Shingles is a reactivation of that chickenpox virus but only in one nerve root. So instead of getting spots all over your body, as you do when you have chickenpox, you get them just in one area of your body. It is almost always just on one side of your body, although it may go right around from front to back, following the skin the nerve affects. The affected skin hurts, and it may start to hurt before the rash appears, and may keep hurting for some time after the rash has gone.
You may feel generally off-colour and not yourself. You can catch chickenpox from someone with shingles if you have not had chickenpox before. But most adults and older children have already had chickenpox and so are immune from catching chickenpox again. You cannot get shingles from someone who has shingles. The shingles rash is contagious for someone else to catch chickenpox until all the blisters vesicles have scabbed and are dry. If the blisters are covered with a dressing, it is unlikely that the virus will pass on to others.
This is because the virus is passed on by direct contact with the blisters. If you have a job, you can return to work once the blisters have dried up, or earlier if you keep the rash covered and feel well enough. Similarly children with shingles can go to school if the rash is covered by clothes and the children do not feel unwell. Pregnant women who have not had chickenpox should avoid people with shingles. See the separate leaflet called Chickenpox Contact in Pregnancy for more details.
Also, if you have a poor immune system immunosuppression , you should avoid people with shingles. See below for a list of people who have a poor immune system. These general rules are to be on the safe side, as it is direct contact with the rash that usually passes on the virus. This one is confusing! You can catch chickenpox from other people, but you can't catch shingles from other people. You only get shingles from a reactivation of your own chickenpox infection in the past.
So if you have shingles, and you come into contact with somebody else, they cannot 'catch' your shingles. But if they have never had chickenpox, it is possible that they could catch chickenpox from you. And if you had chickenpox, and came into contact with somebody else who had never had chickenpox, they could catch chickenpox.
But they couldn't 'catch' shingles from your chickenpox. To put it another way, no, you don't 'catch' shingles. It comes from a virus hiding out in your own body, not from someone else. But if you have shingles, you may be infectious, as it is possible for people to catch chickenpox from you. Only people who have never had chickenpox are likely to be at risk of catching chickenpox from your shingles.
People who have had chickenpox should be immune from catching it again. If the rash is in a covered area of skin, the risk of anyone with whom you are not in close contact catching chickenpox is very low. Shingles is an infection of a nerve and the area of skin supplied by the nerve. It is caused by a virus called the varicella-zoster virus. It is the same virus that causes chickenpox.
Anyone who has had chickenpox in the past may develop shingles. Shingles is sometimes called herpes zoster. Note : this is very different to genital herpes which is caused by a different virus called herpes simplex. About 1 in 4 people have shingles at some time in their lives. It can occur at any age but it is most common in older adults over the age of 50 years.
After the age of 50, it becomes increasingly more common as you get older. It is uncommon to have shingles more than once but some people do have it more than once. Most people have chickenpox at some stage usually as a child. The virus does not completely go after you have chickenpox. Some virus particles remain inactive in the nerve roots next to your spinal cord. They do no harm there and cause no symptoms. For reasons that are not clear, the virus may begin to multiply again reactivate.
This is often years later. The reactivated virus travels along the nerve to the skin to cause shingles. In most cases, an episode of shingles occurs for no apparent reason. Sometimes a period of stress or illness seems to trigger it. A slight ageing of the immune system may account for it being more common in older people.
The immune system keeps the virus inactive and prevents it from multiplying. A slight weakening of the immune system in older people may account for the virus reactivating and multiplying to cause shingles. The risk of getting shingles increases in people with a poor immune system immunosuppression. Loose-fitting cotton clothes are best to reduce irritating the affected area of skin. Pain may be eased by cooling the affected area with ice cubes wrapped in a plastic bag , wet dressings, or a cool bath.
A non-adherent dressing that covers the rash when it is blistered and raw may help to reduce pain caused by contact with clothing. Simple creams emollients may be helpful if the rash is itchy. Calamine lotion can help to cool the skin and reduce mild itchiness. Painkillers - for example, paracetamol , or paracetamol combined with codeine such as co-codamol , or anti-inflammatory painkillers such as ibuprofen - may give some relief.
