eMedicine Specialties > Ophthalmology > Infectious Disease

Herpes Zoster

Author: Manolette R Roque, MD, MBA, DPBO, FPAO, President and CEO, Chief of Service, Ocular Immunology and Uveitis, Consulting Staff, Cornea and Refractive Surgery, Eye Republic Ophthalmology Clinic; General Manager, Ophthalmic Consultants Philippines Co; Consulting Staff, CME Liaison, Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center
Coauthor(s): Barbara L Roque, MD, Full Partner, Ophthalmic Consultants Philippines Co, Chief of Service, Pediatric Ophthalmology and Strabismus, Consulting Staff, Orbit and Eye Plastics, Eye Republic Ophthalmology Clinic; 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
Contributor Information and Disclosures

Updated: Oct 28, 2008

Introduction

Background

Varicella-zoster virus (VZV) is a member of the Herpesviridae family. It is the etiologic agent of varicella (chickenpox), the primary infection, and herpes zoster, the reactivation.1,2

Herpes zoster ophthalmicus involves the tissues innervated by the ophthalmic division of the trigeminal nerve and accounts for 10-25% of all cases of shingles. The sequelae of herpes zoster ophthalmicus can be devastating and include chronic ocular inflammation, visual loss, and debilitating pain.3,4,5,6,7

Herpes zoster oticus involves the inner, middle, and external ear. Herpes zoster oticus presents as excruciating otalgia with an associated cutaneous vesicular eruption (external canal and pinna). When associated facial paralysis is present, the disease is called Ramsay Hunt syndrome.8,9

Pathophysiology

After primary infection, VZV enters the dorsal root ganglia (trigeminal = herpes zoster ophthalmicus, geniculate = herpes zoster oticus), where it remains latent for the lifetime of the individual.10

The frequency of dermatologic involvement in herpes zoster is similar to the centripetal distribution of the initial varicella lesions. This pattern may suggest that the latency arises from contiguous spread of the virus during varicella from infected skin cells to sensory nerve endings with subsequent ascent to the ganglia. It also may suggest that the ganglia are infected hematogenously during the viremic phase of varicella and that the frequency of the dermatome involvement in herpes zoster reflects the ganglia most often exposed to reactivating stimuli.

In immunocompetent patients, specific antibodies (immunoglobulins G, M, and A) appear more rapidly and reach higher titers during reactivation (herpes zoster) than during the primary infection.

The appearance of the cutaneous rash due to herpes zoster coincides with a profound VZV-specific T-cell proliferation. Interferon-alpha production appears with the resolution of herpes zoster. The patient has a long-lasting, enhanced, cell-mediated immunity response to VZV.11,12,13

Frequency

United States

Regarding primary infection, more than 90% of the population is infected by adolescence, and approximately 100% are infected by 60 years of age14

Herpes zoster affects about 10-20% of the population15 The rate is approximately 131 per 100,000 person-years in white individuals.

According to Pavan-Langston's review, 1 million consultations for herpes zoster occur per year; approximately 250,000 of the patients thus examined develop herpes zoster ophthalmicus. A subset of 50% of these patients develops complications of herpes zoster ophthalmicus.

Ramsay Hunt syndrome is the cause of as many as 12% of all cases of facial paralysis.


Mortality/Morbidity

  • In the United States, as many as 10,000 hospitalizations and approximately 100 deaths occur per year as a result of complications from VZV infection. Morbidity and mortality affect mostly immunosuppressed individuals, including elderly persons, individuals who are immunosuppressed (eg, those with HIV infection or AIDS), persons receiving immunosuppressive therapy, and persons with primary infection in utero or in early infancy.
    • CNS complications: Meningoencephalitis, myelitis, cranial nerve palsies, and granulomatous angiitis may result in the development of a cerebrovascular accident.16
    • Disseminated zoster: Hematogenous spread may result in the involvement of multiple dermatomes and visceral involvement and may lead to death due to encephalitis, hepatitis, or pneumonitis.
  • In herpes zoster ophthalmicus, complications may be associated with inflammatory changes (infiltrative, eg, keratitis, or vasculitic, eg, episcleritis/scleritis, iritis, ischemic papillitis, orbital vasculitis)17,18,19,20,21,22,23,24,25,26,27,28,29,30,31   Other complications occur as a result of nerve damage (eg, neurotrophic keratitis, some ocular motor palsies, neuralgia) and tissue scarring (eg, lid deformities, neuralgia, lipid keratopathy)32,33,34,35,36,37,38,39 Ramsay Hunt syndrome (zoster involving cranial nerves V, IX, and X) usually causes symptoms more severe than those of Bell palsy.8,40 In numerous studies, only 10-22% of individuals with significant facial paralysis had complete recovery. However, in one report, 66% of patients with incomplete paralysis had complete recovery.
  • Secondary bacterial infection, typically streptococcal or staphylococcal, may occur at the site of the rash41 Secondary bacterial infections may lead to deep, unsightly scars. They may be avoided by maintaining good hygiene and by preventing scratching, which may lead to untimely scab removal and tissue repair disruption. 
  • Postherpetic neuralgia (ie, pain that persists for more than 1 month after resolution of the vesicular rash) is a common and oftentimes excruciating complication of herpes zoster. This is more common in patients older than 50 years42,43,34,44,45

Race

In 1995, Schmader et al reported that the lifetime incidence of herpes zoster in whites is twice that of African Americans.

Sex

No known sex predilection exists.

