Chickenpox

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Chickenpox
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ICD-10 B01
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ICD-9 052
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Chickenpox, also spelled chicken pox, is the common name for Varicella simplex, classically one of the childhood infectious diseases caught and survived by most children.

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, moderate fever 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.

Effects

Child with varicella disease.

Chickenpox has a two-week incubation period and is highly contagious by air transmission two days before symptoms appear. Therefore, chickenpox spreads quickly through schools and other places of close contact. Once someone has been infected with the disease, they usually develop protective immunity for life. It is fairly rare to get the chickenpox multiple times, but it is possible for people with irregular immune systems. As the disease is more severe if contracted by an adult, parents have been known to ensure their children become infected before adulthood.

The disease can be fatal. Pregnant women and those with immune system depression are more at risk. Death is usually from varicella pneumonia. In the US, 55 percent of chickenpox deaths were in the over-20 age group. Pregnant women not known to be immune and who come into contact with chickenpox should contact their doctor immediately, as the virus can cause serious problems for the fetus. 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.

Later in life, viruses remaining in the nerves can develop into the painful disease shingles, particularly in people with compromised immune systems, such as the elderly, and perhaps even those suffering sunburn. Some of these will develop zoster-associated pain or post-herpetic neuralgia, described usually as "horrible" or "excruciating". A chickenpox vaccine has been available since 1995, and is now required in some countries for children to be admitted into elementary school. In addition, effective medications (e.g. aciclovir) are available to treat chickenpox in healthy and immunocompromised persons.

Symptomatic treatment—calamine lotion to ease itching and paracetamol to reduce fever—is widely used. Aspirin is contraindicated in children, as it can lead to Reye's syndrome.

History

One history of medicine book claims Giovanni Filippo (1510–1580) of Palermo the first description of varicella (chickenpox). Subsequently in the 1600s, an English physician named Richard Morton described what he thought was 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:

  • the specks that appear looked as though the skin was picked by chickens,
  • the disease was named after chick peas, from a supposed similarity in size of the seed to the lesions
  • Samuel Johnson suggested that the disease was "no very great danger," thus a "chicken" version of the pox
  • 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.

In 1998, Dr. Charles F. Grose and Dr. Richard Santos discovered a Mutant form of Chickenpox. This is phenotypic ally different from VZV 32, which is the wild type. The Mutant forms of viruses can often be attributed to contamination of the wild-type in nature. Mutant forms are becoming more frequent with time.

Infection

Chickenpox is highly infectious and 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 1-2 days before the rash appears and until all blisters have formed scabs. This may take between 5-10 days.[1] It takes from 10-21 days after contact with an infected person for someone to develop chickenpox.[2]

The chickenpox lesions (blisters) start as a 2-4 mm red papule which develops an irregular outline (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 8-12 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 7 days sometimes leaving a craterlike scar. Although one lesion goes through this complete cycle in about 7 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 sent back to school until all lesions have crusted over.[3]


Second infections with chickenpox occur in immunocompetent individuals, but are uncommon. Such second infections are rarely severe. A soundly-based conjecture being carefully assessed in countries with low prevalence of chickenpox due to immunisation, low birth rates, and increased separation is that immunity has been reinforced by sub-clinical challenges and this is now less common. This is more dangerous with shingles. There have been reported cases of repeat infections.[4][5]

Congenital defects in babies

These may occur if the child's mother was exposed to VZV during pregnancy. Effects to 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 cup, 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: zig zag (cicatricial) skin lesions, hypopigmentation

Vaccination

Japan was among the first countries to routinely vaccinate for chickenpox. Routine vaccination against varicella zoster virus is also performed in the United States, and the incidence of chickenpox has been dramatically reduced there (from 4 million cases per year in the pre-vaccine era to approximately 400,000 cases per year as of 2005). In Europe most countries do not currently vaccinate against varicella, though the vaccine is gaining wider acceptance. Australia, Canada, and other countries have now adopted recommendations for routine immunization of children and susceptible adults against chickenpox. Other countries, such as Germany and The United Kingdom have targeted recommendations for the vaccine, e.g. for susceptible health care workers at risk of varicella exposure.

