Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Swayback”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMedDate not supplied

Cytochrome-c oxidase isolated from the brain of swayback-diseased sheep displays unusual structure and uncharacteristic kinetics.

Swayback disease, a neurodegenerative disorder of lambs, and Menkes disease, the human equivalent, are caused by a deficiency of dietary copper. Reports of low enzymic activity suggest that several copper-containing enzymes, including cytochrome-c oxidase (COX), may influence the progress of these diseases. To investigate its role in the development of neurodegenerative disorders, in particular swayback disease, we isolated COX from the brains and livers of swayback-diseased lambs. Comparative sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) combined with densitometric analysis revealed that whereas the structure of COX from the liver of diseased animals was normal, the corresponding brain enzyme was subunits II-, III-, and IV-deficient; the deficiency was 55, 30, and 65% respectively. The activities of liver and brain COX from normal and diseased lambs were compared by polarographic assay at low ionic strength. Whereas the enzyme from normal brains and both forms of the liver enzyme yielded characteristic biphasic Eadie-Hofstee plots, the brain enzyme from diseased animals displayed a single phase with a K(m) of 4.7 +/- 2.4 x 10(-6) M: the K(m) values of COX from the normal brain were 12 +/- 2.5 x 10(-6) and 5.5 +/- 0.5 x 10(-7) M. We conclude that the altered enzyme structure accounts for the uncharacteristic kinetics and low activity we have observed for the isolated brain enzyme. We also conclude that the altered enzyme structure partly accounts for the low oxidase activity and decreased ATP synthesis that has been widely reported for brain tissue from swayback-diseased animals. We postulate that the subunit deficiency probably results from incomplete crosslinking between the subunits and the membrane, and predict that similar structural and kinetic factors may also account for low COX activity in Menkes disease.

Animals↗
PubMed1980

Studies on viral leukoencephalomyelitis and swayback in goats.

Six kid goats with CNS disease were studied by a variety of techniques. All had morphological evidence of Viral Leukoencephalomyelitis of Goats. (VLG) characterized by demyelinating encephalomyelitis and pneumonitis. Attempts were made to isolate a virus from 5 of these goats by direct culture of CNS and visceral tissues. Syncytial formation was found in some lung, spleen and bone marrow cultures but syncytia were found to be free of complete virus by electron microscopy. When newborn goats were inoculated with syncytia forming cells, a visna-like virus was found in bone marrow cultures of 1 goat 8 days post inoculation. Bone marrow cells from a twin goat 3 months after inoculation produced syncytia without complete virus. it is suggested that complete virus might be present in goats shortly after infection, while persisting in an incomplete form. Three of the 6 goats studied also had lesions of swayback with diffuse encephalomyelopathy and low liver copper levels. Control copper levels in kids with non-neurological disease were variable, occasionally being as low as swayback animals. The experience of others that swayback in the goat and low copper status are poorly correlated is confirmed. Discrepancies inherent in assaying formalin preserved tissues for copper are described.

Animals↗
PubMed1983

Menkes' disease and swayback. A comparative study of two copper deficiency syndromes.

The neuropathological findings in two siblings with Menkes' disease were compared with representative material obtained from lambs suffering from swayback (enzootic ataxia). The aim of the study was to demonstrate the similarity of lesions in a genetic and a nutritional form of copper deficiency in support of the view that all lesions in Menkes' disease could be ascribed to simple hypocupraemia. All lesions of Menkes' disease were shown to have their counterpart in swayback, with exception of the abnormal arborisations of the Purkinje cell dendrites. These have often been interpreted as malformations and cited in evidence of the prenatal origin of the cerebral lesions. They are, however, non-specific and similar lesions have been reported in conditions arising in later life. While there is abundant collateral evidence of disturbed copper metabolism in utero, the problem of the prenatal versus postnatal origin of cerebral damage remains unresolved.

Animals↗
PubMed1986

Delayed swayback in goat kids, a study of 23 cases.

