Fifteen bald eagles (Haliaeetus leucocephalus) and 3
golden eagles (Aquila chrysaetos) were diagnosed with West Nile disease based on 1) presence of lesions in brain, eyes, and heart, 2)
viral antigen detection in brain, eyes, heart, kidney, and/or liver by immunohistochemical staining, 3) detection of
viral RNA in tissue samples and/or cerebrospinal fluid (CSF) by polymerase chain reaction, and/or 4) detection of West Nile virus (WNV)-specific
antibodies in CSF by serum neutralization assay. West Nile virus-associated gross lesions included cerebral pan-
necrosis with
hydrocephalus ex vacuo (7/15 bald eagles),
fibrin exudation into the fundus in 1 golden eagle,
retinal scarring in 1 bald eagle, and myocardial pallor and rounded heart apex in 4 bald eagles. Histologic lesions included lymphoplasmacytic
encephalitis, most prominently in the cerebrum (17 eagles), lymphoplasmacytic pectenitis and
choroiditis (15 and 8 eagles, respectively), and
myocarditis (12 eagles). West Nile virus
antigen was detected in the majority of the eagles in neurons of the brain (cerebrum and cerebellum), and less commonly present in neurons of the retina, tubular epithelial cells of the kidney, and cardiomyocytes. West Nile disease was diagnosed in 2 bald eagles based on the presence of cerebral pan-
necrosis and WNV-specific
antibodies in the CSF despite lacking
viral antigen and
RNA. In conclusion,
WNV infection causes a fatal disease in bald and
golden eagles. A variety of gross and histologic lesions are highly suggestive of WN disease in most eagles. A combination of detection of
viral antigen and/or
RNA or virus-specific
antibodies proved useful in confirming the diagnosis.