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Cobalt deficiency in Animals
- 1. Cobalt Deficiency Dr. MuhammadAvais Associate Professor Department of Clinical Medicine and Surgery University of Veterinary and Animal Sciences, Lahore, Pakistan
- 2. Etiology • Cobalt deficiencyis a disease of ruminants caused by: – ingesting a diet deficient in cobalt – required for the synthesis of vitamin B12 • Characterized clinically: – Inappetence, loss of body weight – reproductive performance
- 3. Epidemiology • Probably occursin many parts of the world: – Australia, NZ, UK, N. America, Netherlands • Large tracts of land unsuitable for: – raising of ruminants – deficiency is extreme • In certain areas suboptimal growth and production: – limiting factors in husbandry of sheep and cattle
- 4. Risk factors Dietary andenvironmental factors; • Pastures containing less than: – 0.07 and 0.04 mg/kg DM cause clinical disease in sheep and cattle, respectively • The daily requirement for sheep at pasture is; – 0.08 mg/kg DM of cobalt – for growing lambs the need is greater • For growing cattle, an intake of 0.04 mg/kg DM in feed is just below requirement levels
- 5. Risk Factors Primary cobaltdeficiency occurs only on soils which are deficient in cobalt
- 6. PATHOGENESIS • Cobalt isunique as an essential trace element in ruminant nutrition because; – stored in body in limited amounts – not in all tissues • In the adult ruminant, its only known function is in the rumen; – be present continuously in the feed.
- 7. PATHOGENESIS • Effect ofcobalt in the rumen is to participate; – production of vitamin B12 • Compared with other spp. vitamin B12 requirement is higher in ruminants; – Sheep 11 ug/d • Animals in advanced stages of cobalt deficiency; – cured by oral administration of cobalt – parenteral administration of vitamin B12
- 8. PATHOGENESIS • Essential defectin cobalt deficiency in ruminants; –an inability to metabolize propionic acid
- 9. PATHOGENESIS • A keybiochemical pathway for propionic acid from rumen fermentation involves adenosyl cobalamin; – cobalt-containing coenzymes of vitamin B12 complex • Required for conversion of; – methylmalonyl coenzyme A to succinyl coenzyme A – Both intermediates in the utilization pathway of propionate • Lack of vitamin B12 results in accumulation of; • methylmalonic acid, measured in the serum
- 10. CLINICAL FINDINGS • Nospecific signs are characteristic of cobalt deficiency: – Gradual decrease in appetite, loss of body weight, emaciation, weakness, Pica • There is marked pallor of the; – mucous membranes, easily fatigued • Growth, lactation, and wool production are severely retarded; – wool may be tender or broken.
- 11. Clinical Signs • Insheep, severe lacrimation is the most important sign in advanced cases • Signs usually become apparent when; – animals on affected areas for about 6 months – death occurs in 3-12 months
- 12. Clinical Signs • Cobaltdeficiency in pregnant ewes; – decreased lambing percentage, increased stillbirths, increased neonatal mortality • Lambs from deficient ewes are ; – slower to start sucking, reduced conc. of serum colostral immunoglobulins – lower serum vitamin B12 – Higher methylmalonic acid conc.
