PubMed2002
BACKGROUND: The first reports of West Nile virus (WNV) infection in the United States in 1999 prompted Ontario to establish a surveillance protocol to monitor for the possible spread of the virus into the province. Surveillance components included evaluation of dead birds, sentinel chickens, mosquito pools and human disease. We report the results of human surveillance in 2000. METHODS: Between July 1 and Oct. 31, 2000, an active surveillance program was undertaken in which designated site coordinators in sentinel hospitals identified patients who met the suspect case definition (fever and fluctuating level of consciousness [encephalopathy], with or without muscle weakness). During the same period, following province-wide distribution of educational material, all other patients tested for WNV antibodies were identified through review of provincial laboratory reports (laboratory-based enhanced passive surveillance). RESULTS: Of the 60 hospitals contacted, 59 agreed to participate in the active surveillance program; 52 provided information on a regular (weekly) basis, and 7 submitted fewer than 8 reports. Thirty-six (61%) of the sentinel sites reported suspect cases. In total, 188 patients were tested (130 identified through active surveillance and 58 through enhanced passive surveillance). Patients identified through active surveillance were more likely than those identified through passive surveillance to meet the suspect case definition (43% [n = 56] v. 7% [n = 4]), to be admitted to hospital (75% [n = 99] v. 16% [n = 9]), to have a longer hospital stay (mean 25 v. 3 days), to have had a second (convalescent) serum sample collected (37% [n = 48] v. 31% [n = 18]), to have had a cerebrospinal fluid (CSF) sample banked (56% [n = 73] v. 14% [n = 8]) and to have had a discharge diagnosis reported (79% [n = 103] v. 28% [n = 16]). Of the 60 patients (32%) who met the suspect case definition, 34 (57% [31 active, 3 passive]) had a discharge diagnosis of encephalitis. Of these, 17 (50% [15 active, 2 passive]) had paired serum samples collected, and 18 (51% [all active]) had a CSF sample banked. The reported causal agents were herpes simplex virus (n = 8), varicelia virus (n = 2), Powassan virus (n = 1), echovirus 30 (n = 1) and group B Streptococcus (n = 1); the cause was unknown in 18 cases. One patient died of encephalitis. The remaining 26 patients who met the suspect case definition were ultimately found to have nonencephalitic infections, vascular events or alcohol- or drug-related illness. The 128 (68%) tested for WNV who did not meet the suspect case definition included 9 patients ultimately discharged with a diagnosis of encephalitis. No cases of WNV infection were identified. INTERPRETATION: Only one-third of the tested patients met the suspect case definition of encephalopathy on admission, and nearly half of them were later found to have another diagnosis; others did not meet the case definition but were later discharged with a diagnosis of encephalitis. This affirms that identification of acute encephalitis on the basis of symptoms at the time of admission is often impossible.