eMedicine Specialties > Infectious Diseases > Viral Infections

Herpes Zoster

James E Moon, MD, Clinical Investigator, Department of Clinical Trials, Walter Reed Army Institute of Research and Assistant Professor, Department of Medicine, Uniformed Service University of Health Sciences
Duane R Hospenthal, MD, PhD, Chief, Infectious Disease Service, San Antonio Military Medical Center, Brooke Army Medical Center; Professor of Medicine, Uniformed Services University of the Health Sciences

Updated: May 1, 2009

Introduction

Background

Herpes zoster (shingles) is 1 of 2 distinctive manifestations of human infection with the varicella-zoster virus (VZV), the other being varicella (chickenpox). Chickenpox is the primary infection, whereas herpes zoster represents reactivation of a previous infection. Herpes zoster has been known since ancient times and, in fact, still carries the name used by Hippocrates. Understanding the connection between herpes zoster, chickenpox, and VZV, however, is the product of more recent research done in the 19th and 20th centuries.

Chickenpox is a common and generally benign illness of childhood that is characterized by an exanthematous vesicular rash. Following resolution of this primary infection, VZV becomes latent in dorsal root ganglia until such time as a decrease in cellular immunity triggers the reactivation of the virus.

Herpes zoster typically manifests as a vesicular rash in a unilateral dermatomal distribution associated with pain. Without treatment, symptoms usually resolve over several weeks to a month. However, up to 20% of patients may experience prolonged and sometimes debilitating sequelae, chiefly postherpetic neuralgia.

Pathophysiology

VZV is an enveloped double-stranded DNA virus belonging to the Herpesviridae family. In humans, primary infection with VZV occurs when the virus comes into contact with the mucosa of the respiratory tract or conjunctiva. From these sites, it is distributed throughout the body via mononuclear cells in the blood stream. In tissue, VZV spreads from cell to cell via direct contact to produce its effects.

After primary infection, the virus migrates along sensory nerve fibers to the satellite cells of dorsal root ganglia where it becomes dormant. This dormancy may be permanent, or the virus may become reactivated by conditions of decreased cellular immunity, resulting in herpes zoster.

Frequency

United States

Prior to the advent of widespread vaccination, an estimated 4 million cases of primary VZV infection occurred annually in the United States alone. Infection was nearly universal by the end of the teenaged years, with studies showing less than 5% of adults aged 20-29 years remaining susceptible to infection. Cumulative over a lifetime, 15-30% of those with primary infections went on to experience episodes of herpes zoster. High-risk groups, such as elderly populations and immunocompromised people, might experience cumulative incidences as great as 50%. Estimated annual incidence of herpes zoster in the United States was at least 500,000 cases.

In 1995, a vaccine to prevent VZV infection was licensed in the United States and was thereafter added to the schedule of routine childhood vaccinations in the United States, as well in many other countries. Since the introduction of widespread vaccination, the incidence of primary infection has been reduced in certain populations by as much as 90%. However, the effect of childhood vaccination on the incidence of herpes zoster has yet to be adequately quantified. So far, various studies and surveillance data have failed to indicate any consistent trend in incidence rates.

Further complicating the issue of zoster frequency is the recently licensed (2006) adult vaccine (Zostavax) to prevent herpes zoster. A major study in adults aged 60 years and older demonstrated that a single dose of this vaccine reduced the incidence of herpes zoster by 51.3% over a median 3-year surveillance period compared with placebo.¹ However, the effects of this vaccine on herpes zoster in the general population have yet to be quantified.

International

No accurate data are available, but incidence likely is similar to that in the United States.

Mortality/Morbidity

Herpes zoster rarely causes fatalities in patients who are immunocompetent, but it can be life threatening in immunocompromised patients.

• One study demonstrated a mortality rate of nearly 10% among bone marrow transplant recipients who later developed herpes zoster.²
• Long-term complications of ophthalmic zoster with corneal involvement occur in over 20% of such patients and may result in blindness.

Race

No clear predominance exists among any race or ethnic group.

Sex

No significant sex predominance has been observed in herpes zoster.