Age

  • Primary infection with VZV is a childhood disease.
  • VZV reactivation or herpes zoster is primarily a disease that affects healthy older adults.
  • Incidence increases with age, peaking in the seventh decade of life.

Clinical

History

Patients with herpes zoster often report a history of chickenpox. In some cases, a present state of immunocompromise may be noted.

Herpes zoster results in a prodrome (ie, fever, malaise, headache, dysesthesia) that occurs 1-4 days before the development of the cutaneous lesions (rashes). Prodromal pain is typically confined to the same dermatomal distribution. The rashes, which are initially vesicular, gradually become pustular and then crust over during a period of 7-10 days. Similar to chickenpox, once crusting occurs, the lesions cease to be infectious. 

Scarring and hypopigmentation or hyperpigmentation may persist for a long period. For infected and manipulated lesions, deep scars may form46

  • Herpes zoster ophthalmicus
    • Acute orbital and globe lesions develop within 3 weeks of the rash. These lesions may resolve rapidly and completely, or they may lead to a chronic course and linger for years.
    • Recurrence is a characteristic feature of herpes zoster ophthalmicus. Relapse may occur as late as 10 years after onset.
    • Symptoms of herpes zoster ophthalmicus may include eye pain, red eye (usually unilateral), decreased vision, skin/eyelid rash and pain, fever, malaise, and tearing.
  • Herpes zoster oticus
    • Usually, patients present with excruciating otalgia.
    • Symptoms include painful burning blisters (in and around the ear, on the face, in the mouth, and/or on the tongue), vertigo, hearing loss, and eye pain.
    • Onset of pain may precede the rash by several hours or days.

Physical

  • Exanthem
    • Grouped vesicles, usually involving 1, but occasionally up to 3, adjacent dermatomes.47,48
    • Vesicles become pustular, and occasionally hemorrhagic, with evolution to crusts in 7-10 days.
  • Herpes zoster ophthalmicus13
    • Vesicular rashes involving the ophthalmic division of the trigeminal nerve. Crusting begins on the fifth to sixth day.
    • In 1864, Hutchinson proposed that the cutaneous involvement in the distribution of the nasociliary nerve heralds ocular involvement. Time has proven him correct (Hutchinson sign). It is now accepted that severe ocular complications can occur with a vesicular rash anywhere on the forehead.49
  • Herpes zoster oticus
    • Examination reveals a vesicular exanthem involving the external auditory canal, concha, and pinna. Other possible areas of involvement can include postauricular skin, lateral nasal wall, soft palate, and anterolateral tongue.
    • Vertigo and sensorineural hearing loss and/or paralysis of the facial nerve may be noted.
    • Clinically, total loss of the ability to wrinkle the ipsilateral brow differentiates a peripheral seventh nerve lesion from a central seventh nerve lesion, which spares the forehead.
    • Other associated findings may include dysgeusia (alteration in taste) and inability to fully close the ipsilateral eye, which may lead to an occasional presenting complaint of eye dryness and irritation.

Causes

Known risk factors for developing herpes zoster relate to the status of cell-mediated immunity to VZV.

  • Various factors can account for the increased incidence of herpes zoster:
    • VZV-specific immunity and cell-mediated immunity, which generally declines with age
    • Immunosuppression (eg, HIV infection, AIDS)50,51,52,53,54,55,56,57,58,59,60,61,62
    • Immunosuppressive therapy63
    • Primary infection in utero or in early infancy, when the normal immune response is decreased
  • VZV virology
    • VZV is a double-stranded DNA virus with a diameter of 150-200 nm, a lipid envelope bearing the host cell membrane, and glycoprotein spikes. These envelope proteins are essential to understanding the VZV-specific immunity and the production of improved vaccines.
    • Intranuclear replication of VZV in the host cell occurs and produces an intranuclear inclusion body. Viral DNA transcription to messenger RNA leads to synthesis of viral proteins in the host cell cytoplasm. These newly synthesized viral proteins are transported to the host cell nucleus. Assembly with replicated viral DNA into nucleocapsids ensues. Finally, an outer envelope is acquired as the assembled virus passes through the cytoplasm prior to its release from the cell.

More on Herpes Zoster

Overview: Herpes Zoster
Differential Diagnoses & Workup: Herpes Zoster
Treatment & Medication: Herpes Zoster
Follow-up: Herpes Zoster
Multimedia: Herpes Zoster
References
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Further Reading

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Keywords

herpes zoster, herpes zoster ophthalmicus, varicella-zoster virus, chickenpox, shingles, varicella, postherpetic neuralgia, herpes zoster oticus, Ramsay Hunt Syndrome, dermatomal zoster, zona, Hutchinson sign, VZV, HZO

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Contributor Information and Disclosures

Author

Manolette R Roque, MD, MBA, DPBO, FPAO, President and CEO, Chief of Service, Ocular Immunology and Uveitis, Consulting Staff, Cornea and Refractive Surgery, Eye Republic Ophthalmology Clinic; General Manager, Ophthalmic Consultants Philippines Co; Consulting Staff, CME Liaison, Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center
Manolette R Roque, MD, MBA, DPBO, FPAO 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.

Coauthor(s)

Barbara L Roque, MD, Full Partner, Ophthalmic Consultants Philippines Co, Chief of Service, Pediatric Ophthalmology and Strabismus, Consulting Staff, Orbit and Eye Plastics, Eye Republic Ophthalmology Clinic
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.

Medical Editor

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.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
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.

Managing Editor

R Christopher Walton, MD, Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, Assistant Dean for Graduate Medical Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital
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.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

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.

 
 
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