A Handbook for the Sheep Clinician 7Th Edition Agnes C

Total Page:16

File Type:pdf, Size:1020Kb

A Handbook for the Sheep Clinician 7Th Edition Agnes C A Handbook for the Sheep Clinician 7th Edition Agnes C. Winter and Michael J. Clarkson Elk A Handbook for the Sheep Clinician 7th Edition D FSC MIX Paper Pent reaperraloie mamba FSC CO13604 This page intentionally left blank A Handbook for the Sheep Clinician 7th Edition Agnes C. Winter and Michael J. Clarkson School of Veterinary Science, University of Liverpool, UK www.cabi.org CABI is a trading name of CAB International CABI CABI Nosworthy Way 875 Massachusetts Avenue Wallingford 7th Floor Oxfordshire OX10 8DE Cambridge, MA 02139 UK USA Tel: +44 (0)1491832111 Tel: +1 6173954056 Fax: +44 (0)1491833508 Fax: +1 6173546875 E-mail: [email protected] E-mail: [email protected] Website: www.cabi.org © CAB International 2012. All rights reserved. No part of this publication may be reproduced in any form or by any means, electronically, mechanically, by photocopying, recording or otherwise, without the prior permission of the copyright owners. Library of Congress Cataloging-in-Publication Data Winter, Agnes C. A handbook for the sheep clinician / A.C. Winter and M.J. Clarkson. -- 7th ed. p. ; cm. Clarkson's name appears first on the earlier edition. Includes bibliographical references and index. ISBN 978-1-84593-973-1 (hardback : alk. paper) -- ISBN 978-1-84593-974-8 (pbk. : alk. paper) I. Clarkson, M. J. II. Title. [DNLM: 1. Sheep Diseases. 2. Sheep -- physiology. 3. Veterinary Medicine. SF 968] 636.3'089758--dc23 2011034290 ISBN-13: 978 1 84593 973 1 (HB) ISBN-13: 978 1 84593 974 8 (PB) Commissioning editor: Sarah Hulbert Editorial assistant: Alexandra Lainsbury Production editor: Holly Beaumont Typeset by SPi, Pondicherry, India. Printed and bound by CPI Group (UK) Ltd, Croydon, CR0 4YY. Contents About the Authors vii Abbreviations ix Preface xi 1 Production 1 2 Reproduction 9 3 Vaccination 17 4Thin Sheep 23 5 The Pregnant Ewe 35 6The Periparturient Ewe 49 7Newborn Lambs 61 8The Lactating Ewe 75 9Growing Lambs 79 10Sudden Death 89 11Lameness 95 12Skin and Wool 107 13Respiratory Diseases 119 14Neurological Diseases 127 15Eyes, Ears and Nose 139 16Ticks and Tick-borne Diseases 143 17Notifiable Diseases and Diseases Exotic to the UK and Northern Europe 149 18Health Schemes 155 v vi Contents Appendix 1 Clinical Examination 161 Appendix 2 Neurological Examination of Sheep 164 Appendix 3 Checklist for Examination of a Sick Lamb 166 Appendix 4 Professional Development 167 Appendix 5 Revision Problems and Questions 169 Appendix 6 Suggested Answers 175 Index 185 About the Authors Agnes Winter grew up on a small family farm in the Yorkshire Dales. After graduating from Liverpool Veterinary School she worked in mixed practice in north Wales where her inter- est in farm animal work, in particular with sheep, developed further. With her Welsh farmer husband she kept a flock of sheep, including a small flock of pedigree Wensleydales with which she had considerable success in the show ring. After some years she returned to Liverpool Veterinary School to undertake a PhD supervized by her co-author Michael Clarkson. After completion of this she became a lecturer, and later senior lecturer, in sheep health. For the last four years of her academic career she was head of the Clinical Department and, on retiring, was made an Honorary Professor in the University. She remains an active member of the UK Sheep Veterinary Society, of which she was President from 1987-88. She has written five other books on various aspects of sheep health and disease and has received several prestigious awards for her contributions to the sheep industry. Agnes C. Winter BVSc, PhD, DSHP, DipECSRHM, FRAgS, MRCVS Honorary