A 61–year–old man with HIV, not currently on highly active antiretroviral therapy, hypertension, and monoclonal gammopathy of unknown significance, presented to the hospital with a worsening erythematous macular rash for six days. The macules initially erupted on his arms and progressed to involve his face and trunk. He denied any pruritis or painful skin lesions. New macules then erupted on his eyelids, thighs, upper palate, and tongue without evidence of blisters or pustules. He denied any fevers, chills, sick contacts, or recent weight loss. He recently had restarted lisinopril for hypertension, and had no history of adverse reactions to this medication. On exam, he was afebrile with normal vital signs. His skin findings included nodular erythematous eruptions on the face, eyelids, chest, stomach, arms, and thighs without a dermatomal distribution. Present were also a few nonulcerative lesions on the upper palate and tongue. Laboratory data was notable for a white blood cell count of 3 × 103 cells/mL3, CD4 count of 524 cells/mL, HIV viral load of 627 copies/mL. Pathology of a skin punch biopsy showed a vesicular dermatitis with viral cytopathic changes in the epidermis, margination of nuclear chromatin, multi–nucleation, and viral inclusions consistent with herpes virus infection. Varicella zoster virus PCR of the patient’s serum and skin biopsy were tested and were positive. A Herpes simplex virus PCR of his serum and skin biopsy were also tested and were negative. The patient was treated with IV acyclovir. An ophthalmologist confirmed that there was no evidence of acute retinal necrosis or retinitis, a leading cause of blindness with Varicella zoster virus infection. The patient was diagnosed with disseminated Varicella zoster.
Varicella zoster characteristically presents clinically as painful, erythematous, macules and papules that develop into clusters of vesicles that evolve into pustules that ulcerate and crust and show varying degrees of maturity. The skin findings are typically dermatomal in distribution and do not cross the midline. In the immunocompromised patient, however, the presentation may be atypical and biopsy and laboratory confirmation may be needed.
This case reminds hospitalists of the potential for atypical Varicella zoster virus skin findings in immunocompromised patients.
Figure 1Skin biopsy demonstrating a vesicular dermatitis with margination of nuclear chromatin, multi–nucleation, and presence of viral inclusions consistent with viral cytopathic changes in the epidermis caused by Varicella zoster virus.