| Literature DB >> 15827215 |
Elliott R Jacobson1, Pamela E Ginn, J Mitchell Troutman, Lisa Farina, Lillian Stark, Kaci Klenk, Kristen L Burkhalter, Nicholas Komar.
Abstract
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 10(8.9) plaque-forming units [PFU]/0.5 cm3), whereas brain and spinal cord had the lowest viral loads (maximum 10(6.6) PFU/0.5 cm3 each). Virus titers in plasma ranged from 10(3.6) to 10(6.5) PFU/ml, exceeding the threshold needed to infect Culex quinquefasciatus mosquitoes (10(5) PFU/ml). Thus, alligators may serve as a vertebrate amplifying host for WNV.Entities:
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Year: 2005 PMID: 15827215 DOI: 10.7589/0090-3558-41.1.96
Source DB: PubMed Journal: J Wildl Dis ISSN: 0090-3558 Impact factor: 1.535