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Herpes zoster

Herpes zoster
Classification & external resources
Herpes zoster blisters on the neck and shoulder
ICD-10 B02.
ICD-9 053
DiseasesDB 29119
MedlinePlus 000858
eMedicine med/1007  derm/180 emerg/823 oph/257 ped/996

Herpes zoster (or zoster), commonly known as shingles, is a viral disease characterised by a painful skin rash with blisters in a limited area on one side of the body. It is caused by varicella zoster virus (VZV), which is also the virus that causes chickenpox. After a chickenpox infection the virus can lodge permanently in nerve cell bodies without causing any symptoms, although it is not known exactly how this happens. At times of reduced immuno-competence, years or decades later, 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 nerve cell bodies of dorsal root, cranial nerve or autonomic ganglion may contain the latent virus,[1] and the virus may spread from one or more ganglia along nerves of an affected segment and infect the corresponding dermatome causing a shingles rash.[2][3] 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.[1]

Throughout the world the incidence rate of herpes zoster ranges from 1.2 to 3.4 per 1,000 person-years among healthy individuals, increasing to 3.9–11.8 per 1,000 person‐years among those older than 65 years.[4][5][6] Antiviral drug treatment can reduce the severity and duration of herpes zoster when a seven to ten day course is started within 72 hours of the appearance of the characteristic rash.[4]


Signs and symptoms

The earliest symptoms of herpes zoster, which include headache, fever, and malaise, are nonspecific. At this stage, herpes zoster is easily confused with other medical conditions.[7][4] These symptoms are commonly followed by sensations of burning pain, itching, and hypersensitivity.[8] The pain may be extreme in the affected nerve below. These sensations are often described as stinging, tingling, aching, numbing or throbbing, and can be interspersed with quick stabs of agonizing pain.[9] In most cases, after 1-2 days (but sometimes as long as 3 weeks) the initial phase is followed by the addition of the characteristic skin rash. The pain and rash most commonly occurs on the torso, but can appear on the face, eyes or other parts of the body. At first, the rash is visually similar to the first appearance of hives; however, unlike hives, herpes zoster causes skin changes limited to a dermatome (an area of skin supplied by one spinal nerve), normally resulting in a stripe or belt-like pattern limited to one side of the body and not crossing the midline.[8]

The rash becomes vesicular, forming small blisters filled with a serous exudate, as the fever and general malaise continue. The painful vesicles eventually become cloudy or darkened as they fill with blood, crust over within seven to ten days, and usually the crusts fall off and the skin heals, but sometimes after severe blistering scarring and discolored skin remain.[8]

Development of the shingles rash
Day 1 Day 2 Day 5 Day 6

Herpes zoster may have additional symptoms, depending on the dermatome involved. Herpes zoster ophthalmicus involves the orbit of the eye and occurs in approximately 10–25% of cases. It is caused by the virus reactivating in the ophthalmic division of the trigeminal nerve. In a minority of patients, symptoms may include conjunctivitis, keratitis, uveitis, and optic nerve palsies that can sometimes cause chronic ocular inflammation, loss of vision, and debilitating pain.[10]

Herpes zoster oticus, also known as Ramsay Hunt syndrome type II, involves the ear. It is thought to result from the virus spreading from the facial nerve to the vestibulocochlear nerve. Symptoms include hearing loss and vertigo (rotational dizziness).[1]

Zoster sine herpete describes a patient that has all symptoms of herpes zoster except the characteristic rash.[11]


  When the rash is present, a differential diagnosis is made on visual examination alone. Very few other diseases produce a rash in a dermatomal pattern (see map). However, herpes simplex virus (HSV) infrequently produces a rash in such a pattern. The Tsanck smear is helpful for diagnosing acute infection with a herpes virus but does not distinguish between HSV and VZV.[12]

When the rash is absent (early or late in the disease, or in the case of zoster sine herpete), herpes zoster can be difficult to diagnose.[13] Apart from the rash, most symptoms can occur also in other conditions.

Laboratory tests are available to diagnose herpes zoster. The most popular test detects VZV-specific IgM antibody in blood. This antibody is detectable only during chickenpox or herpes zoster, not while the virus is dormant.[14] In larger laboratories, lymph collected from a blister is tested with a polymerase chain reaction for VZV DNA or examined with an electron microscope for virus particles.[15]



The causative agent for herpes zoster is varicella zoster virus (VZV). Most people are infected with this virus as a child, as it causes chicken pox. 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.