Professor, School of Veterinary Science, University of Liverpool 2 Fossbridge House, Walmgate, York, YO1 9SY E-mail: [email protected] Michael Clarkson was born in Yorkshire and graduated from Liverpool Veterinary School. He undertook specialist studies in the Liverpool School of Tropical Medicine where he taught veterinary parasitology and did research on turkey coccidiosis, cattle trypanosomia- sis, liver fluke infection in cattle and sheep and a number of zoonotic infections, especially hydatid disease. Michael has worked in several countries including Kenya, Zambia, Peru, Chile and Libya. He was appointed Professor of Farm Animal Medicine by Liverpool Veterinary School and studied the epidemiology of a number of important sheep diseases including parasitic gastroenteritis, chlamydial and toxoplasma abortion and fasciolosis and continued his interest in hydatid disease. He taught sheep and cattle medicine and worked on a number of sheep farms developing sheep health programmes. He was appointed Emeritus Professor on his retirement and still undertakes research work at the Veterinary School. He has been a member of the UK Sheep Veterinary Society for many years, edited its Proceedings for 25 years, and was President of the Society from 1986-87. vii viii About the Authors Michael J. Clarkson BSc, PhD, DVSc, DSHP, MRCVS Emeritus Professor, School of Veterinary Science, University of Liverpool Leahurst Campus, Neston, CH64 7TE E-mail: [email protected] Agnes Winter and Michael Clarkson were the first two Royal College of Veterinary Surgeons Diplomates in Sheep Health and Production and the first two RCVS-recognized sheep specialists. Abbreviations AADs Amino-acetonitrile derivatives AGID Agar gel immunodiffusion test AHVLA Animal Health and Veterinary Laboratories Agency AI Artificial insemination BDV Border disease virus BLUP Best linear unbiased prediction BOHB Betahydroxybutyrate BSE Bovine spongiform encephalopathy BTV Bluetongue virus BVA British Veterinary Association BVDV Bovine virus diarrhea virus BZ Benzimidazole CAE Caprine arthritis encephalitis CaMD Calcium borogluconate, magnesium and dextrose CAP Common Agricultural Policy CCN Cerebrocortical necrosis CF Complement-fixing CK Creatine kinase CLA Caseous lymphadenitis CNS Central nervous system CODD Contagious ovine digital dermatitis CP Crude protein CS Condition score CSF Cerebrospinal fluid D value Digestibility value DET Dry ewe therapy DM Dry matter EAE Enzootic abortion of ewes EBLEX English Beef and Lamb Executive EBV Estimated breeding value ELISA Enzyme-linked immunosorbent assay ix x Abbreviations EM Electron microscope/microscopy EU European Union FMD Foot and mouth disease FRFootrot GGT Gammaglutamyl transferase GSHPx Glutathione peroxidase ID Interdigital dermatitis IM Intramuscular IV Intravenous LA Long acting LM Levamisole and morantel (drugs) MAP Mycobacterium avium subspecies paratuberculosis ME Metabolizable energy MJ Megajoule ML Macrocyclic lactones MLC Meat and Livestock Commission MOET Multiple ovulation embryo transfer MRI Magnetic resonance imaging MV Maedi visna NADIS National Animal Disease Information Service NSA National Sheep Association NSAID Non-steroidal anti-inflammatory drug NSP National Scrapie Plan OP organophosphate OPA Ovine pulmonary adenocarcinoma PCV Packed cell volume PGE Parasitic gastroenteritis PI3 Parainfluenza virus type 3 PME Post-mortem examination PMSG Pregnant mare's serum gonadotrophin PrP Prion protein PT Pregnancy toxaemia RCVS The Royal College of Veterinary Surgeons SAC Scottish Agricultural College SAHPS Animal Health Planning System SC Subcutaneous SCOPS Sustainable Control of Parasites of Sheep SFP Single Farm Payment SP Synthetic pyrethroid SPA Sheep pulmonary adenomatosis SVS Sheep Veterinary Society