Strong painkillers such as oxycodone and tramadol may be needed in some cases. Some painkillers are particularly useful for nerve pain. If the pain during an episode of shingles is severe, or if you develop postherpetic neuralgia PHN , you may be advised to take:.
If an antidepressant or anticonvulsant is advised, you should take it regularly as prescribed. It may take up to two or more weeks for it to become fully effective to ease pain. In addition to easing pain during an episode of shingles, they may also help to prevent PHN. See the separate leaflet called Postherpetic Neuralgia for more information.
Antiviral medicines used to treat shingles include aciclovir , famciclovir and valaciclovir. An antiviral medicine does not kill the virus but works by stopping the virus from multiplying. So, it may limit the severity of symptoms of the shingles episode. An antiviral medicine is most useful when started in the early stages of shingles within 72 hours of the rash appearing. However, in some cases your doctor may still advise you have an antiviral medicine even if the rash is more than 72 hours old - particularly in elderly people with severe shingles, or if shingles affects an eye.
Antiviral medicines are not advised routinely for everybody with shingles. As a general rule, the following groups of people who develop shingles will normally be advised to take an antiviral medicine:. Steroids help to reduce swelling inflammation.
A short course of steroid tablets prednisolone may be considered in addition to antiviral medication. This may help to reduce pain and speed healing of the rash. However, the use of steroids in shingles is controversial. Your doctor will advise you. Steroids do not prevent PHN. Tests are not usually done for shingles.
The rash can be recognised by its typical pattern and symptoms. It is usually worth seeing a doctor to be certain about the diagnosis and to see if you need treatment or not. Ideally you should see a doctor as soon as possible after the rash appears. Management of herpes zoster shingles and postherpetic neuralgia. Am Fam Physician. Pain, pain, go away: antidepressants and pain management.
Psychiatry Edgmont. Santee JA. Corticosteroids for herpes zoster: what do they accomplish? Am J Clin Dermatol. Pavan-Langston D. Herpes zoster antivirals and pain management. Presentation and management of herpes zoster shingles in the geriatric population. Diphenhydramine Topical. National Library of Medicine. Updated February 15, Ayoade F, Kumar S. Varicella Zoster Chickenpox [Updated Dec 16]. In: StatPearls [Internet].
Reg Anesth Pain Med. Topical capsaicin high concentration for chronic neuropathic pain in adults. Cochrane Database Syst Rev. Herpes zoster ophthalmicus. Curr Treat Options Neurol. Anti-inflammatory activities of colloidal oatmeal Avena sativa contribute to the effectiveness of oats in treatment of itch associated with dry, irritated skin.
J Drugs Dermatol. Chickenpox: Overview. National Sleep Foundation's sleep time duration recommendations: methodology and results summary. Sleep Health. Evid Based Complement Alternat Med. Psychological stress as a trigger for herpes zoster: might the conventional wisdom be wrong?
Clin Infect Dis. TENS - an alternative to antiviral drugs for acute herpes zoster treatment and postherpetic neuralgia prevention. Swiss Med Wkly. Lasting pain after shingles. Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood. Cancer Chemother Pharmacol. Billigmann P. A controlled study of patients].
Fortschr Med. National Institute of Neurological Disorders and Stroke. Shingles: Hope through research. Billigmann, P. A Controlled Study of Patients. Feb 10, ; 4 National Institute on Aging. Dec 31, Table of Contents View All. Table of Contents. Over-the-Counter Therapies. Home Remedies and Lifestyle. Complementary Medicine CAM. Frequently Asked Questions. Next in Shingles Guide. Shingles Doctor Discussion Guide Get our printable guide for your next doctor's appointment to help you ask the right questions.
Download PDF. Email the Guide Send to yourself or a loved one. Sign Up. Shingles can make you feel feverish, tired, and generally unwell. Was this page helpful? Thanks for your feedback! What are your concerns? Article Sources. Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles.
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The histologic features were interpreted as most consistent with tumid lupus erythematosus TLE Fig 1 , B. He was prescribed desoximetasone 0. After 2 weeks of using the topical steroid cream, tingling developed on the right side of his face.