Herpes zoster occurs only in people who have had chickenpox, also caused by varicella zoster virus. It can occur at any age but the vast majority of patients diagnosed with it are more than 50 years old.[16] The virus survives latent in nerve cells of the nerve ganglia.[17] The disease results from the virus reactivating in a single sensory ganglion.[3] In contrast to Herpes simplex virus the latency of VZV is poorly understood. The virus has not been recovered from human nerve cells by cell culture and the location and structure of the viral DNA is not known. Virus-specific proteins continue to be made by the infected cells during the latent period so true latency, as opposed to chronic infection, has not been proven.[18][19]

Unless the immune system is compromised, it suppresses reactivation of the virus, so herpes zoster does not occur. Why this suppression sometimes fails is poorly understood,[5] but herpes zoster is more likely to occur in people whose immune system is impaired due to aging, immunosuppressive therapy, psychological stress, or other factors.[20] Upon reactivation, the virus replicates in the nerve cells, and virions are shed from the cells and carried down the axons to the area of skin served by that ganglion. In the skin, the virus causes local inflammation with the formation of blisters. The pain caused by acute herpes zoster and the long-lasting nature of post herpetic neuralgia result from widespread growth of the virus in, and consequent inflammation of, the infected nerves.[21]

The symptoms of herpes zoster cannot be transmitted to another person.[22] However, during the blister phase, direct contact with the rash can spread VZV to a person who has no immunity to the virus. This newly-infected individual may then develop chickenpox, but they will not immediately develop shingles. Once the rash has developed crusts, a person is no longer contagious. A person is also not infectious before blisters appear, or during postherpetic neuralgia (pain after the rash is gone).[8]

Although VZV has been detected in autopsies of nervous tissue,[23] there are no methods to find dormant virus in the ganglia in live people.

The pain characteristic of herpes zoster is thought to be due to irritation of the sensory nerve fibers in which the virus reproduces.[8]


The aims of treatment are to limit the severity and duration of pain, shorten the duration of a shingles episode, and reduce complications. After a shingles episode the herpes zoster virus will again become dormant in the nerve cell bodies of ganglia, and occasionally the virus may become reactivated to cause subsequent attacks of shingles. Symptomatic treatment is often needed for the complication of postherpetic neuralgia.[24]

Antiviral drugs inhibit VZV replication and reduce the severity and duration of herpes zoster with minimal side effects, but do not reliably prevent postherpetic neuralgia. Of these drugs, aciclovir had been the standard of care; the new drugs valaciclovir and famciclovir demonstrate similar or superior efficacy or safety/tolerability.[24] The drugs are used both as prophylaxis (for example, AIDS patients) and as therapy during the acute phase. Antiviral treatment is recommended for all immunocompetent individuals with herpes zoster over 50 years old, preferably within 72 hours of the appearance of the rash.[25] Complications in Immunocompromised individuals with herpes zoster may be reduced with treatment of intravenous aciclovir. In people who are at high risk for recurrences, five daily oral doses of aciclovir are usually effective.[1] Administering gabapentin along with antivirals may offer further protection against postherpetic neuralgia.[24]

Patients with mild to moderate pain can be treated with over-the-counter analgesics (painkillers). Topical lotions containing calamine can be used on the rash or blisters and may be soothing. Occasionally, severe pain may require an opioid medication, such as morphine. Once the lesions have crusted over, capsaicin cream (Zostrix) may be applied. Topical lidocaine and nerve blocks may also be effective in reducing pain.[26]

Orally administered corticosteroids are frequently used in treatment of the infection, despite the results of clinical trials of this treatment being unconvincing. Prednisone administered with aciclovir reduces the pain associated with herpes zoster and improves the quality of life. In addition, because of the risks of corticosteroid treatment, it is recommended that this combination of drugs only be used in people more than 50 years of age, due to their greater risk of postherpetic neuralgia.[27]


The rash and pain usually subside within three to five weeks, but about one in five patients develop a painful condition called postherpetic neuralgia, which is often difficult to manage. In some patients, herpes zoster can reactivate presenting as zoster sine herpete: pain radiating along the path of a single spinal nerve (a dermatomal distribution), but without an accompanying rash. This condition may involve complications that affect several levels of the nervous system and cause multiple cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. Other serious effects that may occur in some cases include partial facial paralysis (usually temporary), ear damage, or encephalitis.[1]

During pregnancy, first infections with VZV, causing chickenpox, may lead to infection of the fetus and complications in the newborn, but chronic infection or reactivation in shingles are not associated with fetal infection.[28][29]

There is a slightly increased risk of developing cancer after a herpes zoster infection. However, the mechanism is unclear and mortality from cancer did not appear to increase as a direct result of the presence of the virus.[30] Instead, the increased risk may result from the immune suppression that allows the reactivation of the virus.[31]

