- Mar 30, 2007
Shingles is a skin rash caused by the same virus that causes chickenpox. The virus responsible for these conditions is called the Varicella zoster virus (VZV). After an individual has chickenpox, this virus lives in the nervous system and is never fully cleared from the body. Under certain circumstances, such as emotional stress, immune deficiency (from AIDS or chemotherapy), or with cancer, the virus reactivates causing shingles. In most cases, however, a cause for the reactivation of the virus is never found. Anyone who has ever had chickenpox is at risk for the development of shingles, although it occurs most commonly in people over the age of 60.
The herpes virus that causes shingles and chickenpox is not the same as the herpes virus that causes genital herpes (which can be sexually transmitted) and herpes mouth sores. Shingles is medically termed Herpes zoster.
Causes : Herpes zoster, or shingles, is caused by the same virus that causes chickenpox. After an episode of chickenpox, the virus becomes dormant in the body. Herpes zoster occurs as a result of the virus re-emerging after many years.
The cause of the re-activation is usually unknown, but seems to be linked to aging, stress, or an impaired immune system. Often only one attack occurs, without recurrence.
If an adult or child is exposed to the herpes zoster virus and has not had chickenpox as a child or received the chickenpox vaccine, a severe case of chickenpox may develop, rather than shingles.
After infection with chickenpox, the virus resides in a non-active state in the nerve tracts that emerge from the spine. When it is re-activated, it spreads along the nerve tract, first causing pain or a burning sensation.
The typical rash appears in 2 to 3 days, after the virus has reached the skin. It consists of red patches of skin with small blisters (vesicles) that look very similar to early chickenpox. The rash often increases over the next 3 to 5 days. Then, the blisters break, forming small ulcers that begin to dry and form crusts. The crusts fall off in 2 to 3 weeks, leaving behind pink healing skin.
Lesions typically appear along a single dermatome (the body area served by a single spinal nerve) and are only on one side of the body (unilateral). The trunk is most often affected, showing a rectangular belt of rash from the spine around one side of the chest to the breastbone (sternum).
Lesions may also occur on the neck or face, particularly along the trigeminal nerve in the face. The trigeminal has three branches that go to the forehead, the mid-face, and the lower face. Which branch is involved determines where on the face the skin lesions will be.
Trigeminal nerve involvement may include lesions in the mouth or eye. Eye lesions may lead to permanent blindness if not treated with emergency medical care.
Involvement of the facial nerve may cause Ramsay Hunt syndrome with facial paralysis, hearing loss, loss of taste in half of the tongue and skin lesions around the ear and ear canal. Shingles may, on occasion, involve the genitals or upper leg.
Shingles may be complicated by a condition known as post-herpetic neuralgia. This is persistence of pain in the area where the shingles occurred that may last from months to years following the initial episode. This pain can be severe enough to be incapacitating. The elderly are at higher risk for this complication.
Herpes zoster can be contagious through direct contact in an individual who has not had chickenpox, and therefore has no immunity. Herpes zoster may affect any age group, but it is much more common in adults over 60 years old, in children who had chickenpox before the age of one year, and in individuals whose immune system is weakened. The disorder is common, with about 600,000 to one million cases in the U.S. per year.
Most commonly, an outbreak of shingles is localized and involves only one dermatome. Widespread or recurrent shingles may indicate an underlying problem with the immune system such as leukemia, Hodgkin's disease and other cancers, atopic dermatitis, HIV infection, or AIDS. People with suppressed immune systems due to organ transplant or treatment for cancer are also at risk.
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. Zoster sine herpete describes a patient who has all of the symptoms of herpes zoster except this characteristic rash.
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 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 few patients, symptoms may include conjunctivitis, keratitis, uveitis, and optic nerve palsies that can sometimes cause chronic ocular inflammation, loss of vision, and debilitating pain. 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).
If the rash has appeared, identifying this disease (making a differential diagnosis) only requires a visual examination, since very few diseases produce a rash in a dermatomal pattern (see map). However, herpes simplex virus (HSV) can occasionally produce 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.
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.
Progression of herpes zoster. A cluster of small bumps turns into blisters . The blisters fill with lymph, break open , crust over , and finally disappear. Postherpetic neuralgia can sometimes occur due to nerve damage.
Progression of herpes zoster. A cluster of small bumps turns into blisters . The blisters fill with lymph, break open , crust over , and finally disappear. Postherpetic neuralgia can sometimes occur due to nerve damage .
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, and it is extremely rare for patients to suffer more than three recurrences.
Herpes zoster occurs only in people who have had chickenpox, and although it can occur at any age, the vast majority of sufferers are more than 50 years old. 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 extremely contagious. A person is also not infectious before blisters appear, or during postherpetic neuralgia (pain after the rash is gone). The person is no longer contagious after the virus has disappeared.
Prognosis: The rash and pain usually subside within three to five weeks, but about one in five patients develops 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. 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.
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. The drugs are used both as prophylaxis (for example in 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 given within 72 hours of the appearance of the rash. 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.
Patients with mild to moderate pain can be treated with over-the-counter analgesics. 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) can be used. Topical lidocaine and nerve blocks may also reduce pain.
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.
Treatment for herpes zoster ophthalmicus is similar to standard treatment for herpes zoster at other sites. A recent trial comparing aciclovir with its prodrug, valaciclovir, demonstrated similar efficacies in treating this form of the disease. 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.