Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Herpes Zoster

  • Author: Camila K Janniger, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Jun 16, 2016
 

Practice Essentials

Reactivation of varicella-zoster virus (VZV) that has remained dormant within dorsal root ganglia, often for decades after the patient’s initial exposure to the virus in the form of varicella (chickenpox), results in herpes zoster (shingles).[1] Although it is usually a self-limited dermatomal rash with pain, herpes zoster can be far more serious; in addition, acute cases often lead to postherpetic neuralgia (PHN) and is responsible for a significant economic burden.[2]  See the image below.

Herpes zoster, unilateral, on trunk. Herpes zoster, unilateral, on trunk.

See 15 Rashes You Need to Know: Common Dermatologic Diagnoses, a Critical Images slideshow, for help identifying and treating various rashes.

Signs and symptoms

The clinical manifestations of herpes zoster can be divided into the following 3 phases:

  • Preeruptive phase (preherpetic neuralgia)
  • Acute eruptive phase
  • Chronic phase (PHN)

The preeruptive phase is characterized by the following:

  • Sensory phenomena along 1 or more skin dermatomes, lasting 1-10 days (average, 48 hours)
  • Phenomena usually are noted as pain or, less commonly, itching or paresthesias [3]
  • Pain may simulate headache, iritis, pleurisy, brachial neuritis, cardiac pain, appendicitis or other intra-abdominal disease, or sciatica
  • Other symptoms, such as malaise, myalgia, headache, photophobia, and, uncommonly, fever

The acute eruptive phase is marked by the following:

  • Patchy erythema, occasionally accompanied by induration, in the dermatomal area of involvement
  • Regional lymphadenopathy, either at this stage or subsequently
  • Grouped herpetiform vesicles developing on the erythematous base (the classic finding)
  • Cutaneous findings that typically appear unilaterally, stopping abruptly at the midline of the limit of sensory coverage of the involved dermatome
  • Vesicular involution: Vesicles initially are clear but eventually cloud, rupture, crust, and involute
  • After vesicular involution, slow resolution of the remaining erythematous plaques, typically without visible sequelae
  • Scarring can occur if deeper epidermal and dermal layers have been compromised by excoriation, secondary infection, or other complications
  • Almost all adults experience pain, typically severe
  • A few experience severe pain without a vesicular eruption (ie, zoster sine herpete)
  • Symptoms tend to resolve over 10-15 days
  • Complete healing of lesions may require up to a month

PHN is characterized by the following:

  • Persistent or recurring pain lasting 30 or more days after the acute infection or after all lesions have crusted (9-45% of all cases) [4]
  • Pain usually is confined to the area of original dermatomal involvement
  • The pain can be severe and incapacitating
  • Pain can persist for weeks, months, or years
  • Slow resolution of pain is especially common in the elderly [5]
  • PHN is observed more frequently after cases of herpes zoster ophthalmicus (HZO) and in instances of upper-body dermatomal involvement
  • Less common postherpetic sequelae include hyperesthesia or, more rarely, hypoesthesia or anesthesia in the area of involvement

Common features of herpes zoster ophthalmicus are as follows:

  • Classic symptoms and lesions of herpes zoster
  • Ophthalmic manifestations including 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

Other forms of herpes zoster include the following:

  • Herpes zoster of maxillary branch of cranial nerve (CN) V
  • Herpes zoster of mandibular branch of CN V
  • Herpes zoster oticus (Ramsay Hunt syndrome)
  • Glossopharyngeal and vagal herpes zoster
  • Herpes occipitocollaris (vertebral nerves C2 and C3 involvement)
  • Herpes zoster encephalomyelitis
  • Disseminated herpes zoster
  • Unilateral herpes zoster involving multiple dermatomes
  • Recurrent herpes zoster
  • Herpes zoster involving urinary bladder, bronchi, pleural spaces, or gastrointestinal tract
  • Herpes zoster with motor complications

See Clinical Presentation for more detail.

Diagnosis

Diagnosis of herpes zoster is based primarily on the history and physical findings. In most cases, confirming the diagnosis via laboratory testing has no utility. In select patient populations, however—particularly immunocompromised patients—the presentation of herpes zoster can be atypical and may require additional testing.

Laboratory studies for VZV include the following:

  • Direct fluorescent antibody (DFA) testing of vesicular fluid or a corneal lesion
  • Polymerase chain reaction (PCR) testing of vesicular fluid, a corneal lesion, or blood
  • Tzanck smear of vesicular fluid (lower sensitivity and specificity than DFA or PCR)

See Workup for more detail.

Management

Episodes of herpes zoster are generally self-limited and resolve without intervention; they tend to be more benign and mild in children than in adults.

Conservative therapy includes the following:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Wet dressings with 5% aluminum acetate (Burrow solution), applied for 30-60 minutes 4-6 times daily
  • Lotions (eg, calamine)

Primary medications for acute zoster–associated pain include the following:

  • Narcotic and nonnarcotic analgesics (both systemic and topical)
  • Neuroactive agents (eg, tricyclic antidepressants [TCAs])
  • Anticonvulsant agents

Steroid treatment for herpes zoster is traditional but controversial. Typically, a substantial dose (eg, 40-60 mg of oral prednisone every morning) typically is administered as early as possible in the course of the disease and is continued for 1 week, followed by a rapid taper over 1-2 weeks.

Antiviral therapy for herpes zoster may decrease the length of time for new vesicle formation, the number of days to attain complete crusting, and the days of acute discomfort. Usually, the earlier antiviral medications are started, the more effective they are in shortening the duration of zoster and in preventing or decreasing the severity of PHN. Ideally, therapy should be initiated within 72 hours of symptom onset.

Oral treatment with the following has been found beneficial:

  • Acyclovir
  • Famciclovir
  • Valacyclovir

Hospital admission should be considered for patients with any of the following:

  • Severe symptoms
  • Immunosuppression
  • Atypical presentations (eg, myelitis)
  • Involvement of more than 2 dermatomes
  • Significant facial bacterial superinfection
  • Disseminated herpes zoster
  • Ophthalmic involvement
  • Meningoencephalopathic involvement

Prevention and treatment of postherpetic neuralgia

Prompt treatment of acute zoster and its associated pain (eg, with antiviral therapy) can prevent the development of PHN. Once PHN has developed, various treatments are available, including the following:

  • Neuroactive agents (eg, TCAs) [6]
  • Anticonvulsant agents (eg, gabapentin, [7] pregabalin)
  • Narcotic and nonnarcotic analgesics, both systemic (eg, opioids) and topical

A live attenuated VZV vaccine introduced in 2005 (Zostavax) has demonstrated a reduction in the incidence rate of herpes zoster. It is approved for use in patients 50 years of age and older and has been judged to be cost-effective.[8]

See Treatment and Medication for more detail.

Next

Background

Herpes zoster (shingles) is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV), a herpesvirus that is the cause of varicella (chickenpox). Differences in clinical manifestations between varicella and herpes zoster apparently depend on an individual's immune status; those with no previous exposure to VZV, most commonly children, develop the clinical syndrome of varicella, whereas those with circulating varicella antibodies develop a localized recrudescence, zoster.

