• Clinical science
  • Clinician

Shingles (Herpes zoster)

Summary

Shingles (herpes zoster) is a dermatomal rash with painful blistering that is caused by the reactivation of the varicella-zoster virus (VZV). The initial infection with VZV usually occurs early in life, presenting as chickenpox (varicella), after which the virus remains dormant in the dorsal root ganglia. Immunocompromised individuals are at increased risk of VZV reactivation. Shingles is generally a clinical diagnosis, although further testing (e.g., PCR) may be indicated in unclear cases. Treatment with antiviral drugs, such as acyclovir, is usually effective. Potential complications include encephalitis and, particularly in the elderly population, painful postherpetic neuralgia. VZV may also affect the cranial nerves. Involvement of the trigeminal nerve may cause visual impairment up to blindness (herpes zoster opthalmicus), while involvement of the facial and vestibulocochlear nerves can cause facial paralysis and hearing loss (herpes zoster oticus). These presentations, in particular, require urgent medical attention to prevent serious complications.

Epidemiology

  • Incidence [1]
    • Overall: 2.5–4/1,000 per year in the US [2]
    • Among individuals ≥ 60 years old: 10/1,000 per year in the US
    • Incidence of recurrence: unknown
  • Prevalence: increasing among adults in the US [1][3]
  • Sex: > [2]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

Pathophysiology

  • Primary infection (chickenpox): respiratory transmission → VZV inoculates the lymphoid tissue of the nasopharynx and, subsequently, regional lymphoid tissue → viremia and chickenpox recovery from chickenpox, but virus remains dormant in dorsal root ganglia (unless reactivated → recurrent infection)
  • Reactivation (shingles): VZV reactivated, often many years after the primary infection (e.g., especially in immunocompromised individuals) → virus replicates in the dorsal root ganglia travels through peripheral sensory nerves to the skin shingles (less contagious than primary infection) [4]

Clinical features

Subtypes and variants

Herpes zoster ophthalmicus [8]

Herpes zoster oticus [10]

Herpes zoster, herpes zoster oticus, and herpes zoster ophthalmicus present with identical rashes.

Diagnostics

Clinical presentation is usually sufficient for a diagnosis. [9][11]

  • PCR of VZV DNA [9][12]
    • Indications: confirmation of herpes zoster, recurrent herpes zoster, atypical presentations
    • May be performed on a variety of specimens
      • Skin lesions (vesicular fluid) [12]
      • CSF
      • Blood
  • Additional tests to consider [9][12]

Treatment

Antiviral therapy [9][11][13]

Antiviral therapy speeds up the resolution of lesions, reduces viral shedding, reduces the formation of new lesions, and decreases pain. Antiviral therapy is most effective if administered within approx. 72 hours or while new lesions are erupting.

Antiviral therapy should be initiated as early as possible since the effectiveness of antiviral treatment decreases as the disease progresses.

Supportive care [9][11][14]

Patients should receive routine wound care. Pain control is vital to maintain patients' quality of life and prevent postherpetic neuralgia.

Anti-inflammatory and analgesic therapy [9][11][14]

Corticosteroids [9]

Consider an adjuvant corticosteroid taper in patients with CNS complications (e.g., Bell palsy or vasculopathy) and/or severe pain.

Admission criteria and disposition [9]

Acute management checklist

Complications

Postherpetic neuralgia [15][11][16]

  • Definition: chronic neuropathic pain persisting for at least three months in the area previously affected by the rash
  • Epidemiology [15]
    • Most common complication (occurs in 10–20% of overall herpes zoster cases)
    • Strong association with age [15]
  • Risk factors [15][11]
  • Clinical features [11]
  • Treatment [11][16][9][14]
  • Prognosis: Pain typically continues to decrease over the first year but may last for months to years. [16]

Herpes zoster encephalitis [9]

Additional complications [9]

We list the most important complications. The selection is not exhaustive.

Prevention

The live herpes zoster vaccine is contraindicated in immunosuppressed individuals.

