eMedicine Specialties > Emergency Medicine > Infectious Diseases

Herpes Zoster

Richard S Krause, MD, Senior Faculty, Department of Emergency Medicine, State University of New York at Buffalo School of Medicine

Updated: Jun 1, 2009

Introduction

Background

Varicella-zoster virus (VZV) is the agent causing chickenpox, the common childhood infection. Following resolution of chickenpox, VZV lies dormant in the spinal dorsal root ganglia until reactivation results in herpes zoster (shingles). "Shingles" is a syndrome characterized by a painful, unilateral vesicular rash, usually restricted to a dermatomal distribution. At times, especially in the immunosuppressed patient, the infection may spread and produce severe systemic illness with involvement of multiple visceral organs and multiple dermatomes (disseminated zoster).

Shingles usually has a benign course, but complications may occur, ranging from mild to life-threatening. Complicated herpes zoster refers to infections occurring in immunosuppressed patients or manifested by ocular involvement. In properly selected patients, early treatment with antivirals and possibly corticosteroids has been shown to decrease the duration of illness and to prevent or ameliorate some complications.

Herpes zoster on the lateral part of the abdomen.

Pathophysiology

Exactly why VZV reactives from latency is not fully understood. However, VZV-specific cell-mediated immunity has been shown to be a major factor in determining reactivation of VZV. Cell-mediated VZV-specific immunity decreases with age and in patients with certain malignancies. These groups have much higher rates of herpes zoster. Patients with hypogammaglobulinemia (a defect of humoral but not cellular immunity) do not have a higher rate of zoster. This supports the concept of an important role for cell-mediated immunity in the pathogenesis of VZV infection.
 
VZV reactivation causes inflammation in the dorsal root ganglion accompanied by hemorrhagic necrosis of nerve cells. The result is neuronal loss and fibrosis. The distribution of the rash corresponds to the sensory fields of the infected neurons within a specific ganglion. The anatomic location of the involved dermatome often determines the specific manifestations (eg, herpes zoster ophthalmicus causing ocular complications when the trigeminal ganglion is involved).

Frequency

United States

Approximately 95% of adults in the United States have antibodies to the varicella-zoster virus and are vulnerable to reactivation infection. A person of any age with a prior varicella infection may develop zoster, but incidence increases with advancing age due to declining immunity. Approximately 4% of patients with zoster will develop a recurrent episode later in life.  

A study of patients in a large health maintenance organization (HMO) in the United States revealed 1075 cases from 1990-1992.¹ The following characteristics were noted:

• Incidence was 215 cases per 100,000 people per year.
• Older patients were more at risk (1424 cases per 100,000 people per year for age >75 y).
• Fewer than 5% of cases were in children and younger adolescents.
• Three of 4 patients with recurrent zoster were HIV positive.

Mortality/Morbidity

• A common complication of herpes zoster is postherpetic neuralgia, pain that persists for longer than 1 month following resolution of the vesicular rash. This complication is more common in patients older than 50 years. Postherpetic neuralgia may develop as a continuation of pain that accompanies acute zoster, or it may develop following apparent resolution of the initial zoster reactivation. The pain of postherpetic neuralgia usually resolves within 6 months. However, 1% of patients continue to have pain for 1 year or longer.
• Herpes zoster may be associated with a secondary bacterial infection at the site of the rash (typically streptococcal or staphylococcal).
• Herpes zoster involving the ophthalmic branch of the trigeminal nerve may be associated with conjunctivitis, keratitis, corneal ulceration, iridocyclitis, glaucoma, and blindness.
• Complications of the Ramsay Hunt syndrome (zoster involving cranial nerves V, IX, and X) may include peripheral facial nerve weakness and deafness.
• Meningoencephalitis secondary to herpes zoster is more likely to be seen in immunocompromised patients than in immunocompetent patients. Other CNS complications may include myelitis, cranial nerve palsies, and granulomatous angiitis. Granulomatous angiitis may result in the development of a cerebrovascular accident.
• Disseminated zoster may be seen in immunocompromised patients. In such cases, hematogenous spread may result in the involvement of multiple dermatomes. Visceral involvement can also occur. Such systemic involvement can lead to death due to encephalitis, hepatitis, or pneumonitis.

Race

Blacks are one-fourth as likely as whites to develop herpes zoster.

Sex

Incidence is equal in males and females.

