Bovine medicine : diseases and husbandry of cattle 0632055960

Table of contents :
Content: List of Colour Plates.List of Contributors.Preface.Preface to the First Edition. PART I: Management: 1. Calf Rearing.2. Suckler Herds.3. Beef Finishing Systems.4. Dairy Farming.5. Heifer Rearing - 12 Weeks to Calving.6. Tropical Cattle Management.7. Ethnoveterinary Medicine in the Tropics.8. Heat Stress in Dairy Cattle.9. Nutrition.10. Alternative Forages. PART II: Disease: 11. Diagnosis and Differential Diagnosis in the Cow The Calf 12. Outline of Clinical Genetics.13. Congenital Conditions.14. Calf Diarrhoea.15. Salmonellosis.16. Digestive Disorders of Calves.17. Calf Respiratory Disease.18. Other Calf Problems Growing Cattle 19. Endoparasites.20. Respiratory Diseases.21. Trace Element Disorders Adult Cattle Mastitis and Teat Conditions 22. Anatomy, Physiology and Immunology of the Udder.23. Mastitis.24. Summer Mastitis.25. Bulk Milk Testing and Mastitis Monitoring.26. The Milking Machine.27. Skin Infections of the Bovine Teat and Udder and their Differential Diagnosis.28. Factors Affecting Milk Quality.29. The Enhancement of Bovine Mammary Gland Immunity through Vaccination.30. Antimicrobial Therapy of Mastitis Lameness 31. Foot Lameness.32. Lameness above the Foot Fertility 33. Reproductive Physiology in Cattle.34. Problems after Calving.35. Problems Associated with Oestrous Cyclicity.36. Failure to Conceive and Embryonic Loss.37. Foetal Loss and Abnormalities of Pregnancy.38. A Summary of Bull Infertility.39. Artificial Insemination and Diseases Transmitted by Semen.40. Embryo Transfer.41. Herd Fertility Management. (a) Beef cattle. (b) Dairy herds.42. Pharmacological Manipulation of Reproduction Major Infectious Diseases 43. Viral Diseases.(a) Blue tongue.(b) Enzootic bovine leukosis.(c) Foot-and-mouth disease.(d) Rinderpest.(e) Vesicular stomatitis.(f) Bovine immunodeficiency virus.44. Bacterial Conditions.45. Ectoparasites, Tick and Arthropod Borne Diseases Metabolic Problems 46. Major Metabolic Disorders.47. Metabolic Profiles System and Miscellaneous Conditions 48. Alimentary Conditions.49. Respiratory Conditions. (a). (b) Contagious Bovine Pleuropneumonia (CBPP).50. Skin Conditions.51. Neurological Disorders.52. Ocular Diseases.53. Other Conditions.54. Major Poisoning Welfare 55. Welfare Therapy and Disease Prevention 56. Health, Housing and Hygiene.57. Biosecurity.58. Immunological Fundamentals.59. Vaccines and Vaccination of Cattle.60. Antiparasitics.61. Antimicrobial Agents.62. Inflammation, Pain and Anti-inflammatory Drugs.63. Growth Promoters in Cattle.64. Injection Damage.65. Alternative Medicine.66. Aspects of Bovine Surgery The Interaction of the Animal, Environment and Management 67. Stress and the Pathogenesis of Disease Global Variation in Cattle Practice 68. Diseases Related to Management in Europe.69. Cattle Disease in Africa.70. Rabies.71. Cattle Practice in Saudi Arabia.72. Bovine Medicine in New Zealand and Australia.73. North American Dairy Production and Veterinary Involvement.74. The North American Beef Industry.75. Cattle Disease in South America. Index

Citation preview

Bovine Medicine Diseases and Husbandry of Cattle Second edition

Edited by

A.H. Andrews with

R.W. Blowey H. Boyd R.G. Eddy

Blackwell Science

Bovine Medicine Diseases and Husbandry of Cattle Second edition

Edited by

A.H. Andrews with

R.W. Blowey H. Boyd R.G. Eddy

Blackwell Science

© 2004 by Blackwell Science Ltd a Blackwell Publishing Company

First published 1992 by Blackwell Science Second edition published 2004 by Blackwell Publishing

