Shingles (Herpes zoster)
Introduction
Shingles (herpes zoster, HZ) is reactivation of latent varicella‑zoster virus (VZV) from sensory ganglia after primary chickenpox. Reactivation causes viral replication in a sensory ganglion with spread down the corresponding nerve, producing a painful, unilateral, dermatomal vesicular eruption.
In the emergency department (ED) most cases are self‑limited, but presentations may signal complications or vulnerable hosts who need admission, urgent specialist input or public‑health action (e.g. post‑exposure prophylaxis for contacts) (UKHSA Green Book).
Pathophysiology
After primary VZV infection the virus remains latent in dorsal root, trigeminal (including ophthalmic/V1) and geniculate ganglia. Decline in VZV‑specific cell‑mediated immunity (ageing, immunosuppression, malignancy, corticosteroids, etc.) may trigger reactivation.
Local ganglionic inflammation produces neuropathic pain; axonal transport spreads virus to the skin producing clustered vesicles in the affected dermatome.
Clinical features
- Prodrome: unilateral neuropathic pain, dysaesthesia or hyperesthesia in the affected dermatome hours to days before rash. Mild systemic symptoms (low‑grade fever, malaise) may occur.
- Rash evolution: erythematous macules → grouped vesicles on an erythematous base → pustulation and crusting. Lesions are usually confined to a single dermatome and do not cross the midline.
- Common sites: thoracic dermatomes are most frequent, followed by trigeminal (notably ophthalmic/V1).
- Timeline: in uncomplicated immunocompetent patients new vesicle formation typically lasts 3-5 days and crusting begins within 7-10 days.