Zoster probably results most often from a failure of the immune system to contain latent VZV replication. Whether other factors, such as radiation, physical trauma, certain medications, other infections, and stress, also can trigger zoster has not been determined with certainty. Nor is it entirely clear why circulating varicella antibodies and cell-mediated immune mechanisms do not prevent recurrent overt disease, as is common with most other viral illnesses.

The incidence of zoster appears to be inversely correlated with the host’s capacity to mount a cellular immune response. However, many patients with zoster apparently have normal immunity. In these patients, zoster is postulated to occur when VZV antibody titers and cellular immunity drop to levels that no longer are completely effective in preventing viral invasion. Evidence for this hypothesis includes the observation that pediatricians, who presumably are routinely reexposed to VZV and thus maintain high levels of immunity, seldom develop zoster.

Herpes zoster manifests in many ways. It should not be considered simply a self-limited dermatomal rash with pain. VZV infection is an acute neurologic disease that warrants immediate evaluation. That VZV is always a benign disorder is a common misperception. Once VZV infection resolves, many individuals continue to suffer pain—a condition known as postherpetic neuralgia (PHN).

Previous
Next

Pathophysiology

VZV infection gives rise to 2 distinct syndromes. The primary infection, chickenpox, is a contagious and usually benign febrile illness. After this infection resolves, viral particles remain in the dorsal root or other sensory ganglia, where they may lay dormant for years to decades.

In this latent period, host immunologic mechanisms suppress replication of the virus, but VZV reactivates when the host mechanisms fail to contain the virus. Such failure may result from a wide spectrum of conditions, ranging from stress to severe immunosuppression; occasionally, it follows direct trauma. VZV viremia occurs frequently with chickenpox but also may arise with herpes zoster, albeit with a lower viral load.

Once VZV is activated at the spinal root or cranial nerve neurons, an inflammatory response occurs that also encompasses the leptomeninges; both plasma cells and lymphocytes are noted. This inflammation in the dorsal root ganglion can be accompanied by hemorrhagic necrosis of nerve cells. The result is neuronal loss and fibrosis.

The frequency of dermatologic involvement is correlated with the centripetal distribution of the initial varicella lesions. This pattern suggests that the latency may arise from contiguous spread of the virus during varicella from infected skin cells to sensory nerve endings, with subsequent ascent to the ganglia. Alternatively, the ganglia may become infected hematogenously during the viremic phase of varicella, and the frequency of the dermatome involvement in herpes zoster may reflect the ganglia most often exposed to reactivating stimuli.

The appearance of the cutaneous rash due to herpes zoster coincides with a profound VZV-specific T-cell proliferation. Production of interferon alfa appears with the resolution of herpes zoster. In immunocompetent patients, specific antibodies (immunoglobulins G, M, and A [IgG, IgM, and IgA]) appear more rapidly and reach higher titers during reactivation (herpes zoster) than during the primary infection. The patient has a long-lasting, enhanced, cell-mediated immunity response to VZV.[9, 10, 11]

The anatomic location of the involved dermatome often determines the specific manifestations. When cervical and lumbar roots are involved, motor involvement, which is often overlooked, may be evident, depending on the virulence or extent of migration. In at least 1 case of motor neuron involvement, lymphocytic infiltration and myelin breakdown were observed with preservation of axons.

Herpes zoster infections are contagious to persons with no previous immunity to VZV. However, herpes zoster is estimated to be only one third as contagious as primary varicella. It is transmitted either via direct contact with the lesions or via the respiratory route.

Organ system involvement

Central nervous system

Whereas herpes zoster is classically described in sensory (dorsal root) ganglia, it can spread to affect any portion of the central nervous system (CNS). Involvement of the anterior horn cells can produce muscular weakness, cranial nerve palsies, diaphragmatic paralysis, neurogenic bladder, and colonic pseudo-obstruction. 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 may be indistinguishable from those of other forms of meningoencephalitis, though other evidence of acute zoster usually is present.[12] Cerebrospinal fluid (CSF) studies frequently reveal pleocytosis without elevated protein. These infections can be life-threatening.

Optical system

Herpes zoster ophthalmicus (HZO), a potentially devastating form of acute herpes zoster, results from the reactivation of VZV in the trigeminal (fifth cranial) nerve. Any branch of the nerve may be affected, though the frontal branch within the first division of the trigeminal nerve is most commonly involved. This branch innervates nearly all of the ocular and periocular structures.

Polymerase chain reaction (PCR) nerve studies have detected latent trigeminal VZV in as many as 87% of patients.[13] Clinical disease has been reported in as few as 8% and as many as 56% of patients in studies focused on ophthalmic involvement.[14]

Auditory system

Herpes zoster oticus (also known as Ramsay Hunt syndrome, geniculate neuralgia, or herpes zoster auricularis) is caused by VZV reactivation involving the facial and auditory nerves. This syndrome may go unnoticed and be difficult to diagnose, especially in elderly patients.

Vesicular eruptions may manifest on the pinna, tragus, or tympanic membrane or in the auditory canal, as well as anywhere in the facial nerve distribution. The patient may experience hearing impairment, nystagmus, vertigo, or a facial nerve palsy mimicking Bell palsy.[15] Patients may lose taste sensation in the anterior two thirds of the tongue.[15]

Clinical phases of disease

The clinical manifestations of herpes zoster can be divided into the following 3 phases:

  • Preeruptive phase (preherpetic neuralgia)
  • Acute eruptive phase
  • Chronic phase (PHN)

The preeruptive 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, photophobia, and, uncommonly, fever.

The acute eruptive phase is marked by the emergence of vesicular eruptions. Patients may also experience some of the other symptoms seen in the preeruptive phase. 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. After they form vesicles, lesions progress through stages in which they rupture, release their contents, ulcerate, and finally crust over and become dry. Patients remain infectious until the lesions have dried.

During this phase, almost all adult patients experience pain (ie, acute neuritis). A few experience severe pain without any evidence of a vesicular eruption (ie, zoster sine herpete), and a small number have a characteristic eruption but do not experience pain. Symptoms and lesions in the acute eruptive phase 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.

PHN, the chronic phase, is characterized by persistent or recurring pain lasting 30 or more days after the acute infection or after all lesions have crusted. It is the most frequent complication of herpes zoster, observed in 9-45% of all cases.[4] Most people report a deep burning or aching pain, paresthesia, dysesthesia, hyperesthesia, or electric shock–like pains. The pain can be severe and incapacitating, and may take a long time to resolve, especially in the elderly; it lasts longer than 12 months in nearly 50% of patients older than 70 years.[5]

Previous
Next

Etiology

Herpes zoster is caused by VZV infection. VZV is an enveloped, double-stranded DNA virus belonging to the Herpesviridae family; its genome encodes approximately 70 proteins. 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. After primary infection, the virus migrates along sensory nerve fibers to the satellite cells of dorsal root ganglia where it becomes dormant.

