Varicella-zoster virus is 1 of 8 viruses in the Herpesviridae family known to infect humans. It is known to cause 2 distinct disease states: varicella (chickenpox) due to a primary infection from the virus, and HZ (shingles) caused by a reactivation of the latent virus in the dorsal root ganglion, which then travels the neural pathway and manifests cutaneously along 1 to 2 dermatomes.1 This recurrence is possible in infants, children, and adults via 1 of 3 routes of exposure.
The overall incidence of HZ is lower in children compared to adults, and the risk dramatically increases in individuals older than 50 years. Evidence also shows that exposure to VZV before 1 year of age increases the lifetime risk for HZ.2,3 Children aged 1 to 18 years who were evaluated for HZ demonstrated a decreased incidence among those who were vaccinated versus those who were not.4,5 Interestingly, there was an increased incidence of HZ among children aged 1 to 2 years who had been vaccinated. Based on PCR analysis, it was noted that HZ was attributed to the vaccine-related strain of VZV in 92% of 1- to 2-year-old patients.4
There is some concern that the varicella vaccination program implemented in 1995 has led to increased rates of HZ. The literature presents mixed reports. Some studies showed an overall increased incidence of HZ,6,7 and 2 other studies showed no increase in the incidence of HZ.4,8 More recent studies have demonstrated that vaccination may have a protective effect against HZ.4-6,9 In a 2013 study in which HZ samples were tested by PCR analysis to determine the strains of VZV that were responsible for an HZ outbreak in children aged 1 to 18 years, the HZ incidence was 48 per 100,000 person-years in patients who were vaccinated versus 230 per 100,000 person-years in patients who were not vaccinated.Among the subset of patients who were vaccinated (n=118), 52% of the HZ lesions were from the wild-type strain.4
The typical presentation of HZ includes grouped vesicles or small bullae on an erythematous base that occur unilaterally within the distribution of a cranial or spinal sensory nerve, occasionally with overflow into the dermatomes above and below, typically without crossing the midline.8 The most frequent distributions in descending order are thoracic, cranial (mostly trigeminal), lumbar, and sacral. Pain in the dermatome may never occur, may precede, may occur during, or may even occur after the eruption. The initial presentation involves papules and plaques that develop blisters within hours of their development. Lesions continue to appear for several days and may coalesce. The lesions may become hemorrhagic, necrotic, or bullous, with or without adenopathy. Rarely, there can be pain without the associated skin eruption (zoster sine herpete). Lesions tend to crust by days 7 to 10.8
Herpes zoster typically affects children to a lesser extent than adults. The disease state often is milder in children with a decreased likelihood of postherpetic neuralgia.10 However, there are documented cases of severe sequelae secondary to zoster infection in pediatric patients, including but not limited to disseminated HZ,8 HZ ophthalmicus,11,12 Ramsay Hunt syndrome,8 and chronic encephalitis.8 In the adult population, ocular involvement will present in 33% to 50% of cases that involve the ophthalmic branch of the trigeminal nerve without clinical involvement of the nasociliary branch of the ophthalmic nerve. Involvement of the nasociliary branch will lead to ocular pathology in an estimated 76% to 100% of adult cases.13,14 It is unknown if this rate is the same in the pediatric population, but it highlights the importance of educating patients and/or guardians about possible complications. It also demonstrates the importance of including HZ in the differential diagnosis for pediatric patients presenting with papular or vesicular skin eruptions, particularly in the area of the ophthalmic branch of the trigeminal nerve.