Repeated West Nile virus epidemic transmission in Kern County, California, 2004-2007.

West Nile virus (WNV) has remained epidemic in Kern County, CA, since its introduction in 2004 through 2007 when the human case annual incidence increased from 6-8 to 17 per 100,000, respectively. The 2007 increase in human infection was associated with contradicting surveillance indicators, including severe drought, warm spring but cool summer temperature anomalies, decreased rural and urban mosquito abundance but increased early season infection in urban Culex quinquefasciatus Say, moderate avian "herd immunity," and declines in the catch of competent (western scrub-jay and house finch) and noncompetent (California quail and mourning dove) avian species. The decline in these noncompetent avian hosts may have increased contact with competent avian hosts and perhaps humans.

Does variation in Culex (Diptera: Culicidae) vector competence enable outbreaks of West Nile virus in California?

Since the invasion of California by West Nile virus (family Flaviviridae, genus Flavivirus, WNV) in 2003, we have annually monitored vector competence for the NY99 strain in Culex tarsalis Coquillett, Culex pipiens quinquefasciatus Say, Culex p. pipiens L., and Culex stigmatosoma Dyar populations from four areas: deserts of Coachella Valley, densely urbanized maritime Los Angeles, southern San Joaquin Valley in Kern County, and southern Sacramento Valley near Davis in Sacramento County.

Vector competence of Culiseta incidens and Culex thriambus for West Nile virus.

The vector competence of Culiseta incidens (Thomson) and Culex thriambus Dyar for West Nile virus (WNV) were compared to Cx. quinquefasciatus Say or Cx. tarsalis Coquillett and Cx.

Role of California (Callipepla californica) and Gambel's (Callipepla gambelii) quail in the ecology of mosquito-borne encephalitis viruses in California, USA.

Gambel's and California quail were infected repeatedly whenever western equine encephalomyelitis virus (WEEV), St. Louis encephalitis virus (SLEV), and (WNV) West Nile virus were active during summer in California. The timing of virus appearance and quail infection coincided well with the appearance of chicks in nature, leading us to hypothesize that large coveys containing these non-immune birds could be important in focal virus amplification in rural settings.

Overwintering of West Nile virus in Southern California.

West Nile virus (family Flaviviridae, genus Flavivirus, WNV) invaded southern California during 2003, successfully overwintered, amplified to epidemic levels, and then dispersed to every county in the state. Although surveillance programs successfully tracked and measured these events, mechanisms that allowed the efficient overwintering and subsequent amplification of WNV have not been elucidated. Our current research provided evidence for three mechanisms whereby WNV may have persisted in southern California during the winters of 2003-2004 and 2004-2005: 1) continued enzootic transmission, 2) vertical transmission by Culex mosquitoes, and 3) chronic infection in birds.

Effects of temperature on the transmission of west nile virus by Culex tarsalis (Diptera: Culicidae).

Culex tarsalis Coquillett females were infected with the NY99 strain of West Nile virus (family Flaviviridae, genus Flavivirus, WNV) and then incubated under constant temperatures of 10-30 degrees C. At selected time intervals, transmission was attempted using an in vitro capillary tube assay. The median time from imbibing an infectious bloodmeal until infected females transmitted WNV (median extrinsic incubation period, EIP50) was estimated by probit analysis.

Encephalitis virus persistence in California birds: experimental infections in mourning doves (Zenaidura macroura).

After-hatching and hatching year, mourning doves were infected by inoculation with either western equine encephalomyelitis (WEE) or St. Louis encephalitis (SLE) viruses; some birds in each group also were treated with the immunosuppressant cyclophosphamide before and during infection. Cyclophosphamide treatment significantly increased the WEE viremia but did not alterthe antibody response.

Effects of immunosuppression on encephalitis virus infection in the house finch, Carpodacus mexicanus.

Immunosuppression of house finches was attempted by blood feeding Culex tarsalis Coquillett mosquitoes or by injecting birds with the corticosteroid dexamethasone or the immunosuppressant drug cyclophosphamide before and after inoculation with western equine encephalomyelitis or St. Louis encephalitis viruses. Mosquito bites (8-37 females blood feeding on each bird over a 3-d period) did not enhance the viremia response or increase the frequency of chronic infection.