Varicella (chickenpox) is an acute
vesicular exanthem caused by the varicella-zoster virus, an agent that
has a worldwide distribution and for which humans are the only known
host.
There are
no animal reservoirs.
VZV (HHV3) is
a neurotrophic alpha-herpesvirus.
Visit:Herpes Simplex Virus Infection
;Herpes Zoster(Shingles)
;Smallpox
VZV is named
after : Varicella, an alternative name for chickenpox (the primary VZV
infection) Zoster, another name for shingles (reactivation of latent
VZV infection).
Although all age groups are
susceptible, in temperate zones chickenpox affects mostly children and
in the tropics mostly young adults.
The virus, which is spread through
inhalation of droplets or by direct contact is highly contagious from
about 24 hours before the initial eruption to a week of more
thereafter.
Although infection with varicella-zoster
virus establishes lifelong immunity and chickenpox does not recur, the
latent viral genome may be activated years later to cause shingles.
Nonimmune persons (usually children)
are susceptible to primary infection with varicella-zoster virus.
Chickenpox begins as a “silent”
infection of the nasopharynx, with local replication of varicella-zoster
virus.
After an incubation period of 10 to 23
days, the virus enters the bloodstream, causing viremia and a sudden
onset of fever, malaise, and anorexia.
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In the circulation it seeds
reticuloendothelial cells, an effect that leads to secondary waves of
viremia.
The virus then disseminates to skin and
viscera, and within 24 hours a red maculopapular eruption develops,
usually on the upper trunk and face.
The papules rapidly become clear
vesicles with an erythematous base.
In the next 24 hours, the vesicles
become cloudy, the eruption begins to itch, and scratching may rupture
the vesicles.
Separate crops appear for 3 to 6 days
and spread peripherally.
After the last crop, the scabs heal
withour scarring.
Though vesicles of the skin are
generally painless, painful lesions may develop on mucous membranes,
such as the cornea and tympanic membrane.
Complications include pneumonia,
encephalitis, hepatitis, carditis, keratitis, orchitis, arthritis,
hemorrhages and acute encephalopathy with fat accumulation in the
viscera (Reye’s syndrome).
Histologically, the skin lesions
initially show ballooning of epidermal cells.
Later, unilocular vesicles containing
proteinaceous fluid, degenerating cells and syncytial giant cells are
seen.
Cowdry type A intranuclear inclusions
are seen in epidermal cells, endothelial cells of superficial
capillaries, reticuloendothelial cells, and fibroblasts.
The affected organs in chicken pox
exhibit spherical foci of coagulative necrosis.
At the margin of these necrotic foci,
surviving cells contain intranuclear inclusions.
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