The only known animal requirement for cobalt is as a constituent of Vitamin B12, which has 4% cobalt in its chemical structure. This means that a cobalt deficiency is really a vitamin B12 deficiency. Reduced liver stores of cobalt are considered indicative of a dietary cobalt deficiency in ruminants (McDowell, 1992) and its measurement is generally considered sufficiently responsive to changes in cobalt intake to be of diagnostic value in cobalt deficiency (Smith, 1987). 

Microorganisms in the rumen are able to synthesize vitamin B12 needs of ruminants if the diet is adequate in cobalt. Normally, cobalt is not stored in the body in significant quantities. The small amount that is stored does not easily pass back into the rumen or intestinal tract where it can be used for vitamin B12 syntheses. Therefore, ruminants must consume cobalt frequently in the diet for adequate B12 synthesis. Injected cobalt is ineffective.

The fact that injected cobalt is ineffective agrees with recent research which suggests that cobalt deficiency in the rumen may be more important then a vitamin B12 deficiency at the tissue level. 

 

Liver B12 As Cobalt Status Indicator

B12 in Fresh Liver (ppm)	Cobalt Status of Animal
Less than 0.07	Severe cobalt deficiency
0.07-0.11	Moderate cobalt deficiency
0.11-0.19	Mild cobalt deficiency
0.19 or more	Sufficiency

                                      W.J. Miller, University of Georgia (1991) ~

Cobalt Requirement and Toxic Levels

Cobalt Requirement in Total Diet (ppm)	Toxic Level in Total Diet (ppm)
0.1-0.2 This level is not known so the level used for sheep is presented	10 This level is not known so the level used for sheep is presented

                                       Levels recommended based on the latest NRC publication on nutrient requirements ~ Cobalt was first shown to be of value to ruminants in 1935. Prior to that time, ruminants could not be successfully produced in many areas of the world because of severe cobalt deficiencies. In these locations, including Florida, cattle were limited to certain areas. Animals in cobalt deficient areas, would respond when transferred to area with adequate cobalt. The discovery of cobalt as the cause of the problems in these areas  was of tremendous value in increasing ruminant productivity throughout the world. Even today, new cobalt deficient areas are being found as livestock production increases in newly developed areas, and as research efforts are increased to determine mineral needs of animals. The University of Florida scientists reported in 1976 that 43% of the 140 forage samples taken throughout Latin America had cobalt levels of 0.1 ppm or less.

Given the current knowledge, the most convincing evidence of a cobalt deficiency is determined by the response of the animal to cobalt feeding. The response is quick, with appetite increasing in about a week, and weight gains quickly follow. The remission of the anemia, however, occurs more slowly.

Cobalt has a relatively low order of toxicity in all animals. Cobalt toxicity in ruminants is rare because toxic levels are about 300 times requirement levels. Excesses should be avoided, however.

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• Starvation has been shown to falsely elevate the levels of vitamin B12 in the liver and kidneys.

• Cobalt has also been shown to be associated with impaired immune function in other species of ruminants, resulting in increased susceptibility to infection and reduced viability of newborn animals (MacPherson et al., 1987; Ferguson et al., 1989; Paterson and MacPherson, 1990; Fisher, 1991; Vellema et al., 1996).