  • 1. CDC. Shingles (Herpes Zoster). https://www.cdc.gov/shingles/. Updated August 19, 2016. Accessed December 28, 2016.
  • 2. Opstelten W, Van Essen GA, Schellevis F, Verheij TJM, Moons KGM. Gender as an Independent Risk Factor for Herpes Zoster: A Population-Based Prospective Study. Ann Epidemiol. 2006; 16(9): pp. 692–695. doi: 10.1016/j.annepidem.2005.12.002.
  • 3. Leung J, Harpaz R, Molinari N-A, Jumaan A, Zhou F. Herpes Zoster Incidence Among Insured Persons in the United States, 1993–2006: Evaluation of Impact of Varicella Vaccination. Clinical Infectious Diseases. 2011; 52(3): pp. 332–340. doi: 10.1093/cid/ciq077.
  • 4. Sampathkumar P, Drage LA, Martin DP. Herpes Zoster (Shingles) and Postherpetic Neuralgia. Mayo Clinic Proceedings. 2009; 84(3): pp. 274–280. doi: 10.4065/84.3.274.
  • 5. Cohen JI. Herpes Zoster. N Engl J Med. 2013; 369(3): pp. 255–263. doi: 10.1056/nejmcp1302674.
  • 6. Shin BS, Na CH, Song IG, Choi KC. A case of human immunodeficiency virus infection initially presented with disseminated herpes zoster. Annals of dermatology. 2010; 22(2): pp. 199–202. doi: 10.5021/ad.2010.22.2.199.
  • 7. Dado D, Chernev I. Gastrointestinal varicella zoster infection. Dissemination or reactivation of a latent virus in the gut?. Endoscopy. 2013; 45(08): pp. 678–678. doi: 10.1055/s-0032-1326632.
  • 8. LIESEGANG T. Herpes Zoster OphthalmicusNatural History, Risk Factors, Clinical Presentation, and Morbidity. Ophthalmology. 2008; 115(2): pp. S3–S12. doi: 10.1016/j.ophtha.2007.10.009.
  • 9. Dworkin RH, Johnson RW, Breuer J, et al. Recommendations for the Management of Herpes Zoster. Clinical Infectious Diseases. 2007; 44(Supplement_1): pp. S1–S26. doi: 10.1086/510206.
  • 10. Gondivkar S, Parikh V, Parikh R. Herpes zoster oticus: A rare clinical entity. Contemporary Clinical Dentistry. 2010; 1(2): pp. 127–9. doi: 10.4103/0976-237X.68588.
  • 11. Saguil A, Kane S, Mercado M, Lauters R. Herpes Zoster and Postherpetic Neuralgia: Prevention and Management. Am Fam Physician. 2017; 96(10): pp. 656–663. pmid: 29431387.
  • 12. Laboratory Testing for VZV. https://www.cdc.gov/chickenpox/lab-testing/index.html. Accessed January 26, 2020.
  • 13. Sauerbrei A. Diagnosis, antiviral therapy, and prophylaxis of varicella-zoster virus infections. European Journal of Clinical Microbiology & Infectious Diseases. 2016; 35(5): pp. 723–734. doi: 10.1007/s10096-016-2605-0.
  • 14. Bates D, Schultheis BC, Hanes MC, et al. A Comprehensive Algorithm for Management of Neuropathic Pain. Pain Medicine. 2019; 20(Supplement_1): pp. S2–S12. doi: 10.1093/pm/pnz075.
  • 15. Harpaz R, Ortega-Sanchez IR, Seward JF, Advisory Committee on Immunization Practices (ACIP) Centers for Disease Control and Prevention (CDC). Prevention of herpes zoster: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports. 2008; 57(RR-5): pp. 1–30; quiz CE2–4. pmid: 18528318.
  • 16. Johnson RW, Rice ASC. Postherpetic Neuralgia. N Engl J Med. 2014; 371(16): pp. 1526–1533. doi: 10.1056/nejmcp1403062.
  • 17. CDC. Child and Adolescent Schedule. https://www.cdc.gov/vaccines/schedules/hcp/imz/child-adolescent.html. Updated February 3, 2020. Accessed June 23, 2020.
  • 18. Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for Use of Herpes Zoster Vaccines. MMWR Morb Mortal Wkly Rep. 2018; 67(3): pp. 103–108. doi: 10.15585/mmwr.mm6703a5.
  • Centers for Disease Control and Prevention. Vaccines and Preventable Diseases - Shingles Vaccination. https://www.cdc.gov/vaccines/vpd/shingles/public/shingrix/index.html. Updated January 25, 2018. Accessed October 27, 2018.
last updated 10/12/2020
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