Reactivation of VZV that has remained dormant within dorsal root ganglia, often for decades after the patient’s initial exposure to the virus in the form of varicella (chickenpox), results in herpes zoster.[1] Exactly what triggers this reactivation has not yet been determined precisely, but likely candidates (alone, or in combination) include the following:

  • External reexposure to the virus
  • Acute or chronic disease processes (particularly malignancies and infections)
  • Medications of various types
  • Emotional stress

The reason why one dorsal root ganglion experiences reactivation of its stored viral load preferentially over another ganglia is unclear. Diminished cellular immunity seems to increase the risk of reactivation, in that the incidence increases with age and in immunocompromised persons.[16]

Zoster can be a presenting symptom of hyperparathyroidism, and it occurs twice as often (frequency, 3.7%) among patients with hypercalcemia as it does among age-matched cohorts of patients older than 40 years who have normal calcium levels.[17]

The cause of PHN also remains a mystery. Rapid initiation of treatment decreases the incidence of PHN substantially, an effect that can be explained by the theory that incessant pain of active zoster sets up a positive feedback loop within the thalamus and the cortex, creating a central pain syndrome similar to phantom leg pain. According to this theory, prompt treatment breaks the loop by providing pain-free periods early in the disease course.

Risk factors

Known risk factors for developing herpes zoster relate to the status of cell-mediated immunity to VZV. Risk factors in children and adults include the following:

  • VZV-specific immunity and cell-mediated immunity, which generally declines with age
  • Immunosuppression (eg, by HIV infection or AIDS) [16, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30]
  • Immunosuppressive therapy [31, 32]
  • Primary VZV infection in utero or in early infancy, when the normal immune response is decreased
  • Anti-tumor necrosis factor (TNF)-a agents (may pose an increased risk) [33]
  • Immune reconstitution inflammatory syndrome (IRIS)
  • Acute lymphocytic leukemia and other malignancies

IRIS is a paradoxical deterioration in clinical status that develops in a patient receiving antiretroviral treatment despite satisfactory control of viral replication and improvement of the patient’s CD4 count. Such patients may have signs and symptoms of a previously subclinical and unrecognized herpes zoster infection, as a paradoxical worsening of treatment response several weeks into therapy in the context of immune recovery on antiretroviral therapy (ART).

The appearance of herpes zoster within an 8- to 12-week period after initiation of ART should prompt consideration of IRIS. Early recognition and prompt treatment, along with continuation of highly active ART, are especially important in such cases.[34]

Research indicates that patients with inflammatory bowel disease (IBD) are at significantly increased risk for herpes zoster.[9] In an analysis of more than 108,000 IBD patients and 430,000 matched controls, the overall annual incidence of herpes zoster per 100,000 person-years was 734 among IBD patients, compared with 437 in non-IBD patients. The elevated risk in IBD patients remained after adjustment for comorbidities and other factors. Treatment with thiopurines, corticosteroids, and biologic antitumor necrosis factor–alpha (anti-TNF) agents was independently associated with an increased risk of herpes zoster.[35, 36]

Patients with multiple myeloma and colon cancer treated with arsenic trioxide may have a propensity to develop herpes zoster (shingles). Arsenic compounds have been suggested as a possible predisposing factor for herpes viral reactivation in these patients.[37]

Ambilateral reactivation of herpes zoster after cataract operations on both eyes has been described.[38]

In a population-based case-control study from the United Kingdom aimed at quantifying the effects of herpes zoster risk factors at various ages, 144,959 adults diagnosed with herpes zoster between 2000 and 2011 were compared with 549,336 age-, sex-, and practice-matched control subjects (median age, 62 years).[39] The following factors were associated with increased risk of zoster:

  • Rheumatoid arthritis (2.1% vs 1.5%)
  • Inflammatory bowel disease (1.3% vs 0.9%)
  • Chronic obstructive pulmonary disease (4.7% vs 3.7%)
  • Asthma (7.1% vs 5.8%)
  • Chronic kidney disease (6.0% vs 5.4%)
  • Depression (4.7% vs 4.0%)

For many of the risk factors evaluated, the relative effects were greater in younger individuals.[39] The greatest risk of zoster was observed in patients with severely immunosuppressive conditions (eg, lymphoma and myeloma), but current vaccines are contraindicated in these individuals.

Previous
Next

Epidemiology

United States statistics

In the United States, approximately 95% of adults—and 99.5% of adults aged 40 years or older—have antibodies to VZV and thus are vulnerable to reactivation of infection.[40] A person of any age with a previous varicella infection may develop zoster, but the incidence increases with advancing age as a consequence of declining immunity.

Approximately 4% of patients with herpes zoster will develop a recurrent episode later in life.[41] Recurrent zoster occurs almost exclusively in people who are immunosuppressed. Approximately 25% of patients with HIV and 7-9% of those receiving renal transplantation or cardiac transplantation experience a bout of zoster.

HZO represents 10-15% of all cases of HZ. Approximately half of these patients develop complications of HZO. The risk of ophthalmic complications in patients with herpes zoster does not seem to correlate with age, sex, or severity of the rash.

Before the advent of widespread vaccination, an estimated 4 million cases of primary VZV infection occurred annually in the United States alone.[40] Infection was nearly universal by the end of the teenage years, with studies showing only 10% of persons older than age 15 years as remaining susceptible to infection.[41]

Over the period of a lifetime, 10-20% of those with primary infections went on to experience episodes of herpes zoster.[42] High-risk groups, such as elderly populations and immunocompromised people, might experience cumulative incidences as high as 50%.[43] The estimated annual number of herpes zoster cases in the United States is approximately 1 million.[17]

Since the introduction of widespread vaccination for varicella in 1995, the incidence of primary VZV infection in the United States has been reduced by up to 90%.[40] However, the effect of this vaccination, as well as that of the subsequently approved vaccination for herpes zoster, on the current and future incidence of herpes zoster remains to be determined.

International statistics

Internationally, the incidence of zoster has not been well studied, but it is probably in the same range as that reported in the United States.[44] A German study of data on patients in the country’s statutory health system (SHI) for the year 2010 estimated that the mean annual incidence of herpes zoster was 5.79 cases per 1000 person-years, equivalent to 403,625 cases annually in the SHI population (which comprised about 85% of the total German population).[45]

Age-related demographics

Herpes zoster is rare in children and young adults, except in younger patients with AIDS, lymphoma, other malignancies, and other immune deficiencies and in patients who have received bone marrow or kidney transplants. Fewer than 10% of zoster patients are younger than 20 years, and only 5% are younger than 15 years. Even though zoster is primarily a disease of adults, it has been noted as early as the first week of life, occurring in infants born to mothers who had primary VZV infection (chickenpox) during pregnancy.

The incidence of herpes zoster increases with age.[46] In the general population, the lifetime incidence rate of herpes zoster is 10-20%, which rises to 50% in those individuals surviving to age 85 years.[16] More than 66% of patients are older than 50 years. The incidence of PHN also rises with advancing age.[47]

Sex-related demographics

Herpes zoster generally has not been considered to have a sex predilection. However, one study reported a higher prevalence in women than in men.[48] Ertunc et al suggested both that zoster frequency is higher in right-handed patients and that the rash appears more frequently on the left side in females.[49] The pathophysiology for these differences is uncertain.

