Ocular Changes Associated with Hypovitaminosis a in Cattle

Barnett, K. C.; Palmer, Alan M.; Abrams, J. T.; Bridge, P. S.; Spratling, F.R.; Sharman, I. M.

doi:10.1016/s0007-1935(17)48070-5

Cited by 21 publications

(7 citation statements)

References 24 publications

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“…Ocular lesions include xerophthalmia, keratitis and retinal degeneration (Hayes 1974). When the developing fetus or young animals become vitamin A deficient, abnormal development can result in retinal dysplasia, as has been reported in piglets and calves on deficient diets (Palludan 1961, Van der Lugt and Prozetsky 1989), and cranial bone abnormalities with a narrowing of the skull foraminae have been reported in calves (Spratling and others 1965, Barnett and others 1970) and in puppies (Mellanby 1941) and piglets (Palludan 1961).…”

Section: Discussionmentioning

confidence: 81%

Retinal dysplasia in wild otters (Lutra lutra)

Williams

Simpson²,

Flindall

2004

Veterinary Record

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Eyes from 88 otters found dead in south-west England between 1990 and 2000, were collected as part of a larger pathological study. Histopathological examination of 131 eyes revealed dysplastic changes such as rosetting and folding in the retinas of 26 of the otters. In the eyes of 42 of the otters there were postmortem and fixation-induced retinal detachment which complicated the differentiation of dysplastic from normal retina, but 11 eyes had folds which probably indicated a dysplastic pathology. The eyes of 18 of the otters had inflammatory or autolytic changes which precluded a definitive evaluation of their dysplastic status. Liver samples from 55 of the otters were analysed for a range of polychlorinated hydrocarbons and for vitamin A. The otters with dysplastic retinas had significantly lower concentrations of vitamin A and higher concentrations of dieldrin than the otters with normal retinas.

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Section: Discussionmentioning

confidence: 81%

Retinal dysplasia in wild otters (Lutra lutra)

Williams

Simpson²,

Flindall

2004

Veterinary Record

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“…There are a number of diseases where similar, but not identical, clinical and/or pathological changes occur in naturally-occumng and experimentally-induced conditions. Vitamin A deficiency in cattle can affect the fetus in utero or the growing calf (Barnett et al, 1970). In both instances affected animals show depressed dark adaptation, papilloedema and blindness; they sometimes collapse or 'faint'.…”

Section: Discussionmentioning

confidence: 99%

A primary demyelinating disorder of young cattle

Palmer¹,

Jackson²,

Blakemore³

1991

Neuropathology Appl Neurobio

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The clinical signs and neuropathological changes are described in six Limousin X calves that, at about one month after birth, showed signs of blindness, nystagmus, rotation of the eyes, opisthotonos, hyperprotraction of the forelegs and, in one case, apparent seizures. Pathologically there was necrosis of the optic chiasma and focal areas of myelin sheath vacuolation or demyelination in certain areas of the brain, especially in the cerebellar peduncles. In one animal, kept alive for 7 months, there was remyelination by Schwann cells of some demyelinated axons in the focal cerebellar lesions, while other axons remained demyelinated. There was no evidence of oligodendrocyte remyelination. The cause of the condition was not determined but a genetic association is likely.

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“…However, the calves reported here were of mixed sex, born to unrelated bulls and there was no evidence of BVD infection. Further, the retinal dysplasia and remodelling of the occipital bone were all classical signs of hypovitaminosis A (Palludan 1961, Hayes and others 1968, Barnett and others 1970, Van der Lugt and Prozesky 1989). However, there was no stillbirth, doming of the skulls or bony constriction of the optic nerves causing papilloedema (Van der Lugt and Prozesky 1989).…”

Section: Calf Significant Clinical Findingsmentioning

confidence: 99%