Difference between revisions of "White Liver Disease - Sheep"
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+ | Also known as: '''''Fatty Liver Disease — Cobalt Deficiency''''' | ||
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==Introduction== | ==Introduction== | ||
− | White liver disease in sheep is a form of fatty liver disease associated with cobalt deficiency. | + | 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. | 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 [[Erythropoiesis#Nutritional factors|formation of new erythrocytes]]. | 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. | ||
− | Disease is most commonly seen in weaned lambs at pasture in late summer/autumn. | + | ==Clinical Signs== |
− | Cobalt deficiency presents as | + | |
− | + | 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 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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− | The liver damage can lead to | ||
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==Diagnosis== | ==Diagnosis== | ||
Clinical signs are suggestive. | Clinical signs are suggestive. | ||
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− | ==Treatment and | + | '''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. | ||
− | + | 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. | |
− | Long-term prevention: | ||
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==References== | ==References== | ||
− | D.G. Pugh (2002) Sheep and Goat Medicine, Elsevier Health Sciences | + | 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 | + | J. Brugère-Picoux (2004) '''Maladies des moutons''' (2nd Edition),'' Editions France Agricole'' |
− | 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 | + | 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 | ||
+ | |||
+ | N. Sargison (2001) '''Cobalt deficiency in lambs,''''' NADIS disease bulletin'' | ||
+ | {{review}} | ||
[[Category:Liver_-_Degenerative_Pathology]] | [[Category:Liver_-_Degenerative_Pathology]] | ||
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[[Category:Liver Diseases - Sheep]] | [[Category:Liver Diseases - Sheep]] | ||
+ | [[Category:Expert Review - Farm Animal]] |
Revision as of 12:54, 5 July 2011
Also known as: Fatty Liver Disease — Cobalt Deficiency
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 and pale mucous membranes.
The liver damage can lead to photosensitisation (scaly ears), diarrhoea and nervous signs (hepatic encephalopathy).
Diagnosis
Clinical signs are suggestive.
Clinical pathology may reveal mild normocytic, normochromic anaemia, elevated liver enzymes (GGT, AST) and reduced serum levels of vitamin B12.
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.
Individual variation in serum vitamin B12 levels is high and a minimum of seven sheep from a flock should be sampled.
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.
Treatment and Prevention
Immediate treatment: vitamin B12 injection or oral cobalt supplementation should be given.
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.
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
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