Cobalt for Animals

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.

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. Traditionally, a breakdown in propionate metabolism at the point in the metabolic pathway where methymalony-CoA is converted to succinyl-CoA, was thought to be the reason for the depression in appetite. However, Kennedy (249) showed that there were massive increases in succinate concentrations in the rumen within two weeks of when sheep were fed a cobalt deficient diet. When sheep were fed a diet with only 0.02 ppm cobalt, succinate accumulation in the rumen began in two days (250). It has been well documented that changes in the rumen microbial population occurs in cobalt deficient ruminants. It now appears that a cobalt deficiency causes a vitamin B₁₂ deficiency which inhibits propionate producing bacteria such as Selenomonas ruminantium.

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 that were known as "healthy areas" (122). Animals in cobalt deficient areas, known as "sick areas" would respond when transferred to "healthy areas." In certain "sick areas" the lack of cobalt could be alleviated by periodic removal of the animals to "healthy areas" for varying periods. The discovery of cobalt as the cause of the problems in "sick 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 (93, 94, 96, 125, 126, 128, 135). 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 (86). Cobalt deficiency is most common in high rainfall areas where the soil is derived from acid igneous rocks such as granite and subject to leaching. Heavy liming of pastures has been associated with increased risk of cobalt deficiency (299).

With 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.

Table 26 provides information that indicates the cobalt status in ruminants as determined by vitamin B₁₂ levels in the liver.

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

Table 27 gives data on the requirements for cobalt by the various classes of animals. It also gives the maximum tolerable level of cobalt as established by the National Research Council. 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 (157). Excesses should be avoided, however.

Class of Animal	Cobalt Requirement in Total Diet (ppm)	Toxic Level in Total Diet (ppm)
Dairy Cattle	0.1	10
Beef Cattle	0.1 (0.07-0.11)	10
Sheep	0.1-0.2	10²
Goats	0.1-0.2	10³

¹Levels recommended based on the latest NRC publication on nutrient requirements of each animal.

Cobalt protects sheep and to a lesser extent cattle, from "Phalaris Staggers," or "Ronpha Staggers," which sometimes occur with the perennial grass Phalaris tuberosa or one of several other related grass species. The toxic principal may be an alkaloid. The detoxification role of cobalt is not related to its role in vitamin B₁₂.

Cobalt deficiency usually occurs after animals have been on a cobalt deficient diet for a considerable time and as vitamin B₁₂ stores in the liver and other tissues are depleted. Cobalt deficiency results in decreased appetite and feed consumption which leads to listlessness, retarded growth, weight loss, and decreased milk production. With an extreme cobalt deficiency, symptoms may include emaciation or wasting of the musculature, paleness of the skin and mucous membranes, muscular incoordination, a stumbling gait, rough hair coat, and high mortality rate among calves. Starvation associated with cobalt deficiency is caused, at least partially, by the animal’s inability to metabolize propionate. This inability results from a lack of vitamin B₁₂, which is needed for the body to utilize propionate. Propionate is a volatile fatty acid, a product of rumen fermentation and an important source of energy for the animal (156).

Generally, 10 ppm cobalt in the diet is accepted as the maximum safe level. However, there are studies indicating that 20 to 30 ppm does not produce adverse effects (91, 156).

The appearance of a cobalt deficient animal is similar to that of a starved one. An early symptom is loss of appetite, which is alleviated quickly following cobalt supplementation if the deficiency symptoms have not advanced too far and caused body organ damage. The decrease in feed consumption results in emaciation and wasting of the musculature. Paleness of the skin and mucous membranes results from the anemia that develops progressively with the severity of the cobalt deficiency (85, 157). Although infertility can always occur as a secondary consequence of poor body condition in cattle, recent research (251) suggests that cobalt deficiency can cause infertility when cows are in good condition.

Cobalt deficiency causes lack of appetite, lack of thrift, severe emaciation, weakness, anemia, decreased fertility, and decreased milk and wool production (155). Weeping eyes, leading to a matting of wool on the face, is another common symptom (299). Sheep are more susceptible to cobalt deficiency than cattle and the accumulation of fat in the liver of B₁₂ deficient sheep, but not cattle, may be related to a methyl-group deficiency affecting liver lipid metabolism (252). Another metabolic anomaly of cobalt deficient lambs is the accumulation of homocysteine in the plasma which leads to an accumulation of oxidation products, depletion of vitamin E, and damage to the mitochondria (249).

Cobalt deficiency symptoms include a loss of appetite, emaciation, weakness, anemia, and decreased production. The 1981 NRC committee on Nutrient Requirements of Goats assumes that a level of 0.1 ppm cobalt in the diet is adequate for goats since it is adequate for sheep (100).

Cobalt deficiency has not been demonstrated in non-ruminant animals. In a few instances where cobalt has created some response, it is assumed that the diet lacked vitamin B12. It should be indicated, however, that non-ruminants also synthesize a limited amount of vitamin B₁₂ in their digestive tract. How much is absorbed is not known, but vitamin B₁₂ would be available in the feces for animals that practice coprophagy. Horses have thrived on pastures so low in cobalt that cattle and sheep confined to them soon waste and die. The utilization of cobalt by the microbial flora in the rabbit is much more efficient than in ruminants. The absorption of vitamin B₁₂ by rabbits is very efficient (88). There is some evidence that cobalt may have a sparing action on zinc in zinc deficiency in pigs (92).

If the diet of non-ruminants is adequate in vitamin B₁₂, there is no evidence to indicate a need for cobalt. It is possible, however, that if dietary vitamin B₁₂ is limiting, a need for cobalt for intestinal synthesis of B₁₂ will be of some importance with non-ruminant animals. All-plant diets contain little or no vitamin B₁₂. Therefore, non-ruminant animals consuming all-plant diets would need some dietary cobalt in order to enable their microflora to synthesize vitamin B₁₂. This fact causes many producers of non-ruminants to supplement diets with 0.1 ppm cobalt just in case the diet might not supply all the vitamin B₁₂ required (87, 92, 93, 95, 141). Therefore, in practice, trace mineralized salt that provides cobalt, which is needed by ruminants, is also used for non-ruminant animals. This eliminates the need for manufacturing a separate trace mineralized salt for non-ruminants that does not contain cobalt. Moreover, the presence of cobalt provides some insurance in case the non-ruminant diet is lacking sufficient vitamin B₁₂.