A 52–year–old woman with history of systemic lupus erythematosus and end–stage renal disease status post cadaveric renal transplant (2008) presented with three days of a progressive vesicular rash. The rash began in her mouth and spread to her face, body and extremities. Her oral cavity was covered with serous vesicles, erythematous papules, fissures, ulcerations and a thin adherent white plaque. Her face, trunk, groin, and extremities had scattered vesicles, some hemorrhagic. Associated symptoms included odynaphagia and fatigue. She revealed a previous diagnosis of genital herpes and recent contact with her mother who had been diagnosed with shingles. Daily medications included hydroxychloroqunine and tacrolimus. She recently completed a course of prednisone for an acute chronic rejection. Abnormal labs consisted of an aspartate aminotransferase level of 4,949 units/liter, alanine aminotransferase level of 3255 units/liter, alkaline phosphatase level of 710 mmol/L, INR of >4.50, hemoglobin of 4.1 g/dL, a hematocrit of 12.3 %, platelet count of 69, a fibrinogen of <100 mg/deciliter, lactic dehydrogenase of 3,377 units/liter, and D–dimers at >26 mg/liter. Tzanck prep showed multinucleated keratinocytes. Direct fluorescent antibody staining was positive for varicella zoster virus. Serology for varicella zoster showed negative IgM and IgG antibodies. Viral culture was positive for herpes simplex virus type 2. The patient expired three days after admission from liver, kidney and heart failure.
Though uncommon, co–infections of herpes simplex virus type 2 (HSV–2) and varicella zoster virus (VZV) have been reported in immunocompromised patients. Immunosupressed patients are at a much greater risk for serious disseminated disease from both VZV and HSV–2 resulting in significant morbidity and mortality. VZV and HSV–2 infection in immunocompromised patients can lead to pneumonia, hepatitis, esophagitis, disseminated intravascular coagulation, and meningitis. VZV and HSV–2 cases marked by liver damage, as in this case, are usually fatal. Immunocompromised patients frequently have more extensive and atypical skin eruption, often associated with hemorrhagic or purpuric vesicles. If HSV–2 or VZV infection is suspected, early initiation of antiviral treatment with intravenous acyclovir is crucial to reduce or eliminate serious disease–associated sequelae.
This case highlights the importance of suspecting multiple causes for a similar clinical presentation. Initially, HSV–2 was the only suspected cause of infection given the past diagnosis of genital herpes. In light of recent contact with shingles, both HSV–2 and VZV infection could explain her vesicular rash and disseminated visceral disease. As a hospitalist, it is important to take a full history and to include many disease processes in differential diagnoses, even when one cause may seem obvious. By focusing in on one diagnosis too quickly, physicians run the risk of misdiagnosis and mistreatment entirely.