Chickenpox: Difference between revisions

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==Treatment==
==Treatment==
[[Chickenpox medical therapy|Medical therapy]] | [[Chickenpox surgery|Surgical options]] | [[Chickenpox primary prevention|Primary prevention]]  | [[Chickenpox secondary prevention|Secondary prevention]] | [[Chickenpox cost-effectiveness of therapy|Financial costs]] | [[Chickenpox future or investigational therapies|Future therapies]]
[[Chickenpox medical therapy|Medical therapy]] | [[Chickenpox surgery|Surgical options]] | [[Chickenpox primary prevention|Primary prevention]]  | [[Chickenpox secondary prevention|Secondary prevention]] | [[Chickenpox cost-effectiveness of therapy|Financial costs]] | [[Chickenpox future or investigational therapies|Future therapies]]
==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 [[conjunctiva]]e or the [[mucosa]]e of the [[upper respiratory tract]]. Viral proliferation occurs in regional [[lymph node]]s 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]] [[Endothelium|endothelial cells]] and the [[Epidermis (skin)|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) [[Antibody|antibodies]]; IgG antibodies persist for life and confer immunity. [[Cell-mediated 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 [[mucosa]]l and [[Epidermis (skin)|epidermal]] lesions to local [[sensory nerve]]s. VZV then remains latent in the [[Dorsal root ganglion|dorsal ganglion]] cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (shingles).


==Diagnosis==
==Diagnosis==

Revision as of 15:38, 27 January 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

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Pathophysiology

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Causes

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Diagnosis

History and Symptoms | Physical Examination | Staging | Laboratory tests | Electrocardiogram | X Rays | CT | MRI Echocardiography or Ultrasound | Other images | Alternative diagnostics

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Diagnosis

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 reposnse. 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 (IgE).[1]

Prenatal diagnosis of foetal 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.[2]

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 5-10 days.[3] It takes from 10-21 days after contact with an infected person for someone to develop chickenpox.[4]

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 be a week before new lesions stop appearing and existing lesions crust over. Children are not to be sent back to school until all lesions have crusted over.[5]

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. People with chickenpox, in fact, 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

Varicella infection in pregnant women can lead to viral transmission via the placenta and infection of the foetus. If infection occurs during the first 28 weeks of gestation, this can lead to foetal varicella syndrome (also known as congenital varicella syndrome). Effects on the foetus can range in severity from underdeveloped toes and fingers to severe anal and bladder malformation. Possible problems include:

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 nenoate 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. [2]

Treatment

Chickenpox infection tends to be milder the younger a child is and symptomatic treatment, with a little sodium bicarbonate in baths or antihistamine medication to ease itching,[6] and paracetamol (acetaminophen) to reduce fever, are widely used. Ibuprofen can also be used on advice of a doctor. However, aspirin or products containing aspirin must not be given to children with chickenpox (or any fever-causing illness), as this risks causing the serious and potentially fatal Reye's Syndrome. [7]

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.[8].

It is important to maintain good hygiene and daily cleaning of skin with warm water to avoid secondary bacterial infection. 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.

Prognosis

Chickenpox infection is milder in young children, and symptomatic treatment, with a sodium bicarbonate baths or antihistamine medication may ease itching.[9] 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), as this risks causing the serious and potentially fatal Reye's Syndrome. [10]

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. [2] Inflammation of the brain, or encephalitis, can occur in immunocompromised individuals, although the risk is higher with herpes zoster.[11]Necrotizing fasciitis[12] 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.

Vaccination

A varicella vaccine has been available 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.[13]

In the UK, varicella antibodies are measured as part of the routine of prenatal care, and by 2005 all NHS healthcare personnel had determined their immunity and been immunised if they were non-immune and have direct patient contact. Population-based immunization against varicella is not otherwise practiced in the UK, because of lack of evidence of lasting efficacy or public health benefit.

Normal Reactions to vaccine are

  • Fever of 101.9 (38.9 C) up to 42 days after Injection
  • Soreness, inching at the site of injection within 2 days
  • Rash occurring at site of injection anywhere form 8 to 19 days after injection. If this happens you are considered contagious.
  • Rash on other parts of body anywhere from 5 to 26 days after injection. If this happens you are considered contagious.

What to do should reaction occur

Control fever and lessen discomfort, take medication containing acetaminophen, (AKA paracetamol) such as

References

  1. McPherson & Pincus: Henry's Clinical Diagnosis and Management by Laboratory Methods, 21st ed., 2007, Chapter 54.
  2. 2.0 2.1 2.2 Royal College of Obstetricians and Gynaecologists (September 2007). "Chickenpox in Pregnancy" (PDF). Retrieved 2008-04-12.
  3. New Zealand Dermatological Society (14 Jan 2006). "Chickenpox (varicella)". Retrieved 2006-08-18.
  4. "General questions about the disease". Varicella Disease (Chickenpox). CDCP. December 2 2001. Retrieved 2006-08-18. Check date values in: |date= (help)
  5. Heather Brannon (December 25, 2005). "Chicken Pox - Varicella Virus Infection". Retrieved 2006-08-18.
  6. Somekh E, Dalal I, Shohat T, Ginsberg GM, Romano O (2002). "The burden of uncomplicated cases of chickenpox in Israel". J. Infect. 45 (1): 54–7. PMID 12217733.
  7. US Centers for Disease Control and Prevention. "Varicella Treatment Questions & Answers". CDC Guidelines. CDC. Retrieved 2007-8-23. Check date values in: |accessdate= (help)
  8. Tebruegge M, Kuruvilla M, Margarson I (2006). "Does the use of calamine or antihistamine provide symptomatic relief from pruritus in children with varicella zoster infection?". Arch. Dis. Child. 91 (12): 1035–6. doi:10.1136/adc.2006.105114. PMID 17119083. Text "format-Abstract" ignored (help)
  9. Somekh E, Dalal I, Shohat T, Ginsberg GM, Romano O (2002). "The burden of uncomplicated cases of chickenpox in Israel". J. Infect. 45 (1): 54–7. PMID 12217733.
  10. US Centers for Disease Control and Prevention. "Varicella Treatment Questions & Answers". CDC Guidelines. CDC. Retrieved 2007-08-23.
  11. "Definition of Chickenpox". MedicineNet.com. Retrieved 2006-08-18.
  12. "Is Necrotizing Fasciitis a complication of Chickenpox or of Cutaneous Vasculitis?". atmedstu.com. Retrieved 2008-01-18.
  13. Chaves SS, Gargiullo P, Zhang JX; et al. (2007). "Loss of vaccine-induced immunity to varicella over time". N Engl J Med. 356 (11): 1121&ndash, 9. PMID 17360990.

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