shingles

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Definition

Shingles, also called herpes zoster, gets its name from both the Latin and French words for belt or girdle and refers to girdle-like skin eruptions that may occur on the trunk of the body. The virus that causes chickenpox, the varicella zoster virus (VSV), can become dormant in nerve cells after an episode of chickenpox and later reemerge as shingles. Initially, red patches of rash develop into blisters. Because the virus travels along the nerve to the skin, it can damage the nerve and cause it to become inflamed. This condition can be very painful. If the pain persists long after the rash disappears, it is known as post-herpetic neuralgia.

Description

Any individual who has had chickenpox can develop shingles. Approximately 300,000 cases of shingles occur every year in the United States. Overall, approximately 20% of those who had chickenpox as children develop shingles at some time in their lives. People of all ages, even children, can be affected, but the incidence increases with age. Newborn infants, bone marrow and other transplant recipients, as well as indivduals with immune systems weakened by disease or drugs are also at increased risk. However, most individuals who develop shingles do not have any underlying malignancy or other immunosuppressive condition.

— David J. Doermann

[Middle English, alteration (influenced by Old French cengles, pl. of cengle, shingles , and by Old French sengle, single, chingle, belt) of Medieval Latin cingulus (translation of Greek zōstēr, girdle, shingles, from the fact that the inflammation often extends around the middle of the body), variant of Latin cingulum, girdle, from cingere, to gird.]

For more information on shingles, visit Britannica.com.

Definition

Shingles is infection by the varicella-zoster virus of the dorsal root ganglia of the spine. Equivalent terms for shingles are herpes zoster, zoster, zona, or acute posterior ganglionitis.

Description

Shingles is an infection of the central nervous system, in particular, the dorsal root ganglia of the spine, which migrates through sensory nerves to the skin. There it manifests (usually on the upper trunk) as painful, bumpy, fluid-filled eruptions or vesicles. Shingles may also cause nerve pain (neuralgia). The affected areas of skin are those supplied by sensory nerves radiating from the infected dorsal root ganglia. Sensory nerves from these ganglia serve non-overlapping, sharply bounded strips or areas of the skin called dermatomes. Because the left and right sides of the body are divided into separate sets of dermatomes, shingles lesions do not cross the midline of the body.

Demographics

The virus that causes shingles is usually contracted in childhood. It is the same virus that causes chicken pox, which is primarily a disease of childhood because it is highly contagious; that is, few individuals live to adulthood without contracting chicken pox. (This statement applies to the temperate zones of the world. For unknown reasons, chicken pox and shingles are less prevalent in tropical regions.) The virus that causes both chicken pox and shingles can, however, be contracted by an individual for the first time in adulthood. First infection, at whatever age it occurs, is called primary infection. Primary infection does not cause shingles; shingles arises from reactivation of virus introduced to the body by an earlier, primary infection.

Shingles arises in individuals who have already had chicken pox, and especially in people with weakened immune systems, such as the elderly or people receiving chemotherapy or bone marrow transplantation. Persons with AIDS are also vulnerable to shingles. Shingles incidence increases steadily with age. Among 10–19 year olds, the rate per 1,000 persons per year is only 1.38. In the 30–49 age range, it rises to 2.29 cases of shingles per 1,000 persons per year. By age 60–79, almost seven cases occur per 1,000 people per year, and this increases to 10 in the 80–89 age group.

Causes and symptoms

Shingles is caused by the varicella-zoster virus (VZV), also known as HHV-3. VZV is genetically similar to the herpes simplex viruses, the type of viruses that causes cold sores and genital herpes. Herpes simplex virus also takes up permanent residence in sensory nerve ganglia, but not in the dorsal root ganglia of the spine, as does VZV. In chicken pox, the virus is inhaled and begins replicating in the upper respiratory tract before spreading to the liver and other body systems.

Following primary infection, VZV remains as a symptomless infection in the dorsal root ganglia of the spinal cord. It may or may not become active again, that is, begin reproducing, later in life. Reactivation occurs more often in older people, probably as a result of decreased immune response with age. Reactivation may be symptomless, but usually causes shingles. Repeat episodes of shingles are rare (occurring in less than 4% of patients) because the immune system's response to VZV is boosted by a first shingles episode.

Chills, fever, malaise, gastrointestinal problems, and pain in the affected skin areas may precede appearance of skin eruptions by several days. Viral particles travel away from the spinal cord along the sensory nerves toward the skin, causing inflammation of those nerves, which may be painful. On the fourth or fifth day, skin vesicles begin to appear. The affected area is usually hypersensitive, and disabling pain (described as sharp, stabbing, or burning) may occur in the affected area. About the fifth day after appearing, the vesicles begin to crust or scab and the disease resolves within the next two weeks. There may be no visible aftereffects, although slight scarring from the vesicles may occur.

Especially in elderly patients, pain may persist for months or years after shingles has otherwise resolved. This pain, postherpetic neuralgia, is caused by damage to the dorsal root ganglia that renders them either spontaneously active (perceived as chronic pain) or hypersensitive to slight stimuli such as light touch.

VZV can become active in the cranial nerves as well as in the spinal ganglia. Involvement of branches of the trigeminal nerve (fifth cranial nerve) is most common. When the ophthalmic branch of the trigeminal nerve is involved, this condition is called herpes zoster ophthalmicus. It can cause swelling of the eyelid, pain, and other complications involving the eye. Herpes zoster ophthalmicus can also lead to weakness or partial paralysis (hemiparesis) on the opposite side of the body from the nerve affected, possibly by inducing irritation of the blood vessels in the brain. Infection of cranial nerves by reactivated VZV can also affect the hearing. When this occurs, it is usually associated with facial palsy and is known as Ramsay-Hunt syndrome.

Large amounts of free virus (i.e., virus not held inside cells) is present in the fluid-filled vesicles or bumps that erupt on the skin during shingles. Thus, people who are not resistant to VZV are easily infected by contact with persons having an outbreak of shingles. A particular strain of VZV can remain latent for decades and then reappear as a new epidemic.

