Shingles in a child

• in contrast to chickenpox, herpes zoster is caused by individual host factors that allow the escape of the latent virus from immunologic control
  • in most healthy children, the effective establishment of latency follows primary infection, and reactivation is unusual until many decades after an episode of varicella
  • the rate of zoster in children younger than 10 years of age has been estimated to be 0.74 - this compares with 3.4 cases in 1,000 persons a year for the general population.
  • herpes zoster may occur in a child when there is no obvious precipitant
    • however herpes zoster may be associated with an immunocompromised state
      • for example in children who have developed herpes zoster then possible triggers include:
        • immunosuppressive diseases, such as malignancy, or require treatment for cancer or organ transplantation or other chronic diseases, such as rheumatoid arthritis, that diminish effective cell-mediated immune responses against VZV
          • Human immunodeficiency virus (HIV) infection also predisposes children to herpes zoster infection
    • exposure to VZV by maternal infection during pregnancy increases the risk of contracting herpes zoster in early childhood, as does the occurrence of varicella in infancy
      
      
  • healthy children rarely have classic herpes zoster
    • when it occurs, rash usually is mild, and most children do not have the symptoms of acute neuropathic pain that are the hallmark of herpes zoster in adults. At the onset of herpes zoster, clusters of vesicular lesions appear, often noticed first next to the spine and in the midline anteriorly in the same thoracic or lumbosacral dermatome; trigeminal reactivations involve the face
      • the period of new lesion formation is brief, usually 3 to 7 days, and healing is complete by 1 to 2 weeks
      • postherpetic neuralgia, the most common complication of herpes zoster in adults, is not described in children
        
        
      • treatment of herpes zoster in healthy children
        • although acyclovir, valaciclovir, and famciclovir have been shown to be effective for the treatment of recurrent VZV infection in healthy adults in placebo-controlled trials, comparable data are not available for healthy children because the incidence of herpes zoster in childhood is so low
        • children who develop herpes zoster ophthalmicus should receive oral acyclovir because of its documented effects on complications, such as anterior uveitis or stromal keratitis
          • herpes zoster in other dermatomes usually is transient and not associated with pain; these episodes usually do not require antiviral therapy (1)
      • treatment of immunocompromised children with herpes zoster (1)
        • immunocompromised children and adolescents benefit from antiviral therapy when they have herpes zoster because the localized cutaneous infection can be severe and viremia may occur
          • risk of visceral dissemination and mortality is much lower with VZV reactivation than with primary VZV infections, even in high-risk patients
          • optimal initial therapy for immunocompromised children with herpes zoster is acyclovir, given intravenously
            • duration of therapy is 7 days or for 2 days after the cessation of the formation of new lesions
            • when acyclovir is started within 72 hours after the onset of the rash, the duration of formation of new lesions is shortened to only about 3 days (whereas new lesions appear for a week or longer in untreated cases) and visceral dissemination is prevented
            • antiviral treatment reduces acute pain, accelerates crusting, and results in complete healing by 2 to 3 weeks
            • because the clinical course of herpes zoster is longer than that of varicella clinical benefit is observed even when therapy is delayed for more than 72 hours
            • any evidence of visceral spread constitutes an indication for initiating intravenous acyclovir
              
              
• post-exposure prophylaxis (PEP) to varicella (2,3):
  • indicated for immunocompromised children - some centres use oral aciclovir alone; others may use intravenous varicella immunoglobulin in additon to oral (or intravenous) aciclovir
  • not usually recommended for immunocompetent children because they are not at high risk of severe infection. However, PEP might be deemed reasonable for immunocompetent previous children in hospital because they might share facilities with immunocompromised childrenand because nosocomial outbreaks can lead to restrictions on admissions. There is controversy about whether PEP is indicated for immunocompromised children who are known to be VZV-IgG positive, but varicella re-infection is well-recognised (and occurred in our study) so some offer PEP to all immunocompromised childhood contacts regardless of VZV-IgG status (3)

Reference:

• 1. Arvin AM. Antiviral therapy for varicellanext term and herpes zoster. Seminars in Pediatric Infectious Diseases 2002; 13 (1): 12-21.
• 2. einstock DM et al. Postexposure prophylaxis against varicella-zoster virus infection among recipients of hematopoietic stem cell transplant: unresolved issues. Infect Control Hosp Epidemiol 2004;25: 603-608.
• 3. Shinjoh M, Takahash T. Varicella zoster exposure on paediatric wards between 2000 and 2007: safe and effective post-exposure prophylaxis with oral aciclovir. Journal of Hospital Infection 2009; 72(2): 163-168.