exanthem. Most often occurs in childhood. Result of primary infection of a susceptible individual. 1.Worldwide in distribution, whereas the proportion of susceptible adults is even higher in Asia, Africa, and the Middle East. 2.No difference in racial or sexual susceptibility. 3.Humans are the only known reservoir. 4.Vectors play no role in transmission. 5.The mean incubation period is 14 or 15 days, with a rarge of 10 to 23 days. 6.The major route by which varicella is acquired and transmitted is thought to be the respiratory tract 7.Airborne droplets constitute an important mechanism of transmission, but can also be spread by direct contact 1.VZV is a member of the herpes virus family. 2.There is only one VZV serotype. 3.A number of antigens are present in the virion and produced infected cells. 4.Studies of molecular biology and its pathogenesis have been hampered. 1.Entry of the virus is through the mucosa of the upper respiratory tract and oropharynx. 2.Initial multiplication at this portal dissemination small amounts of virus blood and lymphatics (primary viremia) by cells of RES. 3.Incubating infection is partially contaired by innate host defenses and by developing immune responses. 4.Virus replication eventually overwhelms these still undeveloped defenses secondary viremia occurs (zweeks often infection) fever and malaise and disseminates throughout the body especially skin and mucous membranes. 5.Cyclic viremia is terminate after about 3 days. 6.Host immune responses terminate viremia and limit the progression of varicella lesions. 7.IgG, IgM, and IgA of VZV are detectable 2 to 5 days after onset of clinical varicella. 8.Reach maximum titers during second or third week decline slowly persist in low levels for life 9.Cell mediated immunity is more important than humoral immunity in recovery from varicella. Prodrome of Varicella 1.Uncommon in young children. 2.In older children and adults, rash preceded by 2 to 3 day of fever , chills, malaise, headache, anorexia, severe backache. Rash of Varicella 1.Benigns on the face and scalp. 2.Spreads rapidy to the trunk, with relative sparing of the extremities. 3.Central in distribution. 4.More profuse in lows and protected parts of the body. 5.Rose colored macules papule vesicles pustules crusts. 6.Vesicle is superficial and thin walled like a drop of water 7.Vesicle can also develop in the mucous membranes 8.Fever that persist is proportional to the severity of rash. 1.Secondary bacterial infection of skin lesion (children). 2.Primary varicella pneumonia (adult). 3.Congenital VZV infection : asymptomatic infection severe congenital malformation. 4.Morbidity and mortality are markedly increased in immuno compromised patients. 5.CNS complication : Reyes syndrome. Acute cerebellar atoxia. Encephalitis or meningoencephalitis. Acute ascending or transverse myelitis. Guillain-barre syndrome. 6.Mild hepatitis. 1.Histologically, cant be distinguished from herpes zoster. 2.Ballooning degeneration (characteristic changes). 1.The development papulo vesikular eruption after a brief and mild (or absent) prodrome symptoms. Characteristic diagnostic include: 2.Appearance of lesions in crops with central distribution. 3.Rapid evolution of lesions. 4.Presence of lesions in all stages of development in any area throughout the acute disease. 5.Presence of lesions in the mucous membranes of the mouth. 1.Routine blood test are not helpful. 2.Asymptomatic elevation in ALT and AST. 3.Punch biopsies more rediable for histologig examinations. 4.Defenitive diagnosis from isolation of virus in cell cultures. 5.Serologic tests. Antiviral agents : Acyclovir. Famciclovir. Laciclovir. Vidarabine. Foscarnet. 1.Generally benign and self- limited. 2.Locally : Cool compresses. Calamine lotion. Orally : Antihistamines. Antipyretics. Antiviral agents. 1.Passive immunization. 2.Chemoprophylactic.