Diagnosis

Diagnosis is based on history and symptoms. The person must have initially had chicken pox in order to have shingles. Definite diagnosis is difficult before eruption of the characteristic vesicles or bumps on the skin. Often persons with early shingles mistake the reddened, painful area as an accidental burn. Once vesicles appear, however, they are hard to mistake because of their dermatome-bounded distribution on the body. In children, shingles (VZV reactivation) must be differentiated from chicken pox (primary VZV infection). This is normally not difficult, as chicken pox vesicles occur widespread on the body and shingles lesions are usually limited to one area on the person's midsection. Herpes simplex virus can also produce vesicle eruptions similar to those of shingles. If there is doubt about which virus is present, virus from the patient can be cultured.

Treatment team

Unless there are complications such as in a person with AIDS, or a child with leukemia, a primary physician can usually treat shingles.

Treatment

Treatment for shingles is primarily with antiviral drugs, traditionally acyclovir but, more recently, famcyclovir and valacyclovir. Additionally, a live attenuated-virus vaccine for chicken pox has been licensed since 1995. The vaccine was developed to immunize children undergoing cancer treatment because chicken pox can cause severe complications in such children.

The pain associated with shingles, and with the postherpetic neuralgia that may linger (especially in older patients, after the condition has otherwise resolved), is best treated using combination therapy based on antivirals, antidepressants, corticosteroids, opioids (morphine), and topical agents (applied directly to the skin). The inexpensive amino acid lysine has also been reported to ease the symptoms of both herpes simplex infections and shingles.

Recovery and rehabilitation

Recovery from shingles for the otherwise healthy patient is straightforward and generally requires no special rehabilitation aid or therapy.

Clinical trials

As of mid 2004, several clinical trials related to shingles are recruiting patients. One is sponsored by the National Center for Research Resources, University of Texas, and titled "Randomized Study of Two Doses of Oral Valacyclovir in Immunocompromised Patients with Uncomplicated Herpes Zoster." The study seeks to investigate the efficacy of higher-than-standard doses of valacyclovir by assessing quality of life, pain level, and utilization of medical resources of patients treated with a higher-than-standard dose of valacylovir as compared to a control group treated with the standard dose. Contact information is University of Texas Medical Branch, Galveston, Texas, 77555-0209; Stephen K. Tyring is the recruiter, telephone: (281) 333-2288.

Another trial recruiting patients as of 2004 is sponsored by the Baylor College of Medicine, Texas Children's Hospital, and titled "Valacyclovir in Immunocompromised Children." The study seeks to learn how the body handles valacyclovir, its efficacy in treating immunocompromised children with shingles, and the side effects of such treatment. The recruiting inquiries in Pennsylvania is Children's Hospital of Philadelphia, Pennsylvania, 19104; Donna Sylvester, RN, phone: (215) 590-3284. The recruiting inquiries in Texas is Texas Children's Hospital, Houston, Texas, 77030; Susan Blaney, MD, phone: (832) 822-4215, e-mail: sblaney@bcm.tmc.edu, or Lisa R Bomgaars, MD, phone: (832) 824-4688, e-mail: lbomgaars@bcm.tmc.edu.

A third study ongoing in 2004 is sponsored by the drug maker NeurogesX and titled "Controlled Study of NGX-4010 for the Treatment of Postherpetic Neuralgia." NGX-4010 consists of a capsaicin dermal (skin) patch. Capsaicin is the active substance in chili peppers, and is used, paradoxically, both as an irritant and for pain relief. The purpose of this clinical trial is to evaluate the efficacy of a capsaicin patch for relief of postherpetic neuralgia. Contact information varies by state but can viewed at the National Institutes of Health Web site at .

Prognosis

Generally, the prognosis for persons with shingles is good. Shingles is almost never a life-threatening disease in otherwise healthy patients, and usually resolves without treatment in a few weeks. However, postherpetic neuralgia, which occurs more often in elderly patients, can be disabling and difficult to treat.

Persons who have an impaired immune system, such as those deficient in cytotoxic T lymphocytes, persons undergoing immune suppression (e.g., for organ transplant), and persons who have AIDS or leukemia may suffer more serious effects from shingles, as the reactivated virus sometimes disseminates from the dorsal root ganglia to other parts of the body. In these cases, complications can resemble those for primary infection of adults with VZV, namely, viral pneumonia, male sterility, acute liver failure, and (in pregnant women) birth defects.

Resources

BOOKS

Glaser, Ronald, and James F. Jones, (eds). Herpes Virus Infections. New York: Marcel Dekker, Inc., 1994.

Strauss, James H., and Ellen G. Strauss. Viruses and Human Disease. New York: Academic Press, Elsevier Science, 2002.

PERIODICALS

Ho, Charles C., "Use of Combination Therapy for Pin Relief in Acute and Chronic Herpes Zoster." Geriatrics (Dec. 1, 2001).

Johns Hopkins Medical Institutions. "Opioid Medications a Good Bet for Shingles-Related Pain." Ascribe Higher Education News Service (Oct. 7, 2002).

Madison, Linda K. "Shingles Update: Common Questions in Caring for a Patient with Shingles." Orthopaedic Nursing (Jan. 1, 2000).

"New Therapies Reduce Morbidity from Herpes Zoster." Ophthalmology Times (Jan. 1, 1999).

Sheff, Barbara, "Microbe of the Month: Varicella-Zoster Virus." Nursing (Nov. 1, 2000).

Smith, Angela D. "Lysine for Herpes Simplex Infections." Medical Update (Nov. 1, 2001).

OTHER

"NINDS Shingles Information Page." National Institute of Neurological Disorders and Stroke. April 28, 2004 (May 27, 2004). http://www.ninds.nih.gov/health_and_medical/disorders/shingles_doc.htm.

