Cobalt deficiency is a disease in ruminants caused by a diet low in cobalt, essential for vitamin B12 synthesis, leading to clinical signs like inappetence, weight loss, and decreased reproductive performance. The condition is particularly prevalent in regions with cobalt-deficient soils, and its diagnosis involves measuring cobalt and vitamin B12 levels in serum. Treatment includes oral cobalt supplementation and vitamin B12 injections, as well as dietary management to prevent deficiencies in livestock.

1. COBALT DEFICIENCY
DR. MUHAMMAD RIZWAN
D.V.M, M.Phil, Ph.D (Medicine)
Lecturer, Department of Clinical Sciences,
BZU, Multan

2. Etiology
• Cobalt deficiency is 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, performance
reproductive

3. Epidemiology
 Probably occurs in many parts of the world:
deficiency is extreme
Australia, NZ, UK, N. America, Netherlands
 Large tracts of land unsuitable for:
raising of ruminants
 Incertain 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;
– be present continuously in the feed.

7. PATHOGENESIS
• Effect 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
• Essential 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
• 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
• 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
important sign in advanced cases
is the most
• Signs usually become apparent when;
– animals on affected areas for about 6 months
– death may 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. of 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 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
• 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 umol/L is normal
– 2-4 umol/L represents subclinical deficiency
– >4 umol/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 ug doses in lambs and
sheep
– at weekly intervals,

21. CONTROL
• Supplement diet with 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 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