| Herpes zoster
|
| ICD-10 code:
| B02
|
| ICD-9 code:
| 053
|
Herpes zoster, colloquially known as shingles, is the reactivation of varicella zoster virus, leading to a crop of painful blisters over the area of a dermatome. It occurs very rarely in children and adults, but its incidence is high in the elderly (over 60), as well as in any age group of immunocompromised patients. It affects some 500,000 people per year in the United States. Treatment is generally with antiviral drugs such as aciclovir. Many patients develop a painful condition called postherpetic neuralgia which is often difficult to manage.
Contents
- 1 Signs and symptoms
- 2 Diagnosis
- 3 Pathophysiology
- 4 Therapy
- 5 Prognosis
- 6 References
- 7 External links
|
Signs and symptoms
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 2-3 crops of red lesions develop, which gradually turn into small blisters filled with serous fluid. A general feeling of unwellness often occurs.
As long as the blisters have not dried out, HZ patients may transmit the virus to others. This could lead to chickenpox in people (mainly young children) who are not yet immune to this virus.
Shingles blisters are unusual in that they only appear on one side of the body. That is because the chickenpox virus can remain dormant for decades, and does so inside the spinal column or a nerve fiber. If it reactivates as shingles, it affects only a single nerve fiber, or ganglion, which can radiate to only one side of the body. 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.
Diagnosis
The diagnosis is visual — very few other diseases mimic herpes zoster. In case of doubt, fluid from a blister may be analysed in a medical laboratory.
Pathophysiology
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 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.
Therapy
Aciclovir (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 valaciclovir and famciclovir. Steroids are often given in severe cases.
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 capscaicin).
A vaccine called live attenuated Oka/Merck VZV that has been developed by Merck & Co. has proven successful in preventing half the cases of herpes zoster in a study of 38,000 people who received the vaccine. The vaccine also reduced by two-thirds the number of cases of postherpetic neuralgia (Oxman et al., 2005). 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. In Massachusetts, herpes zoster incidence increased 90%, from 2.77/1000 to 5.25/1000 in the period of increasing varicella vaccination 1999-2003 (Yih et al., 2005). 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 (Goldman, 2005).
Often the same treatment given to burn victims relieves the pain of shingles. [1] One example is Vitacel GH7 - an herbal supplement. The same effect can also be achieved with over-the-counter moist burn pads.
Prognosis
The rash and pain usually subside within 3 to 5 weeks. 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.
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. However, those with active blisters can spread chickenpox to others who have never had that condition or who have not been vaccinated against it.
References
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}} Universal varicella vaccination: efficacy trends and effect on herpes zoster}
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|, International Journal of Toxicology
|, 24
|(4)
|: 205-213 PMID 16126614
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}} A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults}
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|, New England Journal of Medicine
|, 253
|(22)
|: 2271-2284 PMID 15930418
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