Abstract
Blood and serum from 3,915 wild and domestic birds (2,590 resident, 139 migrant, and 1,186 captive), representing 56 species collected in central Florida from 1989 through 1997, were analyzed for evidence of St. Louis encephalitis (SLE) virus transmission. All sera were tested for SLE hemagglutination inhibition (HI) antibody. Selected sera and bloods were tested for SLE neutralizing (NT) antibody and virus. The reproductive success of resident birds was highest from 1990-1992 and lowest from 1994-1997. Transmission of SLE to resident birds, especially mourning doves (Zenaida macroura), peaked during the summer of 1990, a year during which a widespread SLE epidemic was recorded in central Florida. The SLE antibody-positive resident birds 1st appeared during September of the epidemic year. Some SLE, HI antibody-positive resident birds were captured throughout 1991, but only 5% were yearlings, compared with 36% in 1990. By 1993, wild resident birds expressing HI and NT antibodies to SLE had nearly disappeared. None of the migrant birds tested were SLE-positive. Sentinel chickens maintained in Indian River County during the epidemic year seroconverted to SLE starting in early July with peak seroconversion rates in August, September, and October. High (> or = 50%) SLE seroconversion rates in sentinel chickens preceded those in wild birds by 10 wk and preceded peak human SLE transmission by at least 8 wk. Major SLE epidemics in south Florida depend on abundant wild bird populations, especially during the amplification phase of the transmission cycle. We propose that hard winter freezes along the temperature-subtropical climatic zone interface in central Florida, at approximately 27 degrees 30' North Latitude, opens foraging and nesting habitats for ground-feeding birds, resulting in high reproductive success and an abundance of seronegative individuals that rapidly amplify the SLE later in the year.
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