Herpes zoster

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"Shingles" redirects here, for other uses of the term, see Shingle.

**Herpes zoster**
*Classification & external resources*

Herpes zoster blisters on the neck and shoulder
ICD-10	B 02.
ICD-9	053
DiseasesDB	29119
MedlinePlus	000858
eMedicine	med/1007

Herpes zoster, colloquially known as shingles, is the reactivation of varicella zoster virus (one of the Herpesviridae group), leading to a crop of painful blisters over the area of a dermatome. In Italy and in Malta, it is sometimes referred to as "St. Anthony's fire". Prior to implementation of the universal varicella vaccination program in the U.S., incidence of shingles increased with advancing age. The incidence rate in children aged less than 10 years was approximately 70 cases/100,000 person-years, increasing to 550 cases/100,000 person-years among adults aged 50 to 59 years. Historically, it was thought that shingles incidence increased due to an age-related decline in immunity; however, recent studies ^[1] suggest that incidence of shingles is linked to the reduced frequency of periodic exogenous (outside) exposures to children with varicella (chickenpox) due to the increasing vaccination of that population. These exposures produced an immunologic boost that helped suppress the reactivation of shingles. Shingles incidence is high in the elderly (over 60), as well as in any age group of immunocompromised patients. It affects some 1 million people per year in the United States and can involve excruciating pain. Many patients develop a painful condition called postherpetic neuralgia which is often difficult to manage.

Treatment is generally with antiviral drugs such as acyclovir (Zovirax), famciclovir (Famvir) or valacyclovir (Valtrex). For the antiviral drugs to be effective, patients typically need to begin taking them within 2-3 days of the appearance of the rash.

In some patients, herpes zoster can reactivate subclinically with pain in a dermatomal distribution without rash. This condition is known as zoster sine herpete and may be more complicated, affecting multiple levels of the nervous system and causing multiple cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis.

The word herpes comes from the Greek word for snake; it is cognate with herpetology.

1 Signs and symptoms
2 Diagnosis
3 Pathophysiology
4 Therapy
5 Prognosis
6 Stages
7 References
8 External links

[edit] Signs and symptoms

The earliest symptoms of shingles include headache, sensitivity to light, flu-like symptoms without fever, as well as itching, tingling, and extreme pain where the rash is developing. Often, pain is the first symptom. This pain can be characterized as stinging, tingling, numbing, or throbbing, and can be pronounced with quick stabs of intensity. Then 1-3 crops of red lesions develop, which gradually turn into small blisters filled with serous fluid. A general feeling of unwellness often occurs. In some cases, the rash does not form blisters, but has an appearance much like urticaria ("hives").

Shingles cannot be passed from one person to another. However, the virus that causes shingles, VZV, can be spread from a person with active shingles to a person who has never had chickenpox through direct contact with the rash. The person exposed would then develop chickenpox, not shingles. The virus is not spread through sneezing, coughing or casual contact. A person with shingles can spread the disease when the rash is in the blister-phase. Once the rash has developed crusts, the person is no longer contagious. A person is not infectious before blisters appear or with post-herpetic neuralgia (pain after the rash is gone).

Chickenpox virus can remain dormant for decades, and does so inside the ganglion near the spinal cord. As the virus is reactivated it spreads down peripheral nerve fibers and produces intense pain. The blisters therefore only affect one area of the body and do not cross the midline. They are most common on the torso, but can also appear on the face (where they are potentially hazardous to vision) or other parts of the body.

Outbreaks occur for many different reasons, most of which are a result of events which decrease the immune system such as aging, severe emotional stress, severe illness or long-term use of corticosteroids. There have been recorded cases of outbreaks occurring due to unmanaged stress or other stresses to the skin such as pinching in more sensitive areas of the skin (nipples, ears, and underarms), scratching, or biting.

[edit] Diagnosis

The diagnosis is visual; very few other diseases mimic herpes zoster, especially in the localization of the rash, which is otherwise quite similar in appearance and initial effect to that of poison oak or poison ivy. In case of doubt, herpes tests can be performed where fluid from a blister may be taken so the cells can be analyzed in a medical laboratory. Herpes test are among many possible forms of testing for the disease. Physicians can take a viral culture of the skin, which involves a microscopic examination of the skin using a Tzanck preparation. While looking at the cell obtained from the blister, the cells infected with the herpes virus will appear very large and contain many dark nuclei. By taking a complete blood count there may be an elevated number of white blood cells, which is an indirect sign of infection. There may also be a rise in the antibody to the virus that will give indication of the virus’ reactivation as well. Lab tests are necessary because, depending on the affected sensory nerve, the pain that is experienced before the onset of the rash may be misdiagnosed as pleurisy, myocardial infarction, appendicitis, cholelithiasis, or a migraine headache.

[edit] Pathophysiology

A course of Shingles

The causative agent for herpes zoster is varicella zoster virus (VZV). Most people are infected with this virus as a child, as it causes chickenpox. The body eliminates the virus from the system, but it remains dormant in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the cranial base.