Age

Incidence of herpes zoster increases with age. Approximately 80% of cases occur in persons older than 20 years. Fewer than 5% of cases are in those younger than 14 years.

Clinical

History

Prodromal pain precedes the rash in approximately 75% of patients, typically confined to the same dermatomal distribution. Initially vesicular, the rash gradually becomes pustular and then crusts over a period of 7-10 days. As with chickenpox, once crusting occurs, the lesion is no longer infectious. Scarring and hypopigmentation or hyperpigmentation may persist for a long period. 

• Most patients describe the pain as burning, throbbing, or stabbing.
• The involved area may be tender to palpation.
• The rash may be pruritic.
• Depending on the involved dermatome, the pain may be attributed to other etiologies such as renal colic, biliary pain, or acute coronary syndrome. 
• Zoster is generally limited to 1 dermatome or at most 2 or 3 adjacent dermatomes in normal hosts.
• The thoracic dermatomes are the most commonly involved sites, followed by the lumbar dermatomes.
• Fewer than 20% of patients have systemic symptoms, such as headache, fever, malaise, or fatigue.
• Pain duration is variable but usually less than 1 month. 
  • Pain lasting longer than 1 month is referred to, by definition, as postherpetic neuralgia.
  • Of patients, 10-15% will have pain for more than 1 month.
  • Zoster sine herpete is defined as pain and paresthesias along the dermatome without the development of visible cutaneous involvement.

Physical

• The primary physical finding is a rash in a unilateral dermatomal distribution; the rash may be erythematous, vesicular, pustular, or crusting, depending on the stage of disease (see Media files 1-2). 

Herpes zoster on the neck.

• The initial rash is typically "herpetic" in appearance: small vesicles grouped on an erythematous base. It has been described as "dew drops on a rose petal."
• Bilateral rash is rare.
• Zoster lesions occur simultaneously and remain in congruent stages of healing.
• Lesions on the tip of the nose signify involvement of the nasociliary nerve; this finding mandates slit-lamp examination with fluorescein stain to look for the dendritic corneal lesions of herpetic keratitis.
• Depending on the dermatome involved, physical examination findings may include the following:  
  • Corneal ulcers, conjunctivitis
  • Regional lymphadenopathy
  • Cranial nerve palsies
  • Peripheral facial nerve palsy
  • Delirium, confusion, coma (in patients with meningoencephalitis)

Causes

Herpes zoster is caused by reactivation of VZV as described in Pathophysiology.

Differential Diagnoses

Other Problems to Be Considered

Coxsackievirus
Superficial pyoderma

Workup

Laboratory Studies

• Diagnosis of herpes zoster is based primarily on clinical findings, specifically the characteristic location and appearance of the skin eruption in association with localized pain. However, in some patients, the presentation of herpes zoster can be atypical and may require additional testing. This is particularly true in immunocompromised patients.
• Varicella-zoster virus can be cultured successfully; this has limited use in the ED due to the long time required for viral growth.
• If necessary, a definitive diagnosis can be confirmed by sending swabs to the laboratory. 
  • Lift the top of the lesion and swab the exposed base. The swab should then be rolled across a sterile glass side, which is air dried and sent to the laboratory for staining with immunofluorescent antibodies.
  • The swab can also be placed in viral transport medium for detection of viral DNA by polymerase chain reaction.
• Tzanck smear can be obtained from the vesicular lesions; however, the smear does not differentiate between varicella-zoster virus and other herpes virus infections such as herpes simplex.
  • A Tzanck smear is a simple test that may be performed by the clinician or in a laboratory.
    • A fresh blister is unroofed and material from the base is smeared on a slide.
    • Wright stain is applied, and the smear is examined under the microscope.
    • A positive result shows distinctive giant cells with multiple nuclei.
    • This test has a significant false-negative rate of at least 20%. Therefore, a negative result does not rule out a herpes virus infection and should not preclude empiric treatment.
• Empiric treatment, when indicated, should not be delayed pending the results of diagnostic tests.

Imaging Studies

No imaging tests are indicated in typical cases of cutaneous VZ infection.

