Kaposi Varicelliform Eruption
A 46-year-old man with HIV infection was hospitalized for evaluation of a nonhealing, tender wound on the right lower extremity. The lesion had been present for 2 months following a minor injury to the leg, but it flared the week before admission. A month before hospitalization, the patient was given trimethoprim/ sulfamethoxazole and minocycline for treatment of the wound, with no improvement. The patient denied fevers, chills, and night sweats. Laboratory studies obtained a month before admission included a bacterial culture that grew methicillinresistant Staphylococcus aureus (MRSA).
On admission, a cutaneous examination revealed multiple, discrete, 2- to 3-mm hemorrhagic punched-out crusted erosions, with several areas that coalesced into large, denuded patches (A). Edema was present and chronic underlying stasis changes were appreciated on his lower extremities, manifested by slightly scaly brown patches. No other significant skin findings were present. The patient was afebrile, with stable vital signs. Dermatology was consulted given the lack of improvement with outpatient antibiotic treatment. Blood cultures exhibited no growth. No leukocytosis was noted. Direct immunofluorescence of the erosion was positive for herpes simplex virus (HSV) and negative for varicella-zoster virus (VZV). A diagnosis of Kaposi varicelliform eruption (KVE) was made. Treatment with intravenous acyclovir was initiated, and the lesions began to involute. Marked improvement was noted by discharge 5 days later (B). The patient continued treatment with oral famciclovir for another 7 days. KVE is a disseminated viral cutaneous infection, usually caused by viruses in the herpesvirus group, that occurs in areas of skin barrierdefect. Although HSV is the most common cause, VZV, coxsackievirus, and vaccinia virus are other etiologic agents.
KVE may present as a primary or recurrent infection with HSV.1 Typically, the primary infection is more severe and patients are often febrile and have generalized lymphadenopathy. Recurrences are usually less severe, involve less body surface area, and resolve quickly (unlike a primary infection). KVE has been reported to occur in various age-groups and in multiple skin conditions where there is disruption of the epidermal barrier, including atopic dermatitis, burns, autoimmune blistering disorders, and ichthyoses.2,3 In this immunocompromised patient, it is likely that stasis dermatitis and a recent leg injury provided the necessary factors for his infection. KVE is often either misdiagnosed as a bacterial infection or attributed to a flare of the underlying skin disease. Anaerobic and aerobic wound cultures should be performed. S aureus, group A streptococci, and Pseudomonas aeruginosa are common isolates; if these pathogens are present, antibiotic therapy should be initiated.4 However, viruses, such as HSV and VZV, should be considered, to prevent unnecessary antibiotic use or a delay in diagnosis.
1. Wheeler CE Jr, Abele DC. Eczema herpeticum, primary and recurrent. Arch Dermatol. 1966;93:162-173.
2. Kramer SC, Thomas CJ, Tyler WB, Elston DM. Kaposi’s varicelliform eruption: a case report and review of the literature. Cutis. 2004;73:115-122.
3. Bork K, Bräuninger W. Increasing incidence of eczema herpeticum: analysis of seventy-five cases. J Am Acad Dermatol. 1988;19:1024-1029.
4. Brook I, Frazier EH, Yeager JK. Microbiology of infected eczema herpeticum. J Am Acad Dermatol. 1998;38:627-629.