Editorial Offices: Blackwell Science Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK Tel: +44 (0)1865 776868 Iowa State Press, a Blackwell Publishing Company, 2121 State Avenue, Ames Iowa 50014-8300 USA Tel: +1 515 292 0140 Blackwell Science Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia Tel: +61 (0)3 8359 1011

Library of Congress Cataloging-in-Publication Data Bovine medicine : diseases and busbandry of cattle / edited by A.H. Andrews ... [et al.]. 2nd ed. p. cm. Includes bibliographical references (p.). ISBN 0-632-05596-0 (alk. paper) 1. Cattle–Diseases. 2. Cattle. I. Andrews, A.H.

The right of the Author to be identified as the Author of this Work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.

SF961.B78 2003 636.2¢0896–dc22 2003063030 ISBN 0-632-05596-0 A catalogue record for this title is available from the British Library Set in 9.5 on 12 pt Times by SNP Best-set Typesetter Ltd., Hong Kong Printed and bound in the UK using acid-free paper by CPI Bath For further information on Blackwell Publishing, visit our website: www.blackwellpublishing.com

Contents

List of Colour Plates

vi

List of Contributors

vii

Preface

xi

Preface to the First Edition

xii

PART 1: MANAGEMENT 1 2

1

Calf Rearing D.M. Allen

3

Suckler Herds D.M. Allen

7

3

Beef Finishing Systems D.M. Allen

14

4

Dairy Farming A.H. Andrews and A. Poole

22

5

Heifer Rearing – 12 Weeks to Calving B. Drew

54

6

Tropical Cattle Management R.D. Fielding and R.W. Matthewman

68

7

Ethnoveterinary Medicine in the Tropics R.D. Fielding

83

8

Heat Stress in Dairy Cattle J.K. Shearer

88

9 Nutrition J.M. Wilkinson 10

Alternative Forages M. Tame and the late P.S. Jarvis

PART 2: DISEASE 11

Diagnosis and Differential Diagnosis in the Cow R.G. Eddy and P.J.N. Pinsent

Congenital Conditions A.H. Andrews

172

14

Calf Diarrhoea P.R. Scott, G.A. Hall, P.W. Jones and J.H. Morgan

185

15

Salmonellosis P.W. Jones, P.R. Watson and T.S. Wallis

215

16

Digestive Disorders of Calves R.W. Blowey

231

17

Calf Respiratory Disease A.H. Andrews

239

18

Other Calf Problems A.H. Andrews

249

Growing Cattle

265

19

Endoparasites S.M. Taylor and A.H. Andrews

267

20

Respiratory Diseases A.H. Andrews

286

21

Trace Element Disorders N.F. Suttle

294

Adult Cattle Mastitis and Teat Conditions 22

95 123

133

135

The Calf

159

12

161

Outline of Clinical Genetics G.B. Young

13

Anatomy, Physiology and Immunology of the Udder K.G. Hibbitt, N. Craven and E.H. Batten

309 311

23

Mastitis P.W. Edmondson and A.J. Bramley

326

24

Summer Mastitis J.E. Hillerton

337

25

Bulk Milk Testing and Mastitis Monitoring D.J. O’Rourke and R.W. Blowey

341

26

The Milking Machine D.J. O’Rourke

353

27

Skin Infections of the Bovine Teat and Udder and Their Differential Diagnosis J.K. Shearer, J.R. Townsend and E.P.J. Gibbs

363

iii

iv

•

Contents

28

Factors Affecting Milk Quality R.W. Blowey and R.A. Laven

29

The Enhancement of Bovine Mammary Gland Immunity Through Vaccination K.P. Kenny, T. Tollersrud and F.D. Bastida-Corcuera

