Abstract

Herpes zoster is caused by reactivation of latent varicella-zoster virus that resides in a dorsal root ganglion. Herpes zoster can develop at any time after a primary infection or varicella vac- cination. The incidence among children is approximately 110 per 100,000 person-years. Clini- cally, herpes zoster is characterized by a painful, unilateral vesicular eruption in a restricted dermatomal distribution. In young children, herpes zoster has a predilection for areas supplied by the cervical and sacral dermatomes. Herpes zoster tends to be milder in children than that in adults. Also, vaccine-associated herpes zoster is milder than herpes zoster after wild-type vari- cella. The diagnosis of herpes zoster is mainly made clinically, based on a distinct clinical ap- pearance. The most common complications are secondary bacterial infection, depigmentation, and scarring. Chickenpox may develop in susceptible individuals exposed to herpes zoster. Oral acyclovir should be considered for uncomplicated herpes zoster in immunocompetent children. Intravenous acyclovir is the treatment of choice for immunocompromised children who are at risk for disseminated disease. The medication should be administered ideally within 72 hours of rash onset.

Highlights

  • Known as shingles, is caused by reactivation of endogenous latent varicella-zoster virus that resides in a sensory dorsal root ganglion usually after primary infection with varicella-zoster virus

  • Herpes zoster can develop at any time after a primary infection or varicella vaccination [1]

  • Infantile herpes zoster is more commonly associated with intrauterine varicella-zoster virus infection than postnatal infection

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Summary

Introduction

Known as shingles, is caused by reactivation of endogenous latent varicella-zoster virus that resides in a sensory dorsal root ganglion usually after primary infection with varicella-zoster virus How to cite this paper: Leung, A.K.C. and Barankin, B. Barankin or chickenpox) [1]. Herpes zoster can develop at any time after a primary infection or varicella vaccination [1]. The activated virus travels back down the corresponding cutaneous nerve to the adjacent skin, causing a painful, unilateral vesicular eruption in a restricted dermatomal distribution

Epidemiology
Pathogenesis
Clinical Manifestations
Complications
Diagnosis
Differential Diagnosis
Prognosis
Management
Findings
10. Prevention
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