Every aspect of our West Nile virus surveillance and control program was evaluated. In order to test for pesticide resistance, our review began by contacting Dr. William Brogdon at the Centers for Disease Control and Prevention. Culex Quinquefasciatus egg rafts were shipped and pesticide resistance tests were conducted on two local populations of this species. Analysis of the two populations showed 64% and 74% less susceptibility to malathion, and 20% and 40% less susceptibility to permethrin when compared with a known insecticide-susceptible population of Cx. Quinquefasciatus.
Mapping known indicators of West Nile virus activity, including infected birds, mosquitoes, and sentinel chickens that tested positive for the virus proved to be very useful for our program. It showed a concentration of transmission activity in the main urban area of Savannah including the Downtown, Victorian, and historic districts, an area occupying approximately 24 square miles. Seven of the nine individuals infected with West Nile virus in 2003 resided within this high risk area. During the 2003 mosquito season, the gravid trap placed at the downtown Savannah location generally collected over 100 adult Cx. Quinquefasciatus per trap night and peaked at over 600 during a single night in November 2003.
Placing critical events that occurred within the high risk area on a timeline gave additional information. Laboratory confirmation by the Southeastern Cooperative Wildlife Disease Study (SCWDS) of the first West Nile virus positive mosquito pool collected on July 22 was received on July 29, 2003. Confirmation of the first human West Nile virus infection was received on September 4 from a presumed onset date of August 1, only 3 days after notification of the first positive mosquito pool. Confirmation (also by SCDWS) of the first West Nile virus positive birds collected on September 11 and 12 within the high risk area was not received until September 23. Finally, confirmation of the first West Nile virus infected sentinel chicken by the University of Georgia, Veterinary Diagnostic and Investigational Laboratory in Tifton, GA, having an exposure date of August 27, was not received until October 1. This delay is the result of the lag time involved between chicken exposure, incubation time before the initial blood sample and analysis, and the re-bleeding and subsequent lab confirmation of the sample. From this timeline, we noted that waiting for these specific viral activity indicators to occur before initiating adult mosquito control operations might not be useful in preventing human cases of West Nile fever/encephalitis. Only three days separated the finding of infected mosquitoes and the first human case, allowing only a minimal amount of time to mount an aggressive control response. Confirmations of West Nile virus infected birds and the single infected sentinel chicken were not received until after notification of the first human case. In fact, during an approximately seven week period (July 30-September 10), 15 positive mosquito pools were collected at a residence before a sentinel chicken, placed at the same residence one night each week, tested positive for West Nile virus. The relatively low reliability of sentinel chickens to detect WNV in advance of human illness has been previously reported from NY and NJ, where the majority of positive seroconversions occurred well after the onset of human cases (Cherry et al. 2001, Komar 2001). We concluded that: sentinel chickens were not adequate indicators of human risk for West Nile fever/encephalitis; dead birds were not good neighborhood-specific indicators of human risk; and infected mosquitoes may indicate an increased risk of human infection, but cannot be relied on to predict the timing of human cases.