Review Question - QID 101304

This rash is most consistent with a Herpes Zoster infection, which is reactivation of a latent virus from a previous infection.

Prior to routine vaccination, most individuals encountered the varicella-zoster virus (VZV) in childhood, when the virus manifested as varicella (chickenpox). Following initial infection, the virus travels along sensory dermatomes to dorsal root ganglia where it remains latent indefinitely. Any weakening of cellular immunity, such as from AIDS, immunocompromising drugs, or aging may allow the virus to reactivate and manifest as herpes zoster, also known as shingles.

Gilden et al. review varicella zoster virus infection. They report that the primary infection usually causes chickenpox (varicella). The virus becomes latent in cranial nerve ganglia, dorsal root ganglia and autonomic ganglia along the entire neuraxis.

Han et al. performed a meta-analysis of the available evidence for or against corticosteroids used acutely during zoster infection. They found that this intervention was ineffective in preventing postherpetic neuralgia with the risks of administration of corticosteroids greater than with placebo.

Johnson and Whitton review the risk factors for postherpetic neuralgia including age, acute pain, rash severity, virus in peripheral blood, and psychosocial stressors.

Figure A shows a classic Herpes Zoster rash along the T3 dermatome.

Incorrect answers:
Answer 1: Excessive fibrosis and collagen deposition causes scleroderma, marked by puffy, taut, sometimes ulcerated skin.
Answer 2: Superficial skin infection, most commonly with S. aureus or S. pyogenes, causes impetigo, marked by painless, honey-colored, crusting blisters.
Answer 3: Autoimmune IgG antibody against desmosomes causes pemphigus vulgaris, marked by flaccid blisters and acantholysis.
Answer 4: Following HPV infection, virally mediated epidermal hyperplasia may cause verrucae, which manifest as tan-colored warts.