PMC6371409_01
(A) Deep infiltrated lesions with tense blisters on the surface; (B) after starting therapy with acyclovir, lesions became necrotic and ulcerated covered with an adherent black eschar; (C) lesions evolved to extensive deep ulcerated areas; (D) three months after initiating therapy, almost complete healing with residual atrophic scars.
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Two months later, the deep infiltrated lesions started to develop tense blisters on the surface (Fig. 1A). Some days after the initial therapy, lesions started to ulcerate, forming confluent necrotic plaques covered with an adherent black eschar which evolved to extensive deep ulcerated areas, as shown in Fig. 1B and C. Another biopsy was performed that showed extensive necrosis and thrombosis of larger vessels, with no signs of viral infection, so the patient was kept on acyclovir prophylaxis (400 mg q12 h) with complete healing and residual atrophic scars after eight months (Fig. 1D).
Intraepidermal blister displaying ballooning and acantholytic keratinocytes and multinucleated cells with nuclear molding. (A) Fibrinoid necrosis (arrow) and thrombosis (arrowhead) of vessels of the hypodermis. (B) Hematoxylin and eosin stain; x200 original magnification.
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Histology revealed an intraepidermal blister with viral cytopathic changes characteristic of herpes HSV/VZV infection (keratinocyte alterations with ballooning, acantholysis, marginalization of the nuclear chromatin and multinucleation; Fig. 2a). Leukocytoclastic vasculitis of the dermal vessels and vascular fibrinoid necrosis of the hypodermis could be seen; thrombosis and adipocyte necrosis were present (Fig. 2b).