Age

People of all ages can be affected, but incidence increases with age, presumably through the general decrease in immune function that occurs with aging. The following data are the incidence rates from 1996:

• People younger than 20 years - 0.4-1.6 cases per 1000 persons
• People aged 20-50 years - 2-3 cases per 1000 persons
• People older than 80 years - 4.5-11 cases per 1000 persons

Clinical

History

The clinical manifestations of herpes zoster can be divided into the pre-eruptive phase (preherpetic neuralgia), acute eruptive phase, and chronic phase (postherpetic neuralgia).

• Pre-eruptive phase
  • This phase is characterized by unusual skin sensations or pain within the affected dermatome that heralds the onset of lesions by 48-72 hours.
  • During this time, patients may also experience other symptoms such as malaise, myalgia, headache, and fever.
• Eruptive phase
  • This phase is marked by the emergence of vesicular eruptions. As in the pre-eruptive phase, patients may also experience symptoms such as malaise, myalgia, headache, and fever.
  • Lesions begin as erythematous macules and papules that quickly develop into vesicles. New lesions tend to form over a period of 3-5 days, sometimes coalescing to form bullae.
    
    

    

    Maculopapular rash due to herpes zoster in a child with a history of leukemia. Courtesy of the CDC.

    
    
  • After they form vesicles, lesions progress through stages in which they rupture, release their contents, ulcerate, and finally crust over and become dry.
  • Almost all adult patients experience pain (ie, acute neuritis) during the eruptive phase. A few experience severe pain without any evidence of a vesicular eruption (ie, zoster sine herpete), and a small number of patients have a characteristic eruption but do not experience pain.
  • Symptoms and lesions tend to resolve over 10-15 days. However, lesions may require up to a month to completely heal, and the associated pain may become chronic (see below).
  • Patients are infectious until lesions are dried. Anyone who has not previously had varicella is at risk of acquiring this readily transmitted virus. Pregnant women and immunosuppressed patients have the highest risk of serious sequelae.
  • Herpes zoster in persons younger than 50 years may be an indicator of an immunocompromised state. Therefore, younger patients with zoster should be assessed for evidence of immunodeficiency, including HIV.
• Chronic phase (postherpetic neuralgia)
  • Postherpetic neuralgia is persistent or recurring pain lasting 30 or more days after the acute infection or after all lesions have crusted.
  • Most people report a deep burning or aching pain, paresthesia, dysesthesia, hyperesthesia, or electric shock–like pains. The pain can be severe and incapacitating.
  • Resolution of pain may require months or even years.
  • The incidence of postherpetic neuralgia increases with age, occurring in the following:
    • 2% of untreated adults younger than 40 years
    • 21% of adults aged 40-60 years
    • 40% or more of adults older than 60 years
• Age is also a risk factor for pain persistence.
  • Up to 50% of patients older than 50 years have pain that persists for more than a month.
  • Pain lasting for more than 1 year occurs in 48% of patients older than 70 years.

Physical

Presentation with a characteristic rash facilitates making the diagnosis of herpes zoster. Other findings can include lymphadenopathy and sensory changes.

