Vesicular eruption coupled with fever

The patient's history of atopy, requiring daily topical immunosuppressant therapy, along with the characteristic punched-out eroded lesions developing rapidly in association with fever and lymphadenopathy, should raise the concern for the diagnosis of eczema herpeticum, a potentially serious complication of...

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The patient’s history of atopy, requiring daily topical immunosuppressant therapy, along with the characteristic punched-out eroded lesions developing rapidly in association with fever and lymphadenopathy, should raise the concern for the diagnosis of eczema herpeticum, a potentially serious complication of herpes simplex virus (HSV) infection. More common in children with severe atopic dermatitis,¹ this infection can occasionally be seen in adults.

In children, eczema herpeticum typically presents with the primary HSV-1 infection; a history of a recent cold sore from a parent or care provider can often be obtained.² In adults, the associated HSV infection may be either primary or recurrent. Although HSV-1 is the more common culprit, cases have been attributed to HSV-2 as well.

Prompt diagnosis is important because of the potential for serious complications: Although the condition may be mild and transient, it may also be associated with keratoconjunctivitis, which can result in blindness and viremia with meningitis/encephalitis, which may be fatal, especially in infants.²

The classic presentation of eczema herpeticum is that of a child with a history of eczema previously well controlled, who is brought in because of an unusually severe flare that is unresponsive to topical corticosteroids. If a history of a recent episode of herpes labialis in a parent or daycare worker can be obtained, the diagnosis is fairly straightforward.² A child with uncomplicated atopic dermatitis tends to be moderately fussy, but those with eczema herpeticum are systemically ill with high fever and adenopathy.²

Clinically, grouped lesions, papules or vesicles typically found on an erythematous base eventually umbilicate and evolve into pustules over several days.² Some lesions may coalesce to form characteristic hemorrhagic ulcers with scalloped borders. The face is the most commonly affected area, but any skin surface with significant eczema is at risk of involvement; the infection may spread to intact skin as well.

The rapidity of disease progression is partially attributed to the impaired epidermal barrier function associated with the pathogenesis of atopic dermatitis, as well as immunologic impairment from topical or systemic immunosuppressive agents._³ Viremia with systemic spread of infection to various organ systems can cause great morbidity and may be fatal.² Any suspicion of ocular involvement requires prompt evaluation by an ophthalmologist to ameliorate risk of blindness. Recurrence of eczema herpeticum is uncommon and generally less severe, especially in children, where it is usually associated with the primary HSV infection.

The diagnosis of eczema herpeticum is mainly clinical and requires a high index of suspicion; however, clinicians should attempt to confirm the diagnosis with laboratory tests. Of the many options available, none is perfect.⁴

Viral culture has been considered the gold standard for confirmation, but timing of the culture and strict requirements for handling the sample impact the test’s sensitivity. A Tzanck smear demonstrating multinucleated giant cells on microscopy may be useful for rapid diagnosis early on. Obtain samples from the base of a freshly uncovered vesicle; this test is less reliable after lesions have evolved to pustules or ulcers.

Direct fluorescent antibody staining and polymerase chain reaction may also be used to confirm diagnosis, but the sensitivity and specificity for these tests have not been well studied, and they are not readily available in all clinical settings.^2,4

A comparable pathologic and morphologic pattern can develop in individuals with pre-existing skin diseases other than eczema that make them similarly susceptible to HSV infection. The term Kaposi’s varicelliform eruption is used to encompass all of these HSV-infected conditions.⁵ Mycosis fungoides, ichthyosis vulgaris, pemphigus, other primary blistering disorders and severe burns can each predispose a person to develop this type of herpetic infection.⁵ Kaposi’s varicelliform eruption is especially difficult to discern in burn lesions since such lesions typically form crusts as well. Burn lesions should be monitored for peripheral vesiculation, which raises the suspicion for HSV.

Given its association with a higher mortality rate, bacterial superinfection is also of great concern in cases of eczema herpeticum or Kaposi’s varicelliform eruption.⁶ A large percentage of patients with moderate-to-severe atopic dermatitis are chronically colonized with pathogenic strains of Staphylococcus aureus.³

Other pathogens associated with super infection include Streptococcus and Pseudomonas species.⁶ Secondary impetiginization of eczema herpeticum — manifesting with a characteristic honey-colored crust — in a patient who is no longer febrile should not be interpreted as a systemic infection or significant cellulitis. Use skin and blood cultures to guide antibiotic treatment in patients with eczema herpeticum suspected of having a superinfection.²

Treat adult patients with an appropriate antiviral agent administered either orally or intravenously for at least one week. Discuss suppressive antiviral therapy, especially in an individual who has frequent HSV outbreaks or is on systemic immune suppression.³

In the pediatric population, eczema herpeticum is considered a true emergency.^2,3 Hospital admission with at least 24 to 48 hours of IV antiviral therapy is necessary, followed by continuous oral antiviral treatment at a therapeutic dose for at least one week and a three- to six-month course of suppressive therapy. ^2,3

Further questioning of this patient established a history of recurrent herpes labialis; the diagnosis of HSV-1 was confimed with a culture. He was treated with valacyclovir (Valtrex) 1 gm b.i.d. for 10 days plus topical mupirocin (Bactroban, Centany) applied t.i.d. The man’s systemic symptoms resolved quickly, and the lesions healed over the ensuing weeks. He has experienced no recurrence while maintaining suppressive antiviral therapy.

William S. Gillen is a fourth-year medical student at Medical College of Virginia Hospitals, Virginia Commonwealth University, in Richmond, where Julia R. Nunley, MD, is a professor of dermatology. Neither author has any relationship to disclose relating to the content of this article.

References

1 Shiohara T, Sato Y, Takahashi R, et al. Increased susceptibility to cutaneous viral infections in atopic dermatitis: the roles of regulatory T cells and innate immune defects. Curr Probl Dermatol. 2011;41:125-135.

2. Mackley CL, Adams DR, Anderson B, Miller JJ. Eczema herpeticum: a dermatologic emergency. Dermatol Nurs. 2002;14:307-310, 323.

3. Kress DW. Pediatric dermatology emergencies. Curr Opin Pediatr. 2011;23:403-406.

4. Cohen PR. Tests for detecting herpes simplex virus and varicella-zoster virus infections. Dermatol Clin. 1994;12:51-68.

5. Nath AK, Sori T, Thappa DM. A case series of Kaposi’s varicelliform eruption in dermatology in-patients in a tertiary-care centre. Indian J Dermatol. 2011;56:110-115.

6. Brook I. Secondary bacterial infections complicating skin lesions. J Med Microbiol 2002;51:808-812.

All electronic documents accessed December 13, 2011.