Fitzgerald S D, Patterson J S, Kiupel M, Simmons H A, Grimes S D, Sarver C F, Fulton R M, Steficek B A, Cooley T M, Massey J P, Sikarskie J G
Diagnostic Center for Population and Animal Health and Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824, USA.
Avian Dis. 2003 Jul-Sep;47(3):602-10. doi: 10.1637/6088.
Since the initial report of West Nile virus in the northeastern United States in 1999, the virus has spread rapidly westward and southward across the country. In the summer of 2002, several midwestern states reported increased cases of neurologic disease and mortality associated with West Nile virus infection in various native North American owl species. This report summarizes the clinical and pathologic findings for 13 captive and free-ranging owls. Affected species were all in the family Strigidae and included seven snowy owls (Nyctea scandiaca), four great-horned owls (Bubo virginianus), a barred owl (Strix varia), and a short-eared owl (Asio flammeus). Neurologic signs identified included head tilt, uncoordinated flight, paralysis, tremors, and seizures. Owls that died were screened for flaviviral proteins by immunohistochemical staining of formalin-fixed tissues, followed by specific polymerase chain reaction assay to confirm West Nile virus with fresh tissues when available. Microscopic lesions were widespread, involving brain, heart, liver, kidney, and spleen, and were typically nonsuppurative with infiltration by predominantly lymphocytes and plasma cells. Lesions in owls were much more severe than those previously reported in corvids such as crows, which are considered highly susceptible to infection and are routinely used as sentinel species for monitoring for the presence and spread of West Nile virus. This report is the first detailed description of the pathology of West Nile virus infection in Strigiformes and indicates that this bird family is susceptible to natural infection with West Nile virus.
自1999年美国东北部首次报告西尼罗河病毒以来,该病毒已迅速向西和向南蔓延至全美。2002年夏季,几个中西部州报告称,北美本土多种猫头鹰感染西尼罗河病毒后,神经系统疾病病例和死亡率有所增加。本报告总结了13只圈养和野生猫头鹰的临床和病理检查结果。受影响的物种均属于鸱鸮科,包括7只雪鸮(矛隼)、4只大角鸮(雕鸮)、1只条纹鸮(长耳鸮)和1只短耳鸮(短耳鸮)。确定的神经症状包括头部倾斜、飞行不协调、麻痹、震颤和癫痫发作。对死亡的猫头鹰,通过对福尔马林固定组织进行免疫组织化学染色来筛查黄病毒蛋白,如有新鲜组织,则随后进行特异性聚合酶链反应检测以确诊西尼罗河病毒。显微镜下病变广泛,累及脑、心、肝、肾和脾,通常为非化脓性,主要有淋巴细胞和浆细胞浸润。猫头鹰的病变比之前在鸦科鸟类(如乌鸦)中报告的病变严重得多,乌鸦被认为对感染高度易感,常被用作监测西尼罗河病毒存在和传播的哨兵物种。本报告首次详细描述了鸱鸮目西尼罗河病毒感染的病理学,表明该鸟类家族易受西尼罗河病毒自然感染。