White Liver Disease - Sheep - Revision history

Bara: Redirected page to Cobalt Deficiency - Sheep

2011-07-25T14:58:22Z

Redirected page to Cobalt Deficiency - Sheep

Lwyasm1: Replaced content with "Category:Delete"

2011-07-25T14:52:37Z

Replaced content with "Category:Delete"

Bara at 12:54, 5 July 2011

2011-07-05T12:54:23Z

HelenD at 08:15, 4 July 2011

2011-07-04T08:15:56Z

Bara at 11:39, 13 May 2011

2011-05-13T11:39:12Z

Bara at 19:46, 20 January 2011

2011-01-20T19:46:22Z

Bara at 19:46, 20 January 2011

2011-01-20T19:46:08Z

Bara: moved White Liver Disease - Ovine to White Liver Disease - Sheep

2010-07-26T22:28:08Z

moved White Liver Disease - Ovine to White Liver Disease - Sheep

Bara: moved Ovine White Liver Disease to White Liver Disease - Ovine

2010-06-28T20:40:24Z

moved Ovine White Liver Disease to White Liver Disease - Ovine

Bara at 20:40, 28 June 2010

2010-06-28T20:40:08Z

← Older revision		Revision as of 14:58, 25 July 2011
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−	[[~~Category:Delete~~]]	+	#redirect[[Cobalt Deficiency - Sheep]]

← Older revision		Revision as of 14:52, 25 July 2011
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−	~~Also known as: '''''Fatty Liver Disease — Cobalt Deficiency'''''~~	+	[[Category:Delete]]
−
−	~~==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 [[Erythropoiesis#Nutritional factors\|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\|photosensitisation]] (scaly ears), [[diarrhoea]] and nervous signs ([[Hepatic Encephalopathy\|hepatic encephalopathy]]).~~
−
−	~~==Diagnosis==~~
−
−	~~Clinical signs are suggestive.~~
−
−	~~'''Clinical pathology''' may reveal mild normocytic, normochromic [[:Category:Anaemia\|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''~~
−
−
−	~~{{review}}~~
−	~~[[Category:Liver_-_Degenerative_Pathology]]~~
−	~~[[Category:Liver Diseases - Sheep]]~~
−	[[Category:~~Expert Review - Farm Animal~~]]

@@ Line 1: / Line 1: @@
 ==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'''.
 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]].
-==Clinical signs==
+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'''.
-Disease is most commonly seen in weaned lambs at pasture in late summer/autumn.
+==Clinical Signs==
-Cobalt deficiency presents as:
-*ill-thrift
+Disease is most commonly seen in '''weaned lambs at pasture''' in '''late summer/autumn'''.
-*anorexia
+Cobalt deficiency presents as ill-thrift, anorexia, emaciation, bilateral serous ocular discharge and pale mucous membranes.
-*emaciation
-*bilateral serous ocular discharge
+The liver damage can lead to [[Photosensitisation|photosensitisation]] (scaly ears), [[diarrhoea]] and nervous signs ([[Hepatic Encephalopathy|hepatic encephalopathy]]).
 ==Diagnosis==
 Clinical signs are suggestive.
-==Treatment and prevention==
+'''Clinical pathology''' may reveal mild normocytic, normochromic [[:Category:Anaemia|anaemia]], elevated liver enzymes (GGT, AST) and reduced serum levels of vitamin B12.
-Immediate treatment: vitamin B12 injection or oral cobalt supplementation <br>
+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 <br>
+D.G. Pugh (2002) '''Sheep and Goat Medicine,''''' Elsevier Health Sciences ''
-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>
+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 <br>
-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
 [[Category:Liver_-_Degenerative_Pathology]]
 [[Category:Liver Diseases - Sheep]]

@@ Line 1: / Line 1: @@
-*Australia and Europe
+==Introduction==
-*young lambs on lush pasture
-*clinical signs
+White liver disease in sheep is a form of fatty liver disease associated with cobalt deficiency.
-**ill thrift
+Disease occurs in areas of low soil cobalt which can be found in parts of the UK and Australia.
-**anorexia
+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]].
-**jaundice
+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.
-**photosensitisation
+Propionate is the major source of glucose in ruminants and thus glucose deficiency and starvation occur.
-*treatment
-**responsive to Vitamin B12 and cobalt
+==Clinical signs==
 [[Category:Liver_-_Degenerative_Pathology]]
 [[Category:To_Do_-_Alimentary]][[Category:To Do - Medium]]
 [[Category:Liver Diseases - Sheep]]

@@ Line 10: / Line 10: @@
 [[Category:Liver_-_Degenerative_Pathology]]
-[[Category:To_Do_-_Clinical]]
+[[Category:To_Do_-_Alimentary]][[Category:To Do - Medium]]
 [[Category:Liver Diseases - Sheep]]

← Older revision		Revision as of 19:46, 20 January 2011
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	[[Category:Liver_-_Degenerative_Pathology]][[Category:Sheep]]		[[Category:Liver_-_Degenerative_Pathology]][[Category:Sheep]]
	[[Category:To_Do_-_Clinical]]		[[Category:To_Do_-_Clinical]]
		+	[[Category:Liver Diseases - Sheep]]

← Older revision	Revision as of 22:28, 26 July 2010
(No difference)

← Older revision	Revision as of 20:40, 28 June 2010
(No difference)

← Older revision		Revision as of 20:40, 28 June 2010
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	[[Category:Liver_-_Degenerative_Pathology]][[Category:Sheep]]		[[Category:Liver_-_Degenerative_Pathology]][[Category:Sheep]]
		+	[[Category:To_Do_-_Clinical]]