Race-related demographics

Blacks are reported to have a significantly lower risk of developing zoster than whites do; however, zoster has been reported as an early manifestation of HIV infection in young Africans. Research has shown that elderly blacks are up to 75% less likely to develop herpes zoster than elderlys.[43] Similar findings have been demonstrated in children.[50] In a meta-analysis of controlled herpes zoster clinical trials, a nonwhite racial group was found to be associated with a younger age at zoster onset.[46]

Previous
Next

Prognosis

The rash usually resolves within 10-15 days. The prognosis for younger and otherwise healthy patients is excellent. Elderly people have a significantly increased risk of complications.

Herpes zoster rarely causes fatalities in patients who are immunocompetent, but it can be life-threatening in severely debilitated or immunocompromised patients. Disseminated zoster in immunocompromised patients can lead to death from encephalitis, hepatitis, or pneumonitis. Patients with active lymphoproliferative malignancies are at particular risk. Mortality rate from disseminated herpes zoster is between 5% and 15%.[42]

Morbidity usually is confined to pain within the affected dermatome, which can range in intensity from uncomfortable to debilitating. PHN can persist well beyond the duration of active disease, though most cases eventually resolve.

Variant presentations of zoster (eg, keratitis and myelitis) may carry additional morbidity. Eye involvement (HZO) can cause temporarily or permanently decreased visual acuity or blindness. Complications such as secondary infection and meningeal or visceral involvement can produce further morbidity in the form of infections and scarring.

Previous
Next

Patient Education

Patients should be informed about the natural progression of herpes zoster and its potential complications.

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.

In regard to treatment, patients should be instructed that treatment should be started within 72 hours of onset if at all possible, not only to speed resolution of the shingles itself but also to prevent PHN. Once PHN begins, treatment is much more difficult and often unsuccessful. Patients should also be told not to scratch the lesions; doing so may predispose them to secondary bacterial infections.

For patient education resources, see the Infections Center, as well as Shingles and Chickenpox.

Previous
 
 
Contributor Information and Disclosures
Author

Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, Rutgers New Jersey Medical School

Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Joseph S Eastern, MD Clinical Assistant Professor, Department of Internal Medicine, Section of Dermatology, University of Medicine and Dentistry of New Jersey; Clinical Assistant Professor, Seton Hall University School of Graduate Medical Education

Joseph S Eastern, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, International Society for Dermatologic Surgery, Medical Society of New Jersey

Disclosure: Nothing to disclose.

Duane R Hospenthal, MD, PhD, FACP, FIDSA, FASTMH Adjunct Professor of Medicine, Department of Medicine, University of Texas Health Science Center at San Antonio

Duane R Hospenthal, MD, PhD, FACP, FIDSA, FASTMH is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society for Infectious Diseases, International Society of Travel Medicine, Medical Mycological Society of the Americas, Armed Forces Infectious Diseases Society, International Society for Human and Animal Mycology, American College of Physicians, American Society for Microbiology, Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

James E Moon, MD, FACP, FIDSA Associate Division Director for Clinical Trials, Division of Experimental Therapeutics, Walter Reed Army Institute of Research and Assistant Professor, Department of Medicine, Uniformed Service University of Health Sciences

James E Moon, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

Wayne E Anderson, DO Assistant Professor of Internal Medicine/Neurology, College of Osteopathic Medicine of the Pacific Western University of Health Sciences; Clinical Faculty in Family Medicine, Touro University College of Osteopathic Medicine; Clinical Instructor, Departments of Neurology and Pain Management, California Pacific Medical Center

Wayne E Anderson, DO is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Law, Medicine & Ethics, California Medical Association, and San Francisco Medical Society

Disclosure: Teva Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Insys Honoraria Speaking and teaching; DepoMed Honoraria Speaking and teaching

Jeffrey Glenn Bowman, MD, MS Consulting Staff, Highfield MRI

Disclosure: Nothing to disclose.

Kevin P Connelly, DO Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University School of Medicine; Medical Director, Paws for Health Pet Visitation Program of the Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc, Chippenham Medical Center

Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose.

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.

Maria M Diaz, MD Staff Physician, Department of Emergency Medicine, Memorial Hospital

Maria M Diaz, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Andrea N Driano, MD Consulting Staff, Department of Emergency Medicine, Children's Hospital and Medical Center, Seattle WA

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte 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.

Franklin Flowers, MD Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, Affiliate Associate Professor of Pediatrics and Pathology, University of Florida College of Medicine

Franklin Flowers, MD, is a member of the following medical societies: American College of Mohs Micrographic Surgery and Cutaneous Oncology

Disclosure: Nothing to disclose.

C Stephen Foster, MD, FACS, FACR, FAAO Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution

C Stephen Foster, MD, FACS, FACR, FAAO is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Association of Immunologists, American College of Rheumatology, American College of Surgeons, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, American Uveitis Society, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Royal Society of Medicine, and Sigma Xi

Disclosure: Nothing to disclose.

Kilbourn Gordon III, MD, FACEP Urgent Care Physician

Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Ryan I Huffman, MD, Staff Physician, Department of Ophthalmology, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, New Jersey Medical School

Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

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.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Cynthia Haeshin Moon, MD Staff Physician, Department of Emergency Medicine, SUNY Downstate Medical Center/Kings County Hospital Center

Disclosure: Nothing to disclose.

Barbara L Roque, MD Full Partner, Ophthalmic Consultants Philippines Co; Service Chief, Pediatric Ophthalmology and Strabismus, Department of Ophthalmology, Asian Hospital and Medical Center; Active Staff, International Eye Institute, St Luke's Medical Center Global City; Visiting Ophthalmologist, AMC Eye Center, Alabang Medical Center

Barbara L Roque, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Cataract and Refractive Surgery, Philippine Academy of Ophthalmology, Philippine Society of Cataract and Refractive Surgery, and Philippine Society of Pediatric Ophthalmology

Disclosure: Nothing to disclose.

Manolette R Roque, MD, MBA General Manager, Full Partner, Ophthalmic Consultants Philippines Co.; President and CEO, Chief Refractive Surgeon, EYE REPUBLIC Ophthalmology Clinic; Section Chief, Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center; Section Chief, Ocular Immunology and Uveitis, International Eye Institute, St Luke's Medical Center Global City; Senior Eye Surgeon, The LASIK Surgery Clinic; Director, AMC Eye Center, Alabang Medical Center; President, Philippine Ocular Inflammation Society

Manolette R Roque, MD, MBA is a member of the following medical societies: American Academy of Ophthalmic Executives, American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, American Society of Ophthalmic Administrators, American Uveitis Society, International Ocular Inflammation Society, Philippine Medical Association, Philippine Ocular Inflammation Society, and Philippine Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD, MMB, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed Director, Regional MS Center of Excellence, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, and Sigma Xi

Disclosure: Nothing to disclose.

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Head of Infectious Disease Fellowship Program, Orlando Regional Medical Center

Mark R Wallace, MD, FACP, FIDSA 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.

R Christopher Walton, MD Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, University of Tennessee College of Medicine

R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society

Disclosure: Nothing to disclose.

Eric L Weiss, MD, DTM&H Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Progressor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

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.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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

  2. Blein C, Gavazzi G, Paccalin M, Baptiste C, Berrut G, Vainchtock A. Burden of herpes zoster: the direct and comorbidity costs of herpes zoster events in hospitalized patients over 50 years in France. BMC Infect Dis. 2015 Aug 19. 15 (1):350. [Medline].

