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vesicles along the sensory nerves to the ganglion, where it remains latent until activated, at which time it progresses down the axon to the skin Multiplication of the virus in epidermal cells causes swelling, vacuolization, and lysis of cell boundaries, leading to the formation of vesicles and so-called Lipschutz inclusion bodies Alternatively, the ganglia could be infected during the viremia of chickenpox, but then one would have to explain why only one or a few sensory ganglia become infected Reactivation of virus is attributed to waning immunity, which would explain the increasing incidence of zoster with aging and with lymphomas, administration of immunosuppressive drugs, AIDS, and radiation therapy The subject of pathogenesis of herpes zoster has been reviewed by Gilden and colleagues, and in a monograph by Rentier who describes the molecular and immune investigations pertaining to VZV Clinical Features As indicated above, the incidence of herpes zoster rises with age Hope-Simpson has estimated that if a cohort of 1000 people lived to 85 years of age, half would have had one attack of zoster and 10 would have had two attacks The notion that one attack of zoster provides lifelong immunity is incorrect, although recurrent attacks are rare and most repeated herpetic eruptions are due to HSV The sexes are equally affected, as is each side of the body Herpes zoster occurs in up to 10 percent of patients with lymphoma and 25 percent of patients with Hodgkin disease particularly in those who have undergone splenectomy or received radiotherapy Conversely, about 5 percent of patients who present with herpes zoster are found to have a concurrent malignancy (about twice the number that would be expected), and the proportion appears to be even higher if more than two adjacent dermatomes are involved The vesicular eruption is usually preceded for several days by itching, tingling, or burning sensations in the involved dermatome(s), and sometimes by malaise and fever as well Or there is severe localized or radicular pain that may be mistaken for pleurisy, appendicitis, cholecystitis, or, quite often, ruptured intervertebral disc, until the diagnosis is clari ed by the appearance of vesicles (nearly always within 72 to 96 h) The rash consists of clusters of tense clear vesicles on an erythematous base, which become cloudy after a few days (due to accumulation of in ammatory cells) and dry, crusted, and scaly after 5 to 10 days In a small number of patients, the vesicles are con uent and hemorrhagic, and healing is delayed for several weeks In most cases pain and dysesthesia last for 1 to 4 weeks; but in the others (7 to 33 percent in different series) the pain persists for months or, in different forms, even for years and presents a dif cult problem in management Impairment of super cial sensation in the affected dermatome(s) is common, and segmental weakness and atrophy are added in about 5 percent of patients In the majority of patients the rash and sensorimotor signs are limited to the territory of a single dermatome, but in some, particularly those with cranial or limb involvement, two or more contiguous dermatomes are involved Rarely (and usually in association with malignancy) the rash is generalized, like that of chickenpox, or altogether absent In half of the cases, the CSF shows a mild increase in cells, mainly lymphocytes, and a modest increase in protein content (although lumbar puncture is not required to establish the diagnosis) The diagnosis can be con rmed by direct immuno uorescence of a biopsied skin lesion, using antibody to VZV, or inferred by nding multinucleated giant cells in scrapings from the base of an early vesicle The spinal uid also contains antibodies to the virus or.

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