Varicella occurs throughout the world but infection occurs at a
younger age in temperate zones compared to the tropics. In temperate regions more
than 90% of adults are immune to varicella while in tropical countries only 60%
of adults are immune to it. Transmission is via the respiratory route and less commonly
by direct contact with the lesions. A susceptible person may develop varicella
following exposure to the lesions of herpes zoster. The severity of the disease
is age-dependent, with adults having more severe disease and more complications.
Varicella confers lasting immunity and second attacks are uncommon, especially
in immunologically healthy people, but clinical reinfection with a mild
varicella-like illness occasionally takes place.
The distinctive features of varicella are the centripetal distribution,
the polymorphism in each affected site and the rapid progression of the individual
lesion from vesicle to crust. Vesicles are common in the mouth, especially on
the palate, and are occasionally seen on other mucous membranes, including the
conjunctiva and genitalia. On the anal mucosa they may be followed by painful
ulcers.
Aciclovir is indicated for varicella in adults
and for severe varicella at any age in the immunocompromised. Therapy does not appear to alter the development of adequate
immunity to reinfection.
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Centripetal distribution
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Resolving rash. The virus is transmitted by droplet infection from the
nasopharynx. A brief first viraemic stage, when the virus can disseminate to
other organs, is followed by a second viraemia coinciding with the onset of the
rash. Patients are infectious to others from about 2 days before to 5 days
after the onset of the rash and most non-immune people will contract the
infection if exposed to someone in the infectious stage of varicella. Vesicle fluid
contains a large amount of virus. Completely dry scabs are not infectious.
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A characteristic feature is the presence of lesions at different
stages in each site. Papules very rapidly become vesicles that appear over around 4 days with centripetal distribution. Vesicles dry rapidly to become crusts within around 4 days. Crusts soon separate leaving shallow pink depressions that normally heal without scarring within around 2 weeks. Hyper- or hypopigmentation may persist for weeks and scars can occur in some.
This page was last updated in August 2014.
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