Naturally Acquired West Nile Virus Encephalomyelitis in Transplant Recipients: Clinical, Laboratory, Diagnostic, and Neuropathological Features | Global Health | JAMA Neurology | JAMA Network
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Original Contribution
August 2004

Naturally Acquired West Nile Virus Encephalomyelitis in Transplant Recipients: Clinical, Laboratory, Diagnostic, and Neuropathological Features

Author Affiliations

Author Affiliations: Departments of Pathology (Dr Kleinschmidt-DeMasters), Neurology (Drs Kleinschmidt-DeMasters and Tyler), and Neurosurgery (Dr Kleinschmidt-DeMasters), Division of Infectious Disease, Department of Medicine (Drs Levi and Tyler), Section of Neuroradiology, Department of Radiology (Dr Escott), Division of Gastroenterology and Hepatology, Department of Medicine (Drs Everson and Laird), and Departments of Microbiology and Immunology (Dr Tyler), University of Colorado Health Sciences Center; Denver Neurologists PC (Dr Marder); and Advanced Neurological Evaluation and Treatment Center PC (Dr McNutt); Denver, Colo.

Arch Neurol. 2004;61(8):1210-1220. doi:10.1001/archneur.61.8.1210

Background  In the 2003 West Nile virus (WNV) epidemic, Colorado reported more WNV cases than any other state, including an unprecedented number in organ transplant recipients.

Methods  Physicians caring for transplant recipients hospitalized with naturally acquired WNV encephalitis provided data to characterize the clinical symptoms, results of diagnostic studies, and outcomes.

Results  Eleven transplant recipients were identified (4 kidney, 2 stem cell, 2 liver, 1 lung, and 2 kidney/pancreas). Seven were directly admitted to 1 of the 2 hospitals in the study, and 4 were referred to 1 of these centers from regional hospitals. All but 1 patient had a prodrome typical of WNV encephalitis in nonimmunosuppressed patients. Ten patients developed meningoencephalitis, which in 3 cases was associated with acute flaccid paralysis. One patient developed acute flaccid paralysis without encephalitis. Six patients had significant movement disorders including tremor, myoclonus, or parkinsonism. All patients had cerebrospinal fluid pleocytosis and WNV-specific IgM in the cerebrospinal fluid and/or serum. Cerebrospinal fluid cytologic studies (n = 5) showed atypical lymphocytes, some resembling plasma cells; however, flow cytometry (n = 3) showed that cells were almost exclusively of T-cell (not B-cell or plasma cell) lineage. Magnetic resonance images of the brain were abnormal in 7 of 8 tested patients, and electroencephalograms were abnormal in 7 of 7, with 2 showing periodic lateralized epileptiform discharges. Nine of 11 patients survived infection, but 3 had significant residual deficits. One patient died 17 days after admission, and autopsy findings revealed severe panencephalitic changes with multifocal areas of necrosis in the cerebral deep gray nuclei, brainstem, and spinal cord as well as diffuse macrophage influx in the periventricular white matter. A second patient died of complications of WNV encephalitis 6 months after hospital admission.

Conclusions  Naturally acquired WNV encephalitis in transplant recipients shows diagnostic, clinical, and laboratory features similar to those reported in nonimmunocompromised individuals, but neuroimaging, electroencephalography, and autopsy results verify that these patients develop neurological damage at the severe end of the spectrum.