Larry Gilman, PhD

Key Terms: Acyclovir, Antibody, Famciclovir, Immunocompromised, Post-herpetic neuralgia.

Description

Herpes zoster, also called shingles, and referred to as "zosteer", gets its name from both the Latin and French words for belt or girdle and refers to belt-like skin eruptions that may occur on the trunk of the body. The virus that causes chickenpox, the varicella zoster virus (VSV), can become dormant in nerve cells after an episode of chickenpox and later re-emerge as shingles. Any individual who has had chickenpox can develop shingles. People of all ages, even children, can be affected, but the incidence increases with age. There are many other conditions which can predispose people to developing shingles, including newborn infants, bone marrow and other transplant recipients, and individuals with immune systems weakened by diseases like HIV or cancer, or drugs, such as those used in chemotherapy.

Shingles erupts along the course of the affected nerve, producing lesions anywhere on the body and may cause severe nerve pain. The most common areas to be affected are the face and trunk, which correspond to the areas where the chickenpox rash is most concentrated. The disease is caused by a reactivation of the chickenpox virus that has been dormant in certain nerves following an episode of chickenpox. Exactly how or why this reactivation occurs is not clear; however, it is believed that the reactivation is triggered when the immune system becomes weakened as in the examples described above. Early signs of shingles are often vague and can easily be mistaken for other illnesses. The condition may begin with fever and malaise (a vague feeling of weakness or discomfort). Within two to four days, severe pain, itching, and numbness/tingling (paresthesia) or extreme sensitivity to touch (hyperesthesia) can develop, usually on the trunk and occasionally on the arms and legs. Pain may be continuous or intermittent, usually lasting from one to four weeks. It may occur at the time of the eruption, but can precede the eruption by days, occasionally making the diagnosis difficult. Signs and symptoms may include the following:

• itching, tingling, or severe burning pain
• red patches that develop into blisters
• grouped, dense, deep, small blisters that ooze and crust
• swollen lymph nodes

Immunocompromised patients usually have a more severe course that is frequently prolonged for weeks to months. They develop shingles frequently and the infection can spread to the skin, lungs, liver, gastrointestinal tract, brain, or other vital organs.

Potentially serious complications can result from herpes zoster. Many individuals continue to experience persistent pain long after the blisters heal. This pain, called post-herpatic neuralgia, can be severe and debilitating. Post-herpetic neuralgia can persist for months or years after the lesions have disappeared.

Other complications include a secondary bacterial infection, and rarely, potentially fatal inflammation of the brain (encephalitis) and the spread of an infection throughout the body. These rare, but extremely serious, complications are more likely to occur in those individuals who have weakened immune systems (immunocompromised).

Causes

Herpes zoster has been reported in patients with many different types of cancer. However, the cancers that affect an individual's immune system, such as leukemia or lymphoma, are the types that place people at particular risk. Herpes zoster is also a particular problem after the various forms of cancer therapy. A study performed in 1998 looked at 766 episodes of herpes zoster infection at a large cancer center from 1972 to 1980. The highest risk of infection was present among patients with lymphoma and leukemia. In those who received radiation treatment and then developed herpes zoster, half of them developed this within seven months. They developed zoster on the area of their body where the radiation was given. This study showed that a period of months can pass before developing zoster as a consequence of radiation. In those who developed zoster after being treated with chemotherapy, half of them developed zoster within a month.

A study in 1999 looked at 215 consecutive patients who had received high-dose chemotherapy and autologous stem cell rescue to help determine what the incidence and severity of herpes zoster infection was. Herpes zoster was developed in 40 people. Over 80% of these infections occurred within six months of receiving the autologous stem cell rescue. Similar rates of herpes zoster have been seen in patients who received bone marrow transplants. A 1996 study looked at 107 children who had received bone marrow transplants for various malignancies. Thirty-three percent of these children developed herpes zoster. Approximately 90% of the cases developed within one year from the time of bone marrow transplant.

Treatments

Shingles almost always resolves spontaneously and may not require any treatment except for the relief of symptoms. In most people, the condition clears on its own in one or two weeks and seldom recurs. The antiviral drugs acyclovir, valacyclovir, and famciclovir can be used to treat shingles. These drugs may shorten the course of the illness. Their use results in more rapid healing of the blisters when drug therapy is started within 72 hours of the onset of the rash. In fact, the earlier the drugs are administered, the better, because early cases can sometimes be stopped. If taken later, these drugs are less effective but may still lessen the pain. Antiviral drug treatment does not seem to reduce the incidence of postherpetic neuralgia, but recent studies suggest famciclovir may cut the duration of post-herpetic neuralgia in half. Side effects of typical oral doses of these antiviral drugs are minor with headache and nausea reported by 8-20% of patients. Severely immunocompromised individuals, such as those with cancer, may require intravenous administration of antiviral drugs. Preventive administration of acyclovir to seropositive patients (people who have evidence in their blood of past infection with varicella) who undergo leukemia induction or bone marrow transplant not only effectively prevents herpes zoster recurrence but also reduces the severity of chemotherapy-induced mucositis. Therefore, acyclovir prophylaxis should be considered in seropositive patients, especially if they have had a recurrence during previous chemotherapy cycles.

Alternative and Complementary Therapies

Cool, wet compresses may help reduce pain. If there are blisters or crusting, applying compresses made with diluted vinegar will make the patient more comfortable. The patient can mix one-quarter cup of white vinegar in two quarts of lukewarm water, and use the compress twice each day for 10 minutes. The patient should stop using the compresses when the blisters have dried up.

Soothing baths and lotions such as colloidal oatmeal baths, starch baths or lotions, and calamine lotion may help to relieve itching and discomfort. The skin should be kept clean, contaminated items should not be re-used. While the lesions continue to ooze, the person should be isolated to prevent infecting other susceptible individuals.

Later, when the crusts and scabs are separating, the skin may become dry, tight, and cracked. If that happens, the patient can rub on a small amount of plain petroleum jelly three or four times a day.

