Clinical meaning
Herpes zoster (shingles) is caused by reactivation of varicella-zoster virus (VZV) that has remained dormant in dorsal root ganglia or cranial nerve ganglia since primary varicella (chickenpox) infection. Reactivation occurs when cell-mediated immunity declines due to aging, immunosuppression, or stress. The virus travels along the sensory nerve to the dermatome it innervates, causing a painful, vesicular rash in a characteristic dermatomal distribution that does NOT cross the midline. The rash progresses through stages: erythematous macules/papules → vesicles on an erythematous base (grouped vesicles often described as 'dewdrops on rose petals') → pustules → crusting (7-10 days). Pain often precedes the rash by 1-5 days (prodromal pain), which can be misdiagnosed as MI, appendicitis, or renal colic depending on the dermatome. The most feared complication is postherpetic neuralgia (PHN): persistent neuropathic pain lasting >90 days after rash onset, affecting up to 30% of patients >60 years. Other complications include herpes zoster ophthalmicus (V1 trigeminal involvement — threatens vision), Ramsay Hunt syndrome (facial nerve/geniculate ganglion — facial paralysis, ear vesicles, hearing loss), and disseminated zoster in immunocompromised patients.