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Shingles

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Overview

Also known as herpes zoster, shingles describes the reactivation of the varicella-zoster virus (VZV), a DNA virus that can cause chickenpox (varicella) and shingles. Chickenpox is a primary infection by VZV, and shingles is its reactivation.

Unlike chickenpox, shingles can occur years-decades after the primary infection and symptoms are usually localised to a specific dermatome. This is because when it reactivates, it travels across sensory nerves to the skin.

Pathophysiology

VZV is highly contagious and spread by the respiratory route. In the skin, its replication can cause epithelial damage, resulting in vesicles containing damaged material and leukocytes. These may burst and spread VZV or resolve. After infection, VZV can remain latent in the dorsal root ganglia. Childhood exposure to chickenpox leads to lifelong immunoglobulin G (IgG) antibodies which persist for life, however, over time, the immune system is less effective at suppressing VZV, resulting in its reactivation and shingles. 

Epidemiology

  • The incidence and severity of shingles increase with age
  • In people <50 years old, the incidence is <2 per 1,000 per year
  • In people ≥80 years, the incidence is 11 cases per 1,000 per year

Risk Factors

  • Increasing age – thought to be due to age-related declines in cell-mediated immunity
  • Immunocompromised states – including HIV, corticosteroids, immunosuppressants 

Presentation

Features of shingles include:

  • A 2-3-day prodrome of burning pain in the affected dermatome
    • Some people may have associated flu-like symptoms (e.g. fever, headache, malaise)
  • Followed by maculopapular lesions that quickly become vesicular over 3-5 days
  • The thoracic and lumbar regions are most commonly affected.

In people with immunocompromised states, shingles can be more severe, prolonged, and may be disseminated.

Other presentations

  • Herpes zoster ophthalmicus – an ophthalmic emergency due to VZV reactivation in the first or second divisions of the trigeminal nerve
  • Intra-oral shingles – involving the palate and tongue, due to VZV reaction in the mandibular division of the trigeminal nerve 
  • Ramsay-Hunt syndrome – due to reactivation of VZV in the geniculate ganglion of the facial nerve

Diagnosis

Diagnosis is clinical.

Management

Overview

Analgesia should be offered:

  • 1st-line: paracetamol and NSAIDs
  • If unresponsive: consider neuropathic pain drugs (e.g. amitriptyline)
  • If still unresponsive + first 2 weeks + immunocompetent: consider oral corticosteroids

Antiviral drugs (e.g. aciclovir) may be prescribed to people who present within 72 hours except if the patient is <50 years old and has a mild rash with mild pain and no risk factors:

  • Antivirals can reduce the incidence of post-herpetic neuralgia

Advise patients that they are still potentially infectious and should avoid contact with at-risk groups including pregnant people and immunocompromised people. Until the vesicles have crusted over (after ~5-7 days), they are infectious.

Complications

Post-herpetic neuralgia – persisting pain for more than 90 days after rash onset. This is one of the most common complications due to VZV-induced peripheral nerve damage. It is more common in older people and rare in people <50 years old.

Skin changes – changes including scarring, keloid formation, and pigment changes can occur after the rash has healed.

Bacterial superinfection – secondary infection of lesions may occur, usually with Staphylococcal and Streptococcal species which can cause cellulitis. 

Herpes zoster ophthalmicus – an ophthalmic emergency due to VZV reactivation in the first or second divisions of the trigeminal nerve. See Herpes Zoster Ophthalmicus.

Ramsay-Hunt syndrome – due to reactivation of VZV in the geniculate ganglion of the facial nerve, causing facial nerve palsy. See Ramsay-Hunt Syndrome.

Central nervous system complications – particularly in people with shingles of the head and neck. Complications can include encephalitis, meningoencephalitis, radiculitis, and cerebrovascular disease. These are more common in immunocompromised people.

Disseminated disease – rare, but serious complication. Can disseminate into the lungs, liver, gut, and brain, leading to pneumonia, hepatitis, and encephalitis. It can also cause disseminated intravascular coagulopathy. This is more likely in people who are severely immunocompromised.

Prognosis

  • Shingles is usually self-limiting, however, in immunocompromised people, it may be prolonged and/or recurrent.

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