Chickenpox or chicken pox is a highly contagious illness caused by primary infection with varicella zoster virus (VZV). It generally begins with a vesicular skin rash 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 an incubation period of 10 to 21 days, and is spread easily through coughs or sneezes 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 has been observed in nonhuman primates, including chimpanzees [1] and gorillas [2] [3].
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Signs and symptoms
Chickenpox is a highly infectious 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 infectious from one to five days before the rash appears. The contagious period continues until all blisters have formed scabs, which may take 5 to 10 days.[1] It takes from 10 to 21 days after contact with an infected person for someone to develop chickenpox.[2]
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.[3]
It is not necessary to have 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 in pregnancy and neonates
For pregnant women, antibodies produced as a result of immunisation or previous infection are transferred via the placenta to the fetus.[4] Women who are immune to chickenpox cannot become infected and do not need to be concerned about it for themselves or their infant during pregnancy.[5]
Varicella infection in pregnant women can lead to viral transmission via the placenta and infection of the fetus. If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella syndrome (also known as congenital varicella syndrome). Effects on the fetus can range in severity from underdeveloped 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
Infection late in gestation or immediately following birth 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 following the birth. The baby 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. [6]
Pathophysiology
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 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), and sometimes Ramsay Hunt syndrome type II.
Diagnosis
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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).[7]
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.[6]
Prevention
A varicella vaccine was first developed by Michiaki Takahashi in 1974 derived from the Oka strain. It has been available in the U.S. since 1995 to inoculate against the disease. Some countries require the varicella vaccination or an exemption before entering elementary school. Protection is not lifelong and further vaccination is necessary five years after the initial immunization.[8]
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.[9][10]
Treatment
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There is no evidence to support the effectiveness of topical application of calamine lotion, a topical barrier preparation containing zinc oxide in spite of its wide usage and excellent safety profile.[11] It is important to maintain good hygiene and daily cleaning of skin with warm water to avoid secondary bacterial infection.[citation needed]. Addition of a small quantity of vinegar to the water is sometimes advocated. [12]
To relieve the symptoms of chicken pox, people commonly use anti-itching creams and lotions. These lotions are not to be used on the face or close to the eyes. An oatmeal bath also might help ease discomfort.[citation needed].
[edit] Children
If oral aciclovir is started within 24 hours of rash onset it decreases symptoms by one day but has no effect on complication rates. Use of acyclovir therefore is not currently recommended. [13]
Adults
Infection in otherwise healthy adults tends to be more severe and active; treatment with antiviral drugs (e.g. aciclovir) is generally advised, as long as it is started within 24-48 hours from rash onset.[citation needed] 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.
[edit] Special populations
If exposure to varicella in certain 'at risk' populations is confirmed (immunosuppressed individuals, pregnant seronegative women, neonates), anti-varicella zosterimmunoglobulin may be given prior to onset of disease symptoms.this is not true for some cases .
Prognosis
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The duration of the visible blistering caused by varicella zoster virus varies in children usually from 4 to 7 days, and the appearance of new blisters begins to subside after the 5th day. Chickenpox infection is milder in young children, and symptomatic treatment, with sodium bicarbonate baths or antihistamine medication may ease itching.[14] Paracetamol (acetaminophen) is widely used to reduce fever. Aspirin, or products containing aspirin, must not be given to children with chickenpox (or any fever-causing illness suspected of being of viral origin), as this risks causing the serious and potentially fatal Reye's Syndrome.[15]
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. [6] Inflammation of the brain, or encephalitis, can occur in immunocompromised individuals, although the risk is higher with herpes zoster.[16] Necrotizing fasciitis[17] 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.[18]
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
Epidemiology
Primary varicella is an endemic disease. Cases of varicella are seen throughout the year but more commonly in winter and early spring. This is unlike enteroviruses and lends some support to the view that, like measles and rubella, varicella is spread mainly by the respiratory route. In contrast, herpes zoster occurs sporadically and evenly throughout the year. Varicella is one of the classic diseases of childhood, with the highest prevalence in the 4–10 age group. Like rubella, it is uncommon in preschool children. Varicella is highly communicable, with an infection rate of 90% in close contacts. Most people become infected before adulthood but 10% of young adults remain susceptible. However, this pattern of infection is not universal, e.g. in rural India, varicella is predominantly a disease of adults, with the mean age of infection 23.4 years. It has been suggested that this could be due to interference by other respiratory viruses that children are exposed to.[19]
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.[19]
History
Chickenpox was first identified by the Persian physician, Muhammad ibn Zakariya ar-Razi (865–925), known to the West as "Rhazes", who clearly distinguished it from smallpox and measles.[20] Giovanni Filippo (1510–1580) of Palermo later provided a more detailed description of varicella (chickenpox). Subsequently in the 1600s, an English physician named Richard Morton described what he thought a mild form of smallpox as "chicken pox". Later, in 1767, a physician named William Heberden, also from England, was the first physician to clearly demonstrate that chickenpox was different from smallpox. However, it is believed the name chickenpox was commonly used in earlier centuries before doctors identified the disease.
There are many explanations offered for the origin of the name chickenpox:
- Persian name: "آبله مرغان" literally means chickens (birds) pox;
- Samuel Johnson suggested that the disease was "less dangerous", thus a "chicken" version of the pox;
- the specks that appear looked as though the skin was pecked by chickens;
- the disease was named after chick peas, from a supposed similarity in size of the seed to the lesions;
- the term reflects a corruption of the Old English word giccin, which meant itching.
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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