Epidemiological and clinico-pathological study of congenital defects in cattle

1985年11月至1986年4月，在日本九州岛发现了2000多头无脑和小脑发育不全的小牛。他们出生时一般都很虚弱，没有父母，不能自己吸奶。几个小时后，大多数小牛还能站立，但它们都没有表现出自吸的样子。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，导致明显的生长迟缓。部分患者表现为持续性脑麻痹。神经症状，如斜拉肌，痉挛和眼球震颤在许多病例中发现。即使他们能走路，也可能因为视力障碍而漫无目的地走着。一种新的病毒——楚赞病毒，最初被怀疑是病原体，后来被证实是病原体。1987年，只收集了53例缺陷小牛。大多数患者被归类为骨骼、心脏和中枢神经系统，但未发现明显的赤叶病或楚赞病毒病的迹象。1988年3月至6月间发现了Akabane病的中度发病，主要发生在低partitus牛中。但在以下几个方面与本病的典型模式有区别：既往无关节挛缩的征象，相对较多的病例伴有holstein，部分病例伴有小脑发育不全。在研究期间，报告了两种遗传缺陷。1972年和1974年，宫崎县的一个地区发生了“8头日本黑牛疑似遗传性出血性糖尿病”，1980年和1982年，鹿儿岛发生了“日本黑牛先天性致死性皮肤缺陷”。每一个都是由一只种公牛引起的，这些公牛后来被淘汰了。然而，这些缺陷仍然很少被发现，可能与隐性基因有关。

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.