Cobalt (Co) Deficiency
Cobalt (Co) deficiency is also known as ovine white liver disease in sheep, hepatic lipidosis in goat and in enzootic marasmus in cattle.
Cobalt plays a vital role in ruminants, because it’s needed for Vitamin B12 synthesis, RBCs production and maturation. Cobalt is stored in liver.
Etiology
Dietary deficiency (<0.007 ppm of Cobalt) cause cobalt (Co) deficiency. Susceptibility is as:
- Sheep more susceptible than cattle
- Lambs & calf more susceptible than adult
- Cattle grazing on granite field
- Grazing on fresh grass
- Cobalt deficient animal predispose to ketosis
Pathogenesis
Cobalt is unique essential trace element in the ruminant, because it store in the body in limited amount only and not in all tissue.
All the cattle require dietary Cobalt for the synthesis of Vit B12 in the rumen, which is necessary for:
- Energy metabolism as Vitamin B12 is required for the metabolism of propionic acid. This propionic acid is the major VFA for glucose precursor in the ruminants. Cobalt deficiency results inability to metabolize propionic acid which leads increased serum methylmalonic acid (MMA) and cause energy deficiency in the animal. Due to the poor performance of this metabolic pathway leads anorexia and ill-thrift.
- Methionine synthesis: It is the major amino acid involved in the growth and DNA synthesis.
Clinical signs
- No specific signs
- Gradual decreases in appetite
- Decreases in body weight
- Weakness, emaciation
- Pica
- Pale MM
- Easily broken wool
- Pregnant animal– still birth and increased neonatal mortality
Differential diagnosis
- Malnutrition
- Parasitism
- Copper/selenium deficiency
Diagnosis
(1) Estimation of Serum and liver cobalt and Vit B12 level
| (In Sheep) | Normal | Deficiency |
|---|---|---|
| Serum Cobalt | 1-3 µg/dl | 0.03 µg/dl |
| Serum Vitamin B12 | – | <0.20 µg/dl |
| Liver Cobalt | 0.03- 0.1 µg/dl | <0.02 µg/g |
(2) Estimation of Methylmalonic acid (MMA)
- Methylmalonic acid (MMA) is the precise indicator for Cobalt deficiency.
- Plasma and urine MMA is good indicator for Cobalt deficiency.
- Estimation of MMA level is potential to distinct between subclinical and clinical form of Cobalt deficiency (But estimation of Vit B12 cannot do).
- Elevation of MMA level can be used as early indicator for Vit B12deficiency.
(3) Estimation of Formiminoglutamic acid (FGA)
- Concentration of Formiminoglutamic acid in urine is a reliable indicator for Cobalt deficiency.
- Formiminoglutamic acid elevation noticed only in later stage of Cobalt deficiency.
- It cannot detect subclinical form of Cobalt deficiency.
- Presences of MMA and Formiminoglutamic acid in urine is positive indicator for Cobalt deficiency. Hence, further quantitative estimation of the MMA and FGA is not necessary.
(4) Hematology
- Anemia but Hemoglobin and RBCs level become normal due to hemoconcentration.
- Normocytic normochromic anemia.
- Decreased glucose and alkaline phosphates level.
(5) Post mortem
- Severe emaciation of the carcass.
- Sheep– white liver diseases- liver become pale and fatty.
- Spleen dark– due to accumulation of hemosiderin.
- High iron level in liver and spleen and low cobalt level.
Treatment
Administration of Cobalt (Cobalt sulfate) and Vitamin B12 is the treatment protocol for Cobalt (Co) deficiency.
- Sheep at 1 mg of Cobalt sulfate per day.
- Vit B12 at 100-300 µg per lamb IM (weekly interval).
- Oral Vitamin B12 is effective than parenteral administration, but it requires more dose and cost effective.
Prevention and Control
- Dietary supplement with cobalt.
- Top dressing of pasture with Cobalt sulfate at 400-600 g/ha annual.
- Cobalt pellet at 5g per sheep & 20g per cattle oral.
- Controlled release of glass bolus.
- Vitamin B12 injection weekly for 4-6 weeks.