There are non-medical methods of prevention and treatment that may speed recovery. For example, getting lots of rest, eating a healthy diet, exercising regularly, and minimizing stress are always helpful in preventing disease. Supplementation with vitamin B₁₂ during the first one to two days and continued supplementation with vitamin B complex, high levels of vitamin C with bioflavonoids, and calcium, are recommended to boost the immune system. Herbal antivirals such as echinacea can be effective in fighting infection and boosting the immune system. Patients should consult physician before taking supplements.

Although no single alternative approach, technique, or remedy has yet been proven to reduce the pain, there are a few options which may be helpful. For example, topical applications of lemon balm (Melissa officinalis) or licorice (Glycyrrhiza glabra) and peppermint (Mentha piperita) may reduce pain and blistering. Homeopathic remedies include Rhus toxicodendron for blisters, Mezereum and Arsenicum album for pain, and Ranunculus for itching. Practitioners of Eastern medicine recommend self-hypnosis, acupressure, and acupuncture to alleviate pain. All of these or similar alternative therapies should be discussed with the treating physician before using.

Resources

Books

Berger, Joseph. Cecil Textbook of Medicine. 21st ed. Philadelphia: W.B. Saunders Company, 2000.

Periodicals

Bilgrami, S., et al. "Varicella zoster virus infection associated with high-dose chemotherapy and autologous stem-cell rescue." Bone Marrow Transplant 23 (March 1999): 469–74.

—David Greenberg, M.D.

(acute posterior ganglionitis, shingles), an acute viral disease involving the dorsal spinal root or cranial nerve and producing vesicular eruption in areas of the skin corresponding to the involved sensory nerve. Pain is a prominent feature and may persist, although skin lesions subside in 1 to 2 weeks.

Herpes zoster. (Ibsen/Phelan, 2000)

Definition

Shingles, also called herpes zoster, gets its name from both the Latin and French words for belt or girdle and refers to girdle-like skin eruptions that may occur on the trunk of the body. The virus that causes chickenpox, the Varicella zoster virus (VSV), can become dormant in nerve cells after an episode of chickenpox and later re-emerge as shingles.

Initially, red patches of rash develop into blisters. Because the virus travels along the nerve to the skin, it can damage the nerve and cause it to become inflamed. This condition can be very painful. If the pain persists long after the rash disappears, it is known as post-herpetic neuralgia (PHN).

Description

Any individual who has had chickenpox can develop shingles. Between 600,000 and one million Americans are diagnosed with shingles each year. Overall, approximately 20% of those who have had chickenpox as children develop shingles at some time in their lives. People of all ages—even children—can be affected, but the incidence increases with age. Newborns, bone marrow and other transplant recipients, and individuals with immune systems weakened by disease or drugs are also at increased risk. However, most individuals who develop shingles do not have any underlying malignancy or other immunosuppressive condition.

Causes & Symptoms

Shingles erupts along the course of the affected nerve, producing lesions anywhere on the body. The condition may cause severe nerve pain. The most common areas to be affected are the face and trunk, which correspond to the areas where the chickenpox rash is most concentrated. There is usually a line of eruptions running from the spine along the path of the affected nerve on one side of the body.

The disease is caused by a reactivation of the chickenpox virus that has lain dormant in certain nerves following an episode of chickenpox. Exactly how or why this reactivation occurs is not clear. In 2002 clinicians pointed out that one of the causes of increasing cases of shingles was actually the success of chicken pox vaccinations. It is believed that the reactivation is triggered when the immune system becomes weakened as a result of age, stress, fatigue, certain medications, chemotherapy, or diseases such as cancer or HIV. Furthermore, in persons with HIV, shingles can be an early sign that the immune system has deteriorated.

Early signs of shingles are often vague and can easily be mistaken for other illnesses. The condition may begin with fever and malaise (a vague feeling of weakness or discomfort). Within two to four days, severe pain, itching, and numbness/tingling (paresthesias) or extreme sensitivity to touch (hyperesthesia) can develop, usually on the trunk and occasionally on the arms and legs.

Pain may be continuous or intermittent, usually lasting one to three weeks. It may occur at the time of the eruption, but can precede the eruption by days, occasionally making the diagnosis difficult.

Signs and symptoms may include the following:

• itching, tingling, or severe burning pain
• red patches that develop into blisters
• dense clusters of small blisters that ooze and crust
• swollen lymph nodes

Diagnosis

Diagnosis usually is not possible until the skin lesions develop. Once they develop, however, the pattern and location of the blisters and the type of cell damage displayed are characteristic of the disease. This feature allows an accurate diagnosis based primarily upon the physical examination. Although tests are rarely necessary, they may include the following:

• Viral culture of skin lesion.
• Microscopic examination using a Tzanck preparation. This involves staining a smear obtained from a blister. Cells infected with the herpes virus appear very large and contain many dark cell centers or nuclei.
• Complete blood count (CBC) may show an elevated white blood cell count (WBC), a nonspecific sign of infection.

Treatment

A person with shingles should immediately see a doctor or health practitioner. Although the condition generally clears up within three to five weeks, treatment can ease the painful symptoms. Alternative medicine remedies and therapies will not cure shingles, but they will provide pain relief, reduce inflammation, and speed recovery.

Herbal Remedies

Many herbs can be used to treat shingles. Some remedies involve brewing tea and then consuming and/or applying it to the affected area. Herbs used to treat shingles include:

• Red pepper, also known as capsicum or cayenne, is so effective that it's an ingredient in commercial ointments approved by the U.S. Food and Drug Administration. Commercial preparations include Zostrix and Capzasin-P. Red pepper is hot, so the ointment should be applied only to healed blisters. Red pepper is useful for treating painful PHN.
• Topical applications of lemon balm, licorice, or peppermint may reduce pain and blistering. These herbs may be brewed as teas and then consumed and applied to the skin.
• Herbal antivirals, such as echinacea, can be effective in fighting infection and boosting the immune system.
• Calendula ointment or lotion works to counter the virus.
• Sedative herbs such as passionflower can be brewed for a tea. Such herbs can help with treatment of post-herpetic neuralgia.
• Vervain helps relieve pain and inflammation. St. John's wort, lavender, chamomile, and marjoram also help relieve inflammation.

