shingles n : eruptions along a nerve path often accompanied by severe neuralgia [syn: herpes zoster, zoster]

English

Etymology

From cingulus, variant of cingulum, translating ζώνη, ζωστήρ.

Pronunciation

/ˈʃɪŋgəlz/

Noun

shingles p

1. (informal) Herpes zostor.
2. Plural of shingle

Herpes zoster (or simply 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. 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,

Signs and symptoms

The earliest symptoms of herpes zoster, which include headache, fever, and malaise, are nonspecific, and may result in an incorrect diagnosis. These symptoms are commonly followed by sensations of burning pain, itching, hyperesthesia, or paresthesia (sensitivity to heat, cold, light or touch). The pain may be extreme in the affected dermatome, with sensations that are often described as stinging, tingling, aching, numbing or throbbing, and can be interspersed with quick stabs of agonizing pain. In most cases, after 1–2 days (but sometimes as long as 3 weeks) the initial phase is followed by the appearance 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 appears 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 that is limited to one side of the body and does not cross the midline.

Later, 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. 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).

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. 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 only appears during chickenpox or herpes zoster and not while the virus is dormant. In larger laboratories, lymph collected from a blister is tested by the polymerase chain reaction for VZV DNA, or examined with an electron microscope for virus particles.

In a recent study, samples of lesions on the skin, eyes, and lung from 182 patients with presumed herpes simplex or herpes zoster were tested with real-time PCR or with viral culture. . In this comparison, viral culture detected VZV with only a 14.3% sensitivity, although the test was highly specific (specificity=100%). By comparison, real-time PCR resulted in 100% sensitivity and specificity. Overall testing for herpes simplex and herpes zoster using PCR showed a 60.4% improvement over viral culture.

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. However, repeated attacks of herpes zoster are rare, The disease results from the virus reactivating in a single sensory ganglion. 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 a chronic low-level infection, has not been proven. Although VZV has been detected in autopsies of nervous tissue, there are no methods to find dormant virus in the ganglia in living people.

Unless the immune system is compromised, it suppresses reactivation of the virus and prevents herpes zoster. Why this suppression sometimes fails is poorly understood, 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. 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 and blisters. The short and long-term pain caused by herpes zoster comes from the widespread growth of the virus in the infected nerves, which causes inflammation.

The symptoms of herpes zoster cannot be transmitted to another person. 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).

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. Instead, the increased risk may result from the immune suppression that allows the reactivation of the virus.

Treatment

The aims of treatment are to limit the severity and duration of pain, shorten the duration of a shingles episode, and reduce complications. Symptomatic treatment is often needed for the complication of postherpetic neuralgia.

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 has been the standard treatment, but the new drugs valaciclovir and famciclovir demonstrate similar or superior efficacy and good safety and tolerability. Complications in immunocompromised individuals with herpes zoster may be reduced with intravenous aciclovir. In people who are at a high risk for repeated attacks of shingles, five daily oral doses of aciclovir are usually effective. Administering gabapentin along with antivirals may offer relief of postherpetic neuralgia.

Orally administered corticosteroids are frequently used in treatment of the infection, despite clinical trials of this treatment being unconvincing. Nevertheless, one trial studying immunocompetent patients older than 50 years of age with localized herpes zoster, suggested that administration of prednisone with aciclovir improved healing time and quality of life. Upon one-month evaluation, aciclovir with prednisone increased the likelihood of crusting and healing of lesions by about two-fold, when compared to placebo. This trial also evaluated the effects of this drug combination on quality of life at one month, showing that patients had less pain, and were more likely to stop the use of analgesic agents, return to usual activities and have uninterrupted sleep. However, when comparing cessation of herpes zoster-associated pain or post herpetic neuralgia, there was no difference between aciclovir plus prednisone, or simply aciclovir alone. 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.. The significant advantage of valciclovir over aciclovir is its dosing of only 3 times/day (compared with acyclovir's 5 times/day dosing), which could make it more convenient for patients and improve adherence with therapy..

Prevention

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. 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. In October 2007 the vaccine was officially recommended in the U.S. for healthy adults aged 60 and over. 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. The UK Health Protection Agency states that while the vaccine is licensed in the UK there are no plans to introduce it into the routine childhood immunization scheme, although it may be offered to healthcare workers who have no immunity to VZV.

A 2006 study of 243 cases and 483 matched controls found that fresh fruit is associated with a reduced 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 association.

Epidemiology

Varicella zoster virus has a high level of infectivity and is prevalent worldwide, and has a very stable prevalence from generation to generation. VZV is a benign disease in a healthy child in developed countries. However, varicella can be lethal to individuals who are infected later in life or who have low immunity. The number of people in this high-risk group has increased, due to the HIV epidemic and the increase in immunosuppressive therapies. Infections of varicella in institutions such as hospitals are also a significant problem, especially in hospitals that care for these high-risk populations.

In general, herpes zoster has no seasonal incidence and does not occur in epidemics. 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. Multiple studies and surveillance data demonstrate no consistent trends in incidence in the U.S. since the chickenpox vaccination program began in 1995. 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. 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. 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.

A 2008 study revealed that people with close relatives who have had shingles are themselves twice as likely to develop it themselves. The study speculates that there are genetic factors in who is more susceptible to VZV.

History

Herpes zoster has a long recorded history, although historical accounts fail to distinguish the blistering caused by VZV and those caused by smallpox, 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.

Until the 1940s, the disease was considered benign, and that serious complications were thought to be very rare. However, by 1942, it was recognized that herpes zoster was a more serious disease in adults than in children and that it 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.

References

External links

• NINDS Shingles Information Page, National Institute of Neurological Disorders and Stroke
• Links to pictures of Shingles (Hardin MD) University of Iowa
• After Shingles—Information about Shingles and Post-Herpetic Neuralgia, from the Visiting Nurses Associations of America
• Facts About The Cornea and Corneal Disease: Herpes Zoster (Shingles), National Eye Institute

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