  3. Goh CL, Khoo L. A retrospective study of the clinical presentation and outcome of herpes zoster in a tertiary dermatology outpatient referral clinic. Int J Dermatol. 1997 Sep. 36(9):667-72. [Medline].

  4. Pasqualucci A, Pasqualucci V, Galla F, De Angelis V, et al. Prevention of post-herpetic neuralgia: acyclovir and prednisolone versus epidural local anesthetic and methylprednisolone. Acta Anaesthesiol Scand. 2000 Sep. 44(8):910-8. [Medline].

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

  6. Zareba G. Pregabalin: a new agent for the treatment of neuropathic pain. Drugs Today (Barc). 2005 Aug. 41(8):509-16. [Medline].

  7. 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. 2009 Mar-Apr. 25(3):185-92. [Medline].

  8. Lopez-Belmonte JL, Cisterna R, Gil de Miguel A, Guilmet C, Bianic F, Uhart M. The use of Zostavax in Spain: the economic case for vaccination of individuals aged 50 years and older. J Med Econ. 2016 Jan 25. 1-29. [Medline].

  9. Ongkosuwito JV, Feron EJ, van Doornik CE, Van der Lelij A, Hoyng CB, La Heij EC, et al. Analysis of immunoregulatory cytokines in ocular fluid samples from patients with uveitis. Invest Ophthalmol Vis Sci. 1998 Dec. 39(13):2659-65. [Medline].

  10. Kumano Y, Manabe J, Hamamoto M, Kawano Y, Minagawa H, Fukumaki Y, et al. Detection of varicella-zoster virus genome having a PstI site in the ocular sample from a patient with acute retinal necrosis. Ophthalmic Res. 1995. 27(5):310-6. [Medline].

  11. Karlin JD. Herpes zoster ophthalmicus: the virus strikes back. Ann Ophthalmol. 1993 Jun. 25(6):208-15. [Medline].

  12. Jemsek J, Greenberg SB, Taber L, Harvey D, Gershon A, Couch RB. Herpes zoster-associated encephalitis: clinicopathologic report of 12 cases and review of the literature. Medicine (Baltimore). 1983 Mar. 62(2):81-97. [Medline].

  13. Pevenstein SR, Williams RK, McChesney D, Mont EK, Smialek JE, Straus SE. Quantitation of latent varicella-zoster virus and herpes simplex virus genomes in human trigeminal ganglia. J Virol. 1999 Dec. 73(12):10514-8. [Medline]. [Full Text].

  14. Pavan-Langston D. Herpes zoster ophthalmicus. Neurology. 1995 Dec. 45(12 Suppl 8):S50-1. [Medline].

  15. Sweeney CJ, Gilden DH. Ramsay Hunt syndrome. J Neurol Neurosurg Psychiatry. 2001 Aug. 71(2):149-54. [Medline]. [Full Text].

  16. Wung PK, Holbrook JT, Hoffman GS, Tibbs AK, Specks U, et al. Herpes zoster in immunocompromised patients: incidence, timing, and risk factors. Am J Med. 2005 Dec. 118(12):1416. [Medline].

  17. Norman J, Politz D. Shingles (varicella zoster) outbreaks in patients with hyperparathyroidism and their relationship to hypercalcemia. Clin Infect Dis. 2008 May 1. 46(9):1452-4. [Medline].

  18. Chronister CL. Review of external ocular disease associated with aids and HIV infection. Optom Vis Sci. 1996 Apr. 73(4):225-30. [Medline].

  19. Foster RE, Petersen MR, Neuss MN, Osher RH. Progressive outer retinal necrosis syndrome in a lymphoma patient with good visual outcome. Am J Ophthalmol. 2001 Jul. 132(1):117-20. [Medline].

  20. Hodge WG, Seiff SR, Margolis TP. Ocular opportunistic infection incidences among patients who are HIV positive compared to patients who are HIV negative. Ophthalmology. 1998 May. 105(5):895-900. [Medline].

  21. Kezuka T. Immune deviation and ocular infections with varicella zoster virus. Ocul Immunol Inflamm. 2004 Mar. 12(1):17-24. [Medline].

  22. Margolis TP, Milner MS, Shama A, Hodge W, Seiff S. Herpes zoster ophthalmicus in patients with human immunodeficiency virus infection. Am J Ophthalmol. 1998 Mar. 125(3):285-91. [Medline].

  23. Peck R, Gimple SK, Gregory DW, Youree B. Progressive outer retinal necrosis in a 73-year-old man: treatment with valganciclovir. AIDS. 2003 May 2. 17(7):1110-1. [Medline].

  24. Purdy KW, Heckenlively JR, Church JA, Keller MA. Progressive outer retinal necrosis caused by varicella-zoster virus in children with acquired immunodeficiency syndrome. Pediatr Infect Dis J. 2003 Apr. 22(4):384-6. [Medline].

  25. Rao NA. Acquired immunodeficiency syndrome and its ocular complications. Indian J Ophthalmol. 1994 Jun. 42(2):51-63. [Medline].

  26. Walton RC, Reed KL. Herpes zoster ophthalmicus following bone marrow transplantation in children. Bone Marrow Transplant. 1999 Jun. 23(12):1317-20. [Medline].

  27. Yau TH, Butrus SI. Presumed bilateral herpes zoster ophthalmicus in an AIDS patient: a case report. Cornea. 1996 Nov. 15(6):633-4. [Medline].

  28. Bert RJ, Samawareerwa R, Melhem ER. CNS MR and CT findings associated with a clinical presentation of herpetic acute retinal necrosis and herpetic retrobulbar optic neuritis: five HIV-infected and one non-infected patients. AJNR Am J Neuroradiol. 2004 Nov-Dec. 25(10):1722-9. [Medline].

  29. Gariano RF, Berreen JP, Cooney EL. Progressive outer retinal necrosis and acute retinal necrosis in fellow eyes of a patient with acquired immunodeficiency syndrome. Am J Ophthalmol. 2001 Sep. 132(3):421-3. [Medline].

  30. Neves RA, Rodriguez A, Power WJ, Muccioli C, Lane L, Belfort R Jr, et al. Herpes zoster peripheral ulcerative keratitis in patients with the acquired immunodeficiency syndrome. Cornea. 1996 Sep. 15(5):446-50. [Medline].

  31. Fernandes NF, Malliah R, Stitik TP, Rozdeba P, Lambert WC, Schwartz RA. Herpes zoster following intra-articular corticosteroid injection. Acta Dermatovenerol Alp Panonica Adriat. 2009 Mar. 18(1):28-30. [Medline].

  32. Benz MS, Glaser JS, Davis JL. Progressive outer retinal necrosis in immunocompetent patients treated initially for optic neuropathy with systemic corticosteroids. Am J Ophthalmol. 2003 Apr. 135(4):551-3. [Medline].

  33. Strangfeld A, Listing J, Herzer P, Liebhaber A, Rockwitz K, Richter C, et al. Risk of herpes zoster in patients with rheumatoid arthritis treated with anti-TNF-alpha agents. JAMA. 2009 Feb 18. 301(7):737-44. [Medline].