TB Tuberculosis TBF Tick-borne fever TSE Transmissible spongiform encephalopathy VLA Veterinary Laboratories Agency (now AHVLA having merged with Animal Health) VMD Veterinary Medicines Directorate Preface The original idea for this book was to produce a concise practical clinical guide to the diagnosis, epidemiology, treatment and control of the common conditions affecting sheep in the UK and an early version appeared in1983.It was first used for teaching veterinary stu- dents at the Liverpool Veterinary School but we were encouraged when a number of veteri- nary surgeons and sheep farmers indicated that they found it helpful and it became well known as the 'Green Book'. The last edition was published in 1997 by the Liverpool University Press, although the document has been updated internally every couple of years since then. The present book has been considerably extended both in the information given on the main conditions and in the geographical range covered. Although the emphasis remains on the common conditions affecting sheep in the UK, we have considered their importance in the countries of northern and southern Europe and elsewhere including Australasia and other southern hemisphere countries and in North America. We have not discussed the conditions of sheep maintained for milk production, however, since that is a specialized area mostly outside our experience. The emphasis has continued to be on the practical clinical aspects of sheep medicine, concentrating on common and important aspects. No attempt has been made to cover more unusual or obscure conditions. Knowledge of the details of pathology and the organisms involved has been assumed or can be sought elsewhere. Where specific drugs are referred to we have used the generic name; availability and legislative aspects of use refer to UK conditions and may vary in other countries. We hope that this book will prove a useful practical handbook for dealing with the com- mon conditions of sheep, both as individuals and in flocks and will be helpful to veterinary students and practitioners and also to farmers and agricultural students and advisors. We are grateful to
Recommended publications
  • Late Onset of Cerebellar Abiotrophy in a Boxer
    SAGE-Hindawi Access to Research Veterinary Medicine International Volume 2010, Article ID 406275, 4 pages doi:10.4061/2010/406275 Case Report Late Onset of Cerebellar Abiotrophy in aBoxerDog Sanjeev Gumber, Doo-Youn Cho, and Timothy W. Morgan Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Skip Bertman Drive, Baton Rouge, LA 70803, USA Correspondence should be addressed to Sanjeev Gumber, [email protected] Received 2 August 2010; Accepted 7 November 2010 Academic Editor: Daniel Smeak Copyright © 2010 Sanjeev Gumber et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cerebellar abiotrophy is a degenerative disorder of the central nervous system and has been reported in humans and animals. This case report documents clinical, histopathological, and immunohistochemical findings of cerebellar abiotrophy in an adult Boxer dog. A 3.5-year-old, female, tan Boxer dog presented with a six-week history of left-sided head tilt. Neurological examination and additional diagnostics during her three subsequent visits over 4.5 months revealed worsening of neurological signs including marked head pressing, severe proprioceptive deficits in all the four limbs, loss of menace response and palpebral reflex in the left eye, and a gradual seizure lasting one hour at her last visit. Based on the immunohistochemical staining for glial fibrillary acidic protein and histopathological examination of cerebellum, cerebellar cortical abiotrophy was diagnosed. This is the first reported case of cerebellar abiotrophy in a Boxer dog to our knowledge.
