Herpes Zoster in the Elderly — Aetiology, Clinical Features and Management

Herpes zoster (shingles) is a localised, painful vesicular eruption caused by reactivation of latent varicella-zoster virus (VZV) from dorsal root and cranial nerve ganglia, where it has lain dormant since primary chickenpox.

The trigger for reactivation is a decline in VZV-specific cell-mediated immunity, which occurs with ageing (immunosenescence) and with immunosuppression from disease or therapy.

Risk factors: increasing age, malignancy (especially lymphoproliferative), HIV, chemotherapy, corticosteroids and other immunosuppressants, transplantation, diabetes, chronic kidney disease, and physical or psychological stress.

Incidence rises sharply with age. In a prospective vaccine trial the incidence in those over 60 was 11.8 cases per 1000 persons per year, against an all-age rate of 1.2–3.4 per 1000 per year.

Zoster occurs in up to half of all individuals surviving to age 85.

Increasing age is the strongest risk factor for postherpetic neuralgia (PHN), which affects more than 40% of those over 60 who develop zoster.

In India, an ICMR estimate places zoster incidence at about 3.3 cases per 1000 persons per year, and seroprevalence studies show over 90% of Indians are VZV-seropositive by age 40 — so essentially the entire older Indian population is at risk.

Prodromal phase (2–7 days): pain, itching, tingling or burning in a dermatome, often with malaise and low-grade fever. In the elderly this is frequently misdiagnosed as myocardial infarction, renal colic, cholecystitis or a disc lesion.

Eruptive phase: grouped vesicles on an erythematous base in a unilateral dermatomal distribution that does not cross the midline; vesicles become pustular, crust in 7–10 days and heal over 2–4 weeks.

Commonest sites: thoracic dermatomes (about half of cases), followed by the ophthalmic division of the trigeminal nerve.

Herpes zoster ophthalmicus: V1 involvement. Hutchinson's sign — vesicles on the tip or side of the nose (nasociliary branch) — predicts ocular involvement and mandates urgent ophthalmology referral; complications include keratitis, uveitis, acute retinal necrosis and blindness.

Ramsay Hunt syndrome (herpes zoster oticus): geniculate ganglion involvement causing ipsilateral facial palsy, vesicles in the external auditory canal or on the palate, vertigo and sensorineural deafness. Recovery of the palsy is poorer than in Bell's palsy.

Disseminated zoster: more than 20 vesicles outside the primary dermatome, with possible visceral involvement (pneumonitis, hepatitis, encephalitis). Suggests significant immunosuppression — investigate for occult malignancy or HIV.

Postherpetic neuralgia: defined as pain persisting 90 days or more after rash onset. It is neuropathic pain — burning, lancinating or electric-shock in character, with allodynia and hyperalgesia. It causes insomnia, depression, weight loss and social withdrawal, and is the principal driver of the disease burden in older people.

Other complications: zoster sine herpete (dermatomal pain without rash), segmental motor palsy, myelitis, meningoencephalitis, VZV vasculopathy causing stroke, and bacterial superinfection.

The diagnosis is clinical in the vast majority. Confirmation, where needed, is by VZV PCR of vesicle fluid or a swab of the base of a de-roofed lesion — the most sensitive test. Tzanck smear shows multinucleate giant cells but cannot distinguish HSV from VZV. Direct fluorescent antibody testing is an alternative.

Antiviral therapy must be started within 72 hours of rash onset. Aciclovir, famciclovir and valaciclovir all reduce acute pain and shorten the duration of chronic pain when started within this window. Beyond 72 hours, still treat if new vesicles are still forming or if there is ophthalmic, motor or disseminated involvement. Valaciclovir 1 g three times daily for 7 days — preferred for compliance Famciclovir 500 mg three times daily for 7 days Aciclovir 800 mg five times daily for 7–10 days — cheapest and most available in India All doses must be reduced for creatinine clearance below 30 ml/min; inadequate dose reduction causes aciclovir neurotoxicity presenting as delirium, which is easily mistaken for the infection itself Intravenous aciclovir 10 mg/kg 8-hourly for disseminated, ophthalmic-severe, or CNS disease 18. Acute pain control: analgesia is important. Paracetamol and NSAIDs for mild pain; those with moderate to severe pain may require opioids. Add gabapentin or corticosteroids if pain persists. Keep lesions clean and dry, and use non-adherent dressings.

Treatment of established PHN: topical lidocaine patch, gabapentin and pregabalin are the FDA-approved agents; nortriptyline and opioids have also been shown to be of benefit, and combination therapy may be necessary. In older adults, start low and titrate slowly; avoid amitriptyline in favour of nortriptyline because of anticholinergic burden, and reduce gabapentinoid doses in renal impairment.

Two vaccines exist. Zostavax, the live attenuated vaccine (FDA 2006), is only about 30% protective and reduced zoster incidence with a hazard ratio of 0.45, ophthalmic zoster HR 0.37 and zoster hospitalisation HR 0.35. Shingrix, the recombinant adjuvanted vaccine (FDA 2016), is about 90% protective.

ACIP recommends two doses of Shingrix for all adults aged 50 and above, given 2–6 months apart, regardless of prior chickenpox and regardless of prior Zostavax. Those who previously received Zostavax should still receive Shingrix.

The three complications that must never be missed: herpes zoster ophthalmicus with Hutchinson's sign, Ramsay Hunt syndrome, and disseminated zoster signalling occult immunosuppression.

Aciclovir neurotoxicity in renal impairment presents as delirium, myoclonus and hallucinations — and is routinely mistaken for the infection itself. Always calculate creatinine clearance before prescribing.

Zoster sine herpete — dermatomal neuropathic pain with no rash. Diagnosed by VZV PCR of CSF or blood, or by serology. Consider it in unexplained unilateral segmental pain in an older person.

VZV vasculopathy is an under-recognised cause of stroke in older adults, particularly after ophthalmic zoster, and is one mechanism proposed to link zoster with dementia.

Zoster in the immunocompromised: Shingrix is non-live and therefore safe in immunocompromised adults (licensed from age 18 in this group) — the key practical advantage over Zostavax.

Nortriptyline over amitriptyline in older people. Tricyclics are on the Beers list; nortriptyline has a substantially lower anticholinergic burden.

Infectivity: zoster transmits VZV to non-immune contacts causing chickenpox, not zoster. Localised zoster requires standard precautions with lesions covered; disseminated or immunocompromised zoster requires airborne plus contact precautions.

"Herpes zoster results from reactivation of latent VZV in the dorsal root ganglia due to waning VZV-specific cell-mediated immunity."

"Age is the strongest risk factor for postherpetic neuralgia, which affects over 40% of patients above 60."

"Antivirals must be started within 72 hours of rash onset, with dose reduction if creatinine clearance is below 30 ml/min."

"Corticosteroids do not reduce the incidence of postherpetic neuralgia."

"Two doses of the recombinant adjuvanted vaccine are recommended for all adults above 50, regardless of previous chickenpox or previous live vaccine."

The distinction line for a top answer: "A 2025 Nature natural experiment in Wales showed zoster vaccination reduced dementia incidence by about 20%, with a randomised trial, DAN-ZOSTER, now under way."