Glávits Róbert, Ferenczi Emoke, Ivanics Eva, Bakonyi Tamás, Mató Tamás, Zarka Péter, Palya Vilmos
Central Veterinary Institute, H-1149 Budapest, Tábornok u. 2, Hungary.
Avian Pathol. 2005 Oct;34(5):408-14. doi: 10.1080/03079450500268039.
The authors investigated an outbreak of West Nile Fever characterized by severe neurological symptoms and death in a flock of 3600 6-week-old geese. Ataxia, intermittent torticollis and opisthotonus, incoordination, rhythmic side-to-side movement of the head, wriggling of the neck and abnormal head position were features of the disease. Death occurred within 4 to 5 days after the clinical signs appeared. The average daily mortality was 5 to 15, reaching 14% (in total) over a period of 6 weeks. There were no consistent gross pathological lesions, but in a few cases yellowish-grey foci of 3 to 6 mm in diameter were observed on the surface or transection of the brain. Histopathology revealed perivascular lymphohistiocytic infiltration and glia cell proliferation in the brainstem, cerebellum, cortex and spinal cord as well as degeneration of neural fibres in the spinal cord. In addition to the lesions caused by the West Nile Virus in the brain, characteristics of circovirus infection such as lymphocyte depletion, vacuolization and basophilic intra-cytoplasmic inclusion bodies containing circovirus-like particles were seen by light and electron microscopy in the cloacal bursa. West Nile Virus infection was confirmed by reverse transcriptase-polymerase chain reaction amplification of virus-specific nucleic acid from tissue samples of the brain. Based on the nucleotide sequence analysis of the polymerase chain reaction products, 99% identity was found on the tested NS5 region with the IS-98 ST1 strain isolated from a stork in Israel in 1998, and with West Nile Virus stains emerging in the USA in 1999. Using an indirect fluorescent antibody test, high antibody titres against the virus were detected in the serum samples submitted from the affected flock. In selected sera this was confirmed by neutralization antibody test as well.
作者对一群3600只6周龄鹅中爆发的以严重神经症状和死亡为特征的西尼罗河热进行了调查。共济失调、间歇性斜颈和角弓反张、运动不协调、头部有节奏的左右摆动、颈部扭动以及头部位置异常是该病的特征。临床症状出现后4至5天内出现死亡。平均每日死亡率为5至15只，在6周内总计达到14%。没有一致的大体病理病变，但在少数情况下，在脑表面或横切面上观察到直径为3至6毫米的黄灰色病灶。组织病理学显示，脑干、小脑、皮质和脊髓有血管周围淋巴细胞组织细胞浸润和神经胶质细胞增生，以及脊髓神经纤维变性。除了脑中由西尼罗河病毒引起的病变外，在泄殖腔法氏囊中通过光学显微镜和电子显微镜观察到了圆环病毒感染的特征，如淋巴细胞耗竭、空泡化和含有圆环病毒样颗粒的嗜碱性胞质内包涵体。通过从脑组织样本中逆转录聚合酶链反应扩增病毒特异性核酸，证实了西尼罗河病毒感染。基于聚合酶链反应产物的核苷酸序列分析，在测试的NS5区域发现与1998年从以色列一只鹳分离的IS-98 ST1株以及1999年在美国出现的西尼罗河病毒株有99%的同一性。使用间接荧光抗体试验，在受影响鹅群提交的血清样本中检测到针对该病毒的高抗体滴度。在选定的血清中，中和抗体试验也证实了这一点。
