Preschooler With Slowly Progressing Rash on One Arm

March 2, 2004
Paul J. Lee, MD
Paul J. Lee, MD

During the past week, a rash on theright thumb and forefinger of a 4-yearoldboy has progressed to involve theentire arm.

During the past week, a rash on the right thumb and forefinger of a 4-year-old boy has progressed to involve the entire arm.

The boy’s parents first noted the digital lesions during a family vacation at a mountain resort where the child had been swimming and playing outdoors. The resort grounds were well maintained; no wild animals had been seen on the premises. All family members had been healthy during the vacation.

The rash on the boy’s fingers spread to the rest of the hand and then up the forearm. The eruption stopped at the shoulder and did not spread to the torso. The rash was not pruritic, but the affected area was painful. The youngster remained afebrile but complained of pain and constant fatigue. His parents treated him with acetaminophen, which diminished the pain, and topical hydrocortisone, which did not help resolve the rash.

The boy’s parents now seek the pediatrician’s advice 7 days after the initial appearance of the lesions. The boy’s vital signs are stable. He appears somewhat tired but remains active. The only notable findings are small vesicles on the right arm with areas of healing and scabbing (Figures 1 and 2). The arm is tender to palpation, but there is no soft tissue swelling or induration. There is full range of motion, but voluntary arm movements are diminished. The patient says the rash is less painful now than it was earlier in the week.

Except for the removal of a branchial cleft cyst at age 2, the child’s medical history is unremarkable. The patient has not had chickenpox; he received live varicella virus vaccine when he was 12 months old.

Herpes zoster secondary to varicella vaccine is diagnosed and is confirmed by a polymerase chain reaction assay. The patient is treated with oral acyclovir, and his lesions and symptoms resolve fully within 2 weeks.




The acute cutaneous infection herpes zoster (shingles) is caused by the reactivation of the latent varicella-zoster virus (VZV)-the herpesvirus that also causes chickenpox.

Chickenpox usually resolves within 2 weeks. Thereafter, VZV becomes dormant and resides in sensory dorsal root ganglia in the spine. The virus may reactivate up to decades later, causing pain and zoster lesions in a dermatomal distribution.

SCOPE OF THE PROBLEM
Between 600,000 and 1 million cases of herpes zoster occur in the United States each year.1 Healthy children are infrequently affected. Fewer than 10% of patients with zoster are younger than 20 years, and only 5% are younger than 15 years. The risk of reactivation increases as cell-mediated immunity declines with advancing age or in immunocompromised states.

The annual incidence of herpes zoster is:

  • 0.74 per 1000 in those younger than 9 years.

  • 1.38 per 1000 in those between 10 and 19 years.

  • 2.58 per 1000 in those in their 20s.

Shingles develops in about 50% of persons older than 80 years, and in as many as 25% of patients with HIV infection, lymphoma, or other immune deficiencies.

Herpes zoster was thought to be a marker for an underlying malignancy; however, recent studies show no increase in the incidence of cancer in children with this infection.2 Approximately 3% of pediatric zoster outbreaks occur in children with malignancies. Therefore, a workup for malignancy is not indicated in an otherwise healthy child who presents with herpes zoster.

PRESENTATION
Patients present with a vesicular rash that generally involves a single unilateral dermatome. Children commonly experience systemic symptoms before the rash erupts; this prodrome may include mild to very severe pain, pruritus, low-grade fever, malaise, and headache.

The lesions resemble those of chickenpox but evolve more slowly and appear as grouped vesicles rather than single lesions. They may be scattered in patches or so numerous that they form a continuous band. Commonly affected areas include the chest, abdomen, and eyes (ophthalmic zoster). Typically, new zoster lesions continue to appear for 2 or 3 days and become pustular and crusted within 14 to 21 days. Roughly one third of patients have a few scattered vesicles in sites that are remote from the primary dermatome. This presentation is likely secondary to viremia and must not be confused with generalized herpes zoster, which occurs in 2% to 10% of patients with herpes zoster.3

VARICELLA VACCINE

Varicella can be prevented by vaccination with the live attenuated Oka vaccine strain of VZV, which was approved by the FDA in 1995. Varicella vaccination is indicated for children older than 12 months who are susceptible to chickenpox. For susceptible persons older than 13 years, 2 doses should be given at least 4 weeks apart.