Chickenpox is most often a mild disease, especially for children. Prior to the introduction of vaccine, there were around 4,000,000 cases per year in the US, mostly children, with typically 100 or fewer deaths. Though mostly children caught it, the majority of deaths (by as much as 80%) were among adults. Additionally, chickenpox involved the hospitalization of about 10,000 people each year.[6] During 2003 and the first half of 2004, the CDC reported eight deaths from varicella, six of whom were children or adolescents. These deaths and hospitalizations have substantially declined in the US due to vaccination,[1][2] though the rate of shingles infection has increased for the same reason. The vaccine has more recently been determined to be effective at preventing shingles (zoster) in persons 60 years of age and older, if administered regularly.[3]

The long-term duration of protection from varicella vaccine is unknown, but there are now persons vaccinated more than thirty years ago with no evidence of waning immunity, while others have become vulnerable in as few as 6 years. Assessments of duration of immunity are complicated in an environment where natural disease is still common, which typically leads to an overestimation of effectiveness, and we are only now entering an era in the US where the long-term efficacy of varicella vaccine can be accurately gauged.[4]

The vaccine is exceedingly safe: approximately 5% of children who receive the vaccine develop a fever or rash, but there have been no deaths yet (as of 1 May 2006) attributable to the vaccine despite more than 40 million doses being administered.[5] Cases of vaccine-related chicken pox have been reported in patients with a weakened immune system,[5][6] but no deaths.

The literature contains several reports adverse reactions following varicella vaccination,[7][8][9][10][11][12][13][14][15][16][17][18][19] including vaccine-strain zoster in children and adults.[20][21] A mean of 2,350 reports per year are attributed to varicella vaccine based on 20,004 cases reported to the Vaccine Adverse Event Reporting System (VAERS) database from May, 1995 through December, 2003. Minor events are known to be under-reported reported to VAERS.

Controversy

Mortality due to primary varicella has declined significantly in countries which make wide use of the varicella vaccine.[1][5] Zoster (shingles) occurs decades after varicella and unsurprisingly zoster incidence has not declined in multiple studies. It is too early to observe the effect on postherpetic neuralgia (PHN).

It has been claimed that shingles may increase after introduction of varicella vaccine.[22][7]. There is yet no evidence this has occurred, and it might occur in the absence of immunisation due to a general decrease in childhood infection for other reasons.[23]

Vaccination is common in the United States. 41 of the 50 states require immunization for children attending government-run schools. The vaccination is not routine in the United Kingdom. Debate continues in the UK on the time when it will be desirable to adopt routine chickenpox vaccination, and in the US opinions that it should be dropped, individually, or along with all immunizations, are also voiced.

Duration of immunity

Some vaccinated children have been found to lose their protective antibody in as little as five to eight years; however, according to the World Health Organization: "After observation of study populations for periods of up to 20 years in Japan and 10 years in the United States, more than 90% of immunocompetent persons who were vaccinated as children were still protected from varicella."[8] As time goes on, boosters may be determined to be necessary, and introduced. Persons infected after vaccine experience milder cases of chicken pox.[9]

Catching wild chickenpox as a child has been thought to commonly result in lifelong immunity, indeed parents have deliberately ensured this in the past with "pox parties" (and similarly for some other diseases such as rubella. See below.) Historically, exposure of adults to contagious children has boosted their immunity, reducing the risk of shingles.[10] Second episodes of chickenpox have been rare, but occur and probably more frequently in the UK latterly[citation needed] and definitely more frequently in the vaccine group. In one study, 30% of children had lost the antibody after five years, and 8% had already caught "wild" chickenpox in that five year period.[11]

The CDC and corresponding national organisations are carefully observing the failure rate which may be high compared with other modern vaccines - large outbreaks of chickenpox having occurred at schools which required their children to be vaccinated.[12][13][14][15][16].

