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Chickenpox
is an acute, systemic, usually childhood infection caused by the
varicella-zoster virus (human herpesvirus type 3). It usually begins
with mild constitutional symptoms that are followed shortly by skin
lesions appearing in crops and characterized by macules, papules, vesicles,
and crusting. Patients at risk of severe neurologic or other systemic complications
(eg, pneumonia) include adults, newborns, and patients who are immunocompromised
or have certain underlying medical conditions. Diagnosis is clinical.
Those at risk of severe complications receive postexposure prophylaxis
with immune globulins, and, if disease develops, treatment with
antiviral drugs (eg, valacyclovir, famciclovir, acyclovir). Vaccination
provides effective prevention.
Chickenpox is caused by the varicella-zoster virus (human herpesvirus type 3), chickenpox being the acute invasive phase of the virus and herpes zoster (shingles) representing reactivation of the latent phase (see Herpesviruses: Herpes Zoster). Chickenpox, which is extremely contagious, is spread by infected droplets and is most communicable during the prodrome and early stages of the eruption. It is communicable from 48 h before the 1st skin lesions appear until the final lesions have crusted. Indirect transmission (by immune carriers) does not occur.
Epidemics occur in winter and early spring in 3- to 4-yr cycles. Some infants may have partial immunity, probably acquired transplacentally, until age 6 mo.
Symptoms,
Signs, and Diagnosis
In immunocompetent children, chickenpox is rarely severe. In adults and immunocompromised children, infection can be serious. Mild headache, moderate fever, and malaise may occur 11 to 15 days after exposure, about 24 to 36 h before lesions appear. This prodrome is more likely in patients > 10 yr and is usually more severe in adults.
The initial rash, a macular eruption, may be accompanied by an evanescent flush. Within a few hours, lesions progress to papules and then characteristic, sometimes pathognomonic, teardrop vesicles, often intensely itchy, on red bases. Lesions initially develop on the face and trunk and erupt in successive crops; some macules appear just as earlier crops begin to crust. The eruption may be generalized (in severe cases) or more limited but almost always involves the upper trunk. Ulcerated lesions may develop on the mucous membranes, including the oropharynx and upper respiratory tract, palpebral conjunctiva, and rectal and vaginal mucosa. In the mouth, vesicles rupture immediately, are indistinguishable from those of herpetic gingivostomatitis, and often cause pain on swallowing. Scalp lesions may produce tender, enlarged suboccipital and posterior cervical lymph nodes. New lesions usually cease to appear by the 5th day, and the majority are crusted by the 6th day; most crusts disappear < 20 days after onset.
Secondary bacterial infection (typically streptococcal or staphylococcal) of the vesicles may occur, causing cellulitis or rarely streptococcal toxic shock. Pneumonia may complicate severe chickenpox in adults, newborns, and immunocompromised patients of all ages but usually not in immunocompetent young children. Myocarditis, transient arthritis or hepatitis, and hemorrhagic complications may also occur.
Encephalopathy occurs in < 1/1000 cases, usually as the disease resolves or within the next 2 wk. Complete neurologic recovery is likely, although rarely persistent deficits or death occurs. One of the most common neurologic complications is acute postinfectious cerebellar ataxia. Transverse myelitis, cranial nerve palsies, and multiple sclerosis–like clinical manifestations have also occurred. Reye's syndrome (see Miscellaneous Disorders in Infants and Children: Reye's Syndrome), a rare but severe childhood complication, may begin 3 to 8 days after onset of the rash; aspirin increases the risk. In adults, encephalitis, which can be life threatening, occurs in 1 to 2/1000 cases of chickenpox.
Chickenpox is suspected in patients with the characteristic rash, which is usually the basis for diagnosis. The rash may be confused with that of other viral skin infections. If the diagnosis is in doubt, laboratory confirmation can be performed; it requires immunofluorescent detection of viral antigen in lesions or culture or serologic findings. Samples are generally obtained with scraping and transported to the laboratory in viral media.
Prognosis
and Treatment
Chickenpox in childhood is rarely severe. Severe or fatal disease is more likely in adults, patients with depressed T-cell immunity (eg, lymphoreticular malignancy), and those receiving corticosteroids or chemotherapy.
Mild cases require only symptomatic treatment. Relief of itching and prevention of scratching, which predisposes to secondary bacterial infection, may be difficult. Wet compresses, or, for severe itching, systemic antihistamines and colloidal oatmeal baths may help. Simultaneous use of large doses of systemic and topical antihistamines can produce encephalopathy and should be avoided.
To prevent secondary bacterial infection, patients should bathe regularly and keep their underclothing and hands clean and their nails clipped. Antiseptics should not be applied unless lesions become infected; infection is treated with antibiotics.
Oral antivirals, when given to immunocompetent hosts within 24 h of the onset of rash, slightly decrease symptom duration and severity. However, because the disease is generally benign in children, antiviral treatment is not routinely recommended. Oral valacyclovir , famciclovir , or acyclovir should be strongly considered for immunocompromised patients and for healthy people at risk for moderate to severe disease, including all patients ≥ 12 yr, those with skin disorders (particularly eczema) or chronic lung disease, and those receiving salicylate or corticosteroid therapy. The dose of famciclovir is 500 mg tid and of valacyclovir is 1 g tid. Acyclovir is a less desirable choice because of its poorer oral bioavailability but can be given at 20 mg/kg qid with a maximum daily dose of 3200 mg. Immunocompromised children > 1 yr should be given 500 mg/m2 q 8 h.
Patients should not return to school or work until the final lesions have crusted.
Prevention
Infection provides lifelong protection. All healthy children and susceptible adults should receive doses of live attenuated varicella vaccine (see Approach to the Care of Normal Infants and Children:Health Supervision of the Well Child Fig. for Fig. 3: Approach to the Care of Normal Infants and Children: Recommended childhood and adolescence immunization schedule. ). Vaccination is particularly important in women of child-bearing age and adults with underlying chronic medical conditions. Serologic testing to determine immune status before vaccination in adults is usually not required. Vaccination is contraindicated in patients with moderate to severe concurrent illness, immunocompromised patients, pregnant women, patients on high doses of systemic corticosteroids, and children using salicylates. Although the vaccine may cause chickenpox in immunocompetent patients, disease is usually mild (< 10 papules or vesicles) and brief and produces few systemic symptoms.
Following exposure, chickenpox can be prevented or attenuated by IM administration of varicella-zoster immune globulin (VZIG), prepared from pooled plasma containing high titers of specific antibody. Candidates for postexposure prophylaxis include people with leukemia, immunodeficiencies, or other severe debilitating illness; susceptible pregnant women; and newborns whose mothers developed chickenpox within 5 days before or 2 days after delivery. VZIG 12.5 units/kg IM (100 units/mL) up to 625 units must be given within 4 days of exposure. Postexposure vaccination may modify or prevent varicella if administered within 3 days (and possibly up to 5 days) after exposure. Vaccination should be given as soon as possible in susceptible patients eligible for vaccination. Potentially susceptible individuals should take strict precautions to avoid people capable of transmitting the infection.
Last full review/revision November 2005
Content last modified November 2005
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