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Patient Story

A 16-year-old-boy with a past medical history significant for atopic dermatitis presented to the Emergency Department with a 1-day history of sudden onset of tender blistering lesions on the face and neck associated with a burning sensation. Associated symptoms included lethargy, headache, and four episodes of vomiting since onset of symptoms. On exam, the boy was noted to be ill-appearing, moderately dehydrated, and febrile to 39°C. He was tachycardic but normotensive, warm, and well perfused. The skin exam revealed pustules, vesicles and crusts over his face, neck, elbows, both hands and both knees (Figure 132-1). He was admitted and treated with intravenous (IV) fluids, IV antibiotics, and IV acyclovir. Viral culture taken from an unroofed vesicular lesion revealed herpes simplex virus type 1. Bacterial cultures taken from the impetiginized lesions grew Staphylococcus aureus.

FIGURE 132-1

Eczema herpeticum in a 16-year-old-boy with a history of severe atopic dermatitis. Eczema herpeticum is a severe HSV infection in a patient with atopic dermatitis. (Used with permission from Camille Sabella, MD.)


Eczema herpeticum is an acutely disseminated herpes simplex virus (HSV) infection associated with systemic symptoms that develops in the setting of underlying skin conditions or epidermal barrier disruption, such as atopic dermatitis. HSV type 1 is most commonly involved, but cases of HSV type 2 infection and other viruses have rarely been implicated.


Kaposi varicelliform eruption.


  • Infants and children with atopic dermatitis are at highest risk.1

Etiology and Pathophysiology

  • Diverse immune mechanisms have been proposed to explain the development of eczema herpeticum in patients with atopic dermatitis:

    • A disruption of the immune response against herpes simplex mediated by T cells.

    • A defect in antibody production against the virus.

    • A decrease in natural killer cells and IL-2 receptors.

    • Inhibition of TH-1 response due to increase in IL-4.

    • Decrease in dendritic cells that produce IL-1.2

  • Another possibility is that viral dissemination is directly favored by the disruption of the skin barrier that exists in atopic dermatitis.3

Risk Factors

  • Early onset of atopic dermatitis and high levels of IgE in atopic patients, based on a retrospective study involving 100 patients with eczema herpeticum.4

  • The use of topical corticosteroids is not a predisposing factor.

  • Patients with chronic skin pathology like Darier disease, cutaneous T cell lymphoma, pityriasis rubra pilaris, benign familial pemphigus, seborrheic dermatitis, Wiskott-Aldrich syndrome, psoriasis, and systemic lupus erythematosis are susceptible to eczema herpeticum. Severe infections may develop even when the dermatitis is inactive.2

  • Other risk factors include conditions where the epidermal barrier has been disrupted, like burns, contact dermatitis, skin grafts, and dermabrasion.



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