Paediatric herpes zoster: Unmasking shingles in the young

EPIDEMIOLOGY

The incidence of HZ in children is relatively low, estimated at 74/100,000 person-years in unvaccinated children and 38/100,000 in vaccinated children.^[1] The risk of paediatric HZ is higher in children who had varicella in infancy or were exposed to the virus in utero. While vaccination has significantly reduced primary varicella infections, breakthrough infections and subsequent HZ cases have been reported, although with a milder course.^[2]

Several factors influence the risk of paediatric HZ, including: Age at primary infection: Infants who contract varicella in the 1^st year of life have an increased risk of developing HZ due to incomplete immune development and inadequate VZV-specific immunity.^[3]

Intrauterine exposure: Maternal varicella during pregnancy can lead to congenital varicella syndrome or asymptomatic foetal infection, which may later manifest as HZ.^[4]

Immunocompromised status: Children with malignancies (e.g., leukaemia, lymphoma), organ transplants, or those undergoing immunosuppressive therapy have an elevated risk of HZ due to impaired cellular immunity.^[5]

Varicella vaccination: Although the vaccine reduces the incidence of varicella and HZ, vaccine-strain VZV can still reactivate, causing HZ in some individuals.^[6]

CLINICAL PRESENTATION

Paediatric HZ typically presents as a unilateral, vesicular rash distributed along a single dermatome. The rash is often preceded by prodromal symptoms such as localised pain, itching, burning, or paraesthesia. The most commonly affected dermatomes include thoracic, cervical and trigeminal nerve distributions.^[7]

KEY CLINICAL FEATURES INCLUDE

Prodrome: Fever, malaise and localised pain or dysaesthesia preceding the rash by 1–3 days.

Acute rash phase: Clusters of vesicles on an erythematous base appearing along a dermatome. The vesicles rupture and crust over within 7–10 days.

Resolution phase: Complete healing occurs within 2–4 weeks, often leaving residual hypopigmentation or scarring.

COMPLICATIONS

Although most cases of paediatric HZ resolve without significant morbidity, complications can arise, particularly in immunocompromised children.

HZ Ophthalmicus (HZO): Involvement of the ophthalmic division of the trigeminal nerve can result in conjunctivitis, keratitis, uveitis, or vision loss if untreated.^[8]

Neurological complications: Meningitis, encephalitis, myelitis and Ramsay Hunt syndrome (involvement of the geniculate ganglion leading to facial paralysis and ear vesicles) have been reported in children with HZ.^[9]

Postherpetic neuralgia (PHN): While rare in children, PHN can cause persistent neuropathic pain lasting months to years after the rash resolves.^[10]

Secondary bacterial infection: Streptococcal or staphylococcal superinfection of the vesicular lesions may require antibiotic treatment.^[11]

DIAGNOSIS

The diagnosis of paediatric HZ is primarily clinical, based on the characteristic rash and dermatomal distribution. However, laboratory confirmation may be required in atypical or complicated cases.

DIAGNOSTIC TOOLS INCLUDE

Polymerase chain reaction: The most sensitive and specific test for detecting VZV DNA from lesion samples.^[12]

Direct fluorescent antibody testing: Rapid identification of VZV in lesion scrapings.

Serology: VZV immunoglobulin G and immunoglobulin M titres may be helpful in assessing immune status but are less useful for acute diagnosis.

TREATMENT

The management of paediatric HZ focuses on symptom relief, antiviral therapy and prevention of complications.

Antiviral therapy: Early initiation of acyclovir (within 72 h of rash onset) can shorten disease duration and reduce complications. Alternative agents include valacyclovir and famciclovir, which offer improved bioavailability and reduced dosing frequency.^[13]

Analgesia: Pain management includes acetaminophen, nonsteroidal anti-inflammatory drugs or, in severe cases, opioid analgesics.^[14]

Topical care: Calamine lotion, oatmeal baths and cool compresses help soothe pruritus and discomfort.

Corticosteroids: May be considered for severe cases involving neurological or ophthalmic complications under specialist guidance.^[15]

PREVENTION

The introduction of the varicella vaccine has significantly reduced the incidence of both varicella and subsequent HZ in children. The Advisory Committee on Immunization Practices recommends two doses of the varicella vaccine:

• First dose: 12–15 months

• Second dose: 4–6 years.^[16]

While the vaccine does not eliminate the risk of HZ, vaccinated individuals who develop HZ generally experience a milder disease course with fewer complications.^[17]

CONCLUSION

Paediatric HZ remains an important clinical entity, particularly in children with a history of early varicella infection, immunosuppression or in utero exposure. While the disease is generally mild in healthy children, complications such as Herpes Zoster Ophthalmicus and neurological involvement necessitate early diagnosis and treatment. The varicella vaccine has played a crucial role in reducing the burden of both primary varicella and subsequent HZ, underscoring the importance of widespread immunisation. Continued research is needed to understand the long-term effects of vaccination on HZ epidemiology and optimise prevention strategies in paediatric populations.