The seroconversion rate associated with varicella vaccine among susceptible children aged 12 months to 12 years is 97%. Among vaccinated persons 13 years or older, 78% seroconvert after the first dose of varicella vaccine and 99% seroconvert after a second dose.

The vaccine has proved to be safe and effective in preventing varicella. However, breakthrough infection-postvaccination chickenpox-has developed in 1% to 4.4% of vaccinated persons. Affected patients usually experience mild illness. The risk of healthy vaccinated persons transmitting vaccine virus to their contacts is minimal; however, the risk of transmission may be higher for patients in whom a varicella-like rash develops following vaccination.

DIAGNOSIS
Patient history and clinical findings are the primary bases for a diagnosis of VZV infection; laboratory tests are necessary for confirmation. A polymerase chain reaction test of vesicular fluid or corneal scrapings and analysis of restriction fragment length polymorphisms of the amplified products can identify the VZV nucleic acid. This technique also provides information on the incidence of vaccine-associated zoster and is the only method that can distinguish the attenuated strain of VZV used in the vaccine from the naturally occurring wild-type strain.

Immunofluorescence staining of skin or vesicle scrapings is another highly sensitive method of making a definitive diagnosis of VZV infection. Viral culture is also diagnostic, but usually infectious virus can only be recovered from vesicles for just a few days.

Occasionally, VZV can reactivate in healthy children and present as herpes zoster. The varicella vaccine confers relative protection from cutaneous herpes zoster. However, preliminary observations show that since routine use of the live attenuated varicella vaccine began in the mid 1990s, zoster is more prevalent in children who have natural exposure to the varicella virus than among those who are vaccinated. Although rare, zoster has been observed in 2.6 of every 100,000 patients who have been vaccinated.4

THERAPY

Herpes zoster generally runs a benign and mild course in children. Rash and symptoms usually resolve within 3 weeks. Although pain may occur, post-herpetic neuralgia is quite rare in this population. Conservative therapy includes NSAIDs; wet dressings with 5% aluminum acetate (Burrow solution) applied for 30 to 60 minutes, 4 to 6 times daily; and topical treatments, such as calamine lotion.

Antiviral therapy may reduce healing time, minimize the eruption of new vesicles, and decrease the duration of pain and viral shedding. For maximal effectiveness, initiate therapy with these agents within 72 hours of the onset of rash. Acyclovir, which has FDA approval for use in children with herpes zoster, has been widely used in this setting and has a good safety profile. In immunocompetent children, acyclovir can be given orally at 80 mg/kg/d in 4 divided doses. Acyclovir can also be used intravenously for severe disease or in immunocompromised children. Valacyclovir and famciclovir have been prescribed for adults with herpes zoster, but these agents are not approved by the FDA for pediatric use.

Those persons not immune to the varicella virus can become infected with VZV. Many school-age children have now been vaccinated against the virus. Zoster is thought to be only one third as contagious as the primary varicella infection. Zoster is transmitted via the respiratory route or by direct contact with the lesions. A child who is recovering from VZV infection can return to school if remaining lesions are covered fully by clothing or dressings.

References:

REFERENCES:


1.

Chartrand SA. Varicella vaccine.

Pediatr ClinNorth Am.

2000;47:373-394.

2.

Wurzel CL, Kahan J, Heitler M, Rubin LG. Prognosisof herpes zoster in healthy children.

Am J DisChild.

1986;140:477-478.

3.

Smith CG, Glaser DA. Herpes zoster in childhood:case report and review of the literature.

PediatrDermatol.

1996;13:226-229.

4.

Uebe B, Sauerbrei A, Burdach S, Horneff G.Herpes zoster by reactivated vaccine varicella zostervirus in a healthy child.

Eur J Pediatr

. 2002;161:442-444.