J. Christian Franson

A Cooper’s hawk (Accipiter cooperii) was found dead in a ditch leading from a heap leach pad at a gold mine in Nevada. Observations at autopsy included an absence of external lesions, traces of subcutaneous and coronary fat, no food in the upper gastrointestinal tract, and no lesions in the viscera. Cyanide concentrations (µg/g ww) were 5.04 in blood, 3.88 in liver, and 1.79 in brain. No bacteria or viruses were isolated from tissues, and brain cholinesterase activity was within the normal range for a Cooper’s hawk.

West Nile virus (WNV) spread to the US western plains states in 2003, when a significant mortality event attributed to WNV occurred in Greater Sage-grouse (Centrocercus urophasianus). The role of avian species inhabiting sagebrush in the amplification of WNV in arid and semiarid regions of the North America is unknown. We conducted an experimental WNV challenge study in Vesper Sparrows (Pooecetes gramineus), a species common to sagebrush and grassland habitats found throughout much of North America. We found Vesper Sparrows to be moderately susceptible to WNV, developing viremia considered sufficient to transmit WNV to feeding mosquitoes, but the majority of birds were capable of surviving infection and developing a humoral immune response to the WNV nonstructural 1 and envelope proteins. Despite clearance of viremia, after 6 mo, WNV was detected molecularly in three birds and cultured from one bird. Surviving Vesper Sparrows were resistant to reinfection 6 mo after the initial challenge. Vesper sparrows could play a role in the amplification of WNV in sagebrush habitat and other areas of their range, but rapid clearance of WNV may limit their importance as competent amplification hosts of WNV.

Wild waterfowl are primary reservoirs of avian influenza viruses (AIV). However the role of sea ducks in the ecology of avian influenza, and how that role differs from freshwater ducks, has not been examined. We obtained and analyzed sera from North Atlantic sea ducks and determined the seroprevalence in those populations. We also tested swab samples from North Atlantic sea ducks for the presence of AIV. We found relatively high serological prevalence (61%) in these sea duck populations but low virus prevalence (0.3%). Using these data we estimated that an antibody half-life of 141 weeks (3.2 years) would be required to attain these prevalences. These findings are much different than what is known in freshwater waterfowl and have implications for surveillance efforts, AIV in marine environments, and the roles of sea ducks and other long-lived waterfowl in avian influenza ecology.

It is unknown how the current Asian origin highly pathogenic avian influenza H5 viruses arrived, but these viruses are now poised to become endemic in North America. Wild birds harbor these viruses and have dispersed them at regional scales. What is unclear is how the viruses may be moving from the wild bird reservoir into poultry holdings. Active surveillance of live wild birds is likely the best way to determine the true distribution of these viruses. We also suggest that sampling be focused on regions with the greatest risk for poultry losses and attempt to define the mechanisms of transfer to enhance biosecurity. Responding to the recent outbreaks of highly pathogenic avian influenza in North America requires an efficient plan with clear objectives and potential management outcomes.

Detection of West Nile virus (WNV) has been reported in a variety of wild ducks in the US, but little is known about the pathogenesis and outcome of exposure of the disease in these species. Previous experimental studies of WNV in ducks either have challenged a small number of ducks with WNV or have tested domesticated ducks. To determine susceptibility and immune response, we challenged 7-wk-old Wood Ducks (Aix sponsa) with a 1999 American Crow (Corvus brachyrhynchos) isolate of WNV. Wood Ducks were susceptible to infection with the virus, and, although clinical signs or mortality were not observed, microscopic lesions were noted, particularly in the heart and brain. West Nile virus viremia peaked on day 2 postinfection (pi) at 10(4.54) plaque-forming units (PFU) of virus/mL serum and WNV was shed orally (between 10(2) and 10(2.9) PFU per swab) and cloacally. Specific anti-WNV antibody response was rapid, with anti-WNV IgM detected on day 3 pi followed on day 5 pi by anti-WNV IgG. Neutralizing antibodies were detected by plaque-reduction neutralization assay in one duck on day 4 pi, and in all sampled ducks on day 5. These results indicate that Wood Ducks are susceptible to WNV, but it is unlikely that significant WNV mortality events occur in Wood Ducks or that they play a significant role in transmission. However, WNV viremia was sufficient, in theory, to infect mosquitoes, and oral and cloacal shedding of the virus may increase the risk of infection to other waterbirds.

