Pathology of fatal West Nile virus infections in native and exotic birds during the 1999 outbreak in New York City, New York

West Nile fever caused fatal disease in humans, horses, and birds in the no rtheastern United States during 1999. We studied birds from two wildlife fa cilities in New York City, New York, that died or were euthanatized and wer e suspected to have West Nile virus infections. Using standard histologic a nd ultrastructural methods, virus isolation, immunohistochemistry, in situ hybridization and reverse-transcriptase polymerase chain reaction, we ident ified West Nile virus as the cause of clinical disease, severe pathologic c hanges, and death in 27 birds representing eight orders and 14 species. Vir us was detected in 23/26 brains (88%), 24/25 hearts (96%), 15/18 spleens (8 3%), 14/20 Livers (70%), 20/20 kidneys (100%), 10/13 adrenals (77%), 13/14 intestines (93%), 10/12 pancreata (83%), 5/12 lungs (42%), and 4/8 ovaries (50%) by one or more methods. Cellular targets included neurons and glial c ells in the brain, spinal cord, and peripheral ganglia; myocardial fibers; macrophages and blood monocytes; renal tubular epithelium; adrenal cortical cells; pancreatic acinar cells and islet cells: intestinal crypt epitheliu m; oocytes; and fibroblasts and smooth muscle cells. Purkinje cells were es pecially targeted, except in crows and magpies. Gross hemorrhage of the bra in, splenomegaly, meningoencephalitis, and myocarditis were the most promin ent lesions. Immunohistochemistry was an efficient and reliable method for identifying infected cases, but the polyclonal antibody cross-reacted with St. Louis encephalitis virus and other flaviviruses. in contrast, the in si tu hybridization probe pWNV-E (WN-USAMRIID99) reacted only with West Nile v irus. These methods should aid diagnosticians faced with the emergence of W est Nile virus in the United States.