Silvano F D, Yoshikawa M, Shimada A, Otsuki K, Umemura T
Department of Veterinary Pathology, Faculty of Agriculture, Tottori University, Japan.
J Vet Med Sci. 1997 Mar;59(3):143-8. doi: 10.1292/jvms.59.143.
Three-day-old, specific-pathogen-free (SPF) chicks were inoculated with the strains of influenza A/whistling swan/Shimane/ 499/83 (H5N3) via the air sac route. The strains had been passaged through air sacs or air sacs and brains of SPF chicks. Two experiments were undertaken to examine the pathogenicity of these strains and the development of brain lesions based on time-interval changes. In experiment 1, original strain (4e) showed low pathogenicity with mild respiratory signs and zero mortality. Air sac passaged strains (18a and 24a) of 4e demonstrated mortalities of 50% and 67%, respectively, and inoculated chicks showed hemorrhages and necrotic lesions in major organs. Air sac-brain passaged strain (24a5b) of 4e produced 100% mortality and severe nervous signs. Severe circulatory disturbance with multiple foci of necrosis in major organs including the brain was found in chicks inoculated with 24a5b. The 24a5b was analogous to highly pathogenic avian influenza virus in regard to its pathogenicity to chicks. Hence, low pathogenic influenza virus (4e) gradually aggravated its pathogenicity to highly pathogenic virus (24a5b) by air sac and brain passages. In experiment 2, chicks were inoculated with 24a5b, and the earliest histological lesion was the enlargement of the vascular endothelial cells at 18 hr post-inoculation (PI) followed by necrotizing encephalitis at 24 to 48 hr PI. Immunohistological staining revealed avian influenza virus antigen initially in the vascular endothelial cells and then in the astrocytes, neurons and ependyma.
三日龄的无特定病原体（SPF）雏鸡通过气囊途径接种甲型流感病毒/啸鸭/岛根/499/83（H5N3）毒株。这些毒株已在SPF雏鸡的气囊或气囊及脑内传代。进行了两项实验，以根据时间间隔变化研究这些毒株的致病性及脑病变的发展情况。在实验1中，原始毒株（4e）致病性低，有轻微呼吸道症状，死亡率为零。4e的气囊传代毒株（18a和24a）死亡率分别为50%和67%，接种雏鸡的主要器官出现出血和坏死病变。4e的气囊-脑传代毒株（24a5b）死亡率达100%，并有严重神经症状。接种24a5b的雏鸡出现严重循环障碍，包括脑在内的主要器官有多个坏死灶。24a5b对雏鸡的致病性与高致病性禽流感病毒相似。因此，低致病性流感病毒（4e）通过气囊和脑传代逐渐使其致病性加重至高致病性病毒（24a5b）。在实验2中，雏鸡接种24a5b，最早的组织学病变是接种后18小时血管内皮细胞肿大，随后在接种后24至48小时出现坏死性脑炎。免疫组织化学染色显示禽流感病毒抗原最初出现在血管内皮细胞，然后出现在星形胶质细胞、神经元和室管膜。