Other Tests

• Monoclonal antibody tests
• Blood mononuclear cell testing for viral DNA (research)

Procedures

• Biopsy for direct immunofluorescence testing (rarely performed)

Treatment

Emergency Department Care

Symptomatic treatment

• Patients with herpes zoster usually experience pain. Antiviral and steroid therapy provides relatively minor relief of pain, and analgesics are often needed.  
  • Initial therapy may include nonsteroidal anti-inflammatory drugs (NSAIDs).
  • In many cases, narcotic analgesia is necessary.
  • A randomized clinical trial of oral analgesics for acute pain in patients with herpes zoster was conducted (n-87; age 50 years or older). Treatment was begun within 6 days of rash onset and with worst pain within 24 hours. Patients were initiated on a 7-day course of famciclovir with controlled-release (CR) oxycodone, gabapentin, or placebo for 28 days. Discontinuing participation, primarily associated with constipation, occurred most frequently in patients randomized to CR-oxycodone (27.6%) compared with placebo (6.9%). Mean worst pain was reduced the first week with CR-oxycodone compared with placebo (p=0.01). Gabapentin did not provide significantly greater pain relief than placebo, although the first week provided a modest reduction of pain.²
  • A randomized, double-blind, placebo-controlled study of extended-release gabapentin (gabapentin ER) demonstrated improvement in average daily pain score in patients with acute herpes zoster. In those taking gabapentin, a reduction of pain of 50% or greater from baseline was reported by 25.5-28.8% compared with 11.8% of patients taking placebo.³
• Wet to dry dressings with tap water or 5% aluminum acetate (Burow solution). Apply to the affected skin for 30-60 minutes 4-6 times per day.
• Bland lotions (ie, Calamine) may help relieve discomfort.

Antiviral therapy for uncomplicated herpes zoster

The goals of antiviral therapy are to decrease pain, to promote healing of skin lesions, and to prevent or reduce the severity of postherpetic neuralgia. Acyclovir and the newer antivirals valacyclovir and famciclovir have been shown to be effective if given within 48-72 hours of the appearance of the rash. The newer agents have better bioavailability and do not need to be given as frequently. Outcomes studied have included time to crusting of skin lesions, duration and severity of acute pain, and duration and incidence of postherpetic neuralgia.⁴  

Acyclovir has been the most studied and widely recommended, but in a blinded, randomized comparison trial, valacyclovir was shown to be superior to acyclovir.^5,6 The trial included more than 1100 patients with uncomplicated zoster who were 50 years or older. Adverse effects were similar in both groups. Outcomes evaluated included resolution of acute pain and the duration of postherpetic neuralgia.

The duration of antiviral treatment in studies has varied from 7-21 days. Based on current literature, for immunocompetent patients, acyclovir for 7-10 days or a 7-day course of the newer agents is appropriate. Longer courses may be needed in immunocompromised patients.

Combined antiviral and corticosteroid therapy for uncomplicated herpes zoster

The addition of corticosteroids has been evaluated in patients treated with acyclovir. The benefit of steroids included accelerated healing of lesions and more rapid resolution of acute pain.⁷ Though statistically significant, the benefits were small. There was no effect on the development or duration of postherpetic neuralgia. 

Steroids have not been studied with valacyclovir of famciclovir, so the benefit is unknown. The addition of steroids should be considered only in patients with severe symptoms. Steroids should not be given alone (without antiviral therapy) due to concern about promotion of viral replication. The effect of steroids on the incidence of secondary skin infection is unknown. Some authors have suggested that they may increase the risk. Prednisone, 40-60 mg/day, is a reasonable choice if steroids are used. The optimal duration of steroid therapy is not known. If prescribed, it seems reasonable for steroids to be used concurrently with antiviral therapy. The duration of steroid use should not extend beyond the period of antiviral therapy.

Treatment of complicated herpes zoster

Patients who are immunosuppressed are at risk for extensive skin involvement or disseminated disease. Although strong evidence is lacking, the following are highlights of some of the current recommendations for treating zoster in these patients.

• Treat all immunosuppressed patients with antivirals, even when the onset of symptoms is more than 72 hours. 
• Valacyclovir should be used if oral therapy is selected.
• Consider treatment with intravenous acyclovir for the following patients:  
  • Transplant patients soon after transplantation or when being treated for rejection
  • Patients with advanced HIV
  • Patients with widespread skin involvement or visceral disease

Treatment of herpes zoster ophthalmicus

Two trials comparing oral acyclovir to famciclovir or valacyclovir in patients with ophthalmic zoster showed comparable outcomes with any of the regimens.⁸ Patients with diagnosed or suspected ophthalmic zoster should receive antivirals and be referred to an ophthalmologist.

