Varicella-Zoster Virus Clinical Presentation

  • Author: Wayne E Anderson, DO; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Jul 11, 2011
 

History

  • Pain and paresthesia are typically the first symptoms. Until the characteristic vesicular rash erupts, diagnosis may be difficult.
  • A prodromal period during which symptoms may vary is common. Pain occurs in 41% of patients, itching in 27%, and paresthesias in 12%.
  • During the acute illness, 90% of patients experience pain, 20% describe helplessness and depression, and 12% experience flulike symptoms.
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Physical

  • Herpes zoster (shingles)
    • The most common presentation is the shingles vesicular rash, which most commonly affects a thoracic dermatome.
    • After a prodromal illness of pain and paresthesias, erythematous macules and papules develop and progress to vesicles within 24 hours. The vesicles eventually crust and resolve.Typical zoster in the vicinity of right popliteal Typical zoster in the vicinity of right popliteal fossa in a vertebral nerve L4 distribution.
    • Pain and sensory loss are the usual symptoms, but motor weakness also occurs and is frequently missed on examination. Motor weakness results when the viral activity extends beyond the sensory root to involve the motor root. Cases of actual monoplegia due to varicella-zoster virus (VZV) brachial plexus neuritis have been reported.
  • Zoster multiplex
    • Shingles may appear in multiple dermatomes, both contiguous and noncontiguous, on either side of the body.
    • They are more common in individuals who are immunocompromised.
    • Terminology depends on the number of involved dermatomes and on whether the condition is unilateral or bilateral. For example, zoster duplex unilateralis refers to the involvement of 2 unilateral dermatomes. Cases of zoster simultaneously occurring in 7 noncontiguous dermatomes have been reported.
  • Zoster sine herpete
    • VZV infection may reactivate without causing cutaneous vesicles. These patients have severe dermatomal pain, possible motor weakness and possible hypesthesia, but no visible rash or vesicles.
    • Studies show that VZV infection may present as acute peripheral facial palsy in 8-25% of patients who have no cutaneous vesicles. This is more common in immunosuppressed patients who use acyclovir (or other agents) as zoster prophylaxis.[1]
  • Myelitis
    • VZV infection may also cause central nervous system deficits.
    • Although deficits are more common in immunocompromised individuals, such presentations do occur in the general population.
    • In one report, the condition began as a typical shingles rash, but spinal cord involvement became apparent 3 weeks after the onset of the initial rash.
    • The manifestations are usually bilateral. The physical findings may progress.
    • The underlying pathology typically progresses for 3 or more weeks. Progression for 6 months in immunocompromised individuals has been reported.
    • With intravenous acyclovir treatment, most cases fully resolve. Recurrence is rare but has been reported.
    • Zoster encephalitis is also rare but is reported in otherwise healthy individuals. Due to the effectiveness of 2-dose vaccinations, fewer cases of VZV encephalitis occur,[2] yet most cases in vaccinated individuals are due to wild type from the vaccine strain.[3]
  • Ramsay-Hunt syndrome
    • This syndrome occurs when the geniculate ganglion is involved.
    • The clinical presentation includes a peripheral facial palsy, pain in the ear and face, and vesicles in the external ear canal.
    • Additional auditory and vestibular symptoms may be present. The vesicles are not present in all cases.
  • Keratitis (herpes ophthalmicus)
    • This is caused by reactivation of VZV infection in the ophthalmic division of the trigeminal nerve.
    • The presentation may include conjunctivitis or corneal ulcers. Complications include blindness.
    • The vesicles do not have to be present.
    • Rarely, in cases of herpes ophthalmicus, the virus migrates along the intracranial branches of the trigeminal nerve, causing thrombotic cerebrovasculopathy with severe headache and hemiplegia.
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Causes

Immunosuppression increases the risk of both typical shingles and atypical presentations, such as myelitis, encephalitis, disseminated disease, and visceral involvement.

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Contributor Information and Disclosures
Author

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: Cephalon Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; King Honoraria Speaking and teaching; Forest Honoraria Speaking and teaching

Specialty Editor Board

Maria D Mileno, MD  Associate Professor of Medicine, Division of Infectious Diseases, The Warren Alpert Medical School of Brown University

Maria D Mileno, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine, and Sigma Xi

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

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.

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.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of prior coauthor Amar Safdar, MD, to the development and writing of this article.

References

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Typical zoster in the vicinity of right popliteal fossa in a vertebral nerve L4 distribution.
 
 
 
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