This article was downloaded by: [Chulalongkorn University] On: 31 December 2014, At: 21:28 Publisher: Taylor & Francis Informa Ltd Registered in England and Wales Registered Number: 1072954 Registered office: Mortimer House, 37-41 Mortimer Street, London W1T 3JH, UK
New Zealand Veterinary Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/tnzv20
Hepatic encephalopathy associated with chronic facial eczema a
a
K.G. Thompson , D.E. Lake & D.O. Cordes a
b
Ruakura Animal Health Laboratory , Private Bag, Hamilton, New Zealand
b
Department of Pathology , Ontario Veterinary College , Guelph, Ontario, Canada , N1G 2W1 Published online: 23 Feb 2011.
To cite this article: K.G. Thompson , D.E. Lake & D.O. Cordes (1979) Hepatic encephalopathy associated with chronic facial eczema, New Zealand Veterinary Journal, 27:10, 221-223, DOI: 10.1080/00480169.1979.34654 To link to this article: http://dx.doi.org/10.1080/00480169.1979.34654
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
221
NEW ZEALAND VETERINARY JOURNAL
1979
CLINICAL COMMUNICATION Hepatic encephalopathy associated with chronic facial eczema K. G. Thompson*, D. E. Lake* and D. O. Cordes*t N.Z. vel.J.2?: 22 J-23
ABSTRACT
CLINICAL HISTORY
Two cows and a ram with severe chronic facial eczema showed nervous signs and histological changes characteristic of hepatic encephalopathy. Clinical signs included dullness and depression, progressing to lateral recumbency with tremor of limbs. Histologically, there was widespread spongy vacuolation of the brain. Hepatic encephalopathy associated with chronic facial eczema may be more common than is currently recognised in sheep and cattle in the North Island of New Zealand.
Case I: In May 1971, a 4-year-old cow was submitted to this laboratory after showing dullness and depression for several weeks. Although still standing, the cow seemed unaware of its surroundings and showed automaton-like movements. Haematology revealed no abnormalities, and neither serum glutamic-oxaloacetic-transminase activity nor bilirubin concentration were elevated. Tests for blood and urinary ketones were negative and the blood glucose concentration was slightly elevated (4.2omo t/1). Case 2: Several heifers in a mob of36 showed photosensitivity and diarrhoea during March 1974. In June of that year, one heifer in poor condition became ataxic, blind and depressed. A urinary ketone test was negative and there was no response to intravenous administration of calcium, magnesium and dextrose. Over a period of 5 days the clinical signs progressed to. recumbency , with paddling oflimbs, and coma. Case 3: In March 1976, 4-year-old ram was submitted to the laboratory in lateral recumbency with a protruding tongue and tremor of all four limbs. These signs were reported to be sudden in onset. All animals were destroyed and examined immediately post mortem.
Downloaded by [Chulalongkorn University] at 21:28 31 December 2014
INTRODUCTION
Clinical signs suggesting disease of the central nervous system (CNS) are not always related to primary lesions in that system. For example, chronic liver disease, terminal renal failure, cardiovascular disorders, musculoskeletal disorders and metabolic imbalances can mimic disease of the CNS. Hepatic encephalopathy has been reported in sheep, cattle, pigs and horses following the ingestion of plants containing hepatotoxic pyrrolizidine alkaloids(8) (II) (13) (19). Other forms of liver damage which have been associated with secondary CNS lesions include chronic copper poisoning(l7)(23), fascioliasis(13), aflatoxicosis(22), metastatic neoplasia(28) and liver necrosis due to anaemia and congestive heart faiIure(ll). Anomalies of the portocaval system have also produced the syndrome in dogs(28) (29). Hepatic encephalopathy is characterised clinically by anorexia, dullness and depression, progressing to terminal recumbency with muscular tremor and involuntary paddling of limbs. Other nervous signs may include ataxia, aggression, convulsions, blindness, headpressing and opisthotonus. Microscopically, there is widespread spongy vacuolation of the CNS
New Zealand Veterinary Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/tnzv20
Hepatic encephalopathy associated with chronic facial eczema a
a
K.G. Thompson , D.E. Lake & D.O. Cordes a
b
Ruakura Animal Health Laboratory , Private Bag, Hamilton, New Zealand
b
Department of Pathology , Ontario Veterinary College , Guelph, Ontario, Canada , N1G 2W1 Published online: 23 Feb 2011.
To cite this article: K.G. Thompson , D.E. Lake & D.O. Cordes (1979) Hepatic encephalopathy associated with chronic facial eczema, New Zealand Veterinary Journal, 27:10, 221-223, DOI: 10.1080/00480169.1979.34654 To link to this article: http://dx.doi.org/10.1080/00480169.1979.34654
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
221
NEW ZEALAND VETERINARY JOURNAL
1979
CLINICAL COMMUNICATION Hepatic encephalopathy associated with chronic facial eczema K. G. Thompson*, D. E. Lake* and D. O. Cordes*t N.Z. vel.J.2?: 22 J-23
ABSTRACT
CLINICAL HISTORY
Two cows and a ram with severe chronic facial eczema showed nervous signs and histological changes characteristic of hepatic encephalopathy. Clinical signs included dullness and depression, progressing to lateral recumbency with tremor of limbs. Histologically, there was widespread spongy vacuolation of the brain. Hepatic encephalopathy associated with chronic facial eczema may be more common than is currently recognised in sheep and cattle in the North Island of New Zealand.
Case I: In May 1971, a 4-year-old cow was submitted to this laboratory after showing dullness and depression for several weeks. Although still standing, the cow seemed unaware of its surroundings and showed automaton-like movements. Haematology revealed no abnormalities, and neither serum glutamic-oxaloacetic-transminase activity nor bilirubin concentration were elevated. Tests for blood and urinary ketones were negative and the blood glucose concentration was slightly elevated (4.2omo t/1). Case 2: Several heifers in a mob of36 showed photosensitivity and diarrhoea during March 1974. In June of that year, one heifer in poor condition became ataxic, blind and depressed. A urinary ketone test was negative and there was no response to intravenous administration of calcium, magnesium and dextrose. Over a period of 5 days the clinical signs progressed to. recumbency , with paddling oflimbs, and coma. Case 3: In March 1976, 4-year-old ram was submitted to the laboratory in lateral recumbency with a protruding tongue and tremor of all four limbs. These signs were reported to be sudden in onset. All animals were destroyed and examined immediately post mortem.
Downloaded by [Chulalongkorn University] at 21:28 31 December 2014
INTRODUCTION
Clinical signs suggesting disease of the central nervous system (CNS) are not always related to primary lesions in that system. For example, chronic liver disease, terminal renal failure, cardiovascular disorders, musculoskeletal disorders and metabolic imbalances can mimic disease of the CNS. Hepatic encephalopathy has been reported in sheep, cattle, pigs and horses following the ingestion of plants containing hepatotoxic pyrrolizidine alkaloids(8) (II) (13) (19). Other forms of liver damage which have been associated with secondary CNS lesions include chronic copper poisoning(l7)(23), fascioliasis(13), aflatoxicosis(22), metastatic neoplasia(28) and liver necrosis due to anaemia and congestive heart faiIure(ll). Anomalies of the portocaval system have also produced the syndrome in dogs(28) (29). Hepatic encephalopathy is characterised clinically by anorexia, dullness and depression, progressing to terminal recumbency with muscular tremor and involuntary paddling of limbs. Other nervous signs may include ataxia, aggression, convulsions, blindness, headpressing and opisthotonus. Microscopically, there is widespread spongy vacuolation of the CNS