The steroid cream was discontinued; however, the paresthesia worsened, and an erythematous rash with vesiculopapules developed on his right cheek and buccal mucosa with sharp demarcation at the midline of his face Fig 1 , C. Both facial and buccal lesions were positive for varicella zoster virus VZV by polymerase chain reaction.
The eruption improved with a 7-day course of valacyclovir. Review of the original biopsy specimen did not show any histologic evidence of VZV infection, and immunohistochemical staining for VZV was negative. A , TLE near right lateral eye consisting of erythematous and edematous plaques. B , Skin biopsy of tumid lupus lesion shows a superficial and deep perivascular and focally interstitial lymphocytic infiltrate.
The areas of pallor correspond to increased dermal mucin. C , Varicella zoster infection in the distribution of cranial nerve V 3. One month after resolution of the herpes zoster, he experienced a recurrence of his tumid lupus. He was started on suppressive valacyclovir, 1 g daily, in preparation for intralesional triamcinolone injection.
One dose was given before triamcinolone injection. One week after he received the intralesional steroids, the vesicular rash reoccurred and subsequently resolved after valacyclovir dose was increased to 3 g daily. Herpes zoster infection is caused by reactivation of VZV and typically presents as a unilateral vesicular and painful rash in a dermatomal distribution. Clinically, TLE appears as erythematous papules and plaques and is characterized histologically by a superficial and deep perivascular lymphocytic infiltrate and increased dermal mucin.
Topical corticosteroids, alone or in combination with systemic immune modulating therapy such as hydroxychloroquine, are the mainstay of treatment for CLE and TLE. Wolf's isotopic response, a phenomenon in which a new skin disorder occurs at the site of a previously healed lesion, could be considered an explanation for this case. However, most reports for this response start with HZ or herpes simplex followed by a secondary lesion, such as skin cancer. Although systemic corticosteroids are known to increase HZ risk, especially in patients with SLE, little is known about the risk of topical medications in reactivation of VZV.
One case report linked the application of topical tacrolimus to the onset of zoster, suggesting topical preparations may be of concern. Corticosteroids decrease cell-mediated immunity, thus raising concern about the reactivation of latent VZV in terminal ganglia. Smith et al 11 argue that relatively large doses of corticosteroids are required for this to occur.
Others have noted that reactivation from topical steroid preparations is unlikely, citing evidence of few side effects from use of oral injections of triamcinolone in patients with herpes labialis and stomatitis. However, our case suggests that in SLE patients, who are at an increased risk of HZ even without immunosuppressive therapy, topical steroids should be used with caution. Further, as vaccination for herpes zoster can decrease rates of virus reactivation in immunosuppressed people, 13 administration of the vaccine before topical steroid treatment may be warranted in SLE patients.
This case presents a nonimmunosuppressed SLE patient who developed HZ in the distribution of topical steroid use followed by HZ recurrence while on suppressive valacyclovir therapy after an intradermal steroid injection. Topical and intradermal steroids should be considered potential risk factors for HZ reactivation in SLE patients. Authors Powell and Hile contributed equally to this article. The rest of the authors have no conflicts to declare.
National Center for Biotechnology Information , U. Published online Dec Michelle Kahlenberg. Author information Article notes Copyright and License information Disclaimer. Michelle Kahlenberg: ude. Key words: herpes zoster, topical steroids.
Published by Elsevier, Inc. This article has been cited by other articles in PMC. Introduction Topical corticosteroids are commonly used in the treatment of a wide range of skin manifestations of systemic lupus erythematosus SLE. Case presentation A year-old man with a 4-year history of SLE, diagnosed by fulfilling American College of Rheumatology criteria 1 antinuclear antibody positive at , positive double-stranded DNA, serositis, thrombocytopenia presented with a 2- to 3-week history of an enlarging erythematous plaque on his right cheek after acute sun exposure Fig 1 , A.
Open in a separate window. Fig 1. Discussion Herpes zoster infection is caused by reactivation of VZV and typically presents as a unilateral vesicular and painful rash in a dermatomal distribution. Footnotes Authors Powell and Hile contributed equally to this article. References 1. Hochberg M. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus.
