Shingles (Herpes Zoster)

Overview 

Shingles is reactivation of latent varicella-zoster virus (VZV) following previous chickenpox or, less commonly, varicella vaccination. After primary infection, VZV remains dormant in the dorsal-root or cranial-nerve ganglia. Reactivation occurs when VZV-specific cell-mediated immunity declines. In Australia, incidence is approximately 560 cases per 100,000 people annually and increases markedly after age 50. Lifetime risk approaches 50% among people living to 80 years. Approximately 13–26% of patients develop a complication. 

Aetiology and Risk Factors

• Previous VZV infection is required.
• Increasing age, particularly over 50 years.
• Immunocompromise:
  • Haematological or solid-organ malignancy
  • HIV
  • Organ or stem-cell transplantation
  • Chemotherapy or radiotherapy
  • Systemic corticosteroids, biologics or other immunosuppressants
• Autoimmune and chronic systemic disease.
• Previous shingles does not provide permanent protection; recurrence is possible.
• Varicella infection during the first year of life may increase later risk.

Pathophysiology

• Primary infection with varicella-zoster virus (VZV) causes chickenpox.
• After recovery, VZV remains latent within the dorsal-root and cranial-nerve sensory ganglia.
• Declining VZV-specific cell-mediated immunity allows the virus to reactivate.
• Reactivation is more common with increasing age, immunosuppression, malignancy or severe illness.
• The virus replicates within the sensory ganglion, causing inflammation and neuronal damage.
• VZV then travels along the sensory nerve to the skin, producing:
  • Dermatomal pain, burning or paraesthesia.
  • A unilateral vesicular rash in the corresponding dermatome.
• The rash usually does not cross the midline because individual sensory nerves supply one side of the body.
• Persistent nerve inflammation and damage may cause postherpetic neuralgia after the skin lesions resolve.
• Spread beyond the sensory ganglion may cause motor weakness, meningitis, encephalitis, vasculopathy or disseminated infection, particularly in immunocompromised patients.

Clinical Manifestations

Prodrome

• Burning, stabbing or aching dermatomal pain
• Tingling, itching or hypersensitivity
• Headache, fatigue or malaise
• Fever is possible but usually mild

Shingles Rash

• Unilateral erythematous papules developing into grouped vesicles.
• Usually affects one or two adjacent dermatomes.
• Commonly affects the thoracic region or face.
• Generally does not cross the midline.
• Vesicles become pustular and crust over within approximately 7–10 days.
• Rash usually heals within 2–4 weeks. 

Important Presentations

• Ophthalmic zoster: forehead, upper eyelid or nose lesions; eye pain, photophobia, redness or reduced vision.
• Hutchinson sign: lesions on the tip or side of the nose suggest nasociliary involvement and increased ocular risk.
• Ramsay Hunt syndrome: painful ear vesicles, ipsilateral facial weakness, hearing loss, tinnitus or vertigo.
• Disseminated disease: widespread vesicles, fever or systemic illness, especially in immunocompromised patients.
• Neurological disease may cause headache, meningism, confusion, weakness or focal deficits.

Diagnosis

• Usually a clinical diagnosis based on unilateral dermatomal pain and grouped vesicles.
• VZV PCR from vesicular fluid, lesion-base swab or crust is preferred when:
  • Presentation is atypical
  • The patient is immunocompromised
  • Disseminated infection is suspected
  • Differentiation from herpes simplex is needed
• Consider bacterial culture if secondary infection is suspected.
• Neurological disease may require lumbar puncture with CSF VZV testing and neuroimaging.

Differential diagnoses 

• herpes simplex
• contact dermatitis
• Impetigo
• insect bites
• autoimmune blistering disorders.

Treatment

Antiviral therapy

Start preferably within 72 hours of rash onset:

• Valaciclovir: 1 g orally three times daily for 7 days.
• Famciclovir: 500 mg orally three times daily for 7 days.
• Aciclovir: 800 mg orally five times daily for 7 days.

Consider treatment after 72 hours if new vesicles are developing or the patient has ophthalmic, neurological, disseminated or immunocompromised disease. Adjust doses for renal impairment and maintain hydration.

Symptomatic management

• Paracetamol ± NSAID where appropriate.
• Short-term stronger analgesia may be required for severe acute pain.
• Neuropathic-pain therapy may include gabapentin, pregabalin or a tricyclic antidepressant.
• Cool compresses, calamine lotion and loose clothing.
• Keep lesions clean, dry and covered.

Hospital treatment / urgent referral

• IV aciclovir for disseminated or visceral disease, severe immunocompromise, encephalitis or inability to take oral treatment.
• Obtain urgent infectious diseases or specialist advice.
• Eye or forehead involvement: same-day ophthalmological assessment.
• Facial weakness, ear vesicles, hearing loss or vertigo: urgent assessment for Ramsay Hunt syndrome.
• Disseminated rash, immunocompromise, pregnancy, severe systemic illness or neurological symptoms: hospital or specialist assessment.
• Corticosteroids must not be used alone without antiviral treatment.

Prevention of shingles

• Recombinant zoster vaccine Shingrix is given as two doses.
• In Australia it is recommended for:
  • Immunocompetent adults aged ≥50 years
  • Immunocompromised adults aged ≥18 years
• It remains recommended after a previous episode of shingles, once the acute illness has resolved and at the guideline-recommended interval. 

Complications and Prognosis

Complications

• Postherpetic neuralgia: persistent burning, stabbing pain or allodynia; most common complication.
• Herpes zoster ophthalmicus:
  • Keratitis
  • Uveitis
  • Glaucoma
  • Retinal disease
  • Permanent visual loss
• Ramsay Hunt syndrome:
  • Facial paralysis
  • Hearing loss
  • Tinnitus or vertigo
• Secondary bacterial skin infection, scarring or pigmentary change.
• Motor neuropathy or segmental weakness.
• Meningitis, encephalitis, myelitis or VZV vasculopathy and stroke.
• Pneumonia or visceral dissemination

Prognosis

• Most immunocompetent patients recover within 2–4 weeks.
• Acute pain may continue after the rash resolves.
• PHN risk rises substantially with age:
  • Approximately 1 in 10 cases in people aged 50–59 years.
  • Approximately 1 in 5 cases in people older than 80 years.
• Poor prognostic factors include older age, severe initial pain, extensive rash, ophthalmic involvement and immunocompromise.
• Recurrence occurs in approximately 6–8% of immunocompetent patients within eight years and is more frequent with immunocompromise.
• Persistent visual, auditory or neurological impairment can occur after complicated disease.

References 

1. Australian Technical Advisory Group on Immunisation. Zoster (herpes zoster). In: Australian Immunisation Handbook [Internet]. Canberra: Australian Government Department of Health and Aged Care; updated 2026 Jan 19.
2. Lim DZJ, Tey HL, Salada BMA, Oon JEL, Seah ED, Chandran NS, et al. Herpes zoster and post-herpetic neuralgia—diagnosis, treatment, and vaccination strategies. Pathogens. 2024;13(7):596. doi:10.3390/pathogens13070596.
3. Centers for Disease Control and Prevention. Clinical overview of shingles (herpes zoster) [Internet]. Atlanta: CDC; 2024.
4. World Health Organization. Shingles (herpes zoster) [Internet]. Geneva: WHO; 2025.
5. NSW Health. Shingles fact sheet [Internet]. Sydney: NSW Government; 2024.