A 34 year old African American man with HIV/AIDS (CD4 13; Viral load 88,000) presented with a rapidly progressive, unilateral growth on the lower right eyelid. The patient underwent a non-diagnostic biopsy and a culture for this non-painful growth, which revealed methicillin-resistant staphylococcus aureus sensitive only to vancomycin. Prior to the results of the culture and sensitivity, he was treated unsuccessfully with topical erythromycin, trimethoprim/sulfamethoxazole, and clindamycin. The patient presented three weeks later to Johns Hopkins Wilmer clinic, where a decision was made to admit him for intravenous vancomycin therapy. Though the lesion had continued to grow and became purulent, the patient was afebrile with no indication of systemic infection.
The patient’s past medical history was significant for chronic, bilateral decreased vision secondary to cyptococcal meningoencephalitis, genital warts, and HIV/AIDS. He had no prior history of herpes simplex virus infection.
The patient was on several medications including highly active anti-retroviral therapy.
Cutaneous examination revealed a single 2cm x 1.5cm fungating, exophytic tumor on the right lower eyelid margin. The lesion exhibited involvement of the palpebral conjunctiva and sparing of the bulbar conjunctiva. The surface was moist with a yellow exudate and hemorrhagic crusting. Upon palpation, the mass was firm and not friable. A shave biopsy of the lesion was sent for histopathology and culture, and the patient continued on intravenous vancomycin. Valacyclovir 500mg orally three times daily was initiated because of concern that this lesion might represent Herpes simplex virus infection.
Histology of the lesion revealed acantholytic and multinucleated keratinocytes that exhibited molding of the nuclei as well as margination of the chromatin consistent with a Herpes virus infection. Immunohistochemical staining specific for Herpes virus confirmed these findings by highlighting multinucleated cells with molded nuclei. Skin biopsy cultures were positive 6 days post-procedure for herpes simplex virus type 2, which was confirmed by direct immunofluorescence. With these laboratory results, the patient was formally diagnosed with pyoderma vegetans secondary to herpes simplex virus type 2 in the setting of HIV/AIDS.
Although the patient was considered to be at significant risk for acyclovir resistant Herpes simplex virus infection (5.3% of HSV infections in patients with HIV/AIDS), he improved quickly on valacyclovir. He was probably still profoundly immunosuppressed as evidenced by the high viral load, low CD4 counts, and only recent initiation of anti-retroviral treatment. Six days post-valacyclovir treatment, cutaneous examination revealed non-exudative, moist granulation tissue at a significantly reduced size indicating acyclovir sensitivity.
1. Reyes M, Shaik NS, Graber JM, et al. Acyclovir-resistant genital herpes among persons attending sexually transmitted disease and human immunodeficiency virus clinics. Arch Intern Med 2003;163:76–80.
Double fluorescent antibody stain for Herpes simplex virus shows prominent staining of cells in the epidermis.