| Co-Investigator(Kenkyū-buntansha) |
MATSUMOTO Mitsuharu Assist.Prof., Dep.Vet.Med., Fac.Agricul., Kagoshima Univ., 農学部, 助手 (30157383)
MOCHIZUKI Masami Assoc.Prof., Dep.Vet.Med., Fac.Agricul., Kagoshima Univ., 農学部, 助教授 (90157834)
NISHIO Akira Professor, Dep.Vet.Med., Facult.Agricul., Kagoshima Univ., 農学部, 教授 (90133181)
SHIMIZU Tsutomu Professor, Dep.Vet.Med., Facult.Agricul., Kagoshima Univ., 農学部, 教授 (50072921)
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| Research Abstract |
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.
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