Compared with acyclovir, valacyclovir may be slightly better at decreasing the severity of pain associated with herpes zoster, as well as the duration of postherpetic neuralgia. Famciclovir is also a DNA polymerase inhibitor. The advantages of famciclovir are its dosing schedule three times daily , its longer intracellular half-life compared with acyclovir and its better bioavailability compared with acyclovir and valacyclovir.
The choice of which antiviral agent to use is individualized. Dosing schedule and cost may be considerations. The recommended dosages for acyclovir, famciclovir and valacyclovir are provided in Table 1. All three antiviral agents are generally well tolerated. The most common adverse effects are nausea, headache, vomiting, dizziness and abdominal pain.
Montvale, N. Cost to the patient will be higher, depending on prescription filling fee. Antiviral agents are not used in combination, and selection of an agent is based on dosage schedule and cost. Orally administered corticosteroids are commonly used in the treatment of herpes zoster, even though clinical trials have shown variable results.
Prednisone used in conjunction with acyclovir has been shown to reduce the pain associated with herpes zoster. Some studies designed to evaluate the effectiveness of prednisone therapy in preventing postherpetic neuralgia have shown decreased pain at three and 12 months. If the use of orally administered prednisone is not contraindicated, adjunctive treatment with this agent is justified on the basis of its effects in reducing pain, despite questionable evidence for its benefits in decreasing the incidence of postherpetic neuralgia.
Given the theoretic risk of immunosuppression with corticosteroids, some investigators believe that these agents should be used only in patients more than 50 years of age because they are at greater risk of developing postherpetic neuralgia. The pain associated with herpes zoster ranges from mild to excruciating.
Patients with mild to moderate pain may respond to over-the-counter analgesics. Patients with more severe pain may require the addition of a narcotic medication. Lotions containing calamine e. Once the lesions have crusted over, capsaicin cream Zostrix may be applied. Topically administered lidocaine Xylocaine and nerve blocks have also been reported to be effective in reducing pain. Ocular herpes zoster is treated with orally administered antiviral agents and corticosteroids, the same as involvement elsewhere.
Although most patients with ocular herpes zoster improve without lasting sequelae, some may develop severe complications, including loss of vision. When herpes zoster involves the eyes, ophthalmologic consultation is usually recommended. The morbidity and mortality of herpes zoster could be reduced if a safe and effective preventive treatment were available.
It is unusual for a patient to develop herpes zoster more than once, suggesting that the first reactivation of varicella-zoster virus usually provides future immunologic protection. Studies are currently being conducted to evaluate the efficacy of the varicella-zoster vaccine in preventing or modifying herpes zoster in the elderly. Although postherpetic neuralgia is generally a self-limited condition, it can last indefinitely. Treatment is directed at pain control while waiting for the condition to resolve.
Pain therapy may include multiple interventions, such as topical medications, over-the-counter analgesics, tricyclic antidepressants, anticonvulsants and a number of nonmedical modalities. Occasionally, narcotics may be required. Dosage recommendations are provided in Table 2. Drug levels for clinical use are not available.
Capsaicin, an extract from hot chili peppers, is currently the only drug labeled by the U. Food and Drug Administration for the treatment of postherpetic neuralgia. Substance P, a neuropeptide released from pain fibers in response to trauma, is also released when capsaicin is applied to the skin, producing a burning sensation. Analgesia occurs when substance P is depleted from the nerve fibers. To achieve this response, capsaicin cream must be applied to the affected area three to five times daily.
Patients must be counseled about the need to apply capsaicin regularly for continued benefit. They also need to be counseled that their pain will likely increase during the first few days to a week after capsaicin therapy is initiated. Patients should wash their hands thoroughly after applying capsaicin cream in order to prevent inadvertent contact with other areas.
Patches containing lidocaine have also been used to treat postherpetic neuralgia. One study found that compared with no treatment, lidocaine patches reduced pain intensity, with minimal systemic absorption. Although lidocaine was efficacious in relieving pain, the effect was temporary, lasting only four to 12 hours with each application. Over-the-counter analgesics such as acetaminophen e. However, these agents are often useful for potentiating the pain-relieving effects of narcotics in patients with severe pain.