Homeopathic Remedies

A person with shingles should consult a homeopath for specific remedies and dosages. Homeopathic remedies include Ranunculus, which is effective for shingles on the trunk. It is also taken for itching. A homeopath may recommend Rhus toxicodendron for blisters and Arsenicum album or Hypericum for pain.

Traditional Chinese Medicine

Practitioners of traditional Chinese medicine (TCM) recommend acupressure and acupuncture to alleviate pain. Acupuncture can help with post-herpetic neuralgia. In addition, a TCM practitioner may recommend herbal remedies such as Chinese gentian root, which is used to treat the liver. In addition, Chinese skullcap root is combined with water and used as a folk remedy for treating shingles in China. Also, certain herbal combinations can treat specific symptoms and contributing causes. For example, Long Dan Xie Gan Tang can quell the accumulation of damp toxic heat in the liver. For damp infected painful eruptions on the torso, Huang Qin Gao can be applied to the surrounding area.

Diet and Nutrition

To boost the immune system, supplement the diet with vitamin B during the first one or two days. Until health returns, continue to supplement with vitamin B complex, high levels of vitamin C with bioflavonoids, and calcium.

Food seasoned with red pepper (capsicum) may provide relief, as may foods containing the amino acid lysine. High-lysine foods include soybeans, black bean sprouts, lentils, parsley, and peas.

Home Remedies

Cool wet compresses may help reduce pain while blisters or crusting is present. Patients may be made more comfortable with the application of a cloth dipped in one-quarter cup (60 ml) of white vinegar mixed in two quarts (1.9 l) of lukewarm water. Compresses should be used twice daily for 10 minutes. When blisters dry up, the compresses may be discontinued.

Soothing treatments such as colloidal oatmeal baths, starch baths or lotions, and calamine lotion may help to relieve itching and discomfort.

When the crusts and scabs are separating, the skin may become dry, tight, and cracked. If that happens, a small amount of plain petroleum jelly can be applied to the area three or four times daily.

Ayurvedic Medicine

Ayurveda is an Indian healing science that is more than 5,000 years old. Treatment is based on maintaining a balance between the body and the world. Treatment for shingles may include applying a turmeric paste to the skin.

Relaxation Techniques

Relaxation techniques can be used to treat symptoms of shingles. Techniques such as hypnotherapy and yoga can help a person relax.

Flower Remedies

Flower remedies are liquid concentrates made by soaking flowers in spring water. Also known as flower essences, 38 remedies were developed by the homeopathic physician Edward Bach during the 1930s. A 39th combination formula, known as Rescue Remedy is taken to relieve stress. The remedy is taken by placing several drops under the tongue four times daily. Alternately, the drops may be added to a glass of water. The patient drinks the mixture throughout the day.

Reflexology

Reflexology is the manipulation of the foot to bring the body into balance. Reflex points on the foot correspond to parts of the body. These points can be treated by a reflexologist or at home by following instructions on a reflex chart.

Allopathic Treatment

The antiviral drugs acyclovir, valacyclovir, and famciclovir can be used to treat shingles. These drugs may shorten the course of the illness. More rapid healing of the blisters results when drug therapy is started within 72 hours of the onset of the rash. In fact, the earlier the drugs are administered the better, because early cases can sometimes be halted. If taken later, these drugs are less effective but may still lessen the pain. Antiviral drug treatment does not seem to reduce the incidence of post-herpetic neuralgia (PHN), but recent studies suggest famciclovir may cut the duration of PHN in half.

Side effects of typical oral doses of these antiviral drugs are minor, with headache and nausea reported by 8–20% of patients. Severely immuno compromised individuals, such as those diagnosed with AIDS, may require intravenous administration of antiviral drugs. Corticosteroids such as prednisone may be used to reduce inflammation but they interfere with the functioning of the immune system. Corticosteroids in combination with antiviral therapy are also used to reduce severe pain and to treat severe infections, such as those affecting the eyes.

After the blisters heal, some people continue to experience PHN for months or even years. This pain can be excruciating. Consequently, the doctor may prescribe tranquilizers, sedatives, or antidepressants to be taken at night. Attempts to treat PHN with famciclovir have shown some promising results. When all else fails, severe pain may require a permanent nerve block.

Expected Results

Shingles usually clears up within three to five weeks and rarely recurs. There have been reports that shingles cleared up several days after licorice ointment was applied to the skin or when the homeopathic remedy Ranunculus was taken.

If the nerves that cause movement are affected, temporary or permanent nerve paralysis and/or tremors may occur. Elderly or debilitated patients may have a prolonged and difficult course and recovery. For them, the eruption is typically more extensive and inflammatory, occasionally resulting in blisters that bleed, areas in which the skin actually dies, secondary bacterial infection, or extensive and permanent scarring.

Similarly, patients with compromised immune systems usually have more severe courses that are often prolonged for weeks to months. They develop shingles frequently and the infection can spread to the skin, lungs, liver, gastrointestinal tract, brain, or other vital organs.

Cases of chronic shingles have been reported in AIDS patients, especially when they have a decreased number of one particular kind of immune cell called CD4 lymphocytes. Depletion of CD4 lymphocytes is associated with more severe, chronic, and recurrent varicella zoster virus infections. Lesions are typical at the onset but may turn into ulcers that do not heal. Herpes zoster can lead to potentially serious complications.

Many individuals continue to experience persistent pain long after the blisters heal. This post-herpetic neuralgia can be severe and debilitating. The incidence of post-herpetic neuralgia increases with age, and episodes in older individuals tend to be of longer duration. Most patients under 30 years of age experience no persistent pain. By age 40, the risk of prolonged pain lasting longer than one month increases to 33%. By age 70, the risk increases to 74%. The pain can adversely affect quality of life, but it usually diminishes over time.

