Diseases information. Disorders. Treatment.

PRIMARY INFECTION
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Primary infection with VZV produces the well-known clinical syndrome of varicella or chickenpox. Low-grade fever may precede the development of the rash by 1 to 2 days. The characteristic rash involves lesions that appear in crops and proceed through a series of well-defined stages. The lesions start as erythematous macules, progress to vesiculation with the classic “dew drop on a rose petal” appearance, become pustular, and finally crust over. The hallmark of the varicella rash is the simultaneous presence of lesions of different stages. The rash tends to appear initially on the trunk, then spread to the face, neck, and extremities. Mucous membranes can be involved. The lesions are intensely pruritic. Systemic manifestations of illness usually are mild or absent. In immunocompetent children, new crops of lesions continue to appear for a few days; by 4 or 5 days, most are crusted over, and new lesions no longer form.
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The severity of illness is related inversely to age. Primary varicella tends to be milder in young children, and teenagers and adults can become seriously ill. For reasons that remain to be elucidated, pregnancy seems to be an independent risk factor for severe varicella, although the association is controversial.
PRENATAL INFECTION

Prenatal infection is uncommon because most women of childbearing age are immune to varicella. Although rare, a congenital varicella syndrome occurs in nearly 2% of infants born to women who con-tract varicella in the first or second trimester of pregnancy. Congenital varicella syndrome is characterized by small infant size, cutaneous scarring, limb hypoplasia, microcephaly, cortical atrophy, chorioretinitis, cataracts, and other anomalies. Approximately 2% of infants who have intrauterine exposure to varicella develop zoster in infancy or early childhood.
PERINATAL INFECTION
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Early studies suggested that the risk of death was as high as 31% among infants whose mothers had onset of primary varicella rash 0 to 4 days before birth. However, most believe that this statistic probably is inflated by selective reporting. The use of varicella zoster immune globulin (VZIG) in these infants has been associated with a markedly better prognosis. There is no evidence to suggest that postnatally acquired varicella infection is any more severe in neonates than it is in older infants.

Varicella zoster virus (VZV) causes varicella, the most common exanthematous disease of childhood. After the acute infection, VZV remains latent in the dorsal root ganglia; reactivation of the virus later in life causes zoster. VZV is ubiquitous, and humans are the only known host. It is estimated that there are 4 million cases per year in the United States, of which 90% occur in children between the ages of 1 and 14 years. Seropositivity reaches 95% by the late teen years and is close to 100% by age 60. The virus is highly contagious, with secondary household infection rates of about 80% to 90%. In temperate climates, a seasonal peak occurs between March and May. There are approximately 6,500 to 9,000 hospitalizations and 100 to 200 deaths in the United States annually from varicella or its complications. Approximately 300,000 cases of zoster are reported annually to the Centers for Disease Control and Prevention (CDC).
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The primary source of infectious material is the fresh cutaneous lesion, which is teeming with virus. Unlike the poxviruses, VZV does not persist in scabs or crusts. It generally is believed that the period of communicability begins 1 to 2 days before the onset of rash and persists for 5 days or until skin lesions are crusting. The incubation period for varicella is approximately 14 days, but it can be as short as 10 or as long as 21 days. VZV infection also can be spread from zoster lesions to susceptible hosts, although the incidence of contagion is lower.

Pathogenesis
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Varicella-zoster virus is an alpha-herpesvirus. Like all herpes group viruses, it is an enveloped, icosahedral virus that contains a double-stranded DNA genome. Chickenpox begins with replication of the virus at sites of contact and is followed by a primary viremia. A secondary viremia occurs after about 1 week, which disseminates the infection to the skin, causing the familiar rash to appear. As the acute disease abates, the virus establishes latency in sensory ganglia. Reactivation of latent infection causes zoster or “shingles,” which produces pain and a vesicular rash in the distribution of one to three dermatomes. Replication of the virus in the ganglia is destructive to ganglion cells, which may account for the pain associated with zoster. Unlike herpes simplex virus (HSV) 1 or 2, which can reactivate frequently, it is uncommon for VZV to reactivate more than once. The exception is chronic or recurrent zoster that has been seen with some frequency in patients who have acquired immunodeficiency syndrome. Exactly what precipitates reactivation of the latent virus is not clear. The incidence of zoster increases with age, however, and this has been correlated with decreasing cell-mediated immunity to VZV. Immunity to varicella appears to be lifelong; that is, second clinical cases of varicella are rare.
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