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childhood.
EPIDEMIOLOGY
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 sexual susceptibility. or
reservoir.
4.Vectors play no role in
transmission.
5.The mean incubation period
transmitted is thought to be
the respiratory tract
ETIOLOGY
been hampered.
PATHOGENESIS
1.Entry of the virus is
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.
CLINICAL MANIFESTATIONS
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.
COMPLICATIONS OF VARICELLA
1.Secondary bacterial infection of skin lesion (children). 2.Primary varicella pneumonia
(adult).
asymptomatic
severe
infection
congenital
malformation.
4.Morbidity and mortality are
markedly
immuno
increased
in
compromised
patients.
5.CNS complication : Reyes syndrome. Acute cerebellar atoxia. Encephalitis or meningoencephalitis. Acute ascending or transverse myelitis. Guillain-barre syndrome. 6.Mild hepatitis.
PATHOLOGY
1.Histologically,
distinguished
cant
from
be
herpes
zoster.
2.Ballooning degeneration
(characteristic changes).
CLINICAL DIAGNOSIS
Characteristic diagnostic include: 1.The development papulo
vesikular eruption after a brief and mild (or absent) prodrome symptoms.
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.
LABORATORY DIAGNOSIS
biopsies for
5.Serologic tests.
TREATMENT
Antiviral agents :
Acyclovir.
Famciclovir. Laciclovir. Vidarabine. Foscarnet.
TREATMENT OF VARICELLA
1.Generally benign and selflimited. 2.Locally : Cool compresses. Calamine lotion. Orally : Antihistamines. Antipyretics. Antiviral agents.
1.Passive immunization.
2.Chemoprophylactic.