Shingles (herpes zoster) is a viral infection of an individual nerve and the skin surface that is served by the nerve (dermatome). It is caused by the reactivation of the varicella-zoster virus, the same virus that causes chickenpox. Following a chickenpox infection, which typically occurs during childhood, the varicella-zoster virus lies dormant in the dorsal root ganglia and reactivates when the immune system is weakened. Unlike chickenpox, which follows the initial infection and causes a generalised rash, shingles occurs years (sometimes decades) after the primary infection and symptoms are usually localised to a specific dermatome. People with active lesions of shingles, particularly if they are immunocompromised, can transmit varicella zoster virus to susceptible people to cause chickenpox. However, there is no evidence that shingles can be acquired from a person who has chickenpox.
Risk factors
- Increasing age - this is thought to result from an age-related decline in virus-specific, cell-mediated immune responses
- Immunocompromise - HIV infection, lymphoproliferative malignancies, immunosuppressive treatment and organ transplantation
- Certain comorbidities - Rheumatoid arthritis, asthma and chronic obstructive pulmonary disease, chronic kidney disease, depression, diabetes mellitus, systemic lupus erythematosus, Wegener's granulomatosis, malignancies
- Psychological factors
- Female sex
- Race/ethnicity
- Statin use
Clinical features
Diagnose shingles on the basis of typical clinical features.
- There is usually a prodromal phase with abnormal skin sensations and pain in the affected dermatome (area of skin served by an individual nerve). The pain can be described as burning, stabbing, or throbbing; can be intermittent or constant, and may be so severe it interferes with sleep and quality of life. Headache, photophobia, malaise, and fever (less common) may also occur as part of the prodromal phase.
- Within 2–3 days (more rarely up to 7 days), a rash typically appears in a dermatomal distribution. It starts as maculopapular lesions then develops into clusters of vesicles, with new vesicles continuing to form over 3–5 days. The rash is usually painful, itchy, and/or tingly, and, unlike other rashes, does not cross the midline of the body. The vesicles then burst, releasing varicella-zoster virus, and crust over within 7–10 days. Healing occurs over 2–4 weeks, and often results in scarring and permanent pigmentation in the affected area.
- In immunocompetent people, the infection usually occurs on the thorax, with dermatomes T1 to L2 most commonly affected. In immunocompromised people, symptoms can be more widespread and affect multiple dermatomes (disseminated disease).
Differential diagnosis
Differential diagnoses of shingles include:
- Herpes simplex virus (HSV) infection
- Candidal skin infection
- Contact dermatitis
- Folliculitis
- Impetigo
- Insect bite or sting
- Scabies
- Urticaria
Differential diagnoses of herpes zoster ophthalmicus include:
- Acute angle closure glaucoma
- HSV ocular infections
- Trigeminal neuralgia
- Ulcerative keratitis
Management
- Seek immediate specialist advice if:
- Serious complications (such as meningitis, encephalitis, or myelitis) are suspected
- The person has shingles in the ophthalmic distribution of the trigeminal nerve, especially those with:
- Hutchinson's sign — a rash on the tip, side, or root of the nose, representing the dermatome of the nasociliary nerve, which is a prognostic factor for subsequent eye inflammation and permanent corneal denervation
- Visual symptoms
- An unexplained red eye
- A severely immunocompromised person has shingles, or an immunocompromised person has shingles where the rash is severe, widespread, or they are systemically unwell
- An immunocompromised child has shingles
- For all other people with shingles:
- Consider the need for oral antiviral treatment
- Prescribe an oral antiviral treatment within 72 hours of rash onset for people with any of the following criteria:
- Immunocompromise (if the level of immunocompromise is not severe, the rash is localised, the person is not systemically unwell, and they can be closely followed up).
- Non-truncal involvement (such as shingles affecting the neck, limbs, or perineum)
- Moderate or severe pain
- Moderate or severe rash
- Consider prescribing oral antiviral treatment within 72 hours of rash onset for all people aged over 50 years to reduce the incidence of post-herpetic neuralgia, which is most common in this age group
- If it is not possible to initiate treatment within 72 hours, consider starting antiviral treatment up to one week after rash onset, especially if the person is at higher risk of severe shingles or complications (for example continued vesicle formation, older age, immunocompromised, or in severe pain)
- Manage pain
- Offer a trial of paracetamol alone or in combination with codeine or a nonsteroidal anti-inflammatory drug (NSAID), such as ibuprofen
- If this is not effective, or the person presents with severe pain, consider offering amitriptyline (off-label use), duloxetine (off-label use), gabapentin, or pregabalin
- Consider oral corticosteroids in the first 2 weeks following rash onset in immunocompetent adults with localised shingles if pain is severe, but only in combination with antiviral treatment
- Give appropriate information and advice
- Explain that only a person who has not had chickenpox or the varicella vaccine can catch chickenpox from a person with shingles. The person with shingles is infectious until all the vesicles have crusted over (usually 5–7 days after rash onset).
- Advise people with shingles to:
- Avoid contact with people who have not had chickenpox, particularly pregnant women, immunocompromised people, and babies younger than 1 month of age.
- Avoid sharing clothes and towels.
- Wash their hands often.
- Wear loose-fitting clothes to reduce irritation.
- Cover lesions that are not under clothes while the rash is still weeping.
- Avoid use of topical creams and adhesive dressings, as they can cause irritation and delay rash healing.
- Keep the rash clean and dry to reduce the risk of bacterial superinfection. They should seek medical advice if there is an increase in temperature, as this may indicate bacterial infection.
- Avoid work, school, or day care if the rash is weeping and cannot be covered. If the lesions have dried or the rash is covered, avoidance of these activities is not necessary.
Complications
A shingles vaccination programme was introduced in September 2013 with the aim of reducing the incidence and severity of shingles disease in adults aged 70 years and older, in whom the risk and severity of disease and of subsequent post-herpetic neuralgia is higher.
- Post-herpetic neuralgia (defined as pain persisting for, or appearing more than, 90 days after rash onset) is the most common complication of shingles and is caused by herpes zoster-induced peripheral nerve damage.
- Other complications of shingles include:
- Skin changes — scarring, changes in pigmentation, and keloid formation may occur after a shingles rash has healed
- Superinfection of skin lesions — secondary infection of the lesions, usually with staphylococcal or streptococcal bacteria, may occur and can result in cellulitis, osteomyelitis, or life-threatening complications (such as necrotising fasciitis and sepsis)
- Herpes zoster oticus (Ramsay Hunt syndrome) — occurs when the virus infects the facial nerve (cranial nerve VII) and characterised by lesions in the ear, facial paralysis, and associated hearing and vestibular symptoms
- Herpes zoster ophthalmicus — occurs when the virus infects the ophthalmic division of the trigeminal nerve and complications include keratitis, corneal ulceration, conjunctivitis, optic neuritis, retinitis, glaucoma, and blindness if untreated
- Peripheral motor neuropathy — occurs when a motor rather than a sensory nerve is involved, and causes loss of movement in the affected area
- Central nervous system (CNS) complications — CNS complications, such as encephalitis, meningoencephalitis, myelitis, cerebellitis, cerebrovascular disease, radiculitis, and Guillain–Barré syndrome, have been reported
- Cardiovascular complications — herpes zoster has been shown to be an independent risk factor for vascular disease, particularly stroke, transient ischaemic attack, and myocardial infarction
- Systemic dissemination is a rare but serious complication of shingles:
- The reactivated virus can, in some cases, disseminate into the lungs, liver, gut, and brain, leading to pneumonia, hepatitis, encephalitis, and disseminated intravascular coagulopathy