Eczema Herpeticum

One week earlier, a 14-month-old girl with a history of eczema was evaluated because of a diffuse rash of excoriated lesions, some of them purulent. She was afebrile. Worsening eczema with secondary infection was diagnosed. Treatment with oral clindamycin was prescribed. At follow-up, the lesions had worsened. The child had multiple excoriated papules, some of which had coalesced into plaques (A). She also had two 5-mm vesicles on her right shoulder (B). Eczema herpeticum was diagnosed clinically. Culture of the vesicles later grew herpes simplex virus (HSV).

This acute disseminated infection is a serious complication of eczema. Before the advent of antiviral drugs, the associated mortality rate ranged from 1% to 9%.¹ Eczema herpeticum is acquired through autoinoculation in a latent host or from an infected contact. HSV is the causative agent in the vast majority of cases; however, cases caused by coxsackievirus A16 and vaccinia virus have also been reported.

The rash begins as a cluster of umbilicated vesiculopustules on skin affected by preexisting dermatitis. The vesiculopustules progress to painful hemorrhagic, crusted, punched-out erosions that coalesce into denuded areas.² These findings help distinguish worsening eczema from eczema herpeticum. Lesions generally heal within 2 to 6 weeks with treatment. Patients are considered infectious as long as active lesions are present. Keratoconjunctivitis and viremia, which can lead to encephalitis, are possible complications.

Characteristic features of eczema herpeticum are an early age at onset of atopic dermatitis, predilection for eczematous skin lesions in the head and neck area, elevated total serum IgE levels, and increased allergen sensitization.³

The differential diagnosis includes impetigo, arthropod bites, scabies, papular urticaria, varicella, and bacterial superinfection. Eczema herpeticum may be misdiagnosed as an exacerbation of underlying atopic dermatitis and subsequently treated with higher-dose corticosteroids, which can lead to serious consequences.

Diagnosis is mainly clinical. The Tzanck test provides the fastest test result but is neither sensitive nor specific for HSV infection.⁴ Direct fluorescent antibody staining is rapid and accurate, although not as sensitive as culture. Viral culture, while both sensitive and specific for HSV infection, requires at least 48 hours for results.²

Acyclovir is the mainstay of treatment. The recommended regimen is 25 mg/kg/d, divided into 5 doses, for 5 to 10 days. Prophylaxis for patients at high risk or with recurrent infection consists of acyclovir or valacyclovir; foscarnet can be used in resistant cases.⁵ Secondary staphylococcal infection is common. Topical antibiotic cream is recommended for all patients to prevent secondary bacterial infection. This patient was treated with oral acyclovir. After 1 week, the rash showed partial resolution.

References:

REFERENCES: 1. Wollenberg A, Wetzel S, Burgdorf WH, Haas J. Viral infections in atopicdermatitis: pathogenic aspects and clinical management. J Allergy Clin Immunol.2003;112:667-674.

2. Braun-Falco O, Plewig G, Wolff HH, Burgdorf WH, eds. Dermatology. 2nd ed. Berlin: Springer-Verlag; 2000.

3. Bussmann C, Peng WM, Bieber T, Novak N. Molecular pathogenesis and clinical implications of eczema herpeticum. Expert Rev Mol Med. 2008;14:e21.

4. Mackley CL, Adams DR, Anderson B, Miller JJ. Eczema herpeticum: a dermatologic emergency. Dermatol Nurs. 2002;14:307-310, 313.

5. Chilukuri S, Rosen T. Management of acyclovir-resistant herpes simplex virus. Dermatol Clin. 2003;21:311-320.