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==Transmission==
==Transmission==

[[Image:A Course of Shingles diagram.png|left|A course of shingles|thumb|250px]]
Most people are infected with VZV as a child, as it causes [[chickenpox]]. The immune system eventually eliminates the virus from most locations, but it remains dormant in the [[ganglion|ganglia]] adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the cranial base.
Most people are infected with VZV as a child, as it causes [[chickenpox]]. The immune system eventually eliminates the virus from most locations, but it remains dormant in the [[ganglion|ganglia]] adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the cranial base.


Revision as of 00:27, 11 December 2007

"Shingles" redirects here, for other uses of the term, see Shingle.
Shingles
SpecialtyInfectious diseases, dermatology, neurology Edit this on Wikidata

Herpes zoster, commonly known as shingles, is a disease caused by the reactivation of a varicella-zoster virus (VZV) infection. This virus, one of the Herpesviridae familly, causes painful blisters over the area of a dermatome.

After an attack of chickenpox, the varicella-zoster virus retreats to nerve cells within the ganglion or the spinal cord, where it lies dormant for several months or several decades.[1] Aging, stress, or disease cause the virus to reactivate and reproduce, the virus travels along the path of a nerve to the skin's surface, where it causes shingles.[2][3][4]

Treatment is generally with antiviral drugs such as aciclovir (Zovirax), or prodrugs such as famciclovir (Famvir), or valaciclovir (Valtrex). The antiviral drugs are most effective if the treatment begins within 72 hours of appearance of definitive symptoms.[5][6][7]

Signs and symptoms

The earliest symptoms (constituting the prodrome) of shingles include headache, sensitivity to light, fever, and malaise, all of which may be followed by itching, tingling, and pain within one to seven days. The pain may be extreme in the affected nerve, where the rash will later develop, and can be characterized as stinging, tingling, aching, numbing, or throbbing, and can be pronounced with quick stabs of intensity. During this phase, herpes zoster is frequently misdiagnosed as other diseases with similar symptoms, including heart attacks and renal colic. Some patients may have these symptoms without developing the characteristic rash. This situation, known as "zoster sine herpete," can delay diagnosis and treatment.[5][8]

The initial phase is followed, in most cases, by development of the characteristic skin rashes of herpes zoster. The rash is visually similar to hives, and follows a distribution near dermatomes, commonly occurring in a stripe or belt-like pattern. The rash evolves into vesicles or small blisters filled with serous fluid. The vesicles are generally painful, and their development is often associated with the occurrence of anxiety and further flu-like symptoms, such as fever, tiredness, and generalized pain. The vesicles eventually become hemorrhagic (filled with blood), and crust over within seven to ten days. As the crusts fall off, patients are rarely left with scarring and pigmented skin.[5]

Shingles cannot be passed from one person to another. However, VZV can be spread from a person with active shingles to a person who has no immunity to the virus by direct contact with the rash, while in the blister phase. The person exposed would then develop chickenpox, not shingles. The virus is not spread through airborne transmission, such as sneezing or coughing. Once the rash has developed crusts, the person is no longer contagious. A person is not infectious before blisters appear or with post-herpetic neuralgia (pain after the rash is gone).[3][5]

Chickenpox virus can remain dormant for decades, and does so inside the ganglion of the spinal cord. As the virus is reactivated it spreads down peripheral nerve fibers and produces intense pain. The blisters therefore only affect one area of the body and do not cross the midline. They are most common on the torso, but can also appear on the face, eyes or other parts of the body.[3][5]

  • Day 1.
    Day 1.
  • Day 2.
    Day 2.
  • Day 5.
    Day 5.
  • Day 6, with characteristic purple color.
    Day 6, with characteristic purple color.

Causes

Shingles can only arise in individuals who have been previously exposed to chickenpox (varicella-zoster). 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.[8][9] The cellular and immunological events that lead to reactivation are poorly understood.[10] 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.[5]

Transmission

Most people are infected with VZV as a child, as it causes chickenpox. The immune system eventually eliminates the virus from most locations, but it remains dormant in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the cranial base.

Generally, the immune system suppresses reactivation of the virus. In the elderly, whose immune response generally tends to deteriorate, as well as in those patients whose immune system is being suppressed, this process fails. The virus starts replicating in the nerve cells, and newly formed viruses are carried down the axons to the area of skin served by that ganglion (a dermatome). Here, the virus causes local inflammation in the skin, with the formation of blisters.[3][5]

The pain characteristic of herpes zoster is thought to be due to irritation of the sensory nerve fibers in which the virus reproduces.[5]

Diagnosis

The diagnosis is visual; very few other diseases mimic herpes zoster, especially in the localization of the rash, which is otherwise quite similar in appearance and initial effect to that of poison oak or poison ivy (although it may not be accompanied by the intense itching so characteristic of those rashes).

