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1 College of Veterinary Medicine, University of Florida, Gainesville, Florida 32610, USA
2 Florida Department of Health Bureau of Laboratories, Tampa, Florida 33612, USA
3 Division of Vector-Borne Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado 80522-2089, USA
5 Corresponding author (email: jacobsone{at}mail.vetmed.ufl.edu)
In September and October 2002, an epizootic of neurologic disease occurred at an alligator farm in Florida (USA). Three affected American alligators (Alligator mississippiensis) were euthanatized and necropsied, and results confirmed infection with West Nile virus (WNV). The most significant microscopic lesions were a moderate heterophilic to lymphoplasmacytic meningoencephalomyelitis, necrotizing hepatitis and splenitis, pancreatic necrosis, myocardial degeneration with necrosis, mild interstitial pneumonia, heterophilic necrotizing stomatitis, and glossitis. Immunohistochemistry identified WNV antigen, with the most intense staining in liver, pancreas, spleen, and brain. Virus isolation and RNA detection by reverse transcription–polymerase chain reaction confirmed WNV infection in plasma and tissue samples. Of the tissues, liver had the highest viral loads (maximum 108.9 plaque-forming units [PFU]/0.5cm3), whereas brain and spinal cord had the lowest viral loads (maximum 106.6 PFU/0.5cm3 each). Virus titers in plasma ranged from 103.6 to 106.5 PFU/ml, exceeding the threshold needed to infect Culex quinquefasciatus mosquitoes (105 PFU/ml). Thus, alligators may serve as a vertebrate amplifying host for WNV.
Key words: Alligator mississippiensis, American alligator, infection, molecular virology, pathology, West Nile Virus.
4 Current address: USDA National Wildlife Research Center, Fort Collins, Colorado 80521, USA
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