Fever and Rash

Posted by • May 10th, 2012

In the latest Case Record of the Massachusetts General Hospital, a 43-year-old woman with a history of atopic dermatitis was admitted to the hospital because of fever and a generalized painful, pruritic rash involving the entire body. Examination revealed vesicles, pustules, and erosions with scalloped borders. A diagnostic test result was received.

The development of cutaneous pain in a patient with a preexisting skin disorder should immediately raise the possibility of KVE, also known as dermatitis herpeticum or eczema herpeticum. In this disorder, a viral infection, usually caused by herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2), is superimposed on inflamed skin, typically atopic dermatitis, although other viruses may cause the same syndrome and other dermatoses may be infected.

Clinical Pearls

• What are the classic findings in KVE ?

The classic initial cutaneous manifestation of KVE is monomorphic vesicles that become pustular, often with a hemorrhagic and erosive component at later stages; erosions appear to be punched out or well demarcated, as seen in our patient. The erosive lesions tend to coalesce, creating large lesions with scalloped borders. Fever, malaise, and lymphadenopathy are often present. KVE can rapidly become fatal; in suspected cases, immediate treatment with intravenous acyclovir must be instituted.

Figure 1. Clinical Photographs of the Patient’s Skin.

• What viral infections are associated with the development of KVE?

Herpes simplex virus (HSV-1 and HSV-2) is most commonly associated with the development of KVE. However, infections with viruses other than HSV may be causative. The two most common are vaccinia virus and coxsackievirus A16. The U.S. military began a smallpox vaccination program in 2002 using the vaccinia virus; patients with atopic dermatitis are excluded from vaccination because of their risk of KVE. Despite this precaution, accidental exposures of persons with atopic dermatitis to recently vaccinated persons have occurred. Hand, foot, and mouth disease, caused by coxsackievirus A16, occurs most commonly in children. Disseminated skin disease after the initial distal vesicular eruption, with features characteristic of KVE, has been reported in a child with atopic dermatitis.

Morning Report Questions

Q: What are the predisposing skin conditions associated with the development of KVE?

A: The development of KVE is more likely in individuals with atopic dermatitis than in those with other inflammatory skin disorders. This predisposition is attributed both to abnormalities in the immune system and to defects in the barrier function of the epidermis that render such persons more susceptible to infection. Other conditions that have been described as substrates for the development of KVE include psoriasis, seborrheic dermatitis, rosacea, tinea cruris, Grover’s disease (transient acantholytic dermatosis), cutaneous T-cell lymphoma, pemphigus foliaceous, Darier’s disease (follicular keratosis), laser resurfacing, ichthyosis, pityriasis rubra pilaris, contact dermatitis, and burns.

Q: How is KVE diagnosed?

A: The diagnosis of KVE can be made by Tzanck testing of vesicular fluid, direct fluorescent antibody staining of vesicular fluid, or viral culture. Most rapid are the bedside Tzanck test and direct fluorescent antibody testing. In the erosive stage, culture of the vesicular fluid is most reliable for making a diagnosis, but this takes days. If the diagnosis of KVE is suspected, it is imperative to initiate treatment while awaiting culture results.

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