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Epidemiological and clinico-pathological study of congenital defects in cattle

牛先天性缺陷的流行病学和临床病理学研究

基本信息

批准号：
61480090
负责人：
HAMANA Katsumi
金额：
$ 3.39万
依托单位：
Kagoshima University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1986
资助国家：
日本
起止时间：
1986 至 1988
项目状态：
已结题

项目摘要

More than 2,000 calves with hydranencephaly and cerebellar hypoplasia was observed in Kyushu island, Japan during November, 1985 and April, 1986. They were generally weak and paretic at birth and could not suck milk by themselves. Most calves could stand several hours later, but none of them showed self-suck. Only a few cases showed self-suck after several days of nursing, but even then it usually was not enough, causing marked retarded growth. Some showed persistent paresis. Nervous signs such as opisthotonus, spasms and nystagmus were found in many cases. Even if they could walk, they only walked aimlessly probably due to disturbance of vision. A new orbi virus, Chuzan virus, was first suspected and later confirmed to be the causative agent.In 1987, only 53 cases of defective calves were collected. Most of them were classified as skeletal, cardial and central nervous system, but no obvious signs of Akabane or Chuzan virus diseases were found.In 1988, the moderate occurrence of Akabane disease mostly in cattle with low paritus was found between March and June. However, they were differentiated from the typical patterns of this disease in the following aspects; no preceding signs of arthrogryposis, relatively many cases of holstein and some cases complicated with cerebellar hypoplasia.During the research periods, two hereditary defects were reported. 'Hereditary hemorrhagic dithesis suspected in eight Japanese black beef calves' occurred in one area of Miyazaki during 1972 and 1974 and ' congenital lethal skin defects in Japanese black cattle' occurred in Kagoshima during 1980 and 1982. Each of them was caused by one stud bull and those bulls were eliminated later. However, these defects are still found rarely probably due to recessive gene.

1985年11月至1986年4月，在日本九州岛观察到2,000多头患有积水性无脑畸形和小脑发育不全的犊牛。他们出生时一般都很虚弱和瘫痪，不能自己吸奶。大多数小牛在几个小时后可以站立，但没有一只出现自吸。只有少数病例在几天的护理后出现自吸，但即使这样通常也不够，导致明显的发育迟缓。有些人表现出持续性麻痹。多数病例出现角弓反张、痉挛和眼球震颤等神经体征。即使他们能走路，也可能是由于视力障碍而漫无目的地行走。一种新的环状病毒，即丘赞病毒，最初被怀疑是该病的病原体，后来被证实是该病的病原体。1988年3 ~ 6月间发现赤羽病中度发病，主要发生在产犊量低的牛中。但与本病的典型表现不同的是，无关节弯曲的先兆，荷斯坦氏综合征较多，部分病例合并小脑发育不全。1972年至1974年期间，在宫崎的一个地区发生了“8头日本黑牛疑似遗传性出血性营养不良”，1980年至1982年期间，在鹿儿岛发生了“日本黑牛先天性致死性皮肤缺陷”。每一个都是由一头种公牛造成的，这些公牛后来被淘汰了。然而，这些缺陷仍然很少发现，可能是由于隐性基因。