|
|
| |||||||||||||||||||||||||||||||||
An 89-year-old man presented to a community hospital in October 2001 with fever and confusion. Except for recurrent hematuria, he had been in good health until the day before admission. After going to sleep unusually early, he awoke confused at 12:30 a.m. and slumped to the floor. His initial evaluation was notable for fever (oral temperature, 38.6°C), disorientation, and difficulty following commands. There was no clear weakness, and the remainder of his physical examination was unrevealing. The white-cell count was 6.9x103 per cubic millimeter (78 percent polymorphonuclear leukocytes, 13 percent lymphocytes, and 8 percent monocytes). Cerebrospinal fluid contained 1785 red cells and 120 white cells per cubic millimeter (75 percent neutrophils); a polymerase-chain-reaction assay for herpes simplex virus was negative. The patient's temperature subsequently rose to 39.4°C. At the time of his transfer to our hospital four days after presentation, he was mute and did not respond to oral commands; the score on the Glasgow Coma Scale was 7 (a score of 1 on the eye-opening category, a score of 1 on the best-verbal-response category, and a score of 5 on the best-motor-response category). Repeated lumbar puncture revealed 39 white cells per cubic millimeter (29 percent neutrophils and 51 percent lymphocytes). Electroencephalography revealed diffuse slowing with triphasic waves. Magnetic resonance imaging showed a small acute infarct in the right cerebellar hemisphere and the absence of meningeal or parenchymal enhancement. The patient had worked on his farm until the week before he became ill. Both his home and farm are located in a town where West Nile virus had been isolated from mosquitoes and horses. Serologic analysis of serum for West Nile virus on the fifth hospital day revealed an IgM titer of at least 1:12,800; the results of a confirmatory plaque-reduction neutralization assay were positive. Measurement of IgG titers in serum samples obtained four days apart showed an increase from 1:1600 to 1:6400. After receiving supportive care for one month, the patient is slowly recovering at this writing. He remains disoriented but can engage in short conversations.
West Nile virus is a flavivirus that can be transmitted by mosquitoes from its host species (birds) to humans. Since the first U.S. cases were described in 1999, human infection has been documented in 10 states, with an additional 17 states reporting the isolation of West Nile virus from mosquitoes, birds, or horses.1,2 Older age is a risk factor for severe neurologic illness and death from West Nile virus infection.3 Currently, there is no specific treatment for West Nile encephalitis; vaccines are being developed.
This case report serves to remind physicians of the importance of screening for endemic arboviruses in the proper clinical setting and to underscore the importance of public health initiatives to reduce the prevalence of mosquito-borne illnesses.
Leigh R. Hochberg, M.D., Ph.D.
John R. Sims, M.D.
Benjamin T. Davis, M.D.
Massachusetts General Hospital
Boston, MA 02114
lhochberg{at}partners.org
References
| |||||||||||||||||||||||||||||||||
HOME | SUBSCRIBE | SEARCH | CURRENT ISSUE | PAST ISSUES | COLLECTIONS | PRIVACY | TERMS OF USE | HELP | beta.nejm.org Comments and questions? Please contact us. The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved. |
Previous