    [Show full text]
  • Canine Hereditary Ataxia in Old English Sheepdogs and Gordon Setters Is Associated with a Defect in the Autophagy Gene Encoding RAB24
    Canine Hereditary Ataxia in Old English Sheepdogs and Gordon Setters Is Associated with a Defect in the Autophagy Gene Encoding RAB24 The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Agler, Caryline, Dahlia M. Nielsen, Ganokon Urkasemsin, Andrew Singleton, Noriko Tonomura, Snaevar Sigurdsson, Ruqi Tang, et al. “Canine Hereditary Ataxia in Old English Sheepdogs and Gordon Setters Is Associated with a Defect in the Autophagy Gene Encoding RAB24.” Edited by Tosso Leeb. PLoS Genet 10, no. 2 (February 6, 2014): e1003991. As Published http://dx.doi.org/10.1371/journal.pgen.1003991 Publisher Public Library of Science Version Final published version Citable link http://hdl.handle.net/1721.1/86370 Terms of Use Creative Commons Attribution Detailed Terms http://creativecommons.org/licenses/by/4.0/ Canine Hereditary Ataxia in Old English Sheepdogs and Gordon Setters Is Associated with a Defect in the Autophagy Gene Encoding RAB24 Caryline Agler1, Dahlia M. Nielsen2, Ganokon Urkasemsin1, Andrew Singleton3, Noriko Tonomura4,5, Snaevar Sigurdsson4, Ruqi Tang4, Keith Linder6, Sampath Arepalli3, Dena Hernandez3, Kerstin Lindblad-Toh4,7, Joyce van de Leemput3, Alison Motsinger-Reif2,8, Dennis P. O’Brien9, Jerold Bell5, Tonya Harris1, Steven Steinberg10, Natasha J. Olby1,8* 1 Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, United States of America, 2 Bioinformatics Research Center, North Carolina State
    [Show full text]
  • Abiotrophy in Domestic Animals: a Review
    Abiotrophy in Domestic Animals: A Review Alexander de Lahunta ABSTRACT and it allows us to concentrate our can be made to normal neuronal efforts on determining the specific development in which many popula- This review of abiotrophies in cytological defect that is present and tions of differentiated neurons die domestic animals has been organized ideally the genetic basis for its prematurely as a normal programmed by the predominate anatomical loca- occurrence. When we use abiotrophy developmental event. Some of the tion of the lesion. Secondary consider- to name a disease, we are only mechanisms may be common to both ations include the major signs of the describing the pathological process processes. This normal developmental clinical disorder and special neuropa- a concept of the mechanism resulting event occurs in the peripheral nervous thological features. Those abiotro- in the degeneration that is described. system when motoneurons from the phies that have an established genetic As the underlying cause of the ventral grey column fail to develop a basis are identifiled but the review abiotrophy is determined, this should normal motor end plate relationship includes degenerative disorders in be used in naming the disease. Using with a skeletal muscle fiber which is which the etiology is not yet the concept of abiotrophy in its the target organ. These neurons established. broadest sense it is applicable to any of degenerate. The ultimate size and the inherited degenerative diseases of shape of the ventral grey column the nervous system. This would reflects this normal degenerative Gowers in 1902 (1) gave a lecture include the numerous cerebellar process (2,3).
    [Show full text]
  • Cerebellar Disease in the Dog and Cat
    CEREBELLAR DISEASE IN THE DOG AND CAT: A LITERATURE REVIEW AND CLINICAL CASE STUDY (1996-1998) b y Diane Dali-An Lu BVetMed A thesis submitted for the degree of Master of Veterinary Medicine (M.V.M.) In the Faculty of Veterinary Medicine University of Glasgow Department of Veterinary Clinical Studies Division of Small Animal Clinical Studies University of Glasgow Veterinary School A p ril 1 9 9 9 © Diane Dali-An Lu 1999 ProQuest Number: 13815577 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a com plete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest ProQuest 13815577 Published by ProQuest LLC(2018). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States C ode Microform Edition © ProQuest LLC. ProQuest LLC. 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106- 1346 GLASGOW UNIVERSITY lib ra ry ll5X C C ^ Summary SUMMARY________________________________ The aim of this thesis is to detail the history, clinical findings, ancillary investigations and, in some cases, pathological findings in 25 cases of cerebellar disease in dogs and cats which were presented to Glasgow University Veterinary School and Hospital during the period October 1996 to June 1998. Clinical findings were usually characteristic, although the signs could range from mild tremor and ataxia to severe generalised ataxia causing frequent falling over and difficulty in locomotion.