• Pre-eruptive phase  
  • Paresthesia or other sensory changes over a dermatomal distribution
  • Lymphadenopathy
• Eruptive phase  
  • The initial rash manifests as a swath of erythematous swollen plaques and patches from which clusters of small vesicles arise. This eruption is virtually diagnostic of shingles.
  • The extent of dermatomal involvement varies among patients and may involve all or part of a dermatome.
  • It usually affects a single unilateral dermatome and rarely crosses the body midline. Involvement of multiple dermatomes or bilateral aspects of the same dermatome (ie, crossing the midline) may indicate disseminated disease or another etiology such as herpes simplex virus (HSV).
  • Variation in vesicle size is common.
  • Only a few vesicles may be present initially, but successive eruptions for 3-5 days may occur.
  • Vesicles either umbilicate or erupt prior to drying and crusting. Crusts generally fall off within 3 weeks.
  • In elderly and immunocompromised patients, the eruptive phase is commonly longer and more extensive. It occasionally results in hemorrhagic blisters, skin necrosis, and secondary bacterial infections.
  • In an uncertain number of cases, zoster may manifest without rash or vesicles, with only pain in a dermatomal distribution (ie, zoster sine herpete).
• Central nervous system involvement  
  • While zoster is classically described in sensory (dorsal root) ganglia, it can spread to affect any portion of the nervous system.
  • Involvement of the anterior horn cells can produce muscular weakness, cranial nerve palsies, diaphragmatic paralysis, neurogenic bladder, and colon pseudoobstruction.
  • Wider involvement of the spinal cord can produce Guillain-Barré syndrome, transverse myelitis, and myositis.
  • In severely ill or immunocompromised patients, general CNS involvement can be observed in the form of meningoencephalitis or encephalitis. Such presentations are indistinguishable from other forms of meningoencephalitis, although other evidence of acute zoster usually is present.³ CSF studies frequently reveal pleocytosis without elevated protein. These infections can be life threatening.
• Herpes zoster ophthalmicus (HZO)  
  • This is potentially the most devastating form of acute zoster.
  • HZO results from the reactivation of varicella-zoster virus (VZV) in the trigeminal (fifth cranial) nerve. Any branch of the nerve may be affected, although the frontal branch within the first division of the trigeminal nerve is most commonly involved. This branch innervates nearly all the ocular and periocular structures.
  • Polymerase chain reaction (PCR) nerve studies have shown latent trigeminal VZV in up to 87% of patients.⁴ However, clinical disease has been reported in only 8-56% of patients in studies focused on ophthalmic involvement.
  • Presentations of HZO are diverse. In addition to the classic symptoms and lesions of herpes zoster, other common manifestations include conjunctivitis, scleritis, episcleritis, keratitis iridocyclitis, Argyll-Robertson pupil, glaucoma, retinitis, choroiditis, optic neuritis, optic atrophy, retrobulbar neuritis, exophthalmos, lid retraction, ptosis, and extraocular muscle palsies.
  • HZO may appear weeks to months after the resolution of other symptoms.
  • Postherpetic neuralgia and long-term sequelae may result.
  • When the nasociliary branch is involved, vesicles may appear on the tip or side of the nose (Hutchinson sign). Such a presentation is a predictor for possible serious complications such as ocular inflammation and corneal denervation.
• Ramsay-Hunt syndrome  
  • Also known as herpes zoster oticus, geniculate neuralgia, or herpes zoster auricularis, it is caused by VZV reactivation involving the facial and auditory nerves.
  • Vesicular eruptions may manifest on the pinna, tragus, in the auditory canal, and on the tympanic membrane, as well as anywhere in the facial nerve distribution.
  • The patient may experience hearing impairment, nystagmus, vertigo, or facial nerve palsy (mimicking Bell palsy).
  • Patients may lose taste sensation in the anterior two thirds of the tongue.
  • It accounts for more than 50% of the cephalic motor neuropathies.
  • It may be unnoticed and difficult to diagnose, especially in elderly patients.

Causes

• Herpes zoster is caused by the reactivation of VZV.
• No identifiable environmental, genetic, or social factors exist.

Differential Diagnoses

Herpes Simplex
Impetigo
Smallpox

Other Problems to Be Considered

Atopic dermatitis
Atypical measles
Poison ivy

Workup

Laboratory Studies

• In almost all cases, herpes zoster can and should be diagnosed by history and physical examination.
• Confirming the diagnosis via laboratory testing usually has no utility because most tests are time-consuming, lack specificity, or are unavailable outside of research facilities.
• When acute diagnostic confirmation is desired, modern tests such as the direct immunofluorescence with fluorescein-tagged antibody (DFA) or PCR (if available) are preferred over the old standard Tzanck smear. These tests have far greater sensitivity and specificity than the Tzanck smear and allow differentiation between HSV and varicella-zoster virus (VZV) infections. Viral culture is another confirmatory option that has the ability to discern between HSV and VZV infections. However, similar to the Tzanck smear, it is less sensitive and has a longer turnaround time than DFA.

Imaging Studies

• Imaging studies are not useful in the diagnosis of shingles.

Procedures

• In cases of atypical lesions, skin biopsy may assist in the diagnosis.

Treatment

Medical Care

Acute herpes zoster

As described above, episodes of herpes zoster are generally self-limited and resolve without intervention. However, effective treatments do exist and can reduce the extent and duration of symptoms as well as the risk of chronic sequelae (ie, postherpetic neuralgia). Treatment is of most benefit in those patient populations at risk for prolonged or severe symptoms, specifically immunocompromised people and those older than 50 years. The benefit of treating younger and healthier populations is unclear.

