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Letter To The Editor

Herpes simplex virus (HSV) is the most common virus involved. Atopic eczema is the commonest predisposing condition but it has been reported to occur in patients with other dermatoses. A 22-year-old male presented with multiple vesicles and crusted lesions all over his face of 4 days’ duration. The lesions had started as a few erythematous papules on his right nasolabial fold. Within 24 hours a sudden crop of vesicles appeared involving the entire face. Crusting appeared over many of them within a day. The lesions were accompanied by high-grade fever lasting for 1 day only. There was no history of oral, genital or eye involvement. There was no family or personal history of atopy, herpes simplex infection, dryness of the skin, blood transfusion, sexual exposure, intravenous drug abuse, recurrent infections, or wasting in the patient. He had not taken any systemic medication or applied anything topically prior to onset of lesions. The patient denied suffering from any skin disease or similar eruption in the past. His general physical and systemic examination was within normal limits. Cutaneous examination revealed multiple, 2–5 mm vesicles covering the entire face. Few scattered, discrete vesicles were present on the neck, chest and arms. The oral cavity, lips, eyes, genitalia, palms and soles were spared. The clinical diagnosis of KVE was made (Fig. 1). His haemogram, liver and renal function tests, routine urine examination and chest X-ray were normal. His HIV serology was negative by ELISA during admission and 1 year later. Tzanck smear from an intact vesicle showed a multinucleated giant cell. Biopsy of an intact vesicle from the neck revealed an intraepidermal vesicle filled mainly with neutrophils and few lymphocytes. Reticular and ballooning degeneration of epidermal cells and secondary acantholysis were present, consistent with HSV or herpes varicella zoster. Herpes simplex virus serology, culture and direct immunofluoresence examination, serum IgE levels and lymphocyte subpopulation studies could not be performed because of lack of facilities in Nepal. The lesions cleared completely without any scarring within 7 days of treatment with oral acyclovir 400 mg three times a day, and local care. His skin was normal 1 year after follow up. The ocurrence of KVE in the normal uninvolved skin of a patient who has acral Darier’s disease has been reported. Our patient was a healthy young male with no past history suggestive of any of the predisposing skin diseases. There was no clinical or laboratory evidence of immunosuppression on routine, easily available and affordable investigation of the patient. We had difficulty in differentiating the condition from an atypical chickenpox. All the lesions were monomorphic, that is in the same stage of development (crusted and umbilicated vesicles) despite 4 days’ history. The abdomen, back, forearms, lower limbs and oral cavity were completely spared. A few scattered lesions numbering less than 10 were present over the neck and arms. There were no papules or pustules or history of repeated crops of lesions. The uniform morphology and distribution of the lesions favoured KVE over atypical chickenpox because, normally, the lesions of chickenpox progress through stages of papules, vesicles, pustules and crust very rapidly within 24 hours. Localization of lesions to the face could not be explained. The case is being reported to highlight the fact that clinicians may encounter similar extensive eruptions occurring in normal individuals in uncommon and unusual distribution. Kaposi’s varicelliform eruption is a potentially fatal disease. The dilemma in differentiating it from chickenpox, typical or otherwise, may delay the institution of therapy, whereas prompt Australasian Journal of Dermatology (2000) 41, 126–127