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Viral skin infections

Herpes zoster

Created 2009.

Learning objectives

  • Identify and manage herpes zoster infections

Clinical features of herpes zoster

Herpes zoster, or shingles, is a painful blistering rash caused by reactivation of the herpes varicella-zoster virus. The primary infection presents as chickenpox (varicella), usually during childhood. Like herpes simplex, the virus persists in selected cells of dorsal root ganglion before it is reactivated.

Herpes zoster can occur in childhood but is much more common in adults, especially the elderly, sick or immune suppressed. It is infectious, resulting in chickenpox in those who have never developed primary immunity, both from virus in the lesions and in some instances the nose and throat.

The first sign of herpes zoster is usually pain, which may be severe, in the areas of one or more sensory nerves, often where they emerge from the spine. The patient usually feels quite unwell with fever, headache and regional lymphadenopathy. Within one to three days of the onset of pain, crops of closely grouped erythematous papules develop within the unilateral dermatome(s). New papules continue to appear for several days, each blistering or becoming pustular then crusting over.

Herpes zoster

The pain and general symptoms subside gradually as the eruption disappears. In uncomplicated cases recovery is complete in 2–3 weeks in children and young adults, and 3–4 weeks in older patients.

The thoracic, cervical, ophthalmic and lumbar/sacral sensory nerve supply regions are most commonly affected at all ages but the frequency of ophthalmic zoster increases with age. Rarely the eruption may affect both sides of the body.

In elderly and undernourished patients the blisters are deeper. Healing may take many weeks and be followed by scarring. Muscle weakness arises in about one in twenty patients because the motor nerves are affected as well as the sensory nerves. Facial nerve palsy is the most common result. There is a 50% chance of complete recovery and in time some improvement can be expected in nearly all cases.

Post-herpetic neuralgia is defined as persistence or recurrence of pain more than a month after the onset of shingles. It becomes increasingly common with age, affecting about a third of patients over 40. It is particularly likely if there is facial infection. The pain may be continuous and burning with increased sensitivity in the affected areas, or a spasmodic shooting type, or, rarely, itching and crawling (formication). The overlying skin is numb or exquisitely sensitive to touch (hyperaesthesia and allodynia).

The incidence and severity of herpes zoster can be reduced by vaccination.


In most cases no investigations are necessary as the clinical features are diagnostic. However, at times the diagnosis should be confirmed in one of the following ways:

  • Basal cells collected from vesicles onto slide for rapid antigen detection by immunofluorescence
  • Viral swab of vesicle fluid or scrapings of vesicles for culture (5–14 days)
  • 5ml plain tube blood or 500 µl serum for serology (immune status IgG and acute phase IgM)

Management of herpes zoster

Treatment of active herpes zoster may include:

  • Rest and analgesics
  • Povidone iodine or calamine lotion applied to blisters
  • Oral aciclovir 800mg 5 times daily for 7 days
  • Systemic steroids for severe infections
  • Oral antibiotics for secondary infection

Post-herpetic neuralgia may be difficult to treat successfully. If paracetamol and soothing local applications are unhelpful, the following may be used:

  • Opioid analgesics
  • Capsaicin cream
  • Local anaesthetics
  • Tricyclic antidepressants
  • Anti-convulsants

The chosen drug should be stopped if it does not produce the desired effect or causes unacceptable side effects at appropriate dose and duration. Polypharmacy can be useful to allow lower doses to achieve analgesia but side effects and drug interactions can be risky.

Opioid analgesics

Tramadol may be quite useful for neuropathic pain as it has serotonergic effects. More potent opioids are sometimes required short term, but can result in escalating dose requirements. If one opiate is ineffective, others are also likely to be ineffective.

Capsaicin cream

Capsaicin reversibly depletes the nerve endings of the neurotransmitter substance P. Compliance is quite poor because it results in a burning discomfort when first applied. It may be required 4 times daily for up to 4 weeks before achieving adequate analgesia. The addition of glyceryl trinitrate seems to reduce the burning discomfort.

Local anaesthetics

These are membrane stabilisers. Lignocaine/prilocaine cream or patches (EMLA) may be useful for localised neuralgia, and should be applied three times daily.

Tricyclic antidepressants

Amitriptyline, imipramine, dothiepin, clomipramine, desipramine and doxepin have been shown to have analgesic effects in patients with neuropathic pain, independent of their antidepressant action. They have an effect on the inhibitory serotonergic pathway, noradrenergic pathway, sodium channels, NMDA receptors and adenosine receptors. They appear to have both central and peripheral effects. As there are differing adverse effects, it is sometimes worth trying several different agents.

Amitriptyline 25 to 150 mg daily is the best studied of this group. It is helpful for neuropathic pain but is not well tolerated. Anticholinergic effects include dry mouth, blurred vision, constipation, urinary hesitancy, tachycardia and ejaculatory difficulty. Histaminergic adverse effects include sedation and weight gain. Alpha blocker action results in orthostatic hypotension. There is significant risk of mortality in overdose.

Tricyclics may also have analgesic effect when used topically, but no topical formulation is available in New Zealand.

Although SSRIs have some analgesic properties and are safer, they appear to be less effective than the tricyclics.

Anti-convulsant medication

These have widely differing methods of action so it is logical to try other agents if the first is unsuccessful.

  • Sodium valproate enhances the synthesis and inhibits the degradation of GABA. It has a low adverse effect profile.
  • Carbamazepine antagonises sodium channels. In doses of up to 500 mg bd it is associated with many adverse effects including severe allergic rashes (toxic epidermal necrolysis), hepatic enzyme induction, hyperlipidaemia, hyponatraemia and weight gain.
  • Lamotrigine has an effect on glutamate relase and on the voltage-gated cation channels. Subsidy requires Special Authority application by a neurologist. The dose should be very slowly increased over six weeks up to 400mg once daily, to reduce the risk of skin rash.
  • Gabapentin may have an action on the alpha delta 2 subunit of a calcium channel and inhibit glutamate release. It is specifically registered to treat neuropathic pain. Subsidy requires Special Authority application by a neurologist. The dose should be rapidly titrated from 300mg at night up to 1200 mg tid. It may cause drowsiness. Other side effects include dry mouth, peripheral oedema, weight gain, abnormal gait, amnesia, confusion, hypaesthesia, abnormal thinking, dyspnoea, amblyopia. Withdrawal reactions may occur on abrupt discontinuation.


Discuss the role of vaccination in the prevention of herpes zoster.


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