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From the Departments of Neurology (L.K., R.J.M.) and Medicine (P.K.), Turku University Hospital, and Department of Virology (T.V., R.V., V.H.), University of Turku, and Department of Neurology (L.K.), Satakunta Central Hospital, Pori, Finland.
Address correspondence and reprint requests to Dr. L. Kupila, Department of Neurology, Turku University Hospital, Kiinamyllynkatu 4-8, 20520 Turku, Finland; e-mail: laura.kupila{at}tyks.fi
Objective: To investigate the etiology of aseptic meningitis and encephalitis in an adult population using modern microbiologic methods.
Methods: Consecutive patients (ages
16) with aseptic meningitis or encephalitis treated in Turku University Hospital, Finland, during 1999 to 2003 were included in the study. Microbiologic tests were performed, including CSF PCR tests for enteroviruses, herpes simplex virus (HSV) 1, HSV-2, and varicella zoster virus (VZV), as well as serum and CSF antibody analysis for these viruses. Antibody testing was also performed for other pathogens commonly involved in neurologic infections. Virus culture was performed on CSF, fecal, and throat swab specimens.
Results: Etiology was defined in 95 of 144 (66%) patients with aseptic meningitis. Enteroviruses were the major causative agents (26%), followed by HSV-2 (17% of all, 25% of females) and VZV (8%). Etiology was identified in 15 of 42 (36%) patients with encephalitis, VZV (12%), HSV-1 (9%), and tick-borne encephalitis virus (9%) being the most commonly involved pathogens. Etiologic diagnosis was achieved by PCR in 43% of the patients with meningitis and in 17% of those with encephalitis.
Conclusions: Enteroviruses and HSV-2 are the leading causes of adult aseptic meningitis, and PCR is of diagnostic value. However, in most cases of encephalitis, the etiology remains undefined.
Supported by the Research Foundation of Orion Corporation, the Finnish Neurological Foundation, and the Finnish Medical Foundation Duodecim.
Disclosure: The authors report no conflicts of interest.
Received June 8, 2005. Accepted in final form September 30, 2005.
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