This report documenting the transmission of rabies virus from an organ donor to multiple recipients underscores the challenges of preventing and detecting transmission of unusual pathogens through transplantation.

Background: Three patients received solid organ transplants from a common donor and were subsequently discharged from the hospital following an uneventful hospital course. Within 30 days, all 3 organ recipients returned to the hospital with varying symptoms that progressed to rapid neurological deterioration, coma, and death.Objective: To describe the clinical, neuroradiological, and pathological findings of rabies virus infection in organ transplant recipients infected from a common donor.Design: Case series involving a common donor and 3 organ recipients ascertained through review of clinical course and autopsy findings. A fourth case was determined by review of pending autopsy cases in which death occurred within the same time interval. Portions of postmortem central nervous system and organ tissues were frozen and formalin-fixed. Fluids and tissues were also collected for cultures, serology, and molecular studies. Postmortem fluids and tissues and antemortem fluids and tissues from all 4 transplant recipients and serum and banked lymphocyte or spleen cells from the donors were sent to the Centers for Disease Control and Prevention for further evaluation.Setting: Transplant unit of an urban teaching hospital.Results: Antemortem cerebrospinal fluid analysis for 3 of the 4 recipients was consistent with a viral etiology. Neuroimaging and electroencephalogram studies were suggestive of an infectious encephalitis or a toxic encephalopathy. Initial laboratory testing did not demonstrate an infectious etiology. Postmortem histologic analysis, immunohistochemistry, electron microscopy, and direct fluorescence antibody testing revealed rabies virus infection. Serological testing done postmortem confirmed rabies virus infection in the common donor.Conclusions: These cases demonstrate a risk for transmitting rabies virus infection through solid organ and tissue transplantation, and this diagnosis should be considered in any rapidly progressing neurological disease.

65-year-old man initially experienced difficulty forming his tie and felt unsteady while driving. Days later, these symptoms were followed by periods of dizziness and vague episodes of confusion that he felt were "out of character." The patient was extremely concerned, especially given a strong family history of strokes. With an unremarkable physical examination, laboratory tests, and brain imaging, the patient's symptoms were attributed to his inadvertent ingestion of codeine-containing medication and to multiple increasing life stressors, including recent prostatectomy for prostate cancer. One week later, the patient returned complaining of significant confusion, problems opening doors, and progressive difficulty performing activities of daily living. Physical examination at this time revealed the patient to be confused with notable psychomotor retardation. Decreased left arm swing was noted on gait exam. An electroencephalogram (EEG) showed findings of right temporal slowing. Because of this finding and the patient's deteriorating mental status, he was admitted for further evaluation. Repeat EEG demonstrated bihemispheric triphasic wave complexes. Cerebrospinal fluid cytology and cultures were normal, but cerebrospinal fluid protein 14-3-3 was abnormally elevated. Magnetic resonance imaging (MRI) of the brain revealed areas of diffusion restriction in the right cerebral cortex and right basal ganglia (Figure 1). No abnormalities were found after extensive laboratory tests, including a metabolic panel and tests for syphilis, HIV, herpes simplex virus, human herpesvirus-6, C-reactive protein, antinuclear antibodies, folate, erythrocyte sedimentation rate, and homocysteine levels. His neurologic condition continued to deteriorate rapidly. Without effective treatment options, he was referred to hospice and succumbed to his disease process approximately 2 months from the time of initial presentation. A limited autopsy of the brain was performed at the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, Ohio. An abnormal prion protein was detected and characterized by Western blot, histopathological studies, and immunohistochemical examinations.

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