Generally, the immune system suppresses reactivation of the virus. In the elderly, whose immune response generally tends to deteriorate, as well as in those patients whose immune system is being suppressed, this process fails. (Some researchers speculate that sunburn and other, unrelated stresses that can affect the immune system may also lead to viral reactivation.) The virus starts replicating in the nerve cells, and newly formed viruses are carried down the axons to the area of skin served by that ganglion (a dermatome). Here, the virus causes local inflammation in the skin, with the formation of blisters.

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

[edit] Therapy

Acyclovir (an antiviral drug) inhibits replication of the viral DNA, and is used both as prophylaxis (e.g., in patients with AIDS) and as therapy for herpes zoster. Other antivirals are valacyclovir and famciclovir. During the acute phase oral acyclovir should be given five times daily for 7 to 10 days. Immunocompromised patients may respond best to intravenous acyclovir. In patients who are at high risk for recurrences, an oral dose of acyclovir, taken twice daily, is usually effective. Use of acylovir is most effective in moderating the progress of the symptoms if taken as early as possible, so medical care should be obtained as soon as the condition is recognized.

It is also reported that the amino acid lysine inhibits the replication of herpes zoster.^[2]

The long term complication postherpetic neuralgia may cause persistent pain that lasts for years. Pain management is difficult as conventional analgesics may be ineffective. Alternative agents are often used, including tricyclic antidepressants (particularly amitriptyline), anticonvulsants (e.g. gabapentin), and/or topical capsaicin.

Zostavax is a vaccine developed by Merck & Co. which has proven successful in preventing half the cases of herpes zoster in a study of 38,000 people who received the vaccine.^[3] The vaccine also reduced by two-thirds the number of cases of postherpetic neuralgia.^[4] However, prior to the vaccine, it has long been known that adults received natural immune boosting from contact with children infected with varicella. This helped to suppress the reactivation of herpes zoster.^[5] In Massachusetts, herpes zoster incidence increased 90%, from 2.77/1000 to 5.25/1000 in the period of increasing varicella vaccination 1999-2003.^[6] The effectiveness of the varicella vaccine itself is dependent on this exogenous (outside) boosting mechanism. Thus, as natural cases of varicella decline, so has the effectiveness of the vaccine.^[7]

Often the same treatment given to burn victims relieves the pain of shingles, including over-the-counter moist burn pads.

[edit] Prognosis

The rash and pain usually subside within 3 to 5 weeks. The most common chronic complication of herpes zoster is postherpetic neuralgia. Pain that persists for longer than one to three months after resolution of the rash is generally accepted as the sign of postherpetic neuralgia. Sometimes serious effects including partial facial paralysis (usually temporary), ear damage, or encephalitis may occur. Shingles on the upper half of the face (the first branch of the trigeminal nerve) may result in eye damage and require urgent ophthalmological assessment. Ocular complications occur in approximately one half of patients with involvement of the ophthalmic division of the trigeminal nerve. These complications include mucopurulent conjunctivitis, episcleritis, keratitis and anterior uveitis. Cranial nerve palsies of the third, fourth and sixth cranial nerves may occur, affecting extraocular motility.

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

[edit] Stages

Back or underarm pain and small rash spots appear
Rash (itchy for some) spreads around the body
More pain develops
Bubbles filled with fluid pop up
After 4-5 days pain is gone and bubbles turn dark purple and peel off

Herpes zoster blisters day 1.

Herpes zoster blisters day 2.

Herpes zoster blisters day 5, pain disappearing.

Herpes zoster blisters day 6, characteristic purple colour.

[edit] References

^ M.N. Oxman et al. The Shingles Prevention Study Group (2005). "A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". New England Journal of Medicine 253 (22): 2271-2284. PMID 15930418.
^ Griffith, RS; Walsh DE, Myrmel KH, Thmpson RW, and Behforooz A (1987). "Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis". Dermatologica 175 (4): 183-190.
^ Oxman MN, Levin MJ, Johnson GR, et al (2005). "A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". New England Journal of Medicine 352 pages=2271–84. PMID 15930418.
^ M.N. Oxman et al. The Shingles Prevention Study Group (2005). "A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". New England Journal of Medicine 253 (22): 2271-2284. PMID 15930418.
^ Brisson M, Gay N, Edmunds W, Andrews N (2002). "Exposure to varicella boosts immunity to herpes-zoster: implications for mass vaccination against chickenpox.". Vaccine 20 (19-20): 2500-7. PMID 12057605.
^ W.K. Yih et al. Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care (2005). "The incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccination coverage, 1998-2003". BMC Public Health 5 (1): 68-68. PMID 15960856.
^ G.S. Goldman. Medical Veritas International Inc. (2005). "Universal varicella vaccination: efficacy trends and effect on herpes zoster". International Journal of Toxicology 24 (4): 205-213. PMID 16126614.