    [Show full text]
  • Berlin-2 17 06 22-Handout.Ppt [Kompatibilitätsmodus]
    25.06.2017 Malformations Important fetal teratogenic virus infections in different species: Feline panleukopenia virus cat cerebellar hypoplasia, hydranencephaly Introduction to Neuropathology – Part II Classical swine fever virus pig dysmyelinogenesis, cerebellar hypoplasia Bovine virus diarrhea virus calf, lamb hydrocephalus. cerebellar hypo- and aplasia, prosencephaly, hypomyelination, porencephaly Malformations Akabane, Cache valley, calf, lamb hydranencephaly, Prof. Dr. W. Baumgärtner and Dr. P. Wohlsein Schmallenberg virus arthrogryposis, Department of Pathology cerebellar hypoplasia, University of Veterinary Medicine porencephaly Hannover, Germany Neurological disease spectrum in dogs Malformations Important fetal teratogenic virus infections in different species: Canine parvovirus dog cerebellar hypoplasia, dysplasia Bluetongue virus lamb, calf hydranencephaly Chuzan virus calf hydranencephaly, cerebellar hypoplasia Aino virus calf arthrogryposis, hydranencephaly, Introduction cerebellar hypoplasia Malformations Border disease virus lamb porencephaly, hypomyelination Wesselsbron virus calf hydranencephaly, Fluehmann et al., 2006; J Small Anim Pract; mod. porencephaly Malformations Malformations ! frequent disorder in domestic animals (5% neonatal death) ! grossly or only microscopically visible Categories of CNS developmental defects: ! defects of neural tube closure Etiology: ! defects of forebrain induction ! primary: spontaneous or hereditary (point gene mutations, ! neuronal migration disorders and sulcation defects chromosomal
    [Show full text]
  • Cerebellar Abiotrophy
    Cerebellar Abiotrophy Affected breeds: Arabian, Bashkir Curly, Danish Sport, Trakehner, Welsh Pony. Equine cerebellar abiotrophy (CA) is an inherited neurological condition and is characterized by the degeneration of a specific cell type in the brain called Purkinje cells; these cells play a fundamental role in controlling movement. CA foals are apparently normal at birth, but between the ages of 6 – 16 weeks develop signs of CA which include head tremor and a lack of balance. Consequently, affected foals may show a splayed stance in an attempt to balance themselves, and may fall and be unable to rise easily. The severity of the signs displayed by affected foals varies widely and symptoms can be confused with other conditions. Affected foals are often euthanized as they are unsafe to ride. Research carried out at the Veterinary Genetics Laboratory in Davis, California has identified a mutation that is associated with CA. CA is found mainly in Arabian horses, but is also seen at a lower level in several other breeds including the Bashkir Curly Horse, Danish Sport Horse, Trakehners and Welsh ponies. The appearance of the defect in these breeds is due to Arabian ancestry; the CA test is therefore recommended for horses that have Arabian horses in their pedigree. CA is inherited in a recessive manner. This means that carrier horses which have one copy of the defective gene appear healthy, but can pass this on to their offspring. The breeding of two carriers will produce CA-affected foals 25% of the time. The breeding of a carrier with a clear horse will not result in affected foals, though 50% of offspring will be carriers themselves.
    [Show full text]
  • Equine Cerebellar Abiotrophy (CA) –
    ARABIAN HORSE FOUNDATION UPDATE Equine Cerebellar Abiotrophy (CA) – Update on UC Davis Research: Indirect DNA Test Available Background: Equine Cerebellar Abiotrophy (CA) is a debilitating degenerative condition of the cerebellum portion of the brain which results in a severe lack of coordination. The degree of severity can vary among individual horses, but most affected horses are euthanized before adulthood, due to the hazard they present to themselves and others, and the current inability to treat or cure the condition. Research has indicated that CA is the result of an autosomal recessive gene mutation. Autosomal means the disorder is not sex linked (both sexes can be affected) and recessive means both parents must contribute the “CA gene” in order to have an affected foal (this is the same mode of inheritance as SCID). Additional information on CA can be found here: http://www.arabianhorses.org/education/genetic/default.asp Indirect DNA Test: The Veterinary Genetics Laboratory at UC Davis has supported CA research for over 6 years. The CA research is being done by Dr. Cecilia Penedo and her graduate student Leah Brault. In 2007, The Horse Genome Project completed the sequencing of the horse genome and this development has enabled tremendous progress for mapping CA to a narrow region of the genome. These advancements have allowed the researchers to identify markers associated with CA and develop an indirect DNA test (early version of a diagnostic test) to help diagnose the defect in suspect foals and to help owners identify carriers in their breeding stock. This test can help guide breeders in making mating selections, with the goal to never produce a CA affected foal.
