Abstract

An epidemiological survey of this nervous disorder of the Brown Swiss breed in the USA did not implicate any geographical or environmental factors. There was no sex predilection. The number of recorded cases increased from four in 1972-76 to 46 in 1977-81. There were 32 cases in 1982-83. Breeding records from over half the cases indicated a familial pattern involving five sires. Studies on 32 affected purebred Brown Swiss cattle obtained from dairy farms throughout the USA are described. Owners supplied histories and breeding records, and blood typing was carried out to confirm parentage. The criteria used to establish a clinical diagnosis were: onset of bilateral hind leg weakness and ataxia between 5 and 8 months of age; deficient proprioceptive reflexes, normal motor and sensory reflexes, with no other clinically detectable neurological abnormality; and absence of clinically significant skeletal or muscular abnormality. Familial relationship was also taken into account. Laboratory studies included at least one blood count, routine serum chemistry, serum enzyme levels, and analysis of CSF, and selected cattle were screened for toxicological abnormalities. Three sires were incriminated in 48.6% of the cases, and one was incriminated in 31.4%. Laboratory analyses revealed no abnormal haematological parameters. Although increased activities of certain serum enzymes were found, these were not considered specific. CSF samples from two cases showed CPK activity. Toxicological analyses of cholinesterase activity and blood Cu levels were not significant.

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