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]Vishal Devarkonda, M.B.B.S[3]
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.
Causes
Shingles can only arise in individuals who have been previously exposed to chickenpox (varicella zoster). After a person recovers from chickenpox, the virus stays in the body in a dormant (inactive) state. Herpes zoster is not caused by the same virus that causes genital herpes, a sexually transmitted disease.The disease arises from various events which depress the immune system, such as aging, severe emotional stress, severe illness, immunosuppression or long-term use of corticosteroids.[18][19] The cellular and immunological events that lead to reactivation are poorly understood.[20] There have been recorded cases of outbreaks occurring due to unmanaged stress or other stresses to the skin such as pinching, biting or scratching of more sensitive areas, such as nipples, ears, and underarms.
Differentiation Herpes zoster from other Diseases
[[Diagnosis might not be possible in the absence of a rash (i.e., before rash or in cases of zoster without rash). It is sometimes confused with herpes simplex, and, occasionally, with impetigo, contact dermatitis, folliculitis, scabies, insect bites, papular urticaria, candidal infection, dermatitis herpetiformis, and drug eruptions.sis]] of Herpes zoster
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).
Risk Factors
Shingels are developed in patients who were previously infected with VZV (through natural infection that caused varicella or varicella vaccination).All older adults in the United States are at risk for herpes zoster as approximately 99.5% of people born in the United States who are 40 years of age and older have had varicella. Common risk factors include increasing age, immunosupression and stress.
Screening
There is no recommended screening guideline for herpes zoster.[21]
Natural History, Complications and Prognosis
Diagnosis
History
A detailed history must be taken regarding the onset of symptoms, distribution and morphologic features of rash, accompanying symptoms, such as fever and pruritus and history of previous chicken pox infection must be obtained.
Physical Examination
The characteristic physical examination finding of herpes zoster is the maculopapular rash. The rash in typically unilateral and its distribution is confined to one or two adjacent dermatomes. As the rash crusts and heals in 7-10 days, a post-inflammatory hyperpigmentation of the skin may result. Other findings, such as cranial and peripheral nerves involvement depend on the location of the dorsal root ganglia involved.
Laboratory Findings
Laboratory testing may be useful in cases with less typical clinical presentations, such as in immunosuppressed persons who may have disseminated Herpes zoster (defined as appearance of lesions outside the primary or adjacent dermatomes).
Electrocardiogram
Herpes zoster infection can simulate chest pain of cardiac origin. These patients have normal electrocardiographic findings. However, in very rare instances, herpes zoster infection can have cardiac complications, such as myocarditis, endocarditis, pericarditis and others.
Chest X-Ray
A chest x-ray may be done to rule out other causes of chest pain.
Other Imaging Findings
Imaging is not routinely done to diagnose herpes zoster infection. However, it may be used as part of the work-up of the several but rare complications of herpes zoster infection.
Other Diagnostic Studies
There are no other diagnostic studies for herpes zoster infection.
Treatment
Medical Therapy
Several antiviral medicines—acyclovir, valacyclovir, and famciclovir—are available to treat shingles. These medicines will help shorten the length and severity of the illness. But to be effective, they must be started as soon as possible after the rash appears. Thus, people who have or think they might have shingles should call their healthcare provider as soon as possible to discuss treatment options. Analgesics (pain medicine) may help relieve the pain caused by shingles. Wet compresses, calamine lotion, and colloidal oatmeal baths may help relieve some of the itching.
Primary Prevention
The only way to reduce the risk of developing shingles and the long-term pain that can follow shingles is to get vaccinated. A vaccine for shingles is licensed for persons aged 60 years and older.[22]
Secondary Prevention
Infection-control measures after exposure to herpes zoster depend on whether the patient with herpes zoster is immunocompetent or immunocompromised and on whether the rash is localized or disseminated. In all cases, standard infection-control precautions should be followed.
Cost-Effectiveness of Therapy
A live vaccine for VZV exists, marketed as Zostavax.[23] A systematic review by the Cochrane Library concluded that Zostavax can reduce the incidence of herpes zoster by almost 50%.[24] A 2007 study found that the zoster vaccine is likely to be cost-effective in the U.S., projecting an annual savings of $82 to $103 million in healthcare costs with cost-effectiveness ratios ranging from $16,229 to $27,609 per quality-adjusted life year gained.[25] In October 2007 the vaccine was officially recommended in the U.S. for healthy adults aged 60 and over.[23][26]
Future of Investigational Therapies
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.
- ↑ Mounsey AL, Matthew LG, & Slawson DC (2005). "Herpes zoster and postherpetic neuralgia: prevention and management". American Family Physician. 72 (6): 1075–1080. PMID 16190505. Retrieved 2007-06-15.
- ↑ {[cite journal|title=What does epidemiology tell us about risk factors for herpes zoster?|author=Thomas SL, Hall AJ|journal= Lancet Infect Dis.|date=2004|volume=4|issue=1|pages=26-33|pmid= 14720565}}
- ↑ Donahue JG, Choo PW, Manson JE, Platt R (1995). "The incidence of herpes zoster". Arch. Intern. Med 155 (15): 1605–9. PMID 7618983
- ↑ United States Preventive Services and Task force. Herpes zoster Screening (2016) https://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=Shigella+ Accessed on October 24th, 2016
- ↑ https://www.cdc.gov/shingles/vaccination.html Accessed on October 24th, 2016
- ↑ 23.0 23.1 Harpaz R, Ortega-Sanchez IR, Seward JF (June 6, 2008). "Prevention of herpes zoster: recommendations of the Advisory Committee on Immunization Practices (ACIP)". MMWR Recomm Rep. 57 (RR–5): 1–30, quiz CE2–4. PMID 18528318. Retrieved 2010-01-04.
- ↑ Gagliardi AM, Gomes Silva BN, Torloni MR, Soares BG (2012). Gagliardi, Anna MZ, ed. "Vaccines for preventing herpes zoster in older adults". Cochrane Database Syst Rev. 10: CD008858. doi:10.1002/14651858.CD008858.pub2. PMID 23076951.
- ↑ Pellissier JM, Brisson M, Levin MJ (2007). "Evaluation of the cost-effectiveness in the United States of a vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". Vaccine. 25 (49): 8326–37. doi:10.1016/j.vaccine.2007.09.066. PMID 17980938.
- ↑ Advisory Committee on Immunization Practices (20 November 2007). "Recommended adult immunization schedule: United States, October 2007 – September 2008". Ann Intern Med. 147 (10): 725–9. doi:10.7326/0003-4819-147-10-200711200-00187. PMID 17947396.