Because of the addictive properties of narcotics, their chronic use is discouraged except in the rare patient who does not adequately respond to other modalities. Tricyclic antidepressants can be effective adjuncts in reducing the neuropathic pain of postherpetic neuralgia.
These agents most likely lessen pain by inhibiting the reuptake of serotonin and norepinephrine neurotransmitters. Tricyclic antidepressants commonly used in the treatment of postherpetic neuralgia include amitriptyline Elavil , nortriptyline Pamelor , imipramine Tofranil and desipramine Norpramin. These drugs are best tolerated when they are started in a low dosage and given at bedtime.
The dosage is increased every two to four weeks to achieve an effective dose. The tricyclic antidepressants share common side effects, such as sedation, dry mouth, postural hypotension, blurred vision and urinary retention. Nortriptyline and amitriptyline appear to have equal efficacy; however, nortriptyline tends to produce fewer anticholinergic effects and is therefore better tolerated. Treatment with tricyclic antidepressants can occasionally lead to cardiac conduction abnormalities or liver toxicity.
The potential for these problems should be considered in elderly patients and patients with cardiac or liver disease. Because tricyclic antidepressants do not act quickly, a clinical trial of at least three months is required to judge a patient's response. The onset of pain relief using tricyclic antidepressants may be enhanced by beginning treatment early in the course of herpes zoster infection in conjunction with antiviral medications.
Phenytoin Dilantin , carbamazepine Tegretol and gabapentin Neurontin are often used to control neuropathic pain. A recent double-blind, placebo-controlled study showed gabapentin to be effective in treating the pain of postherpetic neuralgia, as well as the often associated sleep disturbance.
The anticonvulsants appear to be equally effective, and drug selection often involves trial and error. Lack of response to one of these medications does not necessarily portend a poor response to another. The dosages required for analgesia are often lower than those used in the treatment of epilepsy. Anticonvulsants are associated with a variety of side effects, including sedation, memory disturbances, electrolyte abnormalities, liver toxicity and thrombocytopenia.
Side effects may be reduced or eliminated by initiating treatment in a low dosage, which can then be slowly titrated upward. There are no specific contraindications to using anticonvulsants in combination with antidepressants or analgesics. However, the risk of side effects increases when multiple medications are used.
Effective treatment of postherpetic neuralgia often requires multiple treatment approaches. In addition to medications, modalities to consider include transcutaneous electric nerve stimulation TENS , biofeedback and nerve blocks.
Herpes zoster and postherpetic neuralgia are relatively common conditions, primarily in elderly and immunocompromised patients. Although the diagnosis of the conditions is generally straightforward, treatment can be frustrating for the patient and physician. Approaches to management include treatment of the herpes zoster infection and associated pain, prevention of postherpetic neuralgia, and control of the neuropathic pain until the condition resolves.
Primary treatment modalities include antiviral agents, corticosteroids, tricyclic antidepressants and anticonvulsants. Already a member or subscriber? Log in. Packer is board certified by the American Board of Family Practice. Reprints are not available from the authors. The views expressed herein are exclusively those of the authors and do not necessarily represent the opinions of the United States Army or Department of Defense.
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Bowsher D. Pathophysiology of postherpetic neuralgia: towards a rational treatment. Goh L, Khoo L. A retrospective study of the clinical presentation and outcome of herpes zoster in a tertiary dermatology outpatient referral clinic. Int J Dermatol. Nurmikko T. Clinical features and pathophysiologic mechanisms of postherpetic neuralgia. Schmader K. Management of herpes zoster in elderly patients. Infect Dis Clin Pract. Zoster-associated chronic pain: an overview of clinical trials with acyclovir.
Scand J Infect Dis Suppl. Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Antimicrob Agents Chemother. Acylclovir with and without prednisone for the treatment of herpes zoster. A randomized, placebo-controlled trial. Ann Intern Med.
The effects of early corticosteroid therapy on the skin eruption and pain of herpes zoster. Keczkes K, Basheer AM. Do corticosteroids prevent post-herpetic neuralgia? Br J Dermatol. Prednisolone does not prevent post-herpetic neuralgia. Lee PJ, Annunziato P. Current management of herpes zoster.
Infect Med. Chronic neuropathic pain and its control by drugs.
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