Herpes zoster overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Herpes zoster (or simply zoster), commonly known as shingles, is a viral disease characterized by a painful skin rash with blisters in a limited area on one side of the body, often in a stripe. The initial infection with varicella zoster virus (VZV) causes the acute (short-lived) illness chickenpox, and generally occurs in children and young people. Once an episode of chickenpox has resolved, the virus is not eliminated from the body but can go on to cause shingles—an illness with very different symptoms—often many years after the initial infection.
Varicella zoster virus can become latent in the nerve cell bodies and less frequently in non-neuronal satellite cells of dorsal root, cranial nerve or autonomic ganglion,[1] without causing any symptoms.[2][3] In an immunocompromised individual, perhaps years or decades after a chickenpox infection, the virus may break out of nerve cell bodies and travel down nerve axons to cause viral infection of the skin in the region of the nerve. The virus may spread from one or more ganglia along nerves of an affected segment and infect the corresponding dermatome (an area of skin supplied by one spinal nerve) causing a painful rash.[4][5] Although the rash usually heals within two to four weeks, some sufferers experience residual nerve pain for months or years, a condition called postherpetic neuralgia. Exactly how the virus remains latent in the body, and subsequently re-activates is not understood.[1]
Throughout the world the incidence rate of herpes zoster every year ranges from 1.2 to 3.4 cases per 1,000 healthy individuals, increasing to 3.9–11.8 per year per 1,000 individuals among those older than 65 years.[6][7][8] Antiviral drug treatment can reduce the severity and duration of herpes zoster, if a seven to ten day course of these drugs is started within 72 hours of the appearance of the characteristic rash.[6][9] [10] [11] [12] [13][14]
Historical Perspective
Herpes zoster has a long recorded history, although historical accounts fail to distinguish the blistering caused by VZV and those caused by smallpox,[15] ergotism, and erysipelas. It was only in the late eighteenth century that William Heberden established a way to differentiate between herpes zoster and smallpox,[16] and only in the late nineteenth century that herpes zoster was differentiated from erysipelas. The first indications that chickenpox and herpes zoster were caused by the same virus were noticed at the beginning of the 20th century. Physicians began to report that cases of herpes zoster were often followed by chickenpox in the younger people who lived with the shingles patients. The idea of an association between the two diseases gained strength when it was shown that lymph from a sufferer of herpes zoster could induce chickenpox in young volunteers. This was finally proved by the first isolation of the virus in cell cultures, by the Nobel laureate Thomas H. Weller in 1953.[17]
Pathophysiology
The causative agent for herpes zoster is varicella zoster virus (VZV), a double-stranded DNA virus related to the Herpes simplex virus group. Most people are infected with this virus as children, and suffer from an episode of chickenpox. The immune system eventually eliminates the virus from most locations, but it remains dormant (or latent) in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the base of the skull.
Epidemiology and Demographics
Before introduction of varicella vaccine in the United States in 1995, varicella was endemic, with virtually all persons being infected by adulthood. Since implementation of the varicella vaccination program, incidence has declined in all age groups, with the greatest decline among children aged 1-4 years. Data from passive and active surveillance have indicated a decline in varicella cases of 70%-84% from 1995 through 2001 (1-3). The downward trend in varicella has continued in the United States through 2005 with an approximately 90% decline in incidence from 1995 in active surveillance sites with high vaccine coverage (CDC, unpublished data).
References
- ↑ 1.0 1.1 Johnson, RW & Dworkin, RH (2003). "Clinical review: Treatment of herpes zoster and postherpetic neuralgia". BMJ. 326 (7392): 748. doi:10.1136/bmj.326.7392.748. PMID 12676845.
- ↑ Kennedy PG (2002). "Varicella-zoster virus latency in human ganglia". Rev. Med. Virol. 12 (5): 327–34. doi:10.1002/rmv.362. PMID 12211045.
- ↑ Kennedy PG (2002). "Key issues in varicella-zoster virus latency". J. Neurovirol. 8 Suppl 2: 80–4. doi:10.1080/13550280290101058. PMID 12491156.
- ↑ Peterslund NA (1991). "Herpesvirus infection: an overview of the clinical manifestations". Scand J Infect Dis Suppl. 80: 15–20. PMID 1666443.
- ↑ Gilden DH, Cohrs RJ, Mahalingam R (2003). "Clinical and molecular pathogenesis of varicella virus infection". Viral Immunology. 16 (3): 243–58. doi:10.1089/088282403322396073. PMID 14583142. Retrieved 2012-02-09.
- ↑ 6.0 6.1 Dworkin RH, Johnson RW, Breuer J; et al. (2007). "Recommendations for the management of herpes zoster". Clin. Infect. Dis. 44 Suppl 1: S1–26. doi:10.1086/510206. PMID 17143845.
- ↑ Donahue JG, Choo PW, Manson JE, Platt R (1995). "The incidence of herpes zoster". Archives of Internal Medicine. 155 (15): 1605–9. PMID 7618983. Retrieved 2012-02-09.
- ↑ Araújo LQ, Macintyre CR, Vujacich C (2007). "Epidemiology and burden of herpes zoster and post-herpetic neuralgia in Australia, Asia and South America". Herpes : the Journal of the IHMF. 14 Suppl 2: 40–4. PMID 17939895. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Cunningham AL, Breuer J, Dwyer DE, Gronow DW, Helme RD, Litt JC, Levin MJ, Macintyre CR (2008). "The prevention and management of herpes zoster". Med. J. Aust. 188 (3): 171–6. PMID 18241179.
- ↑ Weaver BA (2007). "The burden of herpes zoster and postherpetic neuralgia in the United States". J Am Osteopath Assoc. 107 (3 Suppl 1): S2–7. PMID 17488884.
- ↑ "National Institute of Allergy and Infectious Diseases Shingles Index" (HTML). Retrieved 2007-05-17.
- ↑ Zamula, Evelyn (2005). "Shingles:An Unwelcome Encore". United States Food and Drug Administration. Retrieved 2007-04-10.
- ↑ Stankus, SJ (2000). "Management of Herpes Zoster (Shingles) and Postherpetic Neuralgia". American Family Physician. 61 (8): 2437–2447. PMID 10794584. Retrieved 2007-04-08. Unknown parameter
|coauthors=ignored (help) - ↑ "Shingles (Herpes Zoster)". Centers for Disease Control. 2006. Retrieved 2007-05-30.
- ↑ Weinberg JM (2007). "Herpes zoster: epidemiology, natural history, and common complications". J Am Acad Dermatol 57 (6 Suppl): S130–5. doi:10.1016/j.jaad.2007.08.046. PMID 18021864
- ↑ Weller TH (2000). Chapter 1. Historical perspective in: Varicella-Zoster Virus: Virology and Clinical Management (Arvin AM & Gershon AA, editors). Cambridge University Press. ISBN 0521660246.
- ↑ Weller TH (1953). "Serial propagation in vitro of agents producing inclusion bodies derived from varicella and herpes zoster". Proc. Soc. Exp. Biol. Med. 83 (2): 340–6. PMID 13064265.