    [Show full text]
  • Identification of Mutation for Cerebellar Degeneration in the Gordon Setter
    North Carolina State University is a land-grant College of Veterinary Medicine university and a constituent institution of The Department of Clinical Sciences University of North Carolina 1060 William Moore Drive Raleigh, North Carolina 27607 Identification of Mutation for Cerebellar Degeneration in the Gordon Setter The mutation causing cerebellar degeneration (also known as cerebellar abiotrophy, cerebellar ataxia, cerebellar cortical degeneration, CA) has been identified in the laboratory of Dr. Natasha Olby at North Carolina State University. Cerebellar degeneration has been documented in the Gordon Setter as an autosomal recessive inherited disorder since at least the 1960s. It causes a progressive loss of coordination resulting in the hallmark ataxic gait characterized by dramatic overstepping, particularly obvious in the forelimbs. Onset of signs ranges from 6 months to 4 years of age and disease progression tends to be slow, occurring over several years. The mutation was identified following extensive mapping of cerebellar degeneration in Old English Sheepdogs. Testing of the mutation discovered in Old English Sheepdogs revealed that both breeds of dog have the same mutation. This implies that it is an old mutation that has existed in these populations of dogs at a very low level until more recent times. The mutation has not been described previously, and to date has only been found in the Old English Sheep dog and the Gordon Setter. Cerebellar degeneration has been seen in Gordon Setters worldwide, including the US, Canada, Europe, and Australia. It has been documented in both conformation and field lines. While the mutation is old and dispersed in the breed, we do not expect it to be present at a high frequency in the breed.
    [Show full text]
  • First Report of Cerebellar Abiotrophy in an Arabian Foal from Argentina
    Open Veterinary Journal, (2016), Vol. 6(3): 259-262 ISSN: 2226-4485 (Print) Case Report ISSN: 2218-6050 (Online) DOI: http://dx.doi.org/10.4314/ovj.v6i3.17 _____________________________________________________________________________________ Submitted: 03/08/2016 Accepted: 09/12/2016 Published: 22/12/2016 First report of cerebellar abiotrophy in an Arabian foal from Argentina S.A. Sadaba1,2, G.J. Madariaga3, C.M. Corbi Botto1,2, M.H. Carino1, M.E. Zappa1, P. Peral García1, S.A. Olguín4, A. Massone3 and S. Díaz1,* 1IGEVET – Instituto de Genética Veterinaria “Ing. Fernando Noel Dulout” (UNLP-CONICET La Plata), Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata, La Plata, Argentina 2Research Fellows from Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET). Av. Rivadavia 1917 (C1033AAJ) CABA, Argentina 3Laboratorio de Patología Especial Veterinaria, Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata, La Plata, Argentina 4Cátedra de Métodos Complementarios de Diagnóstico, Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata, La Plata, Argentina _____________________________________________________________________________________________ Abstract Evidence of cerebellar abiotrophy (CA) was found in a six-month-old Arabian filly with signs of incoordination, head tremor, wobbling, loss of balance and falling over, consistent with a cerebellar lesion. Normal hematology profile blood test and cerebrospinal fluid analysis excluded infectious encephalitis, and serological testing for Sarcocystis neurona was negative. The filly was euthanized. Postmortem X-ray radiography of the cervical cephalic region identified not abnormalities, discounting spinal trauma. The histopathological analysis of serial transverse cerebellar sections by electron microscopy revealed morphological characteristics of apoptotic cells with pyknotic nuclei and degenerate mitochondria, cytoplasmic condensation and areas with absence of Purkinje cells, matching with CA histopathological characteristics.