30

Antimicrobial Therapy of Mastitis D.J. O’Rourke and J.D. Baggot

373

31

Lameness in the Foot R.W. Blowey

409

Lameness Above the Foot A.D. Weaver

435

Fertility

469

33

Reproductive Physiology in Cattle P.J. Hartigan

471

34

The Postpartum Period I.M. Sheldon, D.C. Barrett and H. Boyd

508

Problems Associated with Oestrous Cyclicity H. Boyd, D.C. Barrett, and M. Mihm

530

36

Failure to Conceive and Embryonic Loss D.C. Barrett, H. Boyd and M. Mihm

552

37

Fetal Loss G. Caldow and D. Gray

577

38

Bull Infertility D.N. Logue and W.M. Crawshaw

594

39

Artificial Insemination and Diseases Transmitted by Semen G.H. Wentink

40 41

42

(c) Foot-and-mouth disease R.P. Kitching

700

(d) Rinderpest E.C. Anderson

707

(e) Vesicular stomatitis R.P. Kitching

710

(f) Bovine immunodeficiency virus A.H. Andrews

713

44

Bacterial Conditions A.H. Andrews and the late B.M. Williams

717

45

Ectoparasites, Tick and Arthropod-borne Diseases S.M. Taylor, A.G. Hunter and A.H. Andrews

391

407

35

693

379

Lameness

32

(b) Enzootic bovine leukosis C. Venables and M.H. Lucas

740

Metabolic Problems

779

46

Major Metabolic Disorders R.G. Eddy

781

47

Metabolic Profiles D.A. Whitaker

804

System and Miscellaneous Conditions

819

48

Alimentary Conditions R.G. Eddy

821

49

Respiratory Conditions A.H. Andrews and R.S. Windsor

860

50

Skin Conditions L.R. Thomsett

875

51

Neurological Disorders P.R. Scott

890

52

Ocular Diseases P.G.C. Bedford

917

627

Embryo Transfer A.K. Smith

634

Herd Fertility Management (a) Beef herds S. Borsberry

652 652

53

Other Conditions A.H. Andrews

927

(b) Dairy herds D.C. Barrett and H. Boyd

662

54

Major Poisonings C.J. Giles and A.H. Andrews

937

678

Welfare

953

55

955

Pharmacological Manipulation of Reproduction J.G. Allcock and A.R. Peters

Welfare D.M. Broom

Major Infectious Diseases

689

43

Viral Diseases

691

Therapy and Disease Prevention

969

(a) Bluetongue R.P. Kitching

691

56

971

Health, Housing and Hygiene D.W.B. Sainsbury

Contents

•

v

57

Biosecurity D.C. Barrett and A.J. Taylor

987

58

Immunological Fundamentals W.P.H. Duffus

996

59

Vaccines and Vaccination of Cattle I.D. Baker

1004

69

Cattle Disease in Africa R.S. Windsor

1156

60

Antiparasitics M.A. Taylor

1019

70

Rabies R.S. Windsor

1164

61

Antimicrobial Agents A.H. Andrews

1035

71

Dairy Farming in Saudi Arabia J.C. Fishwick

1172

62

Inflammation and Pain J.L. Fitzpatrick, A.M. Nolan, P. Lees and S.A. May

1045

72

Bovine Medicine in New Zealand and Australia N.D. Sargison and J.J. Vermunt

1177

Growth Promoters in Cattle K. Lawrence

1067

1183

Injection Damage J.H. Pratt

1078

North American Dairy Production and Veterinary Involvement T.W. Graham

65

Alternative Medicine C.E.I. Day

1081

66

Aspects of Bovine Surgery G. Wyn-Jones

1105

63 64

68

73

74

Diseases Related to Management in Europe G.H. Wentink and A. de Kruif

The North American Beef Industry D. Sjeklocha and S. Sweiger

Index Colour plates appear between pages 468 and 469

The Interaction of the Animal, Environment and Management

1131

67

1133

Stress and the Pathogenesis of Disease P.J. Hartigan

Global Variation in Cattle Practice

1149 1151

1188

1193

List of Colour Plates All colour plates appear between 468 and 469. 16.1

Hair loss over legs and perineum associated with steatorrhea and diarrhoea. 16.2 Alopecia due to poorly dispersed fats from milk subsitute. 16.3 Rumen bloat and chