Cobalt deficiency, Biology

Cobalt deficiency

The deficiency of cobalt is more commonly seen in ruminants fed on diets deficient in this essential micronutrient. Cobalt is stored only in limited amounts and needs to be supplied in diet continuously for synthesis of vitamin B12 in the rumen. Diet deficient in cobalt may reduce the vitamin B12 synthesis by over 90%. The deficiency is clinically characterized by loss of body weight, inappetance, pica and reduced production. Naturally occurring diseases such as ‘coast disease of sheep’ and ‘wasting disease’ or ‘marasmus of cattle’ in Australia have been reported to be associated with cobalt deficiency.

Aetiology: Ruminants essentially require cobalt in their diet at the concentrations ranging from 0.04 mg/kg DM to 0.10 mg/kg DM depending on the physiological needs. Primary cobalt deficiency occurs when cobalt content in soils is low, and the grasses grown over such soils contain markedly low cobalt concentration. Pastures containing less than 0.07 and 0.04 mg cobalt/kg DM may induce clinical disease in sheep and cattle, respectively. Rapidly growing grasses contain low level of cobalt and can predispose the deficiency.

Clinical findings: Cattle and sheep are affected alike and present similar clinical sings. Cobalt deficiency in ruminants impairs oxidation of propionate as lack of vitamin B12 inhibits conversion of methylmelonyl coenzyme- A to succinyl coenzyme- A, the intermediates in the pathway of propionic utilization. Despite provision of abundant green feed, animals on cobalt deficient diets exhibit gradual decline in appetite, loss of body weight, emaciation, and weakness. Cattle show signs of pica and reduced milk yield. The mucous membrane is pale. Wool production in sheep is retarded both quantitatively and qualitatively. Severe lachrymation, usually matting wool of face is an important sign of cobalt deficiency in sheep. Stillbirths, increased neonatal mortality and birth to weak lambs are other consequences of cobalt deficiency.

Diagnosis: Cobalt deficiency must be differentiated from Helminthoses, and  deficiencies of copper, selenium and vitamin D, which are also manifested by signs of ill- thrift. Clinico-pathological changes include normocytic-normochromic anaemia, significantly low concentration of vitamin B12  and cobalt in serum and liver, and elevated methylmalonic acid (MMA) in plasma and forminoglutamic acid (FIGLU) in urine. Low levels of serum Vitamin B12 (<0.2 mg/ml) and cobalt (0.03-0.41 µmol/ l) indicate cobalt deficiency. Estimation of MMA in plasma and urine is a good diagnostic and prognostic indicator. Measurement of FIGLU in urine is also useful.Commercial kits are available for these tests.

Treatment and Prevention: Oral dosing with cobalt and vitamin B12 or intramuscular administration of vitamin B12 are effective therapies. Accumulated weekly dose, calculated on the basis of 1 mg cobalt daily in copper sulphate, can be given to sheep. Monthly dose of 300 mg cobalt can prevent mortality in lambs. Vitamin B 12 can be given in 100-300 µg doses in lambs and sheep at weekly interval.

Supplementation of cobalt in diet @ 0.06-0.07 mg/kg dry matter can prevent cobalt deficiency in cattle and sheep. Top dressing of pastures using copper sulphate 400- 600 g/ha annually in cobalt deficient areas is recommended. Controlled cobalt releasing boluses, or cobalt-heavy pellets are available for oral administration in ruminants. These boluses are lodged in reticulum from where cobalt is slowly released. Addition of cobalt with anthelmintics is also an effective preventive measure.

Posted Date: 9/19/2012 2:13:46 AM | Location : United States

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