Cytomegalovirus Ulcer

A 47-year-old man with multiple-drug–resistant AIDS was admitted to Yale–New Haven Hospital for evaluation of mental status and neuromotor changes and a 6-week history of a painful, nonhealing, enlarging ulcer on the lower extremity that the patient attributed to minor trauma. The patient had received outpatient wound care and several courses of oral antibiotics, but he was taking neither antiretroviral medications nor prophylaxis for opportunistic infections. The patient’s most recent CD4 cell count was less than 20/μL with a viral load of 715000 copies/mL. He had a history of successfully treated cytomegalovirus (CMV) retinitis and Pneumocystis carinii pneumonia. On admission, he displayed clinical and radiologic features consistent with cerebral toxoplasmosis. He had no history of diabetes mellitus, peripheral vascular disease, or neuropathic disease. During his hospital stay, the patient received intravenous and oral antibiotics (ampicillin sodium– sulbactam sodium, aztreonam, and clindamycin) for presumed bacterial infection of the ulcer, and a skin care nurse treated the wound daily with bacitracin zinc and dry dressings. After 4 days in the hospital with no improvement, dermatology consultation was requested. On physical examination, there was a tender 3.0 2.0-cm ulcer on the right lateral part of the heel with surrounding erythema and induration (Figure 1). The border was well demarcated and not elevated, undermined, or scalloped. The base contained granulation tissue and necrotic debris. The patient had no oral, ocular, or anogenital ulcers. The remainder of the lower extremity examination was significant for 1+ pitting ankle edema, adequate capillary refill time, palpable dorsalis pedis pulses, and no evidence of compromised circulation or peripheral neuropathy. The patient also had molluscum contagiosum on his chest. A punch biopsy specimen from the edge of the ulcer showed hyperplastic epidermis and numerous thickwalled blood vessels in the dermis, as well as a perivascular lymphocytic infiltrate. Among normal endothelial cells were many large, irregularly shaped endothelial cells with large basophilic intranuclear inclusions, in some cells surrounded by clear halos. Intracytoplasmic basophilic inclusions were also present (Figure 2). Immunohistochemical studies showed CMV antigen reactivity within the endothelial cells. Direct immu