Dermatology MCQ - Viral Infections - Eczema herpeticum

A 4-year-old boy with a history of severe atopic dermatitis presents with a sudden onset of widespread, monomorphic vesicles and punched-out erosions over his face, neck, and trunk. He has a high fever and appears toxic. Eczema herpeticum

9/3/20252 min read

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A 4-year-old boy with a history of severe atopic dermatitis presents with a sudden onset of widespread, monomorphic vesicles and punched-out erosions over his face, neck, and trunk. He has a high fever and appears toxic. A Tzanck smear from a vesicle shows multinucleated giant cells. Which of the following is the most likely diagnosis and the immediate management step?

A) Impetigo; start oral cephalexin
B) Eczema herpeticum; start intravenous acyclovir
C) Staphylococcal scalded skin syndrome; start intravenous vancomycin
D) Varicella; start oral valacyclovir
E) Eczema vaccinatum; administer vaccinia immune globulin (VIG)

Correct Answer: B) Eczema herpeticum; start intravenous acyclovir

Explanation

This presentation is classic for eczema herpeticum (EH), a disseminated cutaneous herpes simplex virus (HSV) infection that complicates pre-existing skin diseases, most commonly atopic dermatitis.

Key Clinical Features of Eczema Herpeticum:

  • Background: Pre-existing skin condition, usually atopic dermatitis.

  • Rash: Monomorphic, punched-out erosions (often umbilicated) and vesicles that appear in clusters and may coalesce. The lesions are typically widespread but concentrated in areas of active or previous dermatitis.

  • Systemic Symptoms: High fever, lethargy, and toxicity due to viremia and potential visceral involvement.

  • Tzanck Smear: Positive for multinucleated giant cells (indicative of herpesvirus infection).

Virologic Cause:

  • Primarily caused by HSV-1 (or HSV-2), not VZV.

  • It represents a widespread cutaneous dissemination of HSV due to breached skin barrier and immune dysregulation in atopic skin.

Immediate Management:

  • Hospitalization is required due to systemic toxicity and risk of complications.

  • Intravenous acyclovir is the first-line treatment to halt viral replication and prevent complications like keratitis, disseminated visceral infection, or sepsis.

  • Supportive care: Hydration, pain control, and management of bacterial superinfection (common with Staphylococcus aureus).

Why Not the Other Options?

  • (A) Impetigo: Causes honey-crusted plaques, not monomorphic vesicles/erosions. No multinucleated giant cells on Tzanck smear.

  • (C) Staphylococcal scalded skin syndrome (SSSS): Caused by S. aureus exfoliative toxin. Presents with widespread erythema and superficial desquamation (Nikolsky sign positive), but no discrete vesicles or erosions. Tzanck smear is negative.

  • (D) Varicella: Causes a generalized vesicular rash in crops (all stages simultaneously), but it is usually not concentrated in areas of dermatitis and lacks the monomorphic appearance. Oral antivirals are used in high-risk cases, but IV acyclovir is preferred for EH due to severity.

  • (E) Eczema vaccinatum: A similar complication but caused by vaccinia virus (e.g., smallpox vaccination or contact with a vaccinated individual). It is clinically indistinguishable from EH but is much rarer. Treated with VIG, not acyclovir.

Complications:

  • Ocular involvement (herpetic keratitis) → urgent ophthalmology consult.

  • Bacterial superinfection (often S. aureus).

  • Disseminated visceral infection (e.g., pneumonitis, encephalitis).

Prognosis:
With prompt IV acyclovir, most patients recover fully. Delayed treatment can be fatal.