Cobalt deficiency in Animals

Cobalt deficiency is a disease of ruminants caused by:
ingesting a diet deficient in cobalt equired for the synthesis of vitamin B12. aracterized clinically:
In appetence, loss of body weight reproductive performance

1. Cobalt Deficiency Dr. Muhammad Avais Associate Professor Department of Clinical Medicine and Surgery University of Veterinary and Animal Sciences, Lahore, Pakistan

2. Etiology Cobalt deficiency is a disease of ruminants caused by: ingesting a diet deficient in cobalt required for the synthesis of vitamin B12 C haracterized clinically: Inappetence , loss of body weight reproductive performance

3. Epidemiology Probably occurs in 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 and environmental 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 cobalt deficiency occurs only on soils which are deficient in cobalt

6. PATHOGENESIS Cobalt is unique 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; b e present continuously in the feed.

7. PATHOGENESIS E ffect of cobalt 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 E ssential defect in cobalt deficiency in ruminants; an inability to metabolize propionic acid

9. PATHOGENESIS A key biochemical pathway for propionic acid from rumen fermentation involves adenosyl cobalamin ; cobalt-containing coenzymes of vitamin B12 complex R equired 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 No specific 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 In sheep, 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 Cobalt deficiency in pregnant ewes; decreased lambing percentage, increased stillbirths, increased neonatal mortality Lambs from deficient ewes are ; slower to start sucking , reduced conc. o f serum colostral immunoglobulins lower serum vitamin B12 Higher methylmalonic acid conc.

13. Ovine white liver disease 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 in goats 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 hepatic cobalt 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 u mol /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 Normal hepatic 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 u mol /L is normal 2-4 u mol /L represents subclinical deficiency >4 u mol /L represents deficiency

19. Treatment Cobalt and vitamin B12 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 B12 should be given in: 100-300 u g doses in lambs and sheep at weekly intervals,

21. CONTROL Supplement diet with cobalt I n cattle, the recommended levels of dietary cobalt to achieve maximum vitamin Bl2 levels are 250 u g/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 release glass 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 B12 injections 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