DIFFERENTIAL IMPACT OF WEST NILE VIRUS ON CALIFORNIA BIRDS.

The strain of West Nile virus (WNV) currently epidemic in North America contains a genetic mutation elevating its virulence in birds, especially species in the family Corvidae. Although dead American Crows (Corvus brachyrhynchos) have been the hallmark of the epidemic, the overall impact of WNV on North America's avifauna remains poorly understood and has not been addressed thoroughly in California. Here, we evaluate variation by species in the effect of WNV on California birds from 2004 to 2007 by using (1) seroprevalence in free-ranging birds, (2) percentage of carcasses of each species reported by the public that tested positive for WNV, (3) mortality determined from experimental infections, and (4) population declines detected by trend analysis of Breeding Bird Survey (BBS) data. Using Bayesian linear models, we extrapolate trends in BBS data from 1980-2003 (pre-WNV) to 2004-2007 (post-WNV). We attribute significant declines from expected abundance trends in areas supporting epiornitics to WNV transmission. We combine risk assessed from each of the four data sets to generate an overall score describing WNV risk by species. The susceptibility of California avifauna to WNV varies widely, with overall risk scores ranging from low for the refractory Rock Pigeon (Columba livia) through high for the susceptible American Crow. Other species at high risk include, in descending order, the House Finch (Carpodacus mexicanus), Black-crowned Night-Heron (Nycticorax nycticorax), Western Scrub-Jay (Aphelocoma californica), and Yellow-billed Magpie (Pica nuttalli). Our analyses emphasize the importance of multiple data sources in assessing the effect of an invading pathogen.

Efficacy of aerial spraying of mosquito adulticide in reducing incidence of West Nile Virus, California, 2005.

Epidemic transmission of West Nile virus (WNV) in Sacramento County, California, in 2005 prompted aerial application of pyrethrin, a mosquito adulticide, over a large urban area. Statistical analyses of geographic information system datasets indicated that adulticiding reduced the number of human WNV cases within 2 treated areas compared with the untreated area of the county. When we adjusted for maximum incubation period of the virus from infection to onset of symptoms, no new cases were reported in either of the treated areas after adulticiding; 18 new cases were reported in the untreated area of Sacramento County during this time. Results indicated that the odds of infection after spraying were approximately 6x higher in the untreated area than in treated areas, and that the treatments successfully disrupted the WNV transmission cycle. Our results provide direct evidence that aerial mosquito adulticiding is effective in reducing human illness and potential death from WNV infection.

West Nile virus infection in tree squirrels (Rodentia: Sciuridae) in California, 2004-2005.

West Nile virus (WNV) transmission generally involves a mosquito vector and an avian reservoir host, with mammals as incidental hosts. Although most mammalian WNV infections cause low or no morbidity or mortality, tree squirrels are susceptible to WNV-associated neurologic disease with infection prevalence comparable to that in dead birds. Positive species included fox squirrel (Sciurus niger), western gray squirrel (S. griseus), and eastern gray squirrel (S. carolinensis). Kidney tissue (dissected and swabbed), and oropharyngeal (oral) swab samples from tree squirrels submitted by California vector control and rehabilitation agencies were tested by reverse transcription-polymerase chain reaction; cycle threshold values were similar for all three samples, ranging from 21.9 to 26.5. Kidney tissue was more sensitive than oral swabs for detecting WNV in squirrels. Three of 36 live neurologic tree squirrels had viremia approximately 5 log(10) plaque-forming units/mL or greater, similar to WNV-infected birds. Tree squirrels are useful in WNV surveillance and provide localized evidence of WNV transmission to mammals.

Field and laboratory evaluation of diagnostic assays for detecting West Nile virus in oropharyngeal swabs from California wild birds.

Three diagnostic assays for detecting West Nile virus (WNV) in avian oral swabs were evaluated in California in 2004 and 2005: two commercial antigen-capture assays, VecTest and Rapid Analyte Measurement Platform (RAMP), and reverse transcriptase-polymerase chain reaction (RT-PCR) of oral swabs in a specialized viral transport medium (VTM). Results from this study demonstrated that VTM was excellent for transportation and maintenance of WNV in avian oral swab samples and allowed for detection by RT-PCR and subsequent confirmation by virus isolation. Oral swabs and kidney tissue in VTM tested by RT-PCR were found to have similar accuracy in detecting WNV in corvids. The two antigen-capture assays, VecTest and RAMP, provided few false positives for corvids, with over 95% specificity. When performed by multiple local agencies throughout the state, VecTest and RAMP were similarly sensitive for oral swabs of American Crows (Corvus brachyrhynchos) (70% and 64%, respectively). Data from known WNV positive corvid oral swabs in VTM tested by antigen-capture assays at a diagnostic laboratory suggested that RAMP was more sensitive than VecTest. Due to high probability of false negatives, neither test is recommended for use on non-corvids. While WNV antigen-capture assays were effective screening tools for corvids, they were markedly less sensitive for Western Scrub Jays (Aphelocoma californica).

West Nile virus in California.

West Nile virus (WNV) was first isolated in California during July 2003 from a pool of Culex tarsalis collected near El Centro, Imperial County. WNV transmission then increased and spread in Imperial and Coachella Valleys, where it was tracked by isolation from pools of Cx. tarsalis, seroconversions in sentinel chickens, and seroprevalence in free-ranging birds. WNV then dispersed to the city of Riverside, Riverside County, and to the Whittier Dam area of Los Angeles County, where it was detected in dead birds and pools of Cx. pipiens quinquefasciatus. By October, WNV was detected in dead birds collected from riparian corridors in Los Angeles, west to Long Beach, and through inland valleys south from Riverside to San Diego County. WNV was reported concurrently from Arizona in mid-August and from Baja, Mexico, in mid-November. Possible mechanisms for virus introduction, amplification, and dispersal are discussed.

Eastern equine encephalomyelitis virus infection in a horse from California.

A yearling quarter horse, which was raised in southern California, received routine vaccinations for prevention of infection by Eastern equine encephalomyelitis virus (EEEV). One week later, severe neurologic signs developed, and the horse was humanely destroyed. A vaccine-related encephalomyelitis was later suspected. A final diagnosis of EEEV infection was established on the basis of acute onset of the neurologic signs, histopathologic and serologic testing, and isolation and molecular characterization of EEEV from brain tissue. The vaccine was extensively tested for viral inactivation. Nucleotide sequences from the vaccine and the virus isolated in the affected horse were also compared. In California, arboviral encephalomyelitides are rarely reported, and EEEV infection has not previously been documented. This report describes the occurrence of EEEV infection in the horse and the investigation to determine the source of infection, which was not definitively identified.