Immunocompromise

The mortality rate in immunocompromised patients with disseminated herpes zoster is 5-15%, with most deaths from pneumonia. Vaccines, unfortunately are less effective among these high-risk patients, as well as being more dangerous because it is an attenuated live virus (see last footnote), but clearly immunisation before immunocompromise would be desirable.

Pox parties

A "pox party" is a party held by parents for the purpose of infecting their children with childhood diseases. Similar ideas have applied to other diseases, e.g. measles, but are now discouraged by doctors and health services. The rationale behind such parties is that guests exposed to the varicella virus will contract the disease and develop strong and persistent immunity, at an age before disaster is likely particularly from chickenpox or rubella. Such parties are now less common in mainstream communities. They are essentially a revival of primitive, pre-vaccination attempts at inoculation.

The first reference to such a practice is the letter of Lady Montagu to Sarah Chiswell describing the parties people in Istanbul made for the purpose of variolation - an effective technique for gaining immunity to smallpox, which she imported to England.

Pox parties have been portrayed in TV cartoons, including South Park ("Chickenpox") and The Simpsons ("Milhouse of Sand and Fog").

See also

  • Cowpox
  • List of diseases
  • List of vaccine-related topics
  • Monkeypox
  • Shingles
  • Smallpox
  • Vaccination schedule
  • Vaccine controversy

References
ISBN links support NWE through referral fees

   * Bernstein, Henry. Who Discovered Chickenpox?. Pediatrics Questions and Answers. Family Education Network. Retrieved on 2005-10-16.
   * Chickenpox (Varicella) Vaccine. Immunization Action Coalition: (October 2005). Retrieved on 2006-06-12.
   * U.S. Census Bureau. Countries Ranked by Population: 2006. International Data Base. Retrieved on 2005-10-16.
   * Centers for Disease Control and Prevention (CDC) (2005). "Varicella-related deaths—United States, January 2003-June 2004." (PDF). MMWR Morb Mortal Wkly Rep 54 (11): 272-4. PMID 15788992.
   * Thomas S, Wheeler J, Hall A (2002). "Contacts with varicella or with children and protection against herpes zoster in adults: a case-control study." (PDF). Lancet 360 (9334): 678-82. PMID 12241874.