Other complications include secondary bacterial infections.

Prevention

Strengthening the immune system by making lifestyle changes is thought to help prevent the development of shingles. These changes include eating a well-balanced diet rich in essential vitamins and minerals, getting enough sleep, exercising regularly, and reducing stress.

In 2002, reports from a large, five-year study showed that researchers might be nearing a workable vaccine for shingles. The vaccine is 10 times stronger than the chickenpox vaccine and similar in nature. Study results were planned for release in mid-2004.

Resources

Books

Cummings, Stephen, and Dana Ullman. Everybody's Guide to Homeopathic Medicines. New York: Putnam, 1997.

Duke, James A. The Green Pharmacy. Emmaus, PA.: Rodale Press, 1997.

Gottlieb, Bill. New Choices in Natural Healing. Emmaus, PA.: Rodale Press, 1995.

Keville, Kathi. Herbs for Health and Healing. Emmaus, PA.: Rodale Press, 1996.

L'Orange, Darlena. Herbal Healing Secrets of the Orient. Paramus, NJ: Prentice Hall, 1998.

Squier, Thomas Broken Bear, with Lauren David Peden. Herbal Folk Medicine. New York: Henry Holt, 1997.

Ullman, Dana. The Consumer's Guide to Homeopathy. New York: Putnam, 1995.

Periodicals

Landers, Susan J. "Rash of Pain: With an Increasingly Large Patient Population at Risk for Shingles, Researchers Focus on Uncovering New Ways to Prevent and Treat this Viral Response." American Medical News (April 1, 2002):32.

MacKenzie, Deborah. "The Hidden Catch: Although Chickenpox is Nasty, Vaccination Might Not be the Answer." New Scientist (May 4, 2002):7.

Organizations

American Academy of Dermatology. 930 N. Meacham Road, P.O. Box 4014, Schaumberg, IL 60168-4014. (708) 330-0230. http://www.aad.org/zoster.html.

American Botanical Council. P.O. Box 201660, Austin TX, 78720. (512) 331-8868. http://www.herbalgram.org.

Herb Research Foundation. 1007 Pearl St., Suite 200, Boulder, CO 80302. (303) 449-2265. http://www.herbs.org.

Other

MotherNature.com Health Encyclopedia.http://www.mothernature.com/ency.

[Article by: Liz Swain; Teresa G. Odle]

"Zoster" redirects here. For the ancient Greek article of dress, see Zoster (costume).

"Shingles" redirects here. For other uses, see Shingle (disambiguation).

Herpes zoster
Classification and 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 simply zoster), commonly known as shingles and also known as zona, 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] 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.^[3][4] 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.^[5][6][7] 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.^[5][8]

Contents 1 Name 2 Signs and symptoms 3 Pathophysiology 4 Diagnosis 5 Prevention 6 Treatment 6.1 Analgesics 6.2 Antivirals 6.3 Steroids 6.4 Herpes zoster ophthalmicus 7 Prognosis 8 Epidemiology 9 History 10 See also 11 References 12 External links

Name

The name herpes zoster comes from Greek zōstēr, meaning "belt" or "girdle", after the characteristic belt-like dermatomal rash.^[9] The name shingles represents Latin cingulus, a variant of Latin cingulum meaning "girdle".

Signs and symptoms

The earliest symptoms of herpes zoster, which include headache, fever, and malaise, are nonspecific, and may result in an incorrect diagnosis.^[5][10] These symptoms are commonly followed by sensations of burning pain, itching, hyperesthesia (oversensitivity), or paresthesia ("pins and needles": tingling, pricking, or numbness).^[11] The pain may be mild to 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.^[12] Herpes Zoster in children is often painless.

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, normally resulting in a stripe or belt-like pattern that is limited to one side of the body and does not cross the midline.^[11] Zoster sine herpete describes a patient who has all of the symptoms of herpes zoster except this characteristic rash.^[13]

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.^[11]

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 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.^[14] 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]

Pathophysiology

Progression of herpes zoster. A cluster of small bumps (1) turns into blisters (2). The blisters fill with lymph, break open (3), crust over (4), and finally disappear. Postherpetic neuralgia can sometimes occur due to nerve damage (5),

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.^[15] Repeated attacks of herpes zoster are rare,^[11] and it is extremely rare for patients to suffer more than three recurrences.^[15]

Herpes zoster occurs only in people who have had chickenpox, and although it can occur at any age, the majority of sufferers are more than 50 years old.^[16] The disease results from the virus reactivating in a single sensory ganglion.^[4] 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.^[2][17] Although VZV has been detected in autopsies of nervous tissue,^[18] 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,^[6] 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.^[19] 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.^[20]

The symptoms of herpes zoster cannot be transmitted to another person.^[21] 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 will not immediately develop shingles. Until 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 rash has disappeared.^[11]

Diagnosis

Herpes zoster on the chest

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.^[22]

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.^[23] 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.^[24] 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.^[25]

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.^[26]

Prevention

A live vaccine for VZV exists, marketed as Zostavax.^[27] 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.^[28] 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.^[29] In October 2007 the vaccine was officially recommended in the U.S. for healthy adults aged 60 and over.^[30][27] As of October 2008^[update], a controlled study is underway to evaluate the effectiveness on those aged 50–59.^[31] 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.^[8][32]

In the United Kingdom and other parts of Europe, population-based immunization is not practised. The rationale is that, until the entire population could be immunized, adults who have previously contracted VZV would derive benefit from occasional exposure to VZV (from children), which serves as a booster to their immunity to the virus, and may reduce the risk of shingles later on in life.^[33] 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.^[34]

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 a risk three times as great as those who consumed more than 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.^[35]

