Cobalt Deficiency - Sheep

Also Known As – Cobalamin Deficiency — Vitamin B12 Deficiency — Secondary Vitamin B12 Deficiency — Ill Thrift — Cobalt deficiency anaemia — Wasting Disease — Coastal Disease — Ovine White Liver Disease — Fatty Liver Disease

Introduction

Cobalt is required by the ruminant for the synthesis of Vitamin B12 – Cobalamin – by the rumenal microflora. Thus a diet deficient in cobalt causes a secondary deficiency in B12 which is required for the metabolism of propionic acid by the liver for energy production via the enzyme Methylmalonyl CoA mutase. Poor utilisation of propionate then leads to reduced appetite and subsequent "ill thrift" - the generic condition in which production and growth are impaired in affected animals. B12 is also used for the metabolism of some sulphur containing amino acids which are then used for wool growth. Thus, cobalt deficient animals often also have poor fleece quality. B12 also has roles in the production of new erythrocytes.

The concentration of cobalt in crops and forages is highly variable and depends on a variety of factors including soil concentration, plant species rate of growth, soil pH and drainage. Soils are generally considered deficient in cobalt if they contain less than 2 parts per million.

Distribution

Cobalt deficient soils are widely distributed across the globe and thus the condition affects sheep internationally, including the UK, Australia, New Zealand and North America. Incidence is higher in coastal areas hence its common name, "Coastal disease".

Signalment

Sheep are most susceptible to cobalt/cobalamin deficiency but cattle, goats and deer can also be affected. This may be partly due to their use of it in optimal wool growth.

Growing lambs are most likely to be clinically affected as their requirements are highest. Pre-ruminant animals have a low requirement for cobalt due to their reliance on glucose as an energy source (rather than propionate) and thus the condition is rarely seen in those younger than 5 weeks. B12 is also present in large amounts in colostrum but far less in milk.

Clinical Signs

Retarded growth, muscular weakness, anaemia, ketosis, poor fleece and poor body condition score are the non-specific hallmarks of the deficiency, usually seen in lambs. A mild conjunctivitis is also common. Anaemia develops and may be clinical in severe cases.

Deficiency in pregnant sheep has been associated with poor milk production and high lamb mortality.

There is also a syndrome known as Ovine White Liver Disease which causes fatty liver degeneration which then leads to subsequent liver failure, hepatic encephalopathy and photosensitisation. This is caused by the accumulation of methylmalonic acid in the absence of adequate cobalt, which is then converted into branch chain fatty acids.

Diagnosis

As many cases are multi-factorial and "ill thrift" is very non-specific in its presentation, diagnosis is difficult. History or identification of low soil cobalt content of poor clover growth may raise suspicion or predict the onset of an outbreak.

Cobalt and Vitamin B12 can both be measured in serum but this is not without difficulty. Because of this, other tests such as methylmalonic acid (MMA) in plasma and urine and formimoglutamic acid (FIGLU) were developed and are now often used. Fresh or formalin fixed liver and serum can also be sent for toxicological analysis of cobalt concentrations.

Affected animals are often anaemic but this may not be evident due to the effects of haemoconcentration on haematology values. Liver enzymes (GGT and AST) are also often raised.

Signs of fatty liver degeneration on pathological examination and histopathology may support clinical signs but this is also non-specific and has many other pathogeneses. Carcasses are generally emaciated and the spleen is often dark due to haemosiderin accumulation.

Diagnosis can also be made, perhaps most accurately, by response to treatment, ideally as a controlled trial with an unsupplemented group from the same population as a comparison, but this is often not practical.

Treatment

Cobalt can be supplemented by spraying pastures and/or top dressing with cobalt salts. This can be performed prior to the turn-out of sheep and lambs.

Vitamin B12 can also be given as individual injections.

Intra-rumenal boluses releasing cobalt or a mixture of trace elements steadily for over one year are also available as a longterm solution for both treatment and prevention. These should obviously be delivered with care and precision to avoid trauma.

Control

Monitoring/testing and management of soil and forage cobalt content is the foundation for prevention of deficiency with appropriate supplementation measures implemented both in the short and longterm if pasture cannot be manipulated.

Cobalt Deficiency - Sheep Learning Resources
Flashcards Test your knowledge using flashcard type questions	Cobalt Deficiency Flashcards Sheep Medicine Q&A 04

References

Pugh, D. G (2002) Sheep and Goat Medicine, Elsevier Health Sciences

Brugère-Picoux, J (2004) Maladies des moutons (2nd Ed), Editions France Agricole

Merck Veterinary Manual, Beef Cattle:Nutritional Requirements, accessed online 24/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/182303.htm&word=cobalt

Mitchell, P. J., McOrist, S., Thomas, K. W., McCausland, I. P (1982) White liver disease of sheep, Australian Veterinary Journal 58, 181-4

Kennedy, S., McConnall, S., Anderson, H., Kennedy, D. G., Young, P. B., Branchflower, W. J (1997) Histopathologic and ultrastructural alterations of white liver disease in sheep experimentally depleted of cobalt, Veterinary Pathology 34, 575-84

Sargison, N (2001) Cobalt deficiency in lambs. NADIS disease bulletin

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