• Topical therapy: The pain and pruritus of zoster can be reduced through judicious use of cool water compresses or baths, as well as the application of over-the-counter lotions containing calamine and other analgesic or antipruritic compounds.
• Analgesics
  • Topical, intradermal, and systemic analgesics may provide relief from the discomfort caused by zoster. Depending on the severity of symptoms, necessary medication may range from basic analgesics such as acetaminophen to powerful narcotic agents.
  • Dworkin et al (2009) recently conducted a randomized clinical trial of oral analgesics for acute pain in 87 adults aged 50 years or older with herpes zoster. Treatment was begun within 6 days of rash onset and during a period in which the patient experience his or her worst pain within the preceding 24 hours. Patients were initiated on a 7-day course of famciclovir, which was combined with a 28-day course of controlled-release (CR) oxycodone, gabapentin, or placebo. Patients who discontinued participation did so primarily because of constipation (27.6% of patients receiving CR oxycodone and 6.9% of patients receiving placebo). CR oxycodone was more successful in reducing the mean worst pain within the first week than placebo (P =0.01). Gabapentin did not provide significantly greater pain relief than placebo, although the drug did provide modest pain reduction in the first week.⁵
  • A randomized, double-blind, placebo-controlled study of extended-release gabapentin (gabapentin ER) conducted by Irving et al (2009) demonstrated improvement in average daily pain scores in patients with acute herpes zoster. In those taking gabapentin, 25.5%-28.8% reported a pain reduction of 50% or more compared with baseline, whereas 11.8% of patients taking placebo reported the same result.⁶
• Antiviral therapy
  • Multiple agents have demonstrated efficacy in reducing symptoms, lesion number, and duration of cutaneous and ophthalmic zoster episodes in immunocompetent and immunocompromised patients. In the United States, antivirals of choice include acyclovir, valacyclovir, and famciclovir. Side effects and dosing regimens for these drugs are described individually below.
  • In general, antiviral therapy has been reported as being most effective if initiated within the first 3 days of symptoms. However, even after 3 days, antiviral therapy has been shown to be efficacious in reducing zoster pain. Thus, antiviral therapy should be considered for acute zoster treatment regimens, regardless of the time of presentation.
  • Acyclovir is a guanine derivative that prevents varicella-zoster virus (VZV) replication through inhibition of the viral DNA polymerase. Valacyclovir and famciclovir are prodrugs converted in vivo into acyclovir and penciclovir, respectively. Both of the prodrugs are as effective as acyclovir in resolving pain, and both appear to promote faster healing of cutaneous lesions. Further, both prodrugs have simpler dosing regimens. However, intravenous acyclovir remains the drug of choice for severe or disseminated disease.
• Corticosteroids: The use of steroids in conjunction with an antiviral for acute zoster is controversial. The results of multiple studies have provided no conclusive evidence that steroids shorten the course of acute infection or have any effect on postherpetic neuralgia.⁷ One study demonstrated that acute neuritis resolved more quickly in patients receiving both corticosteroids and acyclovir compared to patients who received acyclovir alone. Another trial showed a clear improvement in quality of life (eg, decreased analgesic requirements, uninterrupted sleep) among patients using a combined steroid/antiviral regimen compared to control subjects.

Chronic herpes zoster (postherpetic neuralgia)

Primary treatments for postherpetic neuralgia include neuroactive agents such as tricyclic antidepressants, anticonvulsant agents such as gabapentin, and narcotic and nonnarcotic analgesics. No standard treatment plans or protocols exist for treating the pain associated with postherpetic neuralgia. Consultation with pain specialists may be required. Sample medications for treatment of postherpetic neuralgia are described below.