Post exposure prophylaxis

Varicella-zoster immune globulin (VZIG) prevents or modifies clinical illness in susceptible, persons who are exposed to varicella or zoster. It should be reserved for patients at risk for complications such as those who are immunocompromised, pregnant, and for neonates.⁹

Consultations

• Consultation is not generally needed in cases of uncomplicated zoster.
• Consultation with an infectious disease or other appropriate specialist should be considered in cases of disseminated zoster, zoster with visceral involvement, or zoster in an immunocompromised patient.
• Patients in whom ophthalmic zoster is present or cannot be confidently ruled out should usually be referred to an ophthalmologist. 

Medication

Goals of therapy in herpes zoster infection are to (1) shorten the clinical course, (2) provide analgesia, (3) prevent complications, and (4) decrease incidence of postherpetic neuralgia. Meta-analyses and randomized controlled trials suggest that the oral antiviral agents acyclovir, famciclovir, and valacyclovir started within 72 hours of the onset of rash reduce both the severity and the duration of acute pain, as well as the incidence of postherpetic neuralgia.

Antiviral agents

Acyclovir antivirals may decrease incidence of postherpetic neuralgia. Famciclovir and valacyclovir (2 antiviral agents with properties similar to those of acyclovir) offer better dosing regimens than acyclovir and yet are less studied.

Acyclovir (Zovirax)

Reduces duration of symptomatic lesions. Indicated for patients who present within 48 h of onset of rash. Treated patients experience less pain and faster resolution of cutaneous lesions.

Dosing

Adult

800 mg PO q4h (5 times/d) for 7-10 d; alternatively, 10 mg/kg/dose or 500 mg/m²/dose IV q8h

Pediatric

250-600 mg/m²/dose PO 4-5 times/d for 7-10 d; alternatively, 10 mg/kg/dose or 500 mg/m²/dose IV q8h

Interactions

Probenecid or zidovudine prolongs half-life and increases CNS toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution with renal failure or coadministration of other nephrotoxic drugs

Famciclovir (Famvir)

Prodrug that, when biotransformed into active metabolite penciclovir, may inhibit viral DNA synthesis/replication.

Dosing

Adult

500 mg PO q8h for 7 d

Pediatric

Not established

Interactions

Probenecid or cimetidine may increase toxicity; increases bioavailability of digoxin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure or coadministration of nephrotoxic drugs

Valacyclovir (Valtrex)

Prodrug rapidly converted to acyclovir before exerting its antiviral activity. More expensive but more convenient dosing regimen than acyclovir.

Dosing

Adult

1000 mg PO q8h for 7 d

Pediatric

Not established

Interactions

Probenecid, zidovudine, or cimetidine prolongs half-life and increases CNS toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure and coadministration of nephrotoxic drugs; associated with onset of hemolytic uremic syndrome

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli. The addition of oral prednisolone to acyclovir treatment has been shown to reduce pain, to speed healing of lesions, and to enable a more rapid return to daily activities.

Prednisone (Deltasone, Orasone, Meticorten)

The addition of a corticosteroid to acyclovir resulted in decreased acute pain but no decrease in long-term pain. One study also demonstrated more rapid initial healing of rash, although time to complete rash resolution was unchanged.

Dosing

Adult

60 mg/d PO tapered over 3 wk

Pediatric

0.05-2 mg/kg PO divided bid/qid; taper over 2 wk

Interactions

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral, fungal, tubercular skin, and connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI bleeding or ulceration

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and enable physical therapy regimens. Most analgesics have sedating properties that are beneficial for patients who have skin lesions.

Acetaminophen (Tylenol, Aspirin-Free Anacin)

DOC for treatment of pain in patients who (1) have documented hypersensitivity to aspirin or NSAIDs, (2) have upper GI disease, or (3) are taking oral anticoagulants. Reduces fever by direct action on hypothalamic heat-regulating centers, which increases dissipation of body heat via vasodilation and sweating.

Dosing

Adult

325-650 mg PO q6h, or 1000 mg tid/qid; not to exceed 4 g/d

Pediatric

<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 650 mg q4h; not to exceed 5 doses in 24 h

Interactions

Rifampin can reduce analgesic effects; barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Contraindications

Documented hypersensitivity; known G-6-P deficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses exceeding recommended maximum dose

Ibuprofen (Motrin, Advil, Nuprin)

DOC for treatment of mild to moderately severe pain, if no contraindications. Inhibits inflammatory reactions and pain, probably by decreasing activity of enzyme cyclooxygenase, in turn, inhibiting prostaglandin synthesis. One of few NSAIDs indicated for reduction of fever.

