Definition and diagnosis of cobalt deficiency in goats

Wallace, Dawn Stella (1993) Definition and diagnosis of cobalt deficiency in goats. PhD thesis, University of Glasgow.

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Abstract

A review of the literature concerning cobalt, vitamin E, and selenium and their effects on immunity in ruminants is included, concentrating particularly on the definition and diagnosis of cobalt deficiency. Five experiments are reported, the first three of which explore the requirement of goats for cobalt to prevent subclinical deficiency. Included in this is the effect of cobalt supplementation on immunity, and also a preliminary investigation of different forms of vitamin E supplementation and their suitability for treating vitamin B deficiency. In each experiment 24 feral cross goats were depleted of cobalt and then assigned to various levels of cobalt supplementation. In experiments 1 and 2 half the goats were supplemented with vitamin E in the last month of the experiment. The symptoms of vitamin B12 deficiency observed included loss of weight, loss of appetite, pale mucous membranes and 'weepy eyes'. Concentrations less than 0.07 mgCo/kgDM in the diet are likely to lead to deficiency and this is between the comparable requirements for cattle (0.04-0.07) and sheep (0.07-0.08). Deficiency is best confirmed by measuring both MMA and vitamin B12 concentrations. Serum MMA concentrations between 15-20 ?mol/1 and serum vitamin B12 concentrations between 50-100 ng/1 were associated with subclinical deficiency, and these differ from the levels associated with subclinical deficiency in sheep (MMA 10-15 mumol/1, Bj2 200-400 ng/1) and cattle (MMA 2-4 mumol/l, B12 150-200 ng/1). Serum succinate was not found to be reliable as an indicator of cobalt status. No effects on immune function were observed. Both oral and injectable vitamin E treatments raised plasma vitamin E concentrations, although the injectable treatment produced a rapid but short lived response, whereas daily oral supplementation produced a more gradual but long term response. Erythrocyte stability appeared to show some promise as a method of detecting vitamin E deficiency, but results were not conclusive. Results of these experiments are discussed and compared with the relevant literature. The fourth experiment investigated different methods of supplementing calves with vitamin E. Twelve calves were depleted of vitamin E and then randomly assigned to three groups, receiving either oral, injectable or no vitamin E supplement. Half the calves on each treatment also received injections of vitamin B12. Again injection of vitamin E was found to produce a rapid, massive but short lived response in plasma vitamin E concentrations; however repeated injections produced an adverse reaction if insufficient time (< 3 weeks) was left between treatments. Oral supplementation produced a more gradual, but sustained response with no adverse reactions. Thus injection is highly suitable for rapid treatment of deficient animals, but oral supplementation is a more long term solution where instant effects are not required. In calves erythrocyte stability was unsuitable as an indicator of vitamin E status. A small increase in % kill of E. coli and C. albicans but not of S. aureus was observed in the vitamin supplemented calves, but no effect of vitamin E status was observed. Results are discussed and compared to other results in this field. The final experiment investigated the effect of cobalt deficiency on appetite preference in sheep, and by means of different treatments, oral cobalt, vitamin B12 injection, and methionine injection, attempted to gain some insight into the metabolic reason behind this phenomenon. Thirteen mature Suffolk cross castrates were maintained on a cobalt deficient diet, until they showed loss of appetite; they were then given one of the three treatments to see if this would restore their appetite. Vitamin B12 injections produced a rapid response, while cobalt treatment was also effective but took longer to work. Methionine treatment failed to improve appetite, suggesting that it is the failure of the propionate to succinate pathway which is responsible for the loss of appetite, and that it is absorbed vitamin which reverses the symptoms and not free cobalt in the rumen. Results are discussed in the light of other work.

Item Type: Thesis (PhD)
Qualification Level: Doctoral
Additional Information: Adviser: Allan MacPherson
Keywords: Animal sciences
Date of Award: 1993
Depositing User: Enlighten Team
Unique ID: glathesis:1993-72292
Copyright: Copyright of this thesis is held by the author.
Date Deposited: 24 May 2019 15:12
Last Modified: 24 May 2019 15:12
URI: http://theses.gla.ac.uk/id/eprint/72292

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