对如东地区肉鸡腹水综合征病因学调查

本文在国内首次报道钠离子过量与肉鸡腹水综合征的关系。作者通过对如东地区肉鸡腹水综合征病鸡群的饲料及饮水分析、临床病理学（包括血液、血液生物化学指标）观察，认为Ｎａ＋摄入过量是当地肉鸡腹水综合征的重要病因之一，佝偻病可能有诱发、加剧腹水综合征的作用     

望江县长江江滩放牧牛蠕虫感染状况调查

为了解安徽省望江县江滩放牧牛寄生蠕虫的感染情况,本研究采用饱和盐水漂浮法、沉淀法、贝尔曼法对此地区的115头放牧牛的新鲜粪便进行检查,同时对虫种感染率以及不同品种、性别、年龄牛感染率进行了统计分析。调查结果显示,当地放牧牛感染的蠕虫有夏伯特线虫、捻转血矛线虫、奥斯特线虫、肝片吸虫以及肺线虫,总感染率达到90.4%(104/115)。其中捻转血矛线虫为感染优势虫种,感染率达70.4%;捻转血矛线虫、夏伯特线虫在雄牛和雌牛中感染率的差异具有显著性统计学意义。调查结果对长江流域江滩放牧牛蠕虫病防治工作以及了解蠕虫与宿主的相互关系具有一定参考意义。     

INVESTIGATION OF EQUINE INFECTIOUS ANAEMIA IN QUEENSLAND USING GEL DIFFUSION

An antigen for the gel diffusion test for equine infectious anaemia (EIA) was prepared from the spleen of a horse experimentally infected with the CQ strain of the virus. The antigen produced a single, distinct line of precipitation when tested against a range of known positive serums, and did not react with pre-inoculation and known negative serums. Extracts prepared from uninfected spleens displayed no reaction when similarly tested. Serum from 34 of 451 Queensland horses contained detectable levels of antibody to EIA virus. The positive serums were from horses in widely separated areas of the State.     

秦岭两侧黄牛群体遗传检测报告

以中心产区系统随机整群抽样对分布在秦岭两侧的秦川，西镇，平利３个地方黄牛品种（总头数各为６４２９３１，７２８４８，１３６４８）就下列遗传标记进行了检测：１．β血红蛋白（Ｈｂ），血清白蛋白（Ａｌｂ），后白蛋白（Ｐａ），运铁蛋白（Ｔｆ），后运铁蛋白ＯＰｔｆ），碱性磷酸酶（ＡＫＰ）６个位点的基因频率；２．Ｂ（黑色），Ｄ（稀释毛色），Ｓ（白斑的有无与类型），Ｂｒ（黧毛），Ｐｓ（皮肤黑斑），Ｉｎ（下腹部白斑     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

The age of the chicken at the time of infection with infectious avian encephalomyelitis virus (IAEV) and the route of the administration of the virus had a marked effect on the development of the clinical disease. Chickens given the virus by intramuscular, intraperitoneal and oral routes exhibited a decreased susceptibility to development of clinical disease with increasing age. Irrespective of age, chickens were consistently susceptible to intracerebral inoculation of IAEV. Chickens infected with the virus at 1-, 7- and 14-days of age developed lower neutralising antibody titres to IAEV than chickens infected at 21 and 28 days. A relationship between the ability to produce specific neutralising antibody to IAEV and susceptibility to the development of clinical disease is discussed.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

Infectious avian encephalomyelitis virus (IAEV) maternal antibody was detected in the serum of chickens for up to 21 days following hatching. This antibody protected chickens against clinical IAE after intracerebral inoculation with van Roekel strain or oral administration of the NSW-1 strain of IAEV. Maternal antibody to IAEV also protected testosterone bursectomised chickens against the development of clinical disease. IAEV maternal antibody also influeced the pattern of virus excretion in faeces and serological responsiveness. This influence on antibody responses persisted beyond the time that IAEV maternal antibody could be detected. The importance of IAEV maternal antibody on the strategy of vaccination against IAE is discussed.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

An association was demonstrated between the development of clinical infectious avian encephalomyelitis (IAE), the persistence and titre of infectious avian encephalomyelitis virus (IAEV) in the brain of the chicken, the duration of detectable viraemia and the age of the chicken at the time of infection with the virus. The older the chicken at the time of infection the milder the disease, the lower the virus titre in the brain and the shorter the period of viraemia. IAEV serum neutralising antibody was produced earlier after infection in older chickens, and its detection was associated with decreasing virus titres in the brain and the cessation of detectable viraemia. Treatment of chickens with testosterone in ova, to inhibit the development of antibody synthesis, prevented the onset of age-associated resistance and testosterone treated birds were as susceptible to clinical IAE as baby chickens. The results suggested that the ability to produce IAEV serum neutralising antibody was an important component of age-associated resistance to IAE.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

Normal chickens given infectious avian encephalomyelitis virus (IAEV) orally at 1, 7 or 14 days of age developed infectious avian encephalomyelitis (IAE), whereas those dosed with the virus at 21, 28 and 35 days of age did not. Chickens in all of these age groups that had been treated with cyclophosphamide or testosterone developed clinical IAE. Intraperitoneal inoculation of IAEV immunoglobulin at the time of dosing with the virus, or 48 hours later, protected normal and immunosuppressed chickens against the onset of clinical IAE. The titre of IAEV serum neutralising antibody was found to be lower in normal chickens given the virus at 1, 7 and 14 days of age in older chickens. These results suggest a significant role for the humoral immune system in the pathogenesis of IAE and in the development of immunity to the disease.