Meteyer C U, Docherty D E, Glaser L C, Franson J C, Senne D A, Duncan R
Biological Resources Division, U.S.G.S., National Wildlife Health Center, Madison, Wisconsin 53711, USA.
Avian Dis. 1997 Jan-Mar;41(1):171-80.
Neurotropic velogenic Newcastle disease (NVND) occurred in juvenile double-crested cormorants, Phalacrocorax auritus, simultaneously in nesting colonies in Minnesota, North Dakota, South Dakota, and Nebraska and in Lakes Michigan, Superior, Huron, and Ontario during the summer of 1992. Mortality as high as 80%-90% was estimated in some of the nesting colonies. Clinical signs observed in 4- to 6-wk-old cormorants included torticollis, tremors, ataxia, curled toes, and paresis or weakness of legs, wings or both, which was sometimes unilateral. No significant mortality or unusual clinical signs were seen in adult cormorants. Necropsy of 88 cormorants yielded no consistent gross observations. Microscopic lesions in the brain and spinal cord were consistently present in all cormorants from which Newcastle disease virus (NDV) was isolated. Characteristic brain lesions provided rapid identification of new suspect sites of NVND. Lesions were also present in the heart, kidney, proventriculus, spleen, and pancreas but were less consistent or nonspecific. NDV was isolated at the National Wildlife Health Center from 27 of 93 cormorants tested. Virus was most frequently isolated from intestine or brain tissue of cormorants submitted within the first 4 wk of the epornitic. Sera collected from cormorants with neurologic signs were consistently positive for NDV antibody. The NDV isolate from cormorants was characterized as NVND virus at the National Veterinary Services Laboratories, Ames, Iowa. The NVND virus was also identified as the cause of neurologic disease in a North Dakota turkey flock during the summer of 1992. Although no virus was isolated from cormorants tested after the first month of submission, brain and spinal cord lesions characteristic of NVND were observed in cormorants from affected sites for 2 mo, at which time nesting colonies dispersed and no more submissions were received. Risk to susceptible populations of both wild avian species and domestic poultry makes early recognition and confirmation of NVND in wild birds a priority.
1992年夏季,嗜神经速发型新城疫(NVND)在明尼苏达州、北达科他州、南达科他州和内布拉斯加州以及密歇根湖、苏必利尔湖、休伦湖和安大略湖的鸬鹚筑巢地同时发生在双冠鸬鹚幼鸟身上。据估计,一些筑巢地的死亡率高达80%-90%。在4至6周龄的鸬鹚身上观察到的临床症状包括斜颈、震颤、共济失调、脚趾卷曲以及腿部、翅膀或两者的轻瘫或无力,有时是单侧的。成年鸬鹚未出现显著死亡率或异常临床症状。对88只鸬鹚进行尸检未发现一致的大体观察结果。在所有分离出新城疫病毒(NDV)的鸬鹚中,脑和脊髓的微观病变始终存在。特征性的脑部病变有助于快速识别NVND的新可疑部位。心脏、肾脏、腺胃、脾脏和胰腺也有病变,但不太一致或不具特异性。在国家野生动物健康中心,93只接受检测的鸬鹚中有27只分离出了NDV。病毒最常从疫病流行最初4周内送检的鸬鹚的肠道或脑组织中分离出来。有神经症状的鸬鹚血清中NDV抗体始终呈阳性。在爱荷华州艾姆斯的国家兽医服务实验室,从鸬鹚分离出的NDV被鉴定为NVND病毒。1992年夏季,该NVND病毒还被确定为北达科他州一群火鸡神经疾病的病因。尽管在送检第一个月后检测的鸬鹚中未分离到病毒,但在受影响地点的鸬鹚中观察到NVND特征性的脑和脊髓病变持续了2个月,此时筑巢地分散,未再收到送检样本。野生鸟类和家禽易感种群面临的风险使得早期识别和确认野生鸟类中的NVND成为当务之急。