Treatment

Herpes zoster on lower back

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.^[36] However, a study on untreated herpes zoster shows that pain once the rash has cleared (post herpetic neuralgia) is very rare in people under 50 and wears off in time; in older people the pain wore off more slowly, but even in people over 70, 85% were pain free one year after their shingles outbreak.^[37]

Analgesics

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.^[38] Administering gabapentin along with antivirals may offer relief of postherpetic neuralgia.^[36]

Antivirals

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, acyclovir has been the standard treatment, but the new drugs valacyclovir and famciclovir demonstrate similar or superior efficacy and good safety and tolerability.^[36] 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.^[39] Complications in immunocompromised individuals with herpes zoster may be reduced with intravenous acyclovir. In people who are at a high risk for repeated attacks of shingles, five daily oral doses of acyclovir are usually effective.^[1]

Steroids

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.^[40] 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 and 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.^[40]

Herpes zoster ophthalmicus

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.^[41] The significant advantage of valciclovir over aciclovir is its dosing of only 3 times/day (compared with aciclovir's 5 times/day dosing), which could make it more convenient for patients and improve adherence with therapy.^[42]

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.^[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.^[43][44]

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.^[45] Instead, the increased risk may result from the immune suppression that allows the reactivation of the virus.^[46]

Epidemiology

Electron micrograph of Varicella zoster virus. Approx. 150,000-fold magnification.

Varicella zoster virus has a high level of infectivity and is prevalent worldwide,^[47] and has a very stable prevalence from generation to generation.^[48] 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.^[49] Infections of varicella in institutions such as hospitals are also a significant problem, especially in hospitals that care for these high-risk populations.^[50]

In general, herpes zoster has no seasonal incidence and does not occur in epidemics.^[19] 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.^[51] 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.^[19]

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.^[5] Similar incidence rates have been observed worldwide.^[5][7] Herpes zoster develops in an estimated 500,000 Americans each year.^[52] Multiple studies and surveillance data, at least when viewed superficially, demonstrate no consistent trends in incidence in the U.S. since the chickenpox vaccination program began in 1995.^[53] However, upon closer inspection, the two studies that showed no increase in shingles incidence were conducted among populations where varicella vaccination was not as yet widespread in the community.^[54][55] A recent study by Patel et al. concluded that since the introduction of the chickenenpox vaccine, hospitalization costs for complications of shingles have increased by more than $700 million annually for those over 60 years.^[56] Another study by Yih et al. reported that as varicella vaccine coverage in children increased, the incidence of varicella decreased and the occurrence of shinges among adults increased 90%.^[57] The results of a further study by Yawn et al. showed a 28% increase in shingles incidence from 1996 to 2001.^[58] Additionally, there was a statistically significant increase in adult shingles cases reported to the Antelope Valley Varicella Active Surviellance Project (VASP) from 2000 to 2003. The 56.1% increase from 237 cases in 2000 to 370 cases in 2002 yields a rate ratio of 1.4 (95% C.I. 1.2–1.7). Increases in cases of shingles reported to VASP occurred in every age category (except 70+) from 2000 to 2001. VASP also reported verified cases of shingles among adults aged 50 years and older increased 27.5% from 2006 to 2007. (Annual Summary, 2001, 2002, 2003, 2006, 2007 Antelope Valley Varicella Active Surveillance Project, Los Angeles County Department of Health Services; Centers for Disease Control and Prevention (CDC) Cooperative Agreement No. U66/CCU911165-10; Mascola L, et al.) 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.^[5]

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.^[59] 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.^[60] 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.^[61]

A 2008 study revealed that people with close relatives who have had shingles are twice as likely to develop it themselves. The study speculates that there are genetic factors in who is more susceptible to VZV.^[62]

History

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,^[63] and only in the late nineteenth century that herpes zoster was differentiated from erysipelas. In 1831, Richard Bright hypothesized that the disease arose from the dorsal root ganglion, and this was confirmed in an 1861 paper by Felix von Bärunsprung.^[64]

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.^[65]

Until the 1940s, the disease was considered benign, and serious complications were thought to be very rare.^[66] 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.^[50] 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 (i.e., 50%) would have at least one attack of herpes zoster, and 10 (i.e., 1%) would have at least two attacks.^[67]

In historical shingles studies, shingles incidence generally increased with age. However, in his 1965 paper, Dr. Hope-Simpson was first to suggest, “The peculiar age distribution of zoster may in part reflect the frequency with which the different age groups encounter cases of varicella and because of the ensuing boost to their antibody protection have their attacks of zoster postponed.” Lending support to this hypothesis that contact with children with chickenpox boosts adult cell-mediated immunity to help postpone or suppress shingles, is the study by Thomas et al. which reported that adults in households with children, had lower rates of shingles than households without children.^[68] Also, the study by Terada et al. indicated that pediatricians reflected incidence rates from 1/2 to 1/8 that of the general population their age.^[69]

See also

• Disseminated herpes zoster
• Inflammatory skin lesions following zoster infection

References

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External links

• NINDS Shingles Information Page, National Institute of Neurological Disorders and Stroke
• Herpes zoster at the Open Directory Project
• Links to pictures of Shingles (Hardin MD) University of Iowa
• Facts About The Cornea and Corneal Disease: Herpes Zoster (Shingles), National Eye Institute

