Dermatology MCQ - Viral Infections - Herpes Zoster

A 72-year-old woman presents with a painful, unilateral vesicular eruption distributed along the T5 dermatome. The rash began 3 days ago with burning pain, followed by the appearance of grouped vesicles on an erythematous base. She reports no recent sick contacts but had chickenpox as a child. Which of the following is the most likely pathophysiological mechanism underlying this condition?

A) Primary infection with herpes simplex virus type 1 (HSV-1)
B) Reactivation of varicella-zoster virus (VZV) from dorsal root ganglia
C) Autoimmune inflammation targeting peripheral nerves
D) Bacterial infection complicating a pre-existing dermatitis
E) Direct inoculation of poxvirus through skin trauma

Correct Answer: B) Reactivation of varicella-zoster virus (VZV) from dorsal root ganglia

Explanation

This presentation is classic for herpes zoster (shingles), caused by the reactivation of varicella-zoster virus (VZV).

Key Clinical Features of Herpes Zoster:

• Presentation: A unilateral, dermatomal distribution of painful vesicles on an erythematous base. The T5 dermatome (thoracic region) is a common site.

• Prodrome: Often begins with burning pain, itching, or paresthesia in the affected dermatome 1-3 days before the rash appears.

• History: Prior history of chickenpox (primary VZV infection) is a prerequisite, as herpes zoster represents reactivation of latent VZV.

Pathophysiological Mechanism:

• Primary Infection: During childhood chickenpox, VZV infects sensory nerve endings and travels retrograde to establish latency in the dorsal root ganglia.

• Reactivation: Decades later, often due to age-related decline in cell-mediated immunity or immunosuppression, the virus reactivates. It replicates and travels anterograde along the sensory nerve to the skin, causing the characteristic painful dermatomal rash.

• Complications:

  • Postherpetic neuralgia (PHN): Persistent pain after the rash resolves, more common in older adults.

  • Ophthalmic involvement (if V1 trigeminal dermatome affected), motor neuropathy, or disseminated disease in immunocompromised hosts.

Why Not the Other Options?

• (A) Primary HSV-1 infection: HSV-1 typically causes gingivostomatitis or herpes labialis (cold sores), not a dermatomal distribution. Reactivation of HSV usually affects mucocutaneous junctions (e.g., lips, genitals) and is not dermatomal.

• (C) Autoimmune inflammation: Conditions like Guillain-Barré syndrome cause symmetric weakness, not a unilateral vesicular rash. Autoimmune bullous diseases (e.g., pemphigus) lack a dermatomal pattern.

• (D) Bacterial infection: Bacterial cellulitis or erysipelas causes erythema, warmth, and tenderness but not grouped vesicles in a dermatomal distribution.

• (E) Poxvirus inoculation: Poxviruses (e.g., vaccinia, orf) cause localized nodules or ulcers at inoculation sites, not dermatomal vesicular eruptions.

Management:

• Antivirals: Oral acyclovir, valacyclovir, or famciclovir started within 72 hours of rash onset to reduce duration and severity.

• Pain control: Analgesics (e.g., NSAIDs, gabapentin for neuropathic pain).

• Prevention: Recombinant zoster vaccine (RZV) recommended for adults ≥50 years to reduce the risk of herpes zoster and PHN.

Prognosis:
Rash typically crusts and heals in 2–4 weeks. PHN can persist for months to years, especially in older adults. Early antiviral treatment may reduce PHN risk.