• Prevention of postherpetic neuralgia
  • Placebo-controlled trials of various antivirals have shown clear reductions in the pain and duration of postherpetic neuralgia among treated populations. In patients older than 50 years, research has demonstrated a clear improvement in quality of life with treatment in both acute herpes zoster and postherpetic neuralgia. Studies involving the ability of antivirals to prevent postherpetic neuralgia in any age group are inconclusive.
  • Aside from antiviral therapy, the other treatment that has shown promise in preventing postherpetic neuralgia in a select population is vaccination. As described above, a large placebo-controlled trial involving a live attenuated VZV vaccine in immunocompetent adults older than 60 years demonstrated a reduction in the incidence of acute herpes zoster by more than 50% and a reduction in the incidence of postherpetic neuralgia of 67% in the treated population. The US Food and Drug Administration (FDA) licensed this vaccine in 2006 for use in adults aged 60 years or older, and the Advisory Committee on Immunization Practices (ACIP) has recommended that nonimmunocompromised, nonpregnant adults aged 60 years or older receive the vaccine, regardless of zoster history.⁸

Surgical Care

Surgical care is not generally indicated for treatment of herpes zoster. In cases of extreme intractable pain, rhizotomy (surgical separation of pain fibers) may be considered.

Consultations

• Consultation with a dermatologist or infectious disease specialist should be obtained if the diagnosis is in doubt.
• Consultation with an ophthalmologist is suggested for disease affecting the face.
• Consult a pain specialist for severe postherpetic neuralgia.

Diet

No specific dietary changes are recommended.

Activity

• Patients with shingles can perform activities as tolerated.
• During the acute phase, patients should be counseled to avoid direct skin contact with immunocompromised persons, pregnant women, and individuals with no history of chickenpox infection. If the patient is hospitalized, contact isolation measures should be considered.

Medication

As stated above, the goals of drug therapy are to reduce the pain and other symptoms of herpes zoster episodes, and if possible, help to shorten the duration, prevent recurrence, and lower the risk of chronic sequelae.

Antivirals

Reduce pain and time to lesion resolution during the acute phase of shingles and may reduce risk or duration of postherpetic neuralgia.

Acyclovir (Zovirax)

Synthetic purine nucleoside analogue with inhibitory activity against HSV types 1 and 2 and VZV.
Adjust dosage in patients with renal insufficiency.

Dosing

Adult

800 mg PO 5 times/d for 7-10 d
500 mg/m² IV or 10 mg/kg IV q8h for 7 d

Pediatric

Immunocompromised children:
250-600 mg/m² PO 4-5 times/d for 7-10 d
500 mg/m² IV or 7.5-10.0 mg/kg IV q8h for 7 d

Interactions

Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity of acyclovir

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Exercise caution in renal failure or when using nephrotoxic drugs

Valacyclovir (Valtrex)

Prodrug rapidly converted to the active drug acyclovir. More expensive but has a more convenient dosing regimen than acyclovir.

Dosing

Adult

1000 mg PO tid for 7 d

Pediatric

Not established

Interactions

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

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Requires dosage adjustment in renal failure; caution in renal failure and coadministration of nephrotoxic drugs; associated with onset of hemolytic uremic syndrome; allogenic bone marrow transplant recipients and renal transplant recipients

Famciclovir (Famvir)

After ingestion, the drug is rapidly biotransformed into the active compound penciclovir and phosphorylated by viral thymidine kinase. By competition with deoxyguanosine triphosphate, penciclovir triphosphate inhibits viral polymerase.
Adjust dose in patients with renal insufficiency or hepatic disease.

Dosing

Adult

500 mg PO tid for 7 d

Pediatric

Not established

Interactions

Coadministration of probenecid and cimetidine may increase toxicity of penciclovir; coadministration 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

Adjust dose in renal insufficiency or hepatic disease; not studied in immunocompromised patients or disseminated disease

Topical anesthetics

Decrease pain associated with postherpetic neuralgia.

Capsaicin (Dolorac, Capsin, Zostrix)

Derived from plants of the Solanaceae family. May render skin and joints insensitive to pain by depleting substance P in peripheral sensory neurons.

Dosing

Adult

Apply to affected area tid/qid

Pediatric

<2 years: Not recommended
>2 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; broken or irritated skin

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

For external use only; avoid contact with eyes, mucous membranes, wounds, or damaged skin; do not use tight bandage; discontinue use if condition worsens or symptoms persist for 14-28 d

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli. May help reduce pain, but reports are inconclusive.

Prednisone (Deltasone, Orasone, Sterapred)

Decreases inflammation by suppressing neutrophils and reversing increased capillary permeability. Also suppresses immune system.