  34. Sharma A, Makrandi S, Modi M, Sharma A, Marfatia Y. Immune reconstitution inflammatory syndrome. Indian J Dermatol Venereol Leprol. 2008 Nov-Dec. 74(6):619-21. [Medline].

  35. Reuters Health. Increased Risk of Herpes Zoster With IBD, Study Confirms. Available at http://www.medscape.com/viewarticle/776280. Accessed: February 21, 2013.

  36. Long MD, Martin C, Sandler RS, Kappelman MD. Increased risk of herpes zoster among 108 604 patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2013 Feb. 37(4):420-9. [Medline].

  37. Nouri K, Ricotti CA Jr, Bouzari N, Chen H, Ahn E, Bach A. The incidence of recurrent herpes simplex and herpes zoster infection during treatment with arsenic trioxide. J Drugs Dermatol. 2006 Feb. 5(2):182-5. [Medline].

  38. Korber A, Franckson T, Grabbe S, Dissemond J. Ambilateral reactivation of herpes zoster V2 following cataract operation of both eyes. J Eur Acad Dermatol Venereol. 2007 May. 21(5):712-3. [Medline].

  39. Forbes HJ, Bhaskaran K, Thomas SL, Smeeth L, Clayton T, Langan SM. Quantification of risk factors for herpes zoster: population based case-control study. BMJ. 2014. 348:g2911. [Full Text].

  40. Marin M, Meissner HC, Seward JF. Varicella prevention in the United States: a review of successes and challenges. Pediatrics. 2008 Sep. 122(3):e744-51. [Medline].

  41. Whitley RJ. Varicella-Zoster Virus. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s Principles and Practices of Infectious Diseases. 7th ed. New York, NY: Churchill Livingstone; 2010:1963-69.

  42. Gnann JW Jr, Whitley RJ. Clinical practice. Herpes zoster. N Engl J Med. 2002 Aug 1. 347(5):340-6. [Medline].

  43. Schmader K, George LK, Burchett BM, Pieper CF. Racial and psychosocial risk factors for herpes zoster in the elderly. J Infect Dis. 1998 Nov. 178 Suppl 1:S67-70. [Medline].

  44. Araújo LQ, Macintyre CR, Vujacich C. Epidemiology and burden of herpes zoster and post-herpetic neuralgia in Australia, Asia and South America. Herpes. 2007 Sep. 14 Suppl 2:40-4. [Medline].

  45. Ultsch B, Köster I, Reinhold T, Siedler A, Krause G, Icks A, et al. Epidemiology and cost of herpes zoster and postherpetic neuralgia in Germany. Eur J Health Econ. 2012 Dec 28. [Medline].

  46. Nagasako EM, Johnson RW, Griffin DR, Elpern DJ, Dworkin RH. Geographic and racial aspects of herpes zoster. J Med Virol. 2003. 70 Suppl 1:S20-3. [Medline].

  47. Schmader K. Herpes zoster in older adults. Clin Infect Dis. 2001 May 15. 32(10):1481-6. [Medline].

  48. Insinga RP, Itzler RF, Pellissier JM, Saddier P, Nikas AA. The incidence of herpes zoster in a United States administrative database. J Gen Intern Med. 2005 Aug. 20(8):748-53. [Medline]. [Full Text].

  49. Ertunç V, Dane S, Karakuzu A, Deniz O. Higher herpes zoster infection frequency in right-handed patients and more frequent appearance in the left body side of females. Acta Derm Venereol. 1997 May. 77(3):245. [Medline].

  50. Tseng HF, Smith N, Marcy SM, Sy LS, Chao CR, Jacobsen SJ. Risk factors of herpes zoster among children immunized with varicella vaccine: results from a nested case-control study. Pediatr Infect Dis J. 2010 Mar. 29(3):205-8. [Medline].

  51. Ono N, Sakabe A, Nakajima M. [Herpes zoster oticus-associated jugular foramen syndrome]. Brain Nerve. 2010 Jan. 62(1):81-4. [Medline].

  52. Edgerton G. Herpes zoster ophthalmicus: a review of the literature. Arch Ophthalmol. 1945;34:40-62; 114-53.

  53. Galil K, Choo PW, Donahue JG, Platt R. The sequelae of herpes zoster. Arch Intern Med. 1997 Jun 9. 157(11):1209-13. [Medline].

  54. Svozílková P, Ríhová E, Diblík P, Kuthan P, Kovarík Z, Kalvodová B. Varicella zoster virus acute retinal necrosis following eye contusion: case report. Virol J. 2005 Aug 31. 2:77. [Medline]. [Full Text].

  55. Westenend PJ, Hoppenbrouwers WJ. [Fatal varicella-zoster encephalitis; a rare complication of herpes zoster]. Ned Tijdschr Geneeskd. 1998 Mar 21. 142(12):654-7. [Medline].

  56. Fabian VA, Wood B, Crowley P, Kakulas BA. Herpes zoster brachial plexus neuritis. Clin Neuropathol. 1997 Mar-Apr. 16(2):61-4. [Medline].

  57. Furuta Y, Fukuda S, Suzuki S, Takasu T, Inuyama Y, Nagashima K. Detection of varicella-zoster virus DNA in patients with acute peripheral facial palsy by the polymerase chain reaction, and its use for early diagnosis of zoster sine herpete. J Med Virol. 1997 Jul. 52(3):316-9. [Medline].

  58. Hong JJ, Elgart ML. Gastrointestinal complications of dermatomal herpes zoster successfully treated with famciclovir and lactulose. J Am Acad Dermatol. 1998 Feb. 38(2 Pt 1):279-80. [Medline].

  59. Cresswell F, Eadie J, Longley N, Macallan D. Severe Guillain-Barré syndrome following primary infection with varicella zoster virus in an adult. Int J Infect Dis. 2010 Feb. 14(2):e161-3. [Medline].

  60. Shapiro JS. Does varicella-zoster virus infection of the peripheral ganglia cause Chronic Fatigue Syndrome?. Med Hypotheses. 2009 Nov. 73(5):728-34. [Medline].

  61. Ogita S, Terada K, Niizuma T, Kosaka Y, Kataoka N. Characteristics of facial nerve palsy during childhood in Japan: frequency of varicella-zoster virus association. Pediatr Int. 2006 Jun. 48(3):245-9. [Medline].

  62. Elkind MS, Hills NK, Glaser CA, Lo WD, Amlie-Lefond C, Dlamini N, et al. Herpesvirus Infections and Childhood Arterial Ischemic Stroke: Results of the VIPS Study. Circulation. 2016 Jan 26. [Medline].

  63. Grose C. Biological Plausibility of a Link Between Arterial Ischemic Stroke and Infection with Varicella-Zoster Virus or Herpes Simplex Virus. Circulation. 2016 Jan 26. [Medline].

  64. Koh MJ, Seah PP, Teo RY. Zosteriform herpes simplex. Singapore Med J. 2008 Feb. 49(2):e59-60. [Medline].

  65. Patel GA, Siperstein RD, Ragi G, Schwartz RA. Zosteriform lymphangioma circumscriptum. Acta Dermatovenerol Alp Panonica Adriat. 2009 Dec. 18(4):179-82. [Medline].