Repeat attacks of herpes zoster are rare.[8] It is extremely rare for patients to suffer more than three recurrences.[17]


A live vaccine for VZV exists, marketed as Zostavax. In a 2005 study of 38,000 older adults it prevented half the cases of herpes zoster and reduced the number of cases of postherpetic neuralgia by two-thirds.[32] 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.[33] In October 2007 the vaccine became recommended in the U.S. for healthy adults aged 60 and over.[34] Adults also receive an immune boost from contact with children infected with varicella, a boosting method that prevents about a quarter of herpes zoster cases among unvaccinated adults, but which is becoming less common in the U.S. now that children are routinely vaccinated against varicella.[35]

A 2006 study of 243 cases and 483 matched controls found that fresh fruit may reduce the risk of developing shingles: people who consumed less than one serving of fruit a day had three times the risk as those who consumed over three servings, after adjusting for other factors such as total energy intake. For those aged 60 or more, vitamins and vegetable intake had a similar lowering of risk.[36] A 2007 study of 112 elderly adults found that those using Tai Chi Chih had higher levels of cell-mediated immunity to VZV and that this effect added to the that of a standard single dose of chickenpox vaccine; it is not known whether these increases protect against herpes zoster.[37]


Varicella zoster virus is an extremely contagious virus that is prevalent worldwide. VZV has an almost 100% rate of consistent prevalence from generation to generation.[38] Varicella zoster epidemics result from the transmission of VZV through respiratory secretions and from the virus filled lesions of infected people to individuals who lack immunity to the virus. VZV is a benign disease in a healthy child in the United States. To those individuals who are infected later in life or who have altered immune states or deficiencies, however, varicella can be lethal. The number of people in this high-risk group grows with the increase in HIV incidence and the increase in immunosuppressive therapies. Nosocomial infections of varicella are a significant problem, especially in hospitals caring for high-risk populations.[39]

In temperate zones chickenpox is a disease of children, with most cases occurring during the winter and spring, most likely due to school contact; there is no evidence for regular epidemics. In the tropics chickenpox typically occurs among older people.[40] Herpes zoster has no seasonal incidence and does not occur in epidemics.[20] Incidence is highest in people who are over age 55, as well as in immunocompromised patients regardless of age group, and in individuals undergoing psychological stress. Non-whites may be at lower risk; it is unclear whether the risk is increased in females. Other potential risk factors include mechanical trauma, genetic susceptibility, and exposure to immunotoxins.[20]

The incidence rate of herpes zoster ranges from 1.2 to 3.4 per 1,000 person-years among healthy individuals, increasing to 3.9–11.8 per 1,000 person‐years among those older than 65 years.[4] Similar incidence rates have been observed worldwide.[6][4] Herpes zoster develops in an estimated 500,000 Americans each year.[41] Multiple studies and surveillance data demonstrate no consistent trends in incidence in the U.S. since the chickenpox vaccination program began in 1995.[42] It is likely that incidence rate will change in the future, due to the aging of the population, changes in therapy for malignant and autoimmune diseases, and changes in chickenpox vaccination rates; a wide adoption of zoster vaccination could dramatically reduce the incidence rate.[4]

In one study, it was estimated that 26% of patients who contract herpes zoster eventually present with complications. Postherpetic neuralgia arises in approximately 20% of patients.[43] A study of 1994 California data found hospitalization rates of 2.1 per 100,000 person-years, rising to 9.3 per 100,000 person-years for ages 60 and up.[44] An earlier Connecticut study found a higher hospitalization rate; the difference may be due to the prevalence of HIV in the earlier study, or to the introduction of antivirals in California before 1994.[45]


  Herpes zoster has a long recorded history, although historical accounts fail to distinguish the blistering caused by VZV and those caused by smallpox,[16] ergotism, and erysipelas. It was only in the late eighteenth century that William Heberden established a way to differentiate between herpes zoster and smallpox,[39] 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.[46]

Until the 1940s, the disease was considered benign, and it was believed that serious complications were very rare.[47] However, 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 1950s on immunosuppressed individuals showed that the disease was not as benign as once thought, and the search for various therapeutic and preventive measures began.[39] By the mid-1960s, several studies identified the gradual reduction in cellular immunity in old age, observing that in a cohort of 1,000 people who lived to the age of 85, approximately 500 would have one attack of herpes zoster and 10 would have two attacks.[48]


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This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Herpes_zoster". A list of authors is available in Wikipedia.
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