West Nile virus infection can result in prolonged subjective complaints of cognitive and functional decline even in the absence of a neuroinvasive form of infection. Persistent cognitive and functional complaints could be a result of general somatic symptoms, emotional distress, or residual central nervous system damage or dysfunction. Most studies of cognition in postacute West Nile virus infection rely on self-report. This descriptive study aimed to document cognitive deficits in a sample of the 2003 infected population reported in New Mexico. Patients with clinically defined neuroinvasive disease or who were impaired on brief mental status screening were seen for comprehensive neuropsychological assessment. We found that one year after symptom onset, more than half of the sample had objectively measurable neuropsychological impairment in at least two cognitive domains. Impairment was not related to subjective complaints of physical or emotional distress, or premorbid intellectual abilities. Persistent cognitive impairment in West Nile virus infection may be due to prolonged or permanent damage to the central nervous system.
Mental status after acute West Nile virus infection has not been examined objectively. We compared Telephone Interview for Cognitive Status scores of 116 patients with West Nile fever or West Nile neuroinvasive disease. Mental status was poorer and cognitive complaints more frequent with West Nile neuroinvasive disease (p = 0.005).
West Nile virus (WNV) myocarditis has been documented pathologically in birds and mammals but has rarely been reported in human clinical syndromes. We describe myocarditis associated with WNV.
A 38-year-old previously healthy male with a 6-month outpatient history of progressive bilateral visual loss, diagnosed as uveitis, presented with severe jaundice and macular rash. The rashes were diffusely distributed over the trunk and extremities, involving the palms and soles. Laboratory studies revealed leukocytosis, thrombocytopenia, anemia, significant transaminitis (maximal alanine aminotransferase [ALT] level, 233 U/liter; aspartate transaminase [AST] level, 90 U/liter), an alkaline phosphatase level of 2,306 U/liter, and a total bilirubin level of 7.3 mg/dl. Additionally, anti-nuclear antibody (ANA) and scleroderma antibody (Ab) test results were positive. HIV was incidentally detected with a Western blot confirmation and an elevated viral load. The patient denied any sexual activity within the past 24 months, resided at home with his children, and was employed as a contractor in the construction business in the southwestern United States. He denied any recent travel history.At presentation, the patient appeared to be jaundiced, and an oral examination revealed adherent white plaques on the tongue. Erythematous scaly macules, confluent with reticulate patches, were diffusely observed on the trunk and extremities. The palms and soles had hyperkeratotic circinate scales on a background of erythema. The neurological examination was significant for revealing blindness, and the results of the remainder of the physical examinations were unremarkable. A liver biopsy with hematoxylin and eosin (H&E) staining demonstrated severe acute hepatitis and hepatocellular necrosis. Warthin-Starry staining did not demonstrate any spirochetes. Leptospira was not considered, since the patient did not have a history of travel, his outdoor activity did not suggest that etiology, and another organism was serologically detected. Further specific immunohistochemical stains for that organism revealed spiral-shaped organisms and are shown in Fig. 1.
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