Difference between revisions of "White Liver Disease - Sheep"

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#redirect[[Cobalt Deficiency - Sheep]]
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==Introduction==
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White liver disease in sheep is a form of fatty liver disease associated with cobalt deficiency.
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Disease occurs in areas of low soil cobalt which can be found in parts of the UK and Australia.
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Cobalt is used by the rumen microflora to synthesise vitamin B12 (cobalamin). Cobalamin is a co-enzyme for methylmalonyl CoA mutase, an enzyme involved in the pathway through which propionate is metabolised into glucose. Vitamin B12 is also important in the [[Erythropoiesis#Nutritional factors|formation of new erythrocytes]].
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Cobalt deficiency leads to the accumulation of methylmalonyl CoA, or methylmalonic acid, which is converted to branched chain fatty acids that accumulate in the liver and cause damage.
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Propionate is the major source of glucose in ruminants and thus glucose deficiency and starvation occur.
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==Clinical signs==
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Disease is most commonly seen in weaned lambs at pasture in late summer/autumn.
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Cobalt deficiency presents as:
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*ill-thrift
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*anorexia
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*emaciation
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*bilateral serous ocular discharge
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*pale mucous membranes
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The liver damage can lead to:
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*[[Photosensitisation|photosensitisation]] (scaly ears)
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*diarrhoea
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*nervous signs ([[Hepatic Encephalopathy]])
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==Diagnosis==
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Clinical signs are suggestive.
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Clinical pathology may reveal:
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*mild normocytic, normochromic anaemia
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*elevated liver enzymes (GGT, AST)
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*reduced serum levels of vitamin B12
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Liver analysis:
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*reduced levels of cobalt and vitamin B12
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*Grossly: pale, fatty and friable parenchyma
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*Histopathology: Hepatic lipidosis, bile duct proliferation
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Flock levels:
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*Individual variation in serum vitamin B12 levels is high and a minimum of 7 sheep should be sampled.
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*There is little variation in liver vitamin B12 concentrations and 3 samples collected from casualty or slaughterhouse animals can be used to monitor the flock cobalt status.
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==Treatment and prevention==
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Immediate treatment: vitamin B12 injection or oral cobalt supplementation <br>
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Long-term prevention: Pasture analysis and identification of cobalt deficient areas.
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Cobalt supplementation via drenches, licks, pasture fertilization, cobalt bolus administration.
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==References==
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D.G. Pugh (2002) Sheep and Goat Medicine, Elsevier Health Sciences <br>
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J. Brugère-Picoux (2004) Maladies des moutons (2nd Edition), Editions France Agricole <br>
 +
P.J. Mitchell et al (1982) White liver disease of sheep, Australian Veterinary Journal 58, 181-4 <br>
 +
S. Kennedy et al (1997) Histopathologic and ultrastructural alterations of white liver disease in sheep experimentally depleted of cobalt, Veterinary Pathology 34, 575-84 <br>
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N. Sargison (2001) Cobalt deficiency in lambs, NADIS disease bulletin
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[[Category:Liver_-_Degenerative_Pathology]]
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[[Category:To_Do_-_Alimentary]][[Category:To Do - Medium]]
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[[Category:Liver Diseases - Sheep]]

Revision as of 08:15, 4 July 2011

Introduction

White liver disease in sheep is a form of fatty liver disease associated with cobalt deficiency. Disease occurs in areas of low soil cobalt which can be found in parts of the UK and Australia. Cobalt is used by the rumen microflora to synthesise vitamin B12 (cobalamin). Cobalamin is a co-enzyme for methylmalonyl CoA mutase, an enzyme involved in the pathway through which propionate is metabolised into glucose. Vitamin B12 is also important in the formation of new erythrocytes. Cobalt deficiency leads to the accumulation of methylmalonyl CoA, or methylmalonic acid, which is converted to branched chain fatty acids that accumulate in the liver and cause damage. Propionate is the major source of glucose in ruminants and thus glucose deficiency and starvation occur.

Clinical signs

Disease is most commonly seen in weaned lambs at pasture in late summer/autumn. Cobalt deficiency presents as:

  • ill-thrift
  • anorexia
  • emaciation
  • bilateral serous ocular discharge
  • pale mucous membranes

The liver damage can lead to:

Diagnosis

Clinical signs are suggestive. Clinical pathology may reveal:

  • mild normocytic, normochromic anaemia
  • elevated liver enzymes (GGT, AST)
  • reduced serum levels of vitamin B12

Liver analysis:

  • reduced levels of cobalt and vitamin B12
  • Grossly: pale, fatty and friable parenchyma
  • Histopathology: Hepatic lipidosis, bile duct proliferation

Flock levels:

  • Individual variation in serum vitamin B12 levels is high and a minimum of 7 sheep should be sampled.
  • There is little variation in liver vitamin B12 concentrations and 3 samples collected from casualty or slaughterhouse animals can be used to monitor the flock cobalt status.

Treatment and prevention

Immediate treatment: vitamin B12 injection or oral cobalt supplementation
Long-term prevention: Pasture analysis and identification of cobalt deficient areas. Cobalt supplementation via drenches, licks, pasture fertilization, cobalt bolus administration.

References

D.G. Pugh (2002) Sheep and Goat Medicine, Elsevier Health Sciences
J. Brugère-Picoux (2004) Maladies des moutons (2nd Edition), Editions France Agricole
P.J. Mitchell et al (1982) White liver disease of sheep, Australian Veterinary Journal 58, 181-4
S. Kennedy et al (1997) Histopathologic and ultrastructural alterations of white liver disease in sheep experimentally depleted of cobalt, Veterinary Pathology 34, 575-84
N. Sargison (2001) Cobalt deficiency in lambs, NADIS disease bulletin