  66. Ozcan A, Senol M, Saglam H, Seyhan M, Durmaz R, Aktas E, et al. Comparison of the Tzanck test and polymerase chain reaction in the diagnosis of cutaneous herpes simplex and varicella zoster virus infections. Int J Dermatol. 2007 Nov. 46(11):1177-9. [Medline].

  67. Kalpoe JS, Kroes AC, Verkerk S, Claas EC, Barge RM, Beersma MF. Clinical relevance of quantitative varicella-zoster virus (VZV) DNA detection in plasma after stem cell transplantation. Bone Marrow Transplant. 2006 Jul. 38(1):41-6. [Medline].

  68. Böer A, Herder N, Blödorn-Schlicht N, Falk T. Herpes incognito most commonly is herpes zoster and its histopathologic pattern is distinctive!. Am J Dermatopathol. 2006 Apr. 28(2):181-6. [Medline].

  69. Homsy J, Katabira E, Kabatesi D, Mubiru F e. Evaluating herbal medicine for the management of Herpes zoster in human immunodeficiency virus-infected patients in Kampala, Uganda. J Altern Complement Med. 1999 Dec. 5(6):553-65. [Medline].

  70. Eaglstein WH, Katz R, Brown JA. The effects of early corticosteroid therapy on the skin eruption and pain of herpes zoster. JAMA. 1970 Mar 9. 211(10):1681-3. [Medline].

  71. Whitley RJ, Weiss H, Gnann JW Jr, Tyring S, Mertz GJ 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. 1996 Sep 1. 125(5):376-83. [Medline].

  72. Wood MJ, Shukla S, Fiddian AP, Crooks RJ. Treatment of acute herpes zoster: effect of early (< 48 h) versus late (48-72 h) therapy with acyclovir and valaciclovir on prolonged pain. J Infect Dis. 1998 Nov. 178 Suppl 1:S81-4. [Medline].

  73. van Wijck AJ, Opstelten W, Moons KG, van Essen GA, Stolker RJ, Kalkman CJ, et al. The PINE study of epidural steroids and local anaesthetics to prevent postherpetic neuralgia: a randomised controlled trial. Lancet. 2006 Jan 21. 367(9506):219-24. [Medline].

  74. Berry JD, Petersen KL. A single dose of gabapentin reduces acute pain and allodynia in patients with herpes zoster. Neurology. 2005 Aug 9. 65(3):444-7. [Medline].

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

  76. Lin PL, Fan SZ, Huang CH, Huang HH, Tsai MC, Lin CJ, et al. Analgesic effect of lidocaine patch 5% in the treatment of acute herpes zoster: a double-blind and vehicle-controlled study. Reg Anesth Pain Med. 2008 Jul-Aug. 33(4):320-5. [Medline].

  77. De Benedittis G, Lorenzetti A. Topical aspirin/diethyl ether mixture versus indomethacin and diclofenac/diethyl ether mixtures for acute herpetic neuralgia and postherpetic neuralgia: a double-blind crossover placebo-controlled study. Pain. 1996 Apr. 65(1):45-51. [Medline].

  78. Semel D, Murphy TK, Zlateva G, Cheung R, Emir B. Evaluation of the safety and efficacy of pregabalin in older patients with neuropathic pain: results from a pooled analysis of 11 clinical studies. BMC Fam Pract. 2010 Nov 5. 11:85. [Medline]. [Full Text].

  79. Huff JC, Bean B, Balfour HH Jr, Laskin OL, Connor JD, Corey L, et al. Therapy of herpes zoster with oral acyclovir. Am J Med. 1988 Aug 29. 85(2A):84-9. [Medline].

  80. Degreef H. Famciclovir, a new oral antiherpes drug: results of the first controlled clinical study demonstrating its efficacy and safety in the treatment of uncomplicated herpes zoster in immunocompetent patients. Int J Antimicrob Agents. 1994. 4(4):241-6. [Medline].

  81. Tyring S, Barbarash RA, Nahlik JE, Cunningham A, Marley J, Heng M, et al. Famciclovir for the treatment of acute herpes zoster: effects on acute disease and postherpetic neuralgia. A randomized, double-blind, placebo-controlled trial. Collaborative Famciclovir Herpes Zoster Study Group. Ann Intern Med. 1995 Jul 15. 123(2):89-96. [Medline].

  82. 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. 1995 Jul. 39(7):1546-53. [Medline]. [Full Text].

  83. 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. 1994 Mar 31. 330(13):896-900. [Medline].

  84. Kumar V, Krone K, Mathieu A. Neuraxial and sympathetic blocks in herpes zoster and postherpetic neuralgia: an appraisal of current evidence. Reg Anesth Pain Med. 2004 Sep-Oct. 29(5):454-61. [Medline].

  85. Ahmed HE, Craig WF, White PF, Ghoname ES, Hamza MA, Gajraj NM, et al. Percutaneous electrical nerve stimulation: an alternative to antiviral drugs for acute herpes zoster. Anesth Analg. 1998 Oct. 87(4):911-4. [Medline].

  86. Strasfeld L, Chou S. Antiviral drug resistance: mechanisms and clinical implications. Infect Dis Clin North Am. 2010 Sep. 24(3):809-33. [Medline].

  87. Decroix J, Partsch H, Gonzalez R, Mobacken H, Goh CL, Walsh L, et al. Factors influencing pain outcome in herpes zoster: an observational study with valaciclovir. Valaciclovir International Zoster Assessment Group (VIZA). J Eur Acad Dermatol Venereol. 2000 Jan. 14(1):23-33. [Medline].

  88. Kurokawa I, Kumano K, Murakawa K. Clinical correlates of prolonged pain in Japanese patients with acute herpes zoster. J Int Med Res. 2002 Jan-Feb. 30(1):56-65. [Medline].

  89. Kubeyinje EP. Cost-benefit of oral acyclovir in the treatment of herpes zoster. Int J Dermatol. 1997 Jun. 36(6):457-9. [Medline].

  90. Ahmed AM, Brantley JS, Madkan V, Mendoza N, Tyring SK. Managing herpes zoster in immunocompromised patients. Herpes. 2007 Sep. 14(2):32-6. [Medline].

  91. Balfour HH Jr, Bean B, et al. Acyclovir halts progression of herpes zoster in immunocompromised patients. N Engl J Med. 1983 Jun 16. 308(24):1448-53. [Medline].

  92. Morgan R, King D. Characteristics of patients with shingles admitted to a district general hospital. Postgrad Med J. 1998 Feb. 74(868):101-3. [Medline]. [Full Text].

  93. 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. 2000 Aug. 107(8):1507-11. [Medline].

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

  95. Acosta EP, Balfour HH Jr. Acyclovir for treatment of postherpetic neuralgia: efficacy and pharmacokinetics. Antimicrob Agents Chemother. 2001 Oct. 45(10):2771-4. [Medline]. [Full Text].

  96. Dworkin RH, Schmader KE. Treatment and prevention of postherpetic neuralgia. Clin Infect Dis. 2003 Apr 1. 36(7):877-82. [Medline].

  97. Whitley RJ, Volpi A, McKendrick M, Wijck Av, Oaklander AL. Management of herpes zoster and post-herpetic neuralgia now and in the future. J Clin Virol. 2010 May. 48 Suppl 1:S20-8. [Medline].