Dosing

Adult

200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric

<16 years: Not recommended because of association with Reye syndrome
>16 years: Administer as in adults

Interactions

Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants (monitor PT closely and instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; may increase phenytoin levels

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Vaccines

These agents elicit active immunization to increase resistance to infection. Vaccines consist of attenuated microorganisms or cellular components, which act as antigens. Administration stimulates antibody production with specific protective properties.

Varicella zoster vaccine (Zostavax)

Lyophilized preparation of Oka/Merck strain of live, attenuated varicella-zoster virus (VZV). Shown to boost immunity against herpes zoster virus (shingles) in older patients. Reduces occurrence of shingles in individuals >60 y by about 50%. For individuals aged 60-69 y, it reduces occurrence by 64%. Also slightly reduces pain compared with no vaccination in those who develop shingles. Indicated for prevention of herpes zoster in patients >60y who have no contraindications.

Dosing

Adult

<60 years: Not established
>60 years: Following reconstitution with entire vial of diluent supplied, use separate sterile needle and syringe to withdraw entire contents of reconstituted vial and administer SC; administer in upper arm

Pediatric

Not indicated

Interactions

None reported

Contraindications

Documented hypersensitivity to vaccine or components (eg, gelatin, neomycin); history of primary or acquired immunodeficiency states (eg, leukemia, lymphomas, malignant neoplasms affecting bone marrow or lymphatic system, AIDS); immunosuppressive therapy including high-dose corticosteroids; active, untreated tuberculosis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Common adverse effects include erythema, pain, tenderness, itching, and inflammation at injection site; may also cause headache; may cause extensive vaccine-associated rash or disseminated disease in individuals on immunosuppressive therapy (see Contraindications); defer vaccination if fever or acute illness present; do not inject intravascularly; administer within 30 min of reconstitution; not a substitute for varicella virus vaccine (Varivax) for children

Follow-up

Deterrence/Prevention

• Theoretically, current varicella vaccines will reduce zoster incidence.
• Vaccines are being tested for prevention of herpes zoster in individuals previously infected with wild varicella-zoster virus.
• Patients with zoster may transmit the virus, causing infections in susceptible persons (who have not had prior infection).
  • Discharge instructions should include patient education to avoid contact with susceptible individuals, especially if they are pregnant (due to concerns about congenital varicella) or immunocompromised.
  • Transmission is by direct contact, and lesions are considered infectious until they are all crusted over.
    

Complications

Complications of herpes zoster may include the following:

• Postherpetic neuralgia
• Ocular involvement with facial zoster
• Meningoencephalitis
• Cutaneous dissemination
• Superinfection of skin lesions
• Hepatitis/pneumonitis
• Peripheral motor weakness/segmental myelitis
• Cranial nerve syndromes, particularly ophthalmic and facial (Ramsay Hunt syndrome)
• Corneal ulceration
• Guillain-Barré syndrome

Prognosis

• Rash usually resolves within 14-21 days.
• Postherpetic neuralgia is defined as pain persisting at least 1 month after the rash has healed. Its incidence increases dramatically with age (ie, 4% in those aged 30-50 years, 50% in those older than 80 years).

Patient Education

• For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center. Also, see eMedicine's patient education articles Shingles and Chickenpox.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize involvement of the nasociliary nerve as demonstrated by lesions on the tip of the nose; therefore, failure to perform a slit-lamp examination with fluorescein stain to identify the dendritic corneal lesions of herpetic keratitis
• Failure to administer antiviral therapy to those who are immunocompromised
• Administration of steroids without concomitant antiviral therapy

Multimedia

Media file 1: Herpes zoster on the neck.

Media file 2: Herpes zoster on the lateral part of the abdomen.

References

1. Donahue JG, Choo PW, Manson JE, Platt R. The incidence of herpes zoster. Arch Intern Med. Aug 1995;155(15):1605-9. [Medline].

2. [Best Evidence] Dworkin RH, Barbano RL, Tyring SK, Betts RF, McDermott MP, Pennella-Vaughan J, et al. A randomized, placebo-controlled trial of oxycodone and of gabapentin for acute pain in herpes zoster. Pain. Apr 2009;142(3):209-17. [Medline].