- 13. Ovine white liverdisease • A specific hepatic dysfunction of sheep has been described; – New Zealand, Australia, UK, Norway • Called 'white liver disease‘ because of; – grayish color of the liver • Clinically, it is manifested by; – photosensitization when the disease is acute – anemia and emaciation when the disease is chronic • It seems likely that the disease is a toxic hepatopathy – against which adequate levels of dietary cobalt are protective
- 14. Hepatic lipidosis ingoats • Hepatic lipidosis has occurred in Goats; – low levels of serum vitamin B12 – low levels cobalt in the liver • are associated with the liver lesion
- 15. Diagnosis Serum and hepaticcobalt and vitamin B12 concentrations Serum cobalt. • Cobalt concentrations in the serum of normal sheep; – 0.17-0.51 umoI/L • in deficient animals these are reduced to; – 0.03-0.41 umol/L
- 16. Diagnosis Serum vitamin B12 •Clinical signs of cobalt deficiency in sheep are associated with; – serum vitamin B12 levels of less than 0.20 mg/mL • Serum vitamin B12 1evels used as a laboratory test of cobalt status – Levels of 0.2-0.25 ug/L indicative of cobalt deficiency
- 17. Diagnosis Hepatic cobalt • Normalhepatic cobalt levels in lambs; – range between 0.03 and 0.1 ug/g • Levels below 0.02 ug/g associated with; – clinical cobalt deficiency • 0.015 ug/g is considered as a critical level
- 18. Diagnosis Serum methylmalonic acid •Measurement of serum MMA as diagnostic measures of cobalt status in cattle indicates that; – <2 umol/L is normal – 2-4 umol/L represents subclinical deficiency – >4 umol/L represents deficiency
- 19. Treatment Cobalt and vitaminB12 • Effected animals respond satisfactorily to: – oral dosing with cobalt or the IM injection of vit. B12. • Oral dosing with vitamin Bl2 is effective but; – much larger doses are required and costly • Oral dosing with cobalt sulfate is @ 1 mg cobalt/d in sheep
- 20. Treatment • Vitamin B12should be given in: – 100-300 ug doses in lambs and sheep – at weekly intervals,
- 21. CONTROL • Supplement dietwith cobalt – In cattle, the recommended levels of dietary cobalt to achieve maximum vitamin Bl2 levels are 250 ug/kg DM • Top dressing of pastures with cobalt – 400-600 g/ha cobalt sulfate annually – or 1.2-1.5 kg/ha every 3-4 years.
- 22. CONTROL • Cobalt-heavy pellet –Use of 'heavy pellets' containing 90% cobalt oxide – 5 g for sheep, 20 g for cattle – lodges in the reticulum • gives off cobalt continuously in very small but adequate amounts
- 23. CONTROL • Controlled releaseglass boluses of cobalt – boluses are retained in the forestomachs for up to several months and slowly release cobalt • Combine cobalt with administration of anthelmintics – Optimum level of cobalt supplementation of an anthelmintic ranges from 20 to 100 mg cobalt per treatment
- 24. CONTROL • Vitamin B12injections – SQ injection of vit. B12 in lambs maintain vitamin B12 status for about 24 days – 2 mg dose of vitamin B12 at least bimonthly in deficient areas
Editor's Notes
- #3 Cobalt deficiency is a disease of ruminants ingesting a diet deficient in cobalt, which is required for the synthesis of vitamin B12. The disease is characterized clinically by inappetence and loss of body weight. Some effects on reproductive performance in sheep have been reported. Cobalt was first shown to be an essential nutrient for sheep and cattle as an outcome of Australian investigations in the 1930s of two naturally occurring diseases, 'coast disease' of sheep, and 'wasting disease‘ or enzootic marasmus, of cattle 1
- #4 Cobalt deficiency occurs in Australia, New Zealand, the UK, North America, the Netherlands/ and probably occurs in many other parts of the world Where the deficiency is extreme, large tracts of land are unsuitable for the raising of ruminants, and in certain areas suboptimal growth and production may be limiting factors in the husbandry of sheep and cattle.
- #5 Risk factors Dietary and environmental factors Pastures containing less than 0.07 and 0.04 mg/kg DM result in clinical disease in sheep and cattle, respectively. The daily requirement for sheep at pasture is 0.08 mg/kg DM of cobalt; for growing lambs the need is somewhat greater and at pasture levels of less than 0.10 mg/kg DM inefficient rates of gain are likely. For growing cattle, an intake of 0.04 mg/kg DM in the feed is just below requirement levels
- #6 Primary cobalt deficiency occurs only on soils which are deficient in cobalt.
- #7 PATHOGENESIS Cobalt is unique as an essential trace element in ruminant nutrition because it is stored in the body in limited amounts only and not in all tissues. In the adult ruminant, its only known function is in the rumen and it must, therefore, be present continuously in the feed.
- #8 The effect of cobalt in the rumen is to participate in the production of vitamin B12 (cyanocobalamin), and compared with other species the requirement for vitamin B12 is very much higher in ruminants. In sheep, the requirement is of the order of 11 ug/d, and probably 500 ug/d are produced in the rumen, most being lost in the process. Animals in the advanced stages of cobalt deficiency are cured by the oral administration of cobalt or by the parenteral administration of vitamin B12·
- #9 The essential defect in cobalt defiCiency in ruminants is an inability to metabolize propionic acid.