In case of doubt, diagnostic tests can be performed. Such tests may be necessary because, depending on the affected sensory nerve, the pain that is experienced before the onset of the rash may be misdiagnosed as pleurisy, myocardial infarction, appendicitis, cholelithiasis, or a migraine headache. Fluid from a blister may be taken and analyzed in a medical laboratory where it is tested by Polymerase chain reaction (PCR) for the presence of VZV DNA or examined by electron microscopy for Herpes virus particles.[11] A physician can also take a viral culture of lymph from a fresh lesion, or perform a microscopic examination of the blister base called a Tzanck test which although inferior to PCR, is a reliable diagnostic method.[12] In a complete blood count there may be an elevated number of white blood cells, which is an indirect sign of infection. The presence of IgM antibody to the virus in the blood would also give indication of the virus’ reactivation.[5]

Treatment

Currently, there is no cure available for Herpes zoster, nor a treatment to effectively eliminate the virus from the body. However, there are some treatments that can mitigate the length of the disease and alleviate certain side effects.

Antiviral drugs

Aciclovir (an antiviral drug) inhibits replication of the viral DNA, and is used both as prophylaxis (e.g., in patients with AIDS) and as therapy for herpes zoster. Other antivirals are valaciclovir and famciclovir. During the acute phase, oral aciclovir should be given. Use of aciclovir is most effective in moderating the progress of the symptoms, and in preventing post-herpetic neuralgia, if started within 24 to 72 hours of the onset of symptoms, so medical care should be obtained as soon as the condition is recognized. Immunocompromised patients may respond best to intravenous aciclovir. In patients who are at high risk for recurrences, an oral dose of aciclovir, taken five times daily, is usually effective.[13] It is also reported that the amino acid lysine inhibits the replication of herpes zoster.[14][7]

Other drugs

Cimetidine, a common component of over-the-counter heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances.[15][16][17] This usage is considered an off-label use of the drug. In addition, cimetidine and probenecid have been shown to reduce the renal clearance of aciclovir.[18] The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of aciclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician.

Prognosis

The rash and pain usually subside within three to five weeks. Many patients develop a painful condition called postherpetic neuralgia, which is often difficult to manage. In some patients, herpes zoster can reactivate subclinically, with pain in a dermatomal distribution without rash. This condition is known as zoster sine herpete, and may be more complicated, affecting multiple levels of the nervous system and causing multiple cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. Sometimes serious effects including partial facial paralysis (usually temporary), ear damage, or encephalitis may occur.[13]

Since shingles is a reactivation of a virus contracted previously—often decades earlier—it cannot be induced by exposure to another person with shingles or chickenpox. Those with active blisters, however, can spread chickenpox to others who have never had that condition and who have not been vaccinated against it.[3]

Shingles on the upper half of the face may result in eye damage and require urgent ophthalmological assessment. Approximately 25% of Herpes zoster cases result in Herpes zoster ophthalmicus, which occurs when the varicella-zoster virus is reactivated in the ophthalmic division of the trigeminal nerve. Patients with this condition exhibit a vesicular rash around the orbit of the eye distributed according to the affected dermatome. A minority of patients may also develop conjunctivitis, keratitis, uveitis, and optic nerve palsies. As a result of this condition, permanent effects include chronic ocular inflammation, loss of vision, and debilitating pain.[19]

Reactivation of the Varicella-zoster virus (VZV) along the Vestibulocochlear nerve which innervate the ear is responsible for HZ oticus, also known as Ramsay Hunt syndrome type II. Symptoms, which include hearing loss and vertigo, are thought to occur as a result of transmission of the virus via direct proximity of vestibulocochlear nerve (cranial nerve VIII) to the facial nerve (cranial nerve VII).[13]

