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| − | Also known as: '''''Fatty Liver Disease — Cobalt Deficiency'''''
| + | #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 ill-thrift, anorexia, emaciation, bilateral serous ocular discharge and pale mucous membranes.
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| − | The liver damage can lead to [[Photosensitisation|photosensitisation]] (scaly ears), [[diarrhoea]] and nervous signs ([[Hepatic Encephalopathy|hepatic encephalopathy]]).
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| − | ==Diagnosis==
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| − | Clinical signs are suggestive.
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| − | '''Clinical pathology''' may reveal mild normocytic, normochromic [[:Category:Anaemia|anaemia]], elevated liver enzymes (GGT, AST) and reduced serum levels of vitamin B12.
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| − | '''Liver analysis''' will show reduced levels of cobalt and vitamin B12. Grossly, the liver will be pale, fatty with a friable parenchyma. On histopathology, there will be hepatic lipidosis and bile duct proliferation.
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| − | Individual '''variation in serum vitamin B12 levels''' is high and a minimum of seven sheep from a flock should be sampled.
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| − | There is '''little variation in liver vitamin B12 concentrations''' and three 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 should be given.
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| − | Long-term prevention: '''pasture analysis''' and identification of cobalt deficient areas is important. If grazing such areas, '''cobalt supplementation''' via drenches, licks, pasture fertilization or cobalt bolus administration should be undertaken.
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| − | ==References==
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| − | D.G. Pugh (2002) '''Sheep and Goat Medicine,''''' Elsevier Health Sciences ''
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| − | J. Brugère-Picoux (2004) '''Maladies des moutons''' (2nd Edition),'' Editions France Agricole''
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| − | P.J. Mitchell et al (1982) '''White liver disease of sheep,''''' Australian Veterinary Journal'' 58, 181-4
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| − | S. Kennedy et al (1997) '''Histopathologic and ultrastructural alterations of white liver disease in sheep experimentally depleted of cobalt,''''' Veterinary Pathology ''34, 575-84
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| − | N. Sargison (2001) '''Cobalt deficiency in lambs,''''' NADIS disease bulletin''
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| − | {{review}}
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| − | [[Category:Liver_-_Degenerative_Pathology]]
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| − | [[Category:Liver Diseases - Sheep]]
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| − | [[Category:Expert Review - Farm Animal]]
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