Pathogenicity of West Nile virus and response to vaccination in sandhill cranes (Grus canadensis) using a killed vaccine.

West Nile virus was introduced into the United States in the vicinity of New York, New York, USA in 1999. The virus has since killed large numbers of birds nationwide, especially, but not limited to, crows (Corvus brachyrhinchos). One sandhill crane (Grus canadensis) at the Bridgeport Zoo (Bridgeport, Connecticut, USA) reportedly died from West Nile virus, so sandhill cranes and endangered whooping cranes (Grus americana), both in the wild and in captive breeding colonies at United States Geological Service (USGS) Patuxent Wildlife Research Center (Laurel, Maryland, USA) were considered at risk. A killed vaccine in sandhill cranes was evaluated by vaccinating and then challenging these cranes with live West Nile virus. No sandhill cranes inoculated with the killed vaccine developed significant titers when compared with unvaccinated controls. No sandhill cranes inoculated with the vaccine and challenged with the virus died from West Nile virus infection. In addition, no unvaccinated challenged sandhill cranes died. However, 2 days postchallenge, vaccinated cranes had significantly less viremia (P < 0.05) than unvaccinated cranes. Seven days postchallenge vaccinated cranes had significantly less cloacal shedding of the virus (P < 0.05) than unvaccinated cranes and significantly less weight loss (P < 0.05) as compared with unvaccinated cranes. Vaccinated sandhill cranes developed significantly higher titers 14 days postchallenge and were viremic for shorter periods of time after challenge than unvaccinated individuals. Unvaccinated challenged cranes had glial cell aggregates in both the brain and brain stem areas, and this was not observed in vaccinated challenged cranes or in vaccinated unchallenged cranes.

Raptor mortality due to West Nile virus in the United States, 2002.

West Nile virus (WNV) has affected many thousands of birds since it was first detected in North America in 1999, but the overall impact on wild bird populations is unknown. In mid-August 2002, wildlife rehabilitators and local wildlife officials from multiple states began reporting increasing numbers of sick and dying raptors, mostly red-tailed hawks (Buteo jamaicensis) and great horned owls (Bubo virginianus). Commonly reported clinical signs were nonspecific and included emaciation, lethargy, weakness, inability to perch, fly or stand, and nonresponse to danger. Raptor carcasses from 12 states were received, and diagnostic evaluation of 56 raptors implicated WNV infection in 40 (71%) of these cases. Histologically, nonsuppurative encephalitis and myocarditis were the salient lesions (79% and 61%, respectively). Other causes of death included lead poisoning, trauma, aspergillosis, and Salmonella spp. and Clostridium spp. infections. The reason(s) for the reported increase in raptor mortality due to WNV in 2002 compared with the previous WNV seasons is unclear, and a better understanding of the epizootiology and pathogenesis of the virus in raptor populations is needed.

Pancreatitis in wild zinc-poisoned waterfowl.

Four waterfowl were collected in the Tri-State Mining District (Oklahoma, Kansas and Missouri, USA), an area known to be contaminated with lead, cadmium and zinc (Zn). They were part of a larger group of 20 waterfowl collected to determine the exposure of birds to metal contamination at the site. The four waterfowl (three Branta canadensis, one Anas platyrhynchos) had mild to severe degenerative abnormalities of the exocrine pancreas, as well as tissue (pancreas, liver) concentrations of Zn that were considered toxic. The mildest condition was characterized by generalized atrophy of exocrine cells that exhibited cytoplasmic vacuoles and a relative lack of zymogen. The most severe condition was characterized by acini with distended lumens and hyperplastic exocrine tissue that completely lacked zymogen; these acini were widely separated by immature fibrous tissue. Because the lesions were nearly identical to the lesions reported in chickens and captive waterfowl that had been poisoned with ingested Zn, and because the concentrations of Zn in the pancreas and liver of the four birds were consistent with the concentrations measured in Zn-poisoned birds, we concluded that these waterfowl were poisoned by Zn. This may be the first reported case of zinc poisoning in free-ranging wild birds poisoned by environmental Zn.