COBALT FOR ANIMALS

GOPI.M M.V.Sc., Scholar, Dept. Of Animal Nutrition.

Introduction
Exists in nature mainly combined with Arsenic & Sulfur. Present in both plants and animals. Legumes contain more Co than cereals. Rich in meat & bone meal.

 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.

 In plants-accumulation of tetrapyrrole (corrinoids) in leaves.

Bio chemical function

It increases the N2 fixation.

In animals-combined with VitB12 & free ions Co ions take part in hemopoiesis. Vit B12 has many function.

Vitamin B12
1. In hemopoiesis-protoporphyrin synthesis. 2. As co-enzyme in Methionine synthesis. 3. Oxygen transfer in enzyme system. 4. Ruminants- mutase enzyme-metabolism of propionic acids. 5. In sheep- CoCl2.-increases the bile secretion. 6. Cobalamine- Adenosylcobalamine & Methylcobaline.

 Animals body-cow-30-60mcg/kg LBW. Blood 3-8mcg% Newborn piglet-150mcg. Chick-1.5-2mcg. Among body organs-liver contain-30100mcg/kg LBW.

Body content

Among total liver content-half of Co combined with Vit B12. If deficiencies-Co found in the form of Vit B12.

Digestion
Co present in the diet in the form of VitB12 & Protein complex.

Digestion Rumen & LI.

Analogues is inactive & not absorbed. Rumen fluid-40ng/ml of Co.(25lit-1mg).

Normally 3%of Co-Vit B12.

In deficient state-13% of Co is converted into Vit B12.

Absorption
Absorption is based on animals need. SI-by Castles intrinsic factor-gastro mucoprotein. Rumen-0.5-5%. SI = 3-20% (Poultry -3-7%, Pig: 5-10%, Horse : 15-20%). Blood has no Co .only in VitB12 form.

Excretion
Based on mode of entrance. Oral-more via feces. Parental route-urine.

In monogastric animals -mostly via urine.

Excretion
ruminants

lactating

non-lactating

feces 86-87%

milk urine feces 11.5-12.5 0.9-1.0% 98-98.5%

urine 1.5-2%

Requirement
Requirement of Co is fact requirement of Rumen MO. Animal feed contain adequate level of Vit B12,no need of Co supplements. Requirement for ruminants is more 1.propionic acid metabolism. 2.Less production by MO. 3.Less absorption.(1-3%)

Requirement
(Georgievskii) Beef cattle-0.10ppm. Dairy cattle-0.10ppm. Sheep-0.10-0.2ppm. Monogastric animals-3-50mcg/kg BW (NRC) ANIMALS CO-mg/KG DM Cattle Sheep Lamb 0.11 0.05-0.06 0.11

Cobalt deficiency
Decreased appetite and feed consumption
Listlessness, retarded growth, weight loss, and decreased milk production. Propionate is a volatile fatty acid, a product of rumen fermentation and an important source of energy for the animal

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

 Anemia 1.Enzootic marasumus 2.Salt disease. 3.Brush disease. 4.Tabes. Bush sickness New Zealand Pining Europe Salt sick - Australia Wasting disease - USA Microcytic hyperchromic anemia. Rough hair coat. Fatty liver condition. In lambs-most susceptible WLD-white liver disease. In sheep-matting of wool - Weight loss.

Deficiencies

 In monogastric animals-Megaloblastic anemia(Pernicious anemia). In chicken-reduced hatchability.

In ruminants-loss of appetite-increase the propionic acid level due to lack of Mutase enzyme. Liver-0.1mcg/gm wet weight of Vit B12-Co deficiency. Cattle urine-methylmelonyl acid-VitB12 defici.

Deficiencies

Sheep:
Sheep are more susceptible to cobalt deficiency than cattle

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

Toxicity
Not likely to occur. Experimentally it produce 1.polycythemia. 2.inappetite

3.Polyuria
4.Lacrimation.

Threshold level
Cow-1.0mg/kg LBW/day. Calf-0.50mg/kg LBW/day. Sheep-2.3mg/kg LBW/day. Chick-3-3.50mg/kg LBW/day.

Treatment
Sheep-2mg biweekly. -7mg/week.

Inj.VitB12-100micgm/week -I/m
Bullet-Co oxide +Fe-in reticulum for slow releasing.

FEED
Grass Hay Soya Sunflower cake Wheat bran Rice bran Molasses

CO-mg/KG DM
0.04 0.12 0.16 0.20 0.8 0.5 1.21

FEED Alfalfa meal Soya Meat meal Fish meal Feather meal

VIT B12-mcg/KG 11.0 1.1 70 185 66

Treatment of cobalt deficiency Immediate treatment for animals

Vitamin B12 injections immediate treatment of deficient animals showing clinical signs of malnutrition.

Injections of 2 mg to lambs and sheep and 4 mg to calves provide adequate vitamin B12 for three months.
Cobalt pellets may also be used for immediate treatment of deficiency and last 12 months.

Long-term treatment and prevention

Cobalt supplementsdrenches, licks, foliar sprays and fertiliser top-dressing, as well as pellets and vitamin B12 injections.

Salt licks or mineral mixes containing cobalt should provide a minimum of 0.05 mg cobalt (equivalent to 0.24 mg cobalt sulphate) per sheep per day.

 Cobalt pellets introduced orally are the most efficient prevention because they continually release trace amounts of the element directly into the rumen and should last the lifetime of the animal.

Thank YOU