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Varicella-zoster virus (VZV) infection causes two clinically distinct forms of disease. Primary infection with VZV results in varicella (chickenpox), characterized by vesicular lesions in different stages of development on the face, trunk, and extremities. Herpes zoster, also known as shingles, results from reactivation of endogenous latent VZV infection within the sensory ganglia. This clinical form of the disease is characterized by a painful, unilateral vesicular eruption, which usually occurs in a restricted dermatomal distribution. This topic will address the clinical manifestations and complications of herpes zoster in immunocompetent and immunosuppressed hosts. The epidemiology, pathogenesis, diagnosis, and treatment of shingles, and the clinical manifestations of chickenpox, are discussed elsewhere. (See "Epidemiology and pathogenesis of varicella-zoster virus infection: Herpes zoster" and "Treatment of herpes zoster in the immunocompetent host" and "Diagnosis of varicella-zoster virus infection" and "Clinical features of varicella-zoster virus infection: Chickenpox" .) CLINICAL MANIFESTATIONS The presenting clinical manifestations of herpes zoster are usually characterized by rash and acute neuritis. Rash The rash of herpes zoster starts as erythematous papules, which quickly evolve into grouped vesicles or bullae (picture 1 ).

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Varicella-zoster virus (VZV) infection causes two clinically distinct forms of disease. Primary infection with VZV results in varicella (chickenpox), characterized by vesicular lesions in different stages of development on the face, trunk, and extremities. Herpes zoster, also known as shingles, results from reactivation of endogenous latent VZV infection within the sensory ganglia. This clinical form of the disease is characterized by a painful, unilateral vesicular eruption, which usually occurs in a restricted dermatomal distribution.This topic will address the clinical manifestations and complications of herpes zoster in immunocompetent and immunosuppressed hosts. The epidemiology, pathogenesis, diagnosis, and treatment of shingles, and the clinical manifestations of chickenpox, are discussed elsewhere. (See "Epidemiology and pathogenesis of varicella-zoster virus infection: Herpes zoster" and "Treatment of herpes zoster in the immunocompetent host" and "Diagnosis of varicella-zoster virus infection" and "Clinical features of varicella-zoster virus infection: Chickenpox".)CLINICAL MANIFESTATIONSThe presenting clinical manifestations of herpes zoster are usually characterized by rash and acute neuritis.RashThe rash of herpes zoster starts as erythematous papules, which quickly evolve into grouped vesicles or bullae (picture 1). Within three to four days, these vesicular lesions can become more pustular or occasionally hemorrhagic (picture 2 and picture 3). In immunocompetent hosts, the lesions crust by 7 to 10 days and are no longer considered infectious. The development of new lesions more than a week after presentation should raise concerns regarding possible underlying immunodeficiency [1]. Scarring and hypo- or hyperpigmentation may persist months to years after herpes zoster infection has resolved [2].Zoster is generally limited to one dermatome in previously healthy hosts, but can occasionally affect two or three neighboring dermatomes (figure 1 and figure 2). Some patients have a few scattered vesicles located at some distance away from the involved dermatome [1,3].Subscribers log in here To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you: Medical Professional or Student Hospital or Institution Group Practices Patient or Caregiver Literature review current through: Mar 2015. | This topic last updated: Sep 8, 2014. The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. 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