3. [Best Evidence] Irving G, Jensen M, Cramer M, Wu J, Chiang YK, Tark M, et al. Efficacy and tolerability of gastric-retentive gabapentin for the treatment of postherpetic neuralgia: results of a double-blind, randomized, placebo-controlled clinical trial. Clin J Pain. Mar-Apr 2009;25(3):185-92. [Medline].

4. Dworkin RH, Johnson RW, Breuer J, Gnann JW, Levin MJ, Backonja M, et al. Recommendations for the management of herpes zoster. Clin Infect Dis. Jan 1 2007;44 Suppl 1:S1-26. [Medline].

5. Beutner KR, Friedman DJ, Forszpaniak C, Andersen PL, Wood MJ. Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Antimicrob Agents Chemother. Jul 1995;39(7):1546-53. [Medline].

6. Colin J, Prisant O, Cochener B, Lescale O, Rolland B, Hoang-Xuan T. Comparison of the efficacy and safety of valaciclovir and acyclovir for the treatment of herpes zoster ophthalmicus. Ophthalmology. Aug 2000;107(8):1507-11. [Medline].

7. Whitley RJ, Weiss H, Gnann JW Jr, Tyring S, Mertz GJ, Pappas PG, et al. Acyclovir with and without prednisone for the treatment of herpes zoster. A randomized, placebo-controlled trial. The National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group. Ann Intern Med. Sep 1 1996;125(5):376-83. [Medline].

8. Tyring S, Engst R, Corriveau C, Robillard N, Trottier S, Van Slycken S, et al. Famciclovir for ophthalmic zoster: a randomised aciclovir controlled study. Br J Ophthalmol. May 2001;85(5):576-81. [Medline].

9. National Center for Immunization and Respiratory Diseases. Varicella Vaccine - Q&A about High Risk. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/vaccines/vpd-vac/varicella/vac-faqs-clinic-highrisk.htm. Accessed December 11, 2008.

10. Brody MB, Moyer D. Varicella-zoster virus infection. The complex prevention-treatment picture. Postgrad Med. Jul 1997;102(1):187-90, 192-4. [Medline].

11. Kost RG, Straus SE. Postherpetic neuralgia--pathogenesis, treatment, and prevention. N Engl J Med. Jul 4 1996;335(1):32-42. [Medline].

12. Nikkels AF, Pierard GE. Recognition and treatment of shingles. Drugs. Oct 1994;48(4):528-48. [Medline].

13. Straus SE. Overview: the biology of varicella-zoster virus infection. Ann Neurol. 1994;35 Suppl:S4-8. [Medline].

14. Wareham DW, Breuer J. Herpes zoster. BMJ. June 2007;334(7605):1211-1215. [Medline].

15. Wood MJ. Current experience with antiviral therapy for acute herpes zoster. Ann Neurol. 1994;35 Suppl:S65-8. [Medline].

16. Wood MJ, Johnson RW, McKendrick MW, Taylor J, Mandal BK, Crooks J. A randomized trial of acyclovir for 7 days or 21 days with and without prednisolone for treatment of acute herpes zoster. N Engl J Med. Mar 31 1994;330(13):896-900. [Medline].

Keywords

herpes zoster, shingles, zona ignea, zona serpiginosa, zoster, herpesvirus, varicella-zoster virus, VZV, VZV infection, VZV reactivation, varicella-zoster virus infection, zoster sine herpete, chickenpox, chicken pox, vesicular rash, zoster keratitis, Ramsay Hunt syndrome, herpeszosteroticus, transitory unilateral facial paralysis, postherpetic neuralgia, conjunctivitis, keratitis, corneal ulceration, iridocyclitis, glaucoma, peripheral facial nerve weakness, peripheral facial nerve palsy, myelitis, cranial nerve palsies, granulomatous angiitis, disseminated zoster, encephalitis, hepatitis, pneumonitis, tingling, burning, trigeminal neuralgia, herniated nucleus pulposus with radiculopathy, erythematous rash, meningoencephalitis, dorsal root ganglion

Contributor Information and Disclosures

Author

Richard S Krause, MD, Senior Faculty, Department of Emergency Medicine, State University of New York at Buffalo School of Medicine
Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey Glenn Bowman, MD, MS, Consulting Staff, Highfield MRI, Columbus, Ohio
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eric L Weiss, MD, DTM&H, Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine
Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Chris D Melton, MD, to the development and writing of this article.

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