  98. Wu CL, Raja SN. An update on the treatment of postherpetic neuralgia. J Pain. 2008 Jan. 9(1 Suppl 1):S19-30. [Medline].

  99. Rauck RL, Irving GA, Wallace MS, Vanhove GF, Sweeney M. Once-Daily Gastroretentive Gabapentin for Postherpetic Neuralgia: Integrated Efficacy, Time to Onset of Pain Relief and Safety Analyses of Data From Two Phase 3 Multicenter, Randomized, Double-Blind, Placebo-Controlled Studies. J Pain Symptom Manage. 2012 Nov 10. [Medline].

  100. Khaliq W, Alam S, Puri N. Topical lidocaine for the treatment of postherpetic neuralgia. Cochrane Database Syst Rev. 2007 Apr 18. CD004846. [Medline].

  101. Gelb LD. Preventing herpes zoster through vaccination. Ophthalmology. 2008 Feb. 115(2 Suppl):S35-8. [Medline].

  102. Kotani N, Kushikata T, Hashimoto H, Kimura F, Muraoka M, Yodono M, et al. Intrathecal methylprednisolone for intractable postherpetic neuralgia. N Engl J Med. 2000 Nov 23. 343(21):1514-9. [Medline].

  103. Paster Z, Morris CM. Treatment of the localized pain of postherpetic neuralgia. Postgrad Med. 2010 Jan. 122(1):91-107. [Medline].

  104. Pavan-Langston D. Herpes zoster antivirals and pain management. Ophthalmology. 2008 Feb. 115(2 Suppl):S13-20. [Medline].

  105. Dahlmann A. Pain management in herpes zoster ophthalmicus. J R Soc Med. 2000 Jun. 93(6):334-5. [Medline]. [Full Text].

  106. Douglas MW, Johnson RW, Cunningham AL. Tolerability of treatments for postherpetic neuralgia. Drug Saf. 2004. 27(15):1217-33. [Medline].

  107. Evans RW, Lee AG. Herpes zoster ophthalmicus, ophthalmoplegia, and trauma. Headache. 2004 Mar. 44(3):286-8. [Medline].

  108. Oxman MN, Levin MJ, Johnson GR, Schmader KE, et al. A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults. N Engl J Med. 2005 Jun 2. 352(22):2271-84. [Medline].

  109. Oxman MN. Zoster vaccine: current status and future prospects. Clin Infect Dis. 2010 Jul 15. 51(2):197-213. [Medline].

  110. Civen R, Chaves SS, Jumaan A, Wu H, Mascola L, Gargiullo P, et al. The incidence and clinical characteristics of herpes zoster among children and adolescents after implementation of varicella vaccination. Pediatr Infect Dis J. 2009 Nov. 28(11):954-9. [Medline].

  111. Sanford M, Keating GM. Zoster vaccine (Zostavax): a review of its use in preventing herpes zoster and postherpetic neuralgia in older adults. Drugs Aging. 2010 Feb 1. 27(2):159-76. [Medline].

  112. Caple J. Varicella-zoster virus vaccine: a review of its use in the prevention of herpes zoster in older adults. Drugs Today (Barc). 2006 Apr. 42(4):249-54. [Medline].

  113. van Hoek AJ, Gay N, Melegaro A, Opstelten W, Edmunds WJ. Estimating the cost-effectiveness of vaccination against herpes zoster in England and Wales. Vaccine. 2009 Feb 25. 27(9):1454-67. [Medline].

  114. [Guideline] Harpaz R, Ortega-Sanchez IR, Seward JF. Prevention of herpes zoster: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2008 Jun 6. 57:1-30; quiz CE2-4. [Medline].

  115. Schmader K, Levin M, Gnann J, McNeil S, Vesikari T, et al. Efficacy, immunogenicity, safety, and tolerability of zoster vaccine (ZV) in subjects 50 to 59 years of age (Poster/Abstract). Infectious Diseases Society of America. The 48th Annual Meeting of the Infectious Diseases Society of America. 10-21-2010;Vancouver, British Columbia, Canada:Ref Type: Abstract: 3363.

  116. Schmader KE, Oxman MN, Levin MJ, Johnson G, et al. Persistence of the efficacy of zoster vaccine in the shingles prevention study and the short-term persistence substudy. Clin Infect Dis. 2012 Nov 15. 55(10):1320-8. [Medline].

  117. Marin M, Güris D, Chaves SS, Schmid S, Seward JF. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2007 Jun 22. 56:1-40. [Medline].

  118. [Guideline] Fashner J, Bell AL. Herpes zoster and postherpetic neuralgia: prevention and management. Am Fam Physician. 2011 Jun 15. 83 (12):1432-7. [Medline].

  119. [Guideline] Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clin Infect Dis. 2014 Jul 15. 59 (2):147-59. [Medline].

  120. [Guideline] Rubin LG, Levin MJ, Ljungman P, Davies EG, Avery R, Tomblyn M, et al. 2013 IDSA clinical practice guideline for vaccination of the immunocompromised host. Clin Infect Dis. 2014 Feb. 58 (3):309-18. [Medline].

  121. [Guideline] Dubinsky RM, Kabbani H, El-Chami Z, Boutwell C, Ali H, Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: treatment of postherpetic neuralgia: an evidence-based report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2004 Sep 28. 63 (6):959-65. [Medline].

  122. [Guideline] Attal N, Cruccu G, Baron R, Haanpää M, Hansson P, Jensen TS, et al. EFNS guidelines on the pharmacological treatment of neuropathic pain: 2010 revision. Eur J Neurol. 2010 Sep. 17 (9):1113-e88. [Medline].

  123. [Guideline] Centers for Disease Control and Prevention (CDC). Update on herpes zoster vaccine: licensure for persons aged 50 through 59 years. MMWR Morb Mortal Wkly Rep. 2011 Nov 11. 60 (44):1528. [Medline].

  124. [Guideline] Hales CM, Harpaz R, Ortega-Sanchez I, Bialek SR, Centers for Disease Control and Prevention (CDC). Update on recommendations for use of herpes zoster vaccine. MMWR Morb Mortal Wkly Rep. 2014 Aug 22. 63 (33):729-31. [Medline].

  125. Lee EG, Lee HJ, Hyun DJ, Min K, Kim DH, Yoon MS. Efficacy of low dose gabapentin in acute herpes zoster for preventing postherpetic neuralgia: a prospective controlled study. Dermatol Ther. 2016 Jan 22. [Medline].

 
Previous
Next
 
Typical zoster in the vicinity of right popliteal fossa in a vertebral nerve L4 distribution.
Suspected zoster of the hand.
Herpes zoster, unilateral, on trunk.
Herpes zoster on lateral part of abdomen.
Maculopapular rash due to herpes zoster in child with history of leukemia. Image courtesy of Centers for Disease Control and Prevention (CDC).
Herpes zoster in ophthalmic (V1) distribution of trigeminal nerve. Note unilateral distribution of rash and how V1 distribution may extend to tip of nose. Though at risk for keratitis with zoster in this distribution, patient had normal ocular examination. Patient consented to picture distribution for educational use; written permission on file. Image courtesy of JS Huff.
Herpes zoster on neck.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.