- #10 A key biochemical pathway for propionic acid from rumen fermentation involves adenosyl cobalamin, one of several cobalt-containing coenzymes of the vitamin B12 complex that is required for the conversion of methylmalonyl coenzyme A to succinyl coenzyme A, both intermediates in the utilization pathway of propionate. Lack of vitamin B12 results in accumulation of methylmalonic acid which can be measured in the serum.
- #11 CLINICAL FIN DINGS No specific signs are characteristic of cobalt deficiency. A gradual decrease in appetite is the only obvious clinical sign. It is accompanied by loss of body weight, emaciation, and weakness, and these are often observed in the presence of abundant green feed. Pica is likely to occur, espeCially in cattle. There is marked pallor of the mucous membranes and affected animals are easily fatigued. Growth, lactation, and wool production are severely retarded, and the wool may be tender or broken.
- #13 Cobalt deficiency in pregnant ewes can result in decreased lambing percentage, increased percentage of stillbirths, and increased neonatal mortality. Lambs from deficient ewes are slower to start sucking, have reduced concentrations of serum colostral immunoglobulins, and have lower serum vitamin B12 and higher methylmalonic acid concentrations than lambs from cobalt-adequate dams.
- #14 Ovine white liver disease A specific hepatic dysfunction of sheep has been described in New Zealand, Australia, the UK, Norway, and in grazing lambs in the Netherlands. It has been called 'white liver disease‘ because of the grayish color of the liver. Clinically, it is manifested by photosensitization when the disease is acute, and anemia and emaciation when the disease is chronic. It seems likely that the disease is a toxic hepatopathy against which adequate levels of dietary cobalt are protective.
- #15 Hepatic lipidosis in goats Hepatic lipidosis has occurred in Omani goats in many parts of Oman for many years but the cause was unknown. It is now known that low levels of serum vitamin B12 or low levels cobalt in the liver are associated with the liver lesion, and it can be experimentally reproduced using low levels of cobalt intake. Abattoir surveys of goat livers found that hepatic lipidosis was one of the most frequent cause of their condemnation.18 Because the goat is the predominant domesticated animal type raised for meat in the Sultanate of Oman, the condemnation of goat livers at slaughter represents a significant economic loss.
- #16 Serum and hepatic cobalt and vitamin B12 concentrations Serum cobalt. Cobalt concentrations in the serum of normal sheep are of the order of 1-3 ug/dL (0.17-0.51 umoI/L), and in deficient animals these are reduced to 0.03-0.41 umol/L
- #17 Serum vitamin B12. Clinical signs of cobalt deficiency in sheep are associated with serum vitamin B12 levels of less than 0.20 mg/mL, and serum vitamin B12 1evels are used as a laboratory test of cobalt status in animals. Levels of 0.2-0.25 ug/L are indicative of cobalt deficiency. These rise rapidly to 0.5-1 .0 ug/L on treatment.
- #18 Hepatic cobalt. Normal hepatic cobalt levels in lambs range between 0.03 and 0.1 ug/g. Levels below 0.02 ug/g are associated with clinical cobalt deficiency, and 0.015 ug/g is considered as a critical level.
- #19 Serum methyl malonic acid Because of some of the difficulties with the interpretation of serum vitamin B12 levels, other biochemical tests, especially methylmalonic acid (MMA) in plasma and urine as diagnostic and prognostic indicators and formiminoglutamic acid (FIGLU) tests are now used. The determination of MMA has the potential to distinguish between subclinically and clinically affected animals, which serum vitamin B12 cannot do. Methylmalonic acid is ordinarily metabolized in ruminants by a vitamin B12 enzyme system. An elevated plasma concentration of MMA is a comparatively early indicator of functional vitamin B12 deficiency.
- #20 Cobalt and vitamin B12 Infected animals respond satisfactorily to oral dosing with cobalt or the IM injection of vitamin B12. Oral dosing with vitamin Bl2 is effective, but much larger doses are required. Oral dosing with cobalt sulfate is usually at the rate of about 1 mg cobalt/d in sheep and can be given in accumulated doses at the end of each week.
- #22 CONTROL Su pplement d iet with cobalt
- #25 The subcutaneous injection of a soluble vitamin Bl2 in lambs was effective in increasing and maintaining the vitamin Bl2 status for about 24 days. In cobalt deficient areas lambs should be given a 2 mg dose of vitamin B12 at least bimonthly to reduce the risk of vitamin B I2 deficiency.