RESUMO
The effects of a single treatment at entry with three anthelmintics on rates of weight gain and feed conversion efficiency over a 70 day period were studied in 200 feedlot steers. None of the anthelmintic treatments used appeared to confer any improvement in the above parameters under the conditions of this experiment. The results are discussed in relation to routine anthelmintic treatment in western Canada.
Assuntos
Anti-Helmínticos/uso terapêutico , Doenças dos Bovinos/tratamento farmacológico , Enteropatias Parasitárias/veterinária , Infecções por Nematoides/veterinária , Animais , Peso Corporal/efeitos dos fármacos , Bovinos , Doenças dos Bovinos/parasitologia , Enteropatias Parasitárias/tratamento farmacológico , Infecções por Nematoides/tratamento farmacológicoRESUMO
The clinical signs and postmortem findings in sheep from two flocks accidentally poisoned with monensin are described. Clinical signs began within 24 hours of exposure to monensin. In the acute stages they consisted of lethargy, stiffness, muscular weakness, a stilted gait and recumbency. Feed refusal was seen in one flock but not in the second. Subacute to chronic clinical signs were decreased muscle volume of the rump and thigh. When forced to run, chronically affected sheep had a stilted, stiff legged, rocking horse gait.Gross postmortem changes were not always visible. Where visible, they affected skeletal muscles and consisted of pale streaking, with atrophy in the chronic stages. Lesions were most severe in muscles of the rump and hind limbs. Microscopically myofiber swelling and hyalinization were seen with interstitial mononuclear cell reaction and extensive sarcoplasmic mineralization in some cases. Chronic lesions consisted of fibrosis and myofiber atrophy. In lambs less than one month old, diffuse gastrointestinal hemorrhage was the only finding.
RESUMO
The clinical and pathological features of a newly recognized, inherited neurodegenerative disorder in horned Hereford calves are described. The disorder is expressed in newborns by tremulous shaking of the head, body and tail, difficulty in rising, a wobbly spastic gait, and aphonia. Transient improvement is followed by deterioration and progressive spastic paraplegia. Generalized tremors can be induced easily by a variety of stimuli, and spinal reflexes may be exaggerated or depressed. The major pathological finding is an excessive accumulation of neurofilaments within neurons of the central, peripheral, and autonomic nervous systems. The involvement of multiple systems of neurons and the similarity with some forms of human motor neuron disease and spinocerebellar degeneration suggest that this unique bovine disease may serve as a suitable animal model for these human neurodegenerative disorders.