v • d • e Diseases of the skin and appendages by morphology Growths Epidermal wart · callus · seborrheic keratosis · acrochordon · molluscum contagiosum · actinic keratosis · squamous cell carcinoma · basal cell carcinoma · merkel cell carcinoma · nevus sebaceous · trichoepithelioma Pigmented Freckles · lentigo · melasma · nevus · melanoma Dermal and subcutaneous epidermal inclusion cyst · hemangioma · dermatofibroma · keloid · lipoma · neurofibroma · xanthoma · Kaposi's sarcoma · infantile digital fibromatosis · granular cell tumor · leiomyoma · lymphangioma circumscriptum · myxoid cyst Rashes With epidermal involvement Eczematous contact dermatitis · atopic dermatitis · seborrheic dermatitis · stasis dermatitis · lichen simplex chronicus · Darier's disease · glucagonoma syndrome · langerhans cell histiocytosis · lichen sclerosus · pemphigus foliaceus · Wiskott-Aldrich syndrome · Zinc deficiency Scaling psoriasis · tinea (corporis · cruris · pedis · manuum · faciei) · pityriasis rosea · secondary syphillis · mycosis fungoides · systemic lupus erythematosus · pityriasis rubra pilaris · parapsoriasis · ichthyosis Blistering herpes simplex · herpes zoster · varicella · bullous impetigo · acute contact dermatitis · pemphigus vulgaris · bullous pemphigoid · dermatitis herpetiformis · porphyria cutanea tarda · epidermolysis bullosa simplex Papular scabies · insect bite reactions · lichen planus · miliaria · keratosis pilaris · lichen spinulosus · transient acantholytic dermatosis · lichen nitidus · pityriasis lichenoides et varioliformis acuta Pustular acne vulgaris · acne rosacea · folliculitis · impetigo · candidiasis · gonococcemia · dermatophyte · coccidioidomycosis · subcorneal pustular dermatosis Hypopigmented tinea versicolor · vitiligo · pityriasis alba · postinflammatory hyperpigmentation · tuberous sclerosis · idiopathic guttate hypomelanosis · leprosy · hypopigmented mycosis fungoides Without epidermal involvement Red Blanchable Erythema Generalized drug eruptions · viral exanthems · toxic erythema · systemic lupus erythematosus Localized cellulitis · abscess · boil · erythema nodosum · carcinoid syndrome · fixed drug eruption Specialized urticaria · erythema (multiforme · migrans · gyratum repens · annulare centrifugum · ab igne) Nonblanchable Purpura Macular thrombocytopenic purpura · actinic purpura Papular disseminated intravascular coagulation · vasculitis Indurated scleroderma/morphea · granuloma annulare · lichen sclerosis et atrophicus · necrobiosis lipoidica Miscellaneous disorders Ulcers Hair telogen effluvium · androgenic alopecia · trichotillomania · alopecia areata · systemic lupus erythematosus · tinea capitis · loose anagen syndrome · lichen planopilaris · folliculitis decalvans · acne keloidalis nuchae Nail onychomycosis · psoriasis · paronychia · ingrown nail Mucous membrane aphthous stomatitis · oral candidiasis · lichen planus · leukoplakia · pemphigus vulgaris · mucous membrane pemphigoid · cicatricial pemphigoid · herpesvirus · coxsackievirus · syphilis · systemic histoplasmosis · squamous cell carcinoma

v • d • e Infectious diseases · Viral diseases (A80–B34, 042–079) Oncovirus DNA virus: HBV (Hepatocellular carcinoma) · HPV (Cervical cancer) · Kaposi's sarcoma-associated herpesvirus (Kaposi's sarcoma) · Epstein-Barr virus (Nasopharyngeal carcinoma, Burkitt's lymphoma, Primary central nervous system lymphoma) · MCPyV (Merkel cell cancer) · SV40 RNA virus: HCV (Hepatocellular carcinoma) · HTLV-I (Adult T-cell leukemia/lymphoma) Immune disorders HIV (AIDS) Central nervous system Encephalitis/ meningitis DNA virus: JCV (Progressive multifocal leukoencephalopathy) RNA virus: MeV (Subacute sclerosing panencephalitis) · LCV (Lymphocytic choriomeningitis) · Arbovirus encephalitis · Orthomyxoviridae (probable) (Encephalitis lethargica) · RV (Rabies) Myelitis Poliovirus (Poliomyelitis, Post-polio syndrome) · HTLV-I (Tropical spastic paraparesis) Eye Cytomegalovirus (Cytomegalovirus retinitis) · HSV (Herpetic keratitis) Cardiovascular CBV (Pericarditis, Myocarditis) Respiratory system/ acute viral nasopharyngitis/ viral pneumonia DNA virus Epstein-Barr virus (EBV infection/Infectious mononucleosis) · Cytomegalovirus RNA virus IV: SARS coronavirus (Severe acute respiratory syndrome) V, Orthomyxoviridae: Influenzavirus A/B/C (Influenza/Avian influenza) V, Paramyxovirus: Human parainfluenza viruses (Parainfluenza) · RSV · hMPV Digestive system Oropharynx/Esophagus MuV (Mumps) · Cytomegalovirus (Cytomegalovirus esophagitis) Gastroenteritis/ diarrhea DNA virus: Adenovirus (Adenovirus infection) RNA virus: Rotavirus · Norovirus · Astrovirus · Coronavirus Hepatitis DNA virus: HBV (B) RNA virus: CBV · HAV (A) · HCV (C) · HDV (D) · HEV (E) · HGV (G) Pancreatitis CBV Skin and mucous membrane lesions, including exanthem DNA virus Herpesviridae HSV (Herpes simplex, Herpetic whitlow) · VZV (Chickenpox, Herpes zoster) · Human herpesvirus 6/Roseolovirus (Exanthema subitum) · KSHV (Kaposi's sarcoma) · Herpes B Virus Poxviridae Variola (Smallpox) · MoxV (Monkeypox) · CV (Cowpox) · VV (Vaccinia) · MCV (Molluscum contagiosum) Other HPV (Wart/Plantar wart) · Parvovirus B19 (Erythema infectiosum, Reticulocytopenia) RNA virus MeV (Measles) · Rubella virus (Rubella, Congenital rubella syndrome) picornavirus: CAV (Hand, foot and mouth disease, Herpangina) · FMDV (Foot-and-mouth disease) Urogenital BK virus · MuV (Mumps) see also DNA antivirals, RNA antivirals, Antiretroviral drug

v • d • e Varicella zoster Infections Chickenpox - Herpes zoster - Postherpetic neuralgia Other Varicella zoster virus - Varicella vaccine - Zostavax - Pox party

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