VARICELLA - ZOSTER DISEASE
VZV causes two diseases, chickenpox (varicella) and shingles (zoster). The for-mer usually occurs in children, the latter in the elderly. In the intervening years, the virus remains latent in neural ganglia but activates due to waning cellular im-munity. Almost 90% of the US population is infected with VZV by the age of 10 years, and the virus is spread primarily by respiratory secretions.
VZV infection is ubiquitous. In temperate climates, nearly all persons contract chick-enpox before they reach adulthood, and 90% of cases occur before the age of 10 years. In contrast, the mean age at infection in tropical countries is over 20 years, and the seroprevalence at age 70 may be only 50%. The virus is highly contagious, with attack rates among susceptible contacts of 75%. Varicella occurs most frequently during the winter and spring months. The incubation period is 11 to 21 days. The major mode of transmission is respiratory, although direct contact with vesicular or pustular lesions may result in transmission. Communicability is greatest 24 to 48 hours before the onset of rash and lasts 3 to 4 days into the rash. Virus is rarely isolated from crusted lesions.
Respiratory spread leads to infection of the contact patient’s upper respiratory tract fol-lowed by replication in regional lymph nodes and primary viremia. The latter results in infection of the reticuloendothelial system and a subsequent secondary viremia associated with T lymphocytes. Following secondary viremia, there is infection of the skin and finally a host immune response.
The relationship between zoster and varicella was first described by Von Bokay in 1892, when he observed several instances of varicella in households after the introduction of a case of zoster. On the basis of these epidemiologic observations, he proposed that zoster and varicella were different clinical manifestations of a single agent. The cultiva-tion of VZV in vitro by Weller in 1954 confirmed Von Bokay’s hypothesis: the viruses isolated from chickenpox and from zoster (or shingles) are identical. Latency of VZV occurs in sensory ganglia, as shown by in situ hybridization methods in dorsal root gan-glia of adults many years after varicella infection. Herpes zoster (shingles) occurs when latent varicella zoster virus reactivates and multiplies within a sensory ganglion and then travels back down the sensory nerve to the skin. The rash of herpes zoster is generally confined to the area of the skin (ie, dermatome) innervated by the sensory ganglion in which reactivation occurs (Fig 38–3).
Both humoral immunity and cell-mediated immunity are important factors in determining the frequency of reinfection and reactivation of varicella–zoster. Circulating antibody pre-vents reinfection, and cell-mediated immunity appears to control reactivation. In patients with depressed cell-mediated immune responses, especially those with bone marrow transplants, Hodgkin’s disease, AIDS, and lymphoproliferative disorders, reactivation can occur, and VZV infections are more frequent and more severe.
The increase in the incidence and severity of herpes zoster observed with increasing age in immunocompetent individuals is correlated with an age-related decrease in VZV-specific cellular immunity. Beginning in the fifth decade of life, there is a marked decline in cellular immunity to VZV, which can be measured by cutaneous delayed hy-persensitivity as well as by a variety of in vitro assays. This occurs many years before there is any generalized decline in cellular immunity.
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