We conducted a retrospective analysis to evaluate demographic and pathologic characteristics in 484 bald eagles (Haliaeetus leucocephalus) and 68 golden eagles (Aquila chrysaetos) diagnosed with lead poisoning at the U.S. Geological Survey National Wildlife Health Center. As part of our analysis, we compared characteristics of lead poisoned eagles with those that died of other causes. Odds of lead poisoning were greater for bald eagles versus golden eagles, females versus males, adults versus juveniles, and eagles from the Mississippi and Central flyways versus the Atlantic and Pacific flyways. In addition to spatial, species, and demographic associations, we detected a distinct temporal trend in the collection date of lead poisoned bald eagle carcasses. These carcasses were found at greater frequency in late autumn and winter than spring and summer. Lesions in lead poisoned birds included emaciation, evidence of bile stasis, myocardial degeneration and necrosis, and renal tubular nephrosis and necrosis. Ingested lead ammunition or fragments were found in 14.2 % of bald eagles and 11.8 % of golden eagles. The overall mean liver lead concentration (wet weight basis) for eagles diagnosed with lead poisoning was 28.9 ± 0.69 SE mg/kg in bald eagles and 19.4 ± 1.84 SE mg/kg in golden eagles. In eagles diagnosed with collision trauma, electrocution, poisoning (other than lead), emaciation, infectious disease, trapping death, other, and undetermined causes, average liver lead concentrations were low (<1 mg/kg) and did not differ among causes of mortality. Thus, based on our data, we found no evidence that lead exposure of eagles predisposed them to other causes of mortality.

Greater sage‐grouse ( Centrocercus urophasianus ; sage‐grouse) are highly susceptible to infection with West Nile virus (WNV), with substantial mortality reported in wild populations and in experimentally infected birds. Although sage‐grouse are hunted throughout much of their range, they have also recently been considered for protection under the Endangered Species Act. We used blood samples collected on filter‐paper strips during the 2006–2010 Oregon, USA, annual sage‐grouse hunt to survey for specific WNV‐neutralizing antibodies that indicate a previous infection with WNV. During this period, hunters submitted 1,880 blood samples from sage‐grouse they harvested. Samples obtained were proportional for all 12 Oregon sage‐grouse hunting units. Laboratory testing of 1,839 samples by the WNV epitope‐blocking enzyme‐linked immunosorbent assay (bELISA) followed by plaque reduction neutralization test on bELISA‐positive samples yielded 19 (1%) and 1 (0.05%) positive samples, respectively. These data provided early baseline information for future comparisons regarding the prevalence of WNV‐specific neutralizing antibodies in sage‐grouse in Oregon. This methodology may provide other states where sage‐grouse (or other species) populations are hunted and where WNV constitutes a species conservation concern with a viable option to track the relative prevalence of the virus in populations. © 2014 The Wildlife Society.

We summarized the cause of death for 2,980 bald eagles ( Haliaeetus leucocephalus ) and 1,427 golden eagles ( Aquila chrysaetos ) submitted to the National Wildlife Health Center in Madison, Wisconsin, USA, for diagnosis between 1975 and the beginning of 2013. We compared the proportion of eagles with a primary diagnosis as electrocuted, emaciated, traumatized, shot or trapped, diseased, poisoned, other, and undetermined among the 4 migratory bird flyways of the United States (Atlantic, Mississippi, Central, and Pacific). Additionally, we compared the proportion of lead‐poisoned bald eagles submitted before and after the autumn 1991 ban on lead shot for waterfowl hunting. Trauma and poisonings (including lead poisoning) were the leading causes of death for bald eagles throughout the study period, and a greater proportion of bald eagles versus golden eagles were diagnosed as poisoned. For golden eagles, the major causes of mortality were trauma and electrocution. The proportion of lead poisoning diagnoses for bald eagles submitted to the National Wildlife Health Center displayed a statistically significant increase in all flyways after the autumn 1991 ban on the use of lead shot for waterfowl hunting. Thus, lead poisoning was a significant cause of mortality in our necropsied eagles, suggesting a continued need to evaluate the trade‐offs of lead ammunition for use on game other than waterfowl versus the impacts of lead on wildlife populations. Published 2014. This article is a U.S. Government work and is in the public domain in the USA.