The results of a retrospective study of 23 goat kids with delayed swayback are reported. Principal clinical signs were ataxia, loss of postural control, spasticity of the hindlimbs, and muscular weakness, often progressing to permanent recumbency. Denervation of skeletal muscles was demonstrated by electromyography in 2 kids. Three kids slowly recovered during hospitalisation. Histopathological changes were characterized by degeneration of selected neuronal populations with their processes within the central and the peripheral nervous system. Affected systems included upper motor neuron, vestibular, general proprioceptive, and lower motor neuron pathways, with additional involvement of the cerebellar cortex in some animals. Our findings, including limited ultrastructural observations, support the notion that the neuraxon rather than the myelin sheath is the prime target of disease in delayed swayback. The available copper values of affected kids and their unaffected herd mates were significantly lower than those of random control goats, which provides further support for a role of copper deficiency in the aetiology of this disease in the goat.

Animals↗
PubMed1985

Multiple sclerosis in research workers studying swayback in lambs: an updated report.

Four out of seven research workers into swayback disease, a neurological disease of lambs, developed symptoms and signs of multiple sclerosis, and were reported in 1947. A further worker later joined the group. All of the original seven have died and two at necropsy had multiple areas of demyelination in the brain and spinal cord. The chance of four or more out of a random group of eight men developing multiple sclerosis is about one in a thousand million. Multiple sclerosis has not occurred in other workers on swayback disease elsewhere.

Adult↗
PubMedDate not supplied

Novel mitochondrial proteins and decreased intrinsic activity of cytochrome-c oxidase. Characteristics of swayback disease in sheep.

Swayback disease (SD), a fatal neurological disorder affecting lambs and kids, is characterized by abnormal mitochondria and low cytochrome-c oxidase activity. The cytochrome-c oxidase content and activity and the protein composition of mitochondria isolated from the brains of SD lambs were investigated. Difference spectra analysis indicated that the cytochrome-c oxidase content of mitochondria from SD animals was lower than normal, and electrophoresis showed that when compared to mitochondria from normal animals, lipid-depleted mitochondria from SD lambs had a different protein composition, particularly, in the 40-55 kDa region. Polarographic studies, using cytochrome-c as substrate, confirmed low intrinsic activity of cytochrome-c oxidase within the mitochondria of SD lambs. These studies also showed that at low ionic strength, such mitochondria did not yield the expected characteristic biphasic Eadie-Hofstee plots.

Animals↗
PubMed1978

California goats with a disease resembling enzootic ataxia or swayback.

In a retrospective study typical signs and lesions of enzootic ataxia or swayback were found in 16 young dairy goats from eight widely scattered herds in California. In addition to the constant appearance of chromatolytic neurons in brainstem and spinal cord, and myelin deficiency in certain tracts of the cord, cerebellar hypoplasia was found frequently. Liver copper was subnormal in six of nine kids tested. The disease is viewed as a developmental defect in which failure of neuronal perikaryon metabolism leads to distal axonopathy with secondary demyelination.

Animals↗
PubMed1974

Swayback (enzootic ataxia) in Alberta lambs.

Swayback (enzootic ataxia), a disease not previously described in Canada, occurred in newborn lambs in Alberta in 1972. Of 100 lambs born in one flock, over 60 succumbed in the enzootic. The diagnosis was based on the presence of a) gross cavitations and gelatinous lesions of the cerebral white matter in 16 of 24 (66.67%) lambs examined, b) central chromatolysis and hyalinization of neurons of the red and vestibular nuclei and reticular formation and of the lateral and ventral horns of the spinal cord, c) myelin deficiencies of the dorsolateral and sulcomarginal funiculi of the spinal cord and d) low hepatic and serum copper levels in affected lambs and low serum copper levels in the ewes. The feeding of sugar beet-(beta saccharifera) top silage to the ewes during pregnancy, lambing and lactation, and its relationship to the enzootic is discussed.

Animals↗