In the United States, approximately 10,000 individuals are hospitalized as a result of Herpes zoster, while approximately 100 deaths occur as a result of complications of the disease. Morbidity and mortality affect those individuals with immunosuppression (particularly those with HIV infection), those who are receiving immunosuppressive therapy, those who are elderly or in early infancy, individuals with in utero primary infections.[10]Cite error: A <ref> tag is missing the closing </ref> (see the help page). In Massachusetts, herpes zoster incidence increased 90%, from 2.77 per 1000 to 5.25 per 100 in the period of increasing varicella vaccination 1999–2003.[20] The effectiveness of the varicella vaccine itself is dependent on this exogenous (outside) boosting mechanism. Thus, as natural cases of varicella decline, so has the effectiveness of the vaccine.[21]

The intake of micronutrients, including antioxidant vitamins, A, C, E and vitamin B group, as well as fresh fruit, may reduce the risk of developing shingles. In one study, patients who consumed less than one serving of fruit a day had three times the risk as those who consumed over three servings per day. For those aged 60 or more, micronutrient and vegetable intake had a similar lowering of risk.[22] A recent study evaluated the effects of two types of behavioral intervention, Tai Chi and health education, on healthy adults, who, after 16 weeks of the intervention, were vaccinated with VARIVAX, a live attenuated Oka/Merck varicella-zoster virus vaccine.[23]

Epidemiology

Before implementation of the universal varicella vaccination program in the U.S., incidence of shingles increased with advancing age in association with a progressive decline in immunity to varicella-zoster virus.[24] Shingles incidence is highest in persons who are over age 55, as well as in immunocompromised patients regardless of age group.[10] The incidence rate of Herpes zoster in persons aged 65 or older is approximately 19 per 1000 individuals per year in the US. The incidence in this age group of a white ethnic background is approximately 3.5 times higher than in the same age group of a Hispanic ethnic background.[25] It can also be seen in immunocompetent individuals undergoing severe emotional stress.[26]

In the United States, herpes zoster affects about 10–20% of the population (although nearly 100% of the population has been exposed to varicella-zoster by age 60). The rate is approximately 131 per 100,000 person-years in white individuals. Similar rates of infection have been observed worldwide.[7]

According to a review of the disease in the United States, one million consultations for herpes zoster occur per year; approximately 250,000 of the patients examined develop herpes zoster ophthalmicus. A subset of 50% of these patients develops complications of herpes zoster ophthalmicus.[27] Ramsay Hunt syndrome is the cause of as many as 12% of all cases of facial paralysis.[13]

History

Herpes zoster has a long recorded history although historical accounts fail to distinguish the blistering caused by VZV and those caused by smallpox. It was only in the late eighteenth century that William Heberden established a way to clinically differentiate between the two diseases.[28] Until the 1940's, the disease was considered benign, and it was believed that serious complications were very rare.[29]

By 1942, it was recognized that zoster was a more serious disease in adults than in children and that Herpes zoster increased in frequency with advancing age. Further studies during the 1950's on immunosuppressed individuals showed that the disease lost much of its benign characteristics and the search for various therapeutic and preventive measures was initiated.[28] By the mid-1960's, several studies identified the gradual reduction in cellular immunity in old age by observing that in a cohort of 1000 people who lived to the age of 85, approximately 500 would have one attack of Herpes zoster and 10 would have two attacks.[30]

