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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.

Recent outbreaks of haemorrhagic nephritis enteritis in geese flocks of 3 to 10 weeks in age in Hungary were investigated. Mortality varied between 4% and 67%. Affected birds generally died suddenly. Occasional clinical signs included tremors of the head and neck, subcutaneous haemorrhages and excretion of faeces containing partly digested blood. At necropsy the most frequent findings were a turgid wall and reddish mucosa of the intestines and reddish discolouration of the swollen kidneys, but oedema and haemorrhages of the subcutaneous connective tissue, hydropericardium and ascites were also seen. In subacute cases, visceral gout was frequently observed. Histological examination revealed zonal necrosis of the tubular epithelial cells with haemorrhages in the kidney. Other histological findings were serous hepatitis with fatty infiltration, necrotizing haemorrhagic enteritis and haemorrhages in the different organs including the brain. Experimental geese infected parenterally with crude liver and spleen homogenates prepared from diseased birds died after 8 to 20 days without premonitory signs, and had typical gross and histological lesions. Attempts to isolate cytopathic virus on different tissue cultures failed. The presence of polyomavirus was proven by polymerase chain reaction. Five isolates were further investigated by analysing their complete VP1 gene sequence. All tested strains were very closely related to each other on the basis of the nucleotide sequence, and they were identical at the deduced amino acid level.