Dosing

Adult

10-50 mg PO qd

Pediatric

Not established

Interactions

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

Contraindications

Documented hypersensitivity; increased susceptibility to infection; peptic ulcer disease; hepatic dysfunction

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

Tricyclic antidepressants

Have been shown to have a role in the treatment of postherpetic neuralgia.

Amitriptyline (Elavil)

Blocks reuptake of norepinephrine and serotonin. Decreases pain by inhibiting spinal neurons involved in pain perception.

Dosing

Adult

10-150 mg PO hs; initially administer as smaller divided increments and gradually titrate up to an effective level with a maximum dosage of 150 mg PO qhs

Pediatric

Not currently recommended for children <12 y

Interactions

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase amitriptyline levels; amitriptyline inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Contraindications

Documented hypersensitivity; administration of MAOIs in past 14 d; history of seizures; cardiac arrhythmias; glaucoma; urinary retention

Precautions

Pregnancy

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

Precautions

Caution in cardiac conduction disturbances, history of hyperthyroidism, and renal or hepatic impairment; avoid using in elderly patients

Vaccines

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.

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

Further Inpatient Care

• Inpatient care is recommended for any patient at risk for dissemination or for those requiring IV medications, as well as any patient demonstrating disseminated disease or ophthalmic or meningoencephalopathic involvement.

Further Outpatient Care

• Follow up until symptoms resolve.
• Inform patients about the natural progression of herpes zoster and its potential complications.
• Pain relief should be a primary concern.
• Patients who develop postherpetic neuralgia should be seen regularly and should receive emotional support in addition to medical therapy.

Transfer

• Patients with disseminated disease, severe immunosuppression, or those unresponsive to therapy should be transferred to a higher level of care.
• If consultation is required but not available at the initial facility, patients should be transferred to a tertiary care medical center.

Deterrence/Prevention

The Advisory Committee on Immunization Practices (ACIP) recently issued updated adult vaccination scheduling guidelines for October 2007 through September 2008. These guidelines include changes for varicella and zoster vaccines.⁸

Prognosis

• The prognosis for younger and otherwise healthy patients is excellent.
• Elderly people have a significantly increased risk of complications, including postherpetic neuralgia, bacterial infections, and scarring.

Patient Education

• During the acute phase, patients are infective to others and should be instructed to avoid contact with elderly people, people who are immunocompromised, pregnant women, or people with no history of chickenpox infection.
• Patients should be instructed to not scratch the lesions, which may predispose them to secondary bacterial infections.
• 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

• Misdiagnosis or failure to treat patients with involvement of the trigeminal nerve may lead to long-term ophthalmic complications.
• Take special care with immunocompromised and debilitated patients. Err on the side of admitting immunosuppressed patients and those with eye or symptomatic CNS involvement.

Multimedia

Media file 1: Maculopapular rash due to herpes zoster in a child with a history of leukemia. Courtesy of the CDC.

References

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Keywords

herpes zoster, shingles, HZ, varicella-zoster virus, VZV, preherpetic neuralgia, postherpetic neuralgia, PHN, varicella, chickenpox, herpes zoster ophthalmicus, HZO, Ramsay-Hunt syndrome, herpes zoster oticus, geniculate neuralgia, herpes zoster auricularis

Contributor Information and Disclosures

Author

James E Moon, MD, Clinical Investigator, Department of Clinical Trials, Walter Reed Army Institute of Research and Assistant Professor, Department of Medicine, Uniformed Service University of Health Sciences
Disclosure: Nothing to disclose.

Coauthor(s)

Duane R Hospenthal, MD, PhD, Chief, Infectious Disease Service, San Antonio Military Medical Center, Brooke Army Medical Center; Professor of Medicine, Uniformed Services University of the Health Sciences
Duane R Hospenthal, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Society for Infectious Diseases, International Society of Travel Medicine, and Medical Mycology Society of the Americas
Disclosure: Nothing to disclose.

Medical Editor

Mark Raymond Wallace, MD, Infectious Disease Fellowship Director, Orlando Regional Healthcare; Clinical Professor of Medicine, Florida State University
Mark Raymond Wallace, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Gordon L Woods, MD, Consulting Staff, Department of Internal Medicine, University Medical Center
Gordon L Woods, MD is a member of the following medical societies: Society of General Internal Medicine
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

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