Notes

  1. ↑ 1.0 1.1 Seward JF, Watson BM, Peterson CL, et al. (2002). Varicella disease after introduction of varicella vaccine in the United States, 1995–2000. JAMA 287 (5): 606–11. PMID 11829699.
  2. ↑ Nguyen HQ, Jumaan AO, Seward JF (2005). Decline in mortality due to varicella after implementation of varicella vaccination in the United States. N Engl J Med 352: 450–8. PMID 15689583.
  3. ↑ Oxman MN, Levin MJ, Johnson GR, et al (2005). A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults. N Engl J Med 352 pages=2271–84. PMID 15930418.
  4. ↑ Goldman GS (2005). Universal varicella vaccination: efficacy trends and effect on herpes zoster. Int J Toxicol 24 (4): 205–213. PMID 16126614.
  5. ↑ 5.0 5.1 5.2 Wise RP, Salive ME, Braun MM, et al. (2000). Postlicensure safety surveillance for varicella vaccine. JAMA 284 (10): 1271–9. PMID 10979114.
  6. ↑ Quinlivan MA, Gershon AA, Nichols RA, La Russa P, Steinberg SP, Breuer J (2006). Vaccine Oka Varicella-oster virus genotypes are monomorphic in single vesicles and polymorphic in respiratory tract secretions. J Infect Dis 193 (7): 927–30. PMID 16518753.
  7. ↑ Ravkina LI, Matsevich GR (1970). Morphological changes in the central nervous system in post-vaccinal encephalomyelitis developing after chickenpox vaccination in children. Zh Nevropatol Psikhiatr Im S S Korsakova 70 (10): 1465–71. PMID 4395233.
  8. ↑ Sunaga Y, Hikima A, Ostuka T, Morikawa A (1995). Acute cerebellar ataxia with abnormal MRI lesions after varicella vaccination. Pediatr Neurol 13 (4): 340–2. PMID 8771172.
  9. ↑ Singer S, Johnson CE, Mohr R, Holowecky C (1995). Urticaria following varicella vaccine associated with gelatin allergy. Vaccine 17 (4): 327–9. PMID 9987170.
  10. ↑ Gerecitano J, Friedman-Kien A, Chazen GD (1997). Allergic reaction to varicella vaccine. Ann Intern Med 126 (10): 833–4. PMID 9148672.
  11. ↑ Sakaguchi M, Yamanaka T, Ikeda K, Sano Y, Fujita H, Miura T, Inouye S (1997). IgE-mediated systemic reactions to gelatin included in the varicella vaccine. J Allergy Clin Immonol 99 (2): 263–4. PMID 9042057.
  12. ↑ Naruse H, Miwata H, Ozaki T, Asano Y, Namazue J, Yamanishi K (1993). Varicella infection complicated with meningitis after immunization. Acta Paediatr Jpn 35 (4): 345–7. PMID 8397466.
  13. ↑ Lee SY, Komp DM, Andiman W (1986). Thrombocytopenic Purpura following varicella-zoster vaccination. Am J Pediatr Hematol Oncol 8 (1): 78–80. PMID 3013041.
  14. ↑ Wrensch M, Weinberg A, Wiencke J, Miike R, Barger G, Kelsey K (2001). Prevalence of antibodies to four herpesviruses among adults with glioma and controls. Am J Epidem 154 (2): 161–5. PMID 11447050.
  15. ↑ Naseri A, Good WV, Cunningham ET Jr (2003). Herpes zoster virus sclerokeratitis and anterior uveitis in a child following varicella vaccination. Am J Ophthalmol 135 (3): 415–7. PMID 12614776.
  16. ↑ Esmaeli-Gutstein B, Winkelman JZ (1999). Uveitis associated with varicella virus vaccine. Am J Ophthalmol 127 (6): 733–4. PMID 10372892.
  17. ↑ Schwab J, Ryan M (2004). Varicella zoster virus meningitis in a previously immunized child. Pediatrics 114 (2): e273–4. PMID 15286270.
  18. ↑ Bronstein DE, Cotliar J, Votava-Smith JK, Powell MZ, Miller MJ, Cherry JD (2005). Recurrent papular urticaria after varicella immunization in a 15-month-old girl. Pediatr Infect Dis J 24 (3): 269–70. PMID 15750467.
  19. ↑ Binder NR, Holland GN, Hosea S, Silverberg ML (2005). Herpes zoster ophthalmicus in an otherwise-healthy child. J AAPOS 9 (6): 597–8. PMID 16414532.
  20. ↑ Matsubara K, Nigami H, Harigaya H, Baba K (1995). Herpes zoster in a normal child after varicella vaccination. Acta Paediatr Jpn 37 (5): 648–50. PMID 8533598.
  21. ↑ Hammerschlag MR, Gershon AA, Steinberg SP, Clarke L, Gelb LD (1989). Herpes zoster in an adult recipient of live attenuated varicella vaccine. J Infect Dis 160 (3): 535–7. PMID 2547882.
  22. ↑ Yih WK, Brooks DR, Lett SM, Jumaan AO, Zhang Z, Clements KM, Seward JF (2005). The incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccination coverage, 1998-2003. BMC Public Health 5 (1): 68-68. PMID 15960856.
  23. ↑ Brisson M, Gay NJ, Edmunds WJ, Andrews NJ (2002). Exposure to varicella boosts immunity to Herpes-zoster: implications for mass vaccination against varicella. Vaccine 20: 2500–7. PMID 12057605.

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