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Wednesday, October 31, 2007


Compiled and Summarized by Anthony
Chickenpox is the common name for Varicella zoster, classically one of the childhood infectious diseases caught by and survived by almost every child.

Chickenpox is caused by the varicella-zoster virus (VZV), also known as human herpes virus 3 (HHV-3), one of the eight herpes viruses known to affect humans. It starts with conjunctival and catarrhal symptoms and then characteristic spots appearing in two or three waves, mainly on the body and head rather than the hands and becoming itchy raw pox (pocks), small open sores which heal mostly without scarring.

Chickenpox has a 14-16 day incubation period and is highly contagious through physical contact two days before symptoms appear. Following primary infection, there is usually lifelong protective immunity from further episodes of chickenpox. Recurrent chickenpox, commonly known as shingles, is fairly rare but more likely in people with compromised immune systems.

Chickenpox is rarely fatal (usually from varicella pneumonia), with pregnant women and those with a suppressed immune system being more at risk. Pregnant women not known to be immune and who come into contact with chickenpox may need urgent treatment as the virus can cause serious problems for the baby. This is less of an issue after 20 weeks.

Later in life, viruses remaining dormant in the nerves can reactivate causing localized eruptions of shingles. This occurs particularly in people with compromised immune systems, such as the elderly, and perhaps even those suffering sunburn. Unlike chickenpox which normally fully settles, shingles may result in persisting post-herpetic neuralgia pain.

Signs and Symptoms

Chickenpox is a highly contagious disease that spreads from person to person by direct contact or through the air from an infected person's coughing or sneezing. Touching the fluid from a chickenpox blister can also spread the disease. A person with chickenpox is contagious from one to two days before the rash appears until all blisters have formed scabs. This may take five to 10 days. It takes from 10-21 days after contact with an infected person for someone to develop chickenpox.

The chickenpox lesions (blisters) start as a two to four millimeter red papule which develops an irregular outline (a rose petal). A thin-walled, clear vesicle (dew drop) develops on top of the area of redness. This "dew drop on a rose petal" lesion is very characteristic for chickenpox. After about eight to 12 hours the fluid in the vesicle gets cloudy and the vesicle breaks leaving a crust. The fluid is highly contagious, but once the lesion crusts over, it is not considered contagious. The crust usually falls off after seven days sometimes leaving a crater-like scar. Although one lesion goes through this complete cycle in about seven days, another hallmark of chickenpox is the fact that new lesions crop up every day for several days. Therefore, it may take about a week until new lesions stop appearing and existing lesions crust over. Children are not to be sent back to school until all lesions have crusted over.

Secondary infections, such as inflammation of the brain, can occur in immunocompromised individuals. This is more dangerous with shingles.

Chickenpox is highly contagious and is spread through the air when infected people cough or sneeze, or through physical contact with fluid from lesions on the skin. Zoster, also known as shingles, is a reactivation of chickenpox and may also be a source of the virus for susceptible children and adults. It is not necessary to have physical contact with the infected person for the disease to spread. Those infected can spread chickenpox before they know they have the disease - even before any rash develops. In fact, people with chickenpox can infect others from about two days before the rash develops until all the sores have crusted over, usually four to five days after the rash starts.

Congenital defects in babies

These may occur if the child's mother was exposed to the zoster virus during pregnancy. Effects on the fetus may be minimal in nature but physical deformities range in severity from under developed toes and fingers, to severe anal and bladder malformation. Possible problems include:

· Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain
· Damage to the eye (optic stalk, optic cap, and lens vesicles), microphthalmia, cataracts, chorioretinitis, optic atrophy
· Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner's syndrome
· Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction
· Skin disorders: (cicatricial) skin lesions, hypopigmentation

Causative Agent

Human herpesvirus 3 (alpha) or varicella zoster virus (VZV) is the causative agent.

Mode of Transmission

Chickenpox transmission is mainly person to person by airborne respiratory droplets but also by direct contact with vesicle fluid of chickenpox cases, or contact with the vesicle fluid of patients with herpes zoster. Indirect contact occurs through articles freshly soiled by discharges from vesicles of infected persons. Scabs are not infective.


Confirmation of the diagnosis is generally only required when the clinical picture is atypical. It is made by:

· isolation of the virus in cell cultures
· visualisation by electron microscopy
· serological tests for antibodies
· immunofluorescence on lesion swab or fluid
· nucleic acid testing or PCR.

Incubation Period

14-16 days (13-17 days in some books)


Little is known about the route and the source of transmission of the virus. VZV is certainly transmissible through the airborne route and does not require close personal contact. The skin lesions are certainly full of infectious virus particles whilst in contrast, it is almost impossible to isolate virus from the upper respiratory tract. It is possible that aerial transmission originates from symptomless oral lesions. The virus is thought to gain entry via the respiratory tract and spreads shortly after to the lymphoid system. After an incubation period of 14 days, the virus arrives at its main target organ, the skin. The virus probably spreads to other organ systems in the body without any ill effect. However, in immunocompromised individuals and neonates, dissemination can cause serious infection of the lungs and brain. Recovery from infection is thought to result in lifelong immunity.

Following the primary infection, the virus remains latent in the cerebral or posterior root ganglia. In 10 - 20% of individuals, a single recurrent infection occurs after several decades. The virus reactivates in the ganglion and tracks down the sensory nerve to the area of the skin innervated by the nerve, producing a varicellaform rash in the distribution of a dermatome. The failure of the host defense mechanisms to contain the virus in the ganglia after such prolonged periods of time is not understood. In immunocompetent individuals, it is probably due to the decline effectiveness of previously acquired immunity with advancing age. Herpes zoster also appears in increasing frequency in immunocompromised individuals such as those with Hodgkin's disease and AIDS, who have defective CMI. Also disseminated herpes zoster is more likely to occur in such people.


Chickenpox is usually acquired by the inhalation of airborne respiratory droplets from an infected host. The highly contagious nature of VZV explains the epidemics of chickenpox that spread through schools as one child who is infected quickly spreads the virus to many classmates. High viral titers are found in the characteristic vesicles of chickenpox; thus, viral transmission may also occur through direct contact with these vesicles, although the risk is lower.

After initial inhalation of contaminated respiratory droplets, the virus infects the conjunctivae or the mucosae of the upper respiratory tract. Viral proliferation occurs in regional lymph nodes of the upper respiratory tract 2-4 days after initial infection and is followed by primary viremia on postinfection days 4-6. A second round of viral replication occurs in the body's internal organs, most notably the liver and the spleen, followed by a secondary viremia 14-16 days postinfection. This secondary viremia is characterized by diffuse viral invasion of capillary endothelial cells and the epidermis. VZV infection of cells of the malpighian layer produces both intercellular edema and intracellular edema, resulting in the characteristic vesicle.

Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity. Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (shingles).


The varicella-zoster virus is spread through direct contact with a person that is infected and through the air with fluid from the rash or respiratory secretions. An infected person can spread the virus from 5 days before the rash develops until all lesions have crusted.

Currently, the best way to prevent illness is by vaccine, which is 85% effective.

People with chickenpox should remain at home until no new lesions are forming and all present lesions have crusted. This is generally a period of four to five days for persons with a healthy immune system.

Infected persons with compromised immune systems may continue to form new lesions and remain infectious for a longer period of time.

People with shingles should cover their rash before leaving the house. Care should be taken to wash hands after touching chickenpox or shingles rashes.


For most health children, chickenpox symptoms can be controlled with soothing baths or antihistamines to decrease itching. Acetaminophen may help control fever, headache, or muscle pain. Do not give aspirin to children with chickenpox, because this can increase the child's risk of Reye syndrome.

A prescription drug called acyclovir is FDA approved to treat the symptoms of chickenpox in persons older than age 2. The drug should help reduce the severity of chickenpox symptoms, especially in older children and teenagers, if taken within 24 hours of the rash's first appearance. However, this drug is generally only used in severe cases of chickenpox and in patients who have weakened immune systems, such as persons with cancer and who have had an organ transplant.

A vaccine to prevent chickenpox is available for children over age 1.

Drug-related information can be found here.


Secondary bacterial infection of skin lesions, manifesting as impetigo, cellulitis, and erysipelas, is the most common complication in healthy children.

o Staphylococci and streptococci are the most commonly implicated bacterial pathogens.
o Bacterial superinfection may predispose to scarring. Localized bacterial superinfection rarely may manifest in septicemia, culminating in secondary bacterial pneumonia, otitis media, or necrotizing fasciitis.

Disseminated primary varicella infection, usually seen in the immunocompromised or adult populations, may have high morbidity. Ninety percent of cases of varicella pneumonia occur in the adult population. Rarer complications of disseminated chickenpox also include myocarditis, hepatitis, and glomerulonephritis.

Central nervous system complications of primary VZV infection may occur, albeit very rarely. Reye syndrome, Guillain-Barré syndrome, acute cerebellar ataxia, and encephalitis have all been documented to occur after VZV infection.

Thrombocytopenia and purpura secondary to VZV infection have been described in more than 100 patients.

o Hemorrhagic complications are more common in the immunocompromised or immunosuppressed populations, although healthy children and adults have been affected. Five major clinical syndromes have been described: febrile purpura, malignant chickenpox with purpura, postinfectious purpura, purpura fulminans, and anaphylactoid purpura.

o These syndromes have variable courses, with febrile purpura being the most benign of the syndromes and having an uncomplicated outcome. In contrast, malignant chickenpox with purpura is a grave clinical condition that has a mortality rate of greater than 70%. The etiology of these hemorrhagic chickenpox syndromes is not known, although an autoimmune pathophysiologic mechanism has been implicated.


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