    [Show full text]
  • From Head Trauma to Toxicity, Cerebellar Disease Diagnosis
    Vet Times The website for the veterinary profession https://www.vettimes.co.uk FROM HEAD TRAUMA TO TOXICITY, CEREBELLAR DISEASE DIAGNOSIS Author : Dan Forster Categories : Vets Date : December 8, 2008 DAN FORSTER examines the clinical pointers indicating a disease that not only affects movement, but also eating, and describes the possible differential diagnoses behind the dysfunction. ANIMALS with cerebellar disease will often present with classic signs of ataxia and dysmetria. However, the aetiology of the cerebellar damage is not always straightforward. This article reviews some of the causes of cerebellar dysfunction that may be encountered in general practice. The cerebellum occupies 10 per cent of the brain parenchyma in dogs and cats, and lies behind the cerebrum. It is connected to the brainstem by three paired cerebellar peduncles on each side, which act as a conduit for both afferent and efferent information related to cerebellar function. It is divided into functional units by a series of transverse fissures. The small flocculonodular node is important for balance, and the caudal lobe is associated with the feedback regulation of motor function. The more rostral lobe receives proprioceptive information. At a cellular level, the inner portion of the cerebellum is the medullary substance that contains the deep nuclei. The outer portion is the cerebellar cortex and is composed of three layers; the molecular cell layer, the Purkinje cell layer and the granule cell layer (Figure 1). The Purkinje cells are large and very active, metabolically, which makes them highly susceptible to ischaemic and toxic damage. 1 / 15 An understanding of the microscopic anatomy is useful when considering how different cerebellar diseases manifest themselves clinically.
    [Show full text]
  • Cerebellar Abiotrophy
    CEREBELLAR ABIOTROPHY What is cerebellar abiotrophy? The cerebellum is the part of the brain that regulates the control and coordination of movement. In this condition, cells in the cerebellum mature normally before birth, but then deteriorate prematurely causing clinical signs associated with poor coordination and lack of balance. The Purkinje cells in the cerebellum are primarily involved; cells in other areas of the brain may also be affected. How is cerebellar abiotrophy inherited? An autosomal recessive mode of inheritance has been confirmed or is strongly suspected for the abiotrophies listed below, with the exception of x-linked cerebellar ataxia in the English pointer, which has an x-linked mode of inheritance. What breeds are affected by cerebellar abiotrophy? Neonatal cerebellar abiotrophy (very rare) - Affected cells start to degenerate before birth, so that signs of cerebellar dysfunction are present at birth or when the pup first walks. Beagle, samoyed Postnatal cerebellar abiotrophy - Cells in the cerebellum are normal at birth and begin to degenerate at variable times thereafter. Australian kelpie, border collie, Labrador retriever - Clinical signs are first seen at 6 to 12 weeks, and the condition worsens quickly (over a few weeks). Airedale - There is early onset (12 weeks of age) and a slow progression of clinical signs. Bern running dog, Bernese mountain dog, bull terrier, German shepherd - Signs are seen by 6 months of age. Gordon setters - Clinical signs develop at 6 months to 2 years of age, and the progression is slow (months to years). Brittany spaniels - The onset of clinical signs is late (average age 10 years), and the condition progresses slowly.
    [Show full text]
  • HSVMA Guide to Congenital and Heritable Disorders in Dogs
    GUIDE TO CONGENITAL AND HERITABLE DISORDERS IN DOGS Includes Genetic Predisposition to Diseases Special thanks to W. Jean Dodds, D.V.M. for researching and compiling the information contained in this guide. Dr. Dodds is a world-renowned vaccine research scientist with expertise in hematology, immunology, endocrinology and nutrition. Published by The Humane Society Veterinary Medical Association P.O. Box 208, Davis, CA 95617, Phone: 530-759-8106; Fax: 530-759-8116 First printing: August 1994, revised August 1997, November 2000, January 2004, March 2006, and May 2011. Introduction: Purebred dogs of many breeds and even mixed breed dogs are prone to specific abnormalities which may be familial or genetic in nature. Often, these health problems are unapparent to the average person and can only be detected with veterinary medical screening. This booklet is intended to provide information about the potential health problems associated with various purebred dogs. Directory Section I A list of 182 more commonly known purebred dog breeds, each of which is accompanied by a number or series of numbers that correspond to the congenital and heritable diseases identified and described in Section II. Section II An alphabetical listing of congenital and genetically transmitted diseases that occur in purebred dogs. Each disease is assigned an identification number, and some diseases are followed by the names of the breeds known to be subject to those diseases. How to use this book: Refer to Section I to find the congenital and genetically transmitted diseases associated with a breed or breeds in which you are interested. Refer to Section II to find the names and definitions of those diseases.
    [Show full text]