References

  1. ^ 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. Retrieved 2007-12-10.
  2. ^ "National Institute of Allergy and Infectious Diseases Shingles Index". Retrieved 2007-05-17.
  3. ^ a b c d e Zamula, Evelyn (2005). "Shingles:An Unwelcome Encore". United States Food and Drug Administration. Retrieved 2007-04-10.
  4. ^ Glaser R & Kiecolt-Glaser JK (2005). "Stress-induced immune dysfunction: implications for health". Nat Rev Immunol. 5 (3): 243–251. doi:10.1038/nri1571. PMID 15738954.
  5. ^ a b c d e f g h i Stankus, SJ (2000). "Management of herpes zoster (shingles) and postherpetic neuralgia". Am Fam Physician. 61 (8): 2437–47. PMID 10794584. Retrieved 2007-04-08. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  6. ^ "Shingles (Herpes Zoster)". Centers for Disease Control. 2006. Retrieved 2007-05-30.
  7. ^ a b c Dworkin RH, Johnson RW, Breuer J, Gnann JW, Levin MJ, Backonja M; et al. (2007). "Recommendations for the management of herpes zoster". Clin Infect Dis. 44 (Suppl 1): 1–26. doi:10.1086/510206. PMID 17143845. Retrieved 2007-12-10. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  8. ^ a b Mounsey AL, Matthew LG, & Slawson DC (2005). "Herpes zoster and postherpetic neuralgia: prevention and management". Am Fam Physician. 72 (6): 1075–80. PMID 16190505. Retrieved 2007-06-15.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Thomas SL, Hall AJ (2004). "What does epidemiology tell us about risk factors for herpes zoster?". Lancet Infect Dis. 4 (1): 26–33. PMID 14720565.
  10. ^ a b c Donahue, JG, Choo, PW, Manson, JE & Platt, R (1995). "The incidence of herpes zoster". Arch Intern Med. 155 (15): 1605–9. PMID 7618983.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ Beards G, Graham C, Pillay D (1998). "Investigation of vesicular rashes for HSV and VZV by PCR". J. Med. Virol. 54 (3): 155–7. PMID 9515761.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Ozcan A, Senol M, Saglam H; et al. (2007). "Comparison of the Tzanck test and polymerase chain reaction in the diagnosis of cutaneous herpes simplex and varicella-zoster virus infections". Int. J. Dermatol. 46 (11): 1177–9. doi:10.1111/j.1365-4632.2007.03337.x. PMID 17988338. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  13. ^ a b c d 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. Retrieved 2007-12-10.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ Griffith, RS (1987). "Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis". Dermatologica. 175 (4): 183–90. PMID 3115841. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  15. ^ Kapinska-Mrowiecka M, &Toruwski G (1996.). "Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation". Pol Tyg Lek. 51 (23–26): 338–9. PMID 9273526. {{cite journal}}: Check date values in: |year= (help)CS1 maint: year (link)
  16. ^ Hayne ST, & Mercer JB (1983). "Herpes zoster: treatment with cimetidine". Can Med Assoc J. 129 (12): 1284–5. PMID 6652595. Retrieved 2007-12-10.
  17. ^ Notmann J, Arieli J, Hart J, Levinsky H, Halbrecht I, & Sendovsky U (1994). "In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine". Asian Pac J Allergy Immunol. 12 (1): 51–8. PMID 7872992.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ De Bony F, Tod M, Bidault R, On NT, Posner J, & Rolan P (2002). "Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite aciclovir". Antimicrob Agents Chemother. 46 (2): 458–63. PMID 11796358. Retrieved 2007-12-10.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ^ Shaikh S, Ta CN (2002). "Evaluation and management of herpes zoster ophthalmicus". Am Fam Physician. 66 (9): 1723–1730. PMID 12449270. Retrieved 2007-12-09.
  20. ^ Yih, WK (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. PMID 15960856. Retrieved 2007-12-10. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  21. ^ Goldman, GS (2005). "Universal varicella vaccination: efficacy trends and effect on herpes zoster". Int J Toxicol. 24 (4): 205–13. PMID 16126614.
  22. ^ Thomas SL, Wheeler JG, Hall AJ (2006). "Micronutrient intake and the risk of herpes zoster: a case-control study". Int J Epidemiol. 35 (2): 307–14. doi:10.1093/ije/dyi270. PMID 16330478. Retrieved 2007-12-10.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ Irwin, MR (2007). "Augmenting immune responses to varicella zoster virus in older adults: a randomized, controlled trial of Tai Chi". J Am Geriatr Soc. 55 (4): 511–7. doi:10.1111/j.1532-5415.2007.01109.x. PMID 17397428. Retrieved 2007-04-08. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  24. ^ Oxman, MN (2005). "A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". N Engl J Med. 253 (22): 2271–84. PMID 15930418. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help) (Free registration required)
  25. ^ Chaves SS, Santibanez TA, Gargiullo P, Guris D (2007). "Chickenpox exposure and herpes zoster disease incidence in older adults in the U.S.". Public Health Rep. 122 (2). PMID 17357357.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ^ Mehta SK, Cohrs RJ, Forghani B, Zerbe G, Gilden DH, & Pierson DL (2004). "Stress-induced subclinical reactivation of varicella zoster virus in astronauts". J Med Virol. 72 (1): 174–9. PMID 14635028.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ Pavan-Langston D (1995). "Herpes zoster opthalmicus". Neurology. 45 (12 Suppl 8): 50–1. PMID 8545020.
  28. ^ a b 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.
  29. ^ Holt LE & McIntosh R (1936). Holt's Diseases of Infancy and Childhood. D Appleton Century Company. pp. 931–3.
  30. ^ Hope-Simpson RE (1965). "The nature of herpes zoster; a long-term study and a new hypothesis". Proc R Soc Med. 58: 9–20. PMID 14267505. Retrieved 2007-12-10.
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