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Shingles (Herpes zoster)


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.


Epidemiological data refers to the US, unless otherwise specified.




  • Primary infection (chickenpox): respiratory transmissionVZV inoculates the lymphoid tissue of the nasopharynx and, subsequently, regional lymphoid tissue → viremia + chickenpox → recovery from chickenpox, but virus remains dormant in dorsal root ganglia (unless reactivated → recurrent infection)
  • Reactivation (shingles): VZV reactivated (e.g., due to immunocompromise)virus replicates in the dorsal root ganglia → travels through peripheral sensory nerves to the skin → shingles (less contagious than primary infection)


Clinical features


Subtypes and variants

Herpes zoster ophthalmicus

Herpes zoster oticus

Herpes zoster ophthalmicus can lead to blindness! Herpes zoster oticus can result in hearing loss and permanent facial paralysis on the affected side!

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



Clinical presentation is usually sufficient for a diagnosis. [12][13]

  • PCR of VZV DNA [12][14]
    • Indications: confirmation of herpes zoster, recurrent herpes zoster, atypical presentations
    • May be performed on a variety of specimens
      • Skin lesions (vesicular fluid) [14]
      • CSF
      • Blood
  • Additional tests to consider [12][14]


Antiviral therapy [12][13][15]

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 [12][13][16]

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 [12][13][16]

Corticosteroids [12]

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

Admission criteria and disposition [12]

Acute management checklist


Postherpetic neuralgia [17][13][18]

  • Definition: chronic neuropathic pain persisting for at least three months in the area previously affected by the rash
  • Epidemiology [17]
    • Most common complication (occurs in 10–20% of overall herpes zoster cases)
    • Strong association with age [17]
  • Risk factors [17][13]
  • Clinical features [13]
  • Treatment [13][18][12][16]
  • Prognosis: Pain typically continues to decrease over the first year but may last for months to years. [18]

Herpes zoster encephalitis [12]

Additional complications [12]

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


The live herpes zoster vaccine is contraindicated in immunosuppressed individuals.