Contagious viral disease producing itchy blisters. It usually occurs in epidemics among young children, causes a low fever, and runs a mild course, leaving patients immune. The blisters can scar if scratched. The virus that causes chickenpox (varicella-zoster virus) can reactivate years later, causing shingles. Zoster immune globulin (ZIG) can prevent chickenpox in children with leukemia or immunodeficiency disorders who are exposed to the virus. A vaccine has also been developed.
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Chickenpox is a highly contagious illness caused by primary infection with varicella zoster virus (VZV). It generally begins 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 pockmarks, small open sores which heal mostly without scarring.
Chickenpox has a 10-21 day incubation period and is spread easily through aerosolized droplets from the nasopharynx of ill individuals or through direct contact with secretions from the rash. Following primary infection there is usually lifelong protective immunity from further episodes of chickenpox.
Chickenpox is rarely fatal, although it is generally more severe in adults than in children. Pregnant women and those with a suppressed immune system are at highest risk of serious complications. The most common late complication of chicken pox is shingles, caused by reactivation of the varicella zoster virus decades after the initial episode of chickenpox.
Chickenpox is a highly contagious disease that spreads from person to person by direct contact or by 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 five days before the rash appears until all blisters have formed scabs. This may take 5 to 10 days. It takes from 10 to 20 days after contact with an infected person for someone to develop chickenpox.
The chicken pox 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 of chickenpox. After about 8 to 12 hours the fluid in the vesicle becomes 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 that new lesions crop up every day for several days. Therefore it may be a week before new lesions stop appearing and existing lesions crust over. Children should not be sent back to school until all lesions have crusted over.
It is not necessary to have physical contact with the infected person for the disease to spread. Infected persons can spread chickenpox before they know they have the disease, i.e. before any rash develops. They can infect others from about two days before the rash develops until all the sores have crusted over, usually four or five days after the rash starts.
Infection late in gestation or immediately post-partum is referred to as neonatal varicella. Maternal infection is associated with premature delivery. The risk of the baby developing the disease is greatest following exposure to infection in the period 7 days prior to delivery and up to 7 days post partum. The neonate may also be exposed to the virus via infectious siblings or other contacts, but this is of less concern if the mother is immune. Newborns who develop symptoms are at a high risk of pneumonia and other serious complications of the disease.
After initial inhalation of contaminated respiratory droplets, the virus infects 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 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 diagnosis of varicella is primarily clinical. In a non-immunized individual with typical prodromal symptoms associated with the appropriate appearing rash occurring in "crops", no further investigation would normally be undertaken.
If further investigation is undertaken, confirmation of the diagnosis can be sought through either examination of the fluid within the vesicles, or by testing blood for evidence of an acute immunologic response. Vesicle fluid can be examined with a Tsanck smear, or better with examination for direct fluorescent antibody. The fluid can also be "cultured", whereby attempts are made to grow the virus from a fluid sample. Blood tests can be used to identify a response to acute infection (IgM) or previous infection and subsequent immunity (IgG).
Prenatal diagnosis of fetal varicella infection can be performed using ultrasound, though a delay of 5 weeks following primary maternal infection is advised. A PCR (DNA) test of the mother's amniotic fluid can also be performed, though the risk of spontaneous abortion due to the amniocentesis procedure is higher than the risk of the baby developing foetal varicella syndrome.
In the United Kingdom, varicella antibodies are measured in women with no history of the disease as part of routine prenatal care. By 2005 all National Health Service personnel had determined their immunity and been immunized if they were non-immune and have direct patient contact. Population-based immunization against varicella is not otherwise practiced in the UK. It is feared that there would be a greater number of cases of shingles in adults, until the vaccination was given to the entire population—because adults who have had chickenpox as a child are less likely to have shingles in later life if they have been exposed occasionally to the chickenpox virus (for example by their children). This is because the exposure acts as a booster vaccine.
If exposure to varicella in certain 'at risk' populations is confirmed (immunosuppressed individuals, pregnant seronegative women, neonates), anti-varicella zoster immunoglobulin may be given prior to onset of disease symptoms.
Infection in otherwise healthy adults tends to be more severe and active; treatment with antiviral drugs (e.g. acyclovir) is generally advised. Patients of any age with depressed immune systems or extensive eczema are at risk of more severe disease and should also be treated with antiviral medication. In the U.S., 55 percent of chickenpox deaths are in the over-20 age group, even though they are a tiny fraction of the cases.
In adults, the disease can be more severe, though the incidence is much less common. Infection in adults is associated with greater morbidity and mortality due to pneumonia, hepatitis, and encephalitis. In particular, up to 10% of pregnant women with chickenpox develop pneumonia, the severity of which increases with onset later in gestation. In England and Wales, 75% of deaths due to chickenpox are in adults. Inflammation of the brain, or encephalitis, can occur in immunocompromised individuals, although the risk is higher with herpes zoster. Necrotizing fasciitis is also a rare complication.
Secondary bacterial infection of skin lesions, manifesting as impetigo, cellulitis, and erysipelas, is the most common complication in healthy children. 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.
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. 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.
Historically, varicella has been a disease predominantly affecting preschool and school-aged children. In adults the pock marks are darker and the scars more prominent than in children.
There are many explanations offered for the origin of the name chickenpox:
As "pox" also means curse, in medieval times some believed it was a plague brought on to curse children by the use of black magic.
During the medieval era, oatmeal was discovered to soothe the sores, and oatmeal baths are today still commonly given to relieve itching.
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