||Herpes zoster is an acute, localized viral infection of the skin. The etiologic agent is the varicella zoster virus, a large, DNA-containing virus of the herpesvirus group. The varicella zoster virus within the cutaneous lesion is contagious, especially to immunosuppressed individuals.
During the course of varicella (chickenpox), the herpesvirus passes from the skin and mucosal lesions to the sensory nerve endings and migrates up the sensory nerves to the sensory ganglia. The virus remains within these ganglia as an asymptomatic latent infection. Under conditions of immunosuppression or local trauma, the latent virus becomes reactivated and travels down the sensory nerve, initially causing neuritis and pain, and then passes into the skin, producing vesicles.
The typical skin lesions are unilateral and confined to a dermatomal distribution. An outbreak is frequently heralded by prior pain. The initial lesion develops as erythematous papules which rapidly progress to bullous vesicles, to pustules, and then crusts after 8 to 10 days. Herpes zoster affecting the auricle arises in those dermatomes that provide segmental innervation to the auricle and external canal (cranial nerves V, VII, X, C2, and C3).
The vesicles of herpes zoster may also involve the skin of the external canal or the outer surface of the tympanic membrane.
The most distressing sequela of herpes zoster is postherpetic neuralgia, a prolonged, severe burning or stabbing pain which may last for many months.
In the early stage several pustules can be seen scattered in the conchal bowl of this patient.