster virus, and herpes simplex.

• Direct fluorescent assay (DFA) from vesicular fluid or corneal lesion can yield the varicella zoster viral antigen.

• A polymerase chain reaction (PCR) from vesicular fluid or corneal scraping can yield the varicella zoster virus nucleic acid.

Other Tests:

• Skin biopsy may be performed and reveals an intraepidermal vesicle with degeneration of epidermal cells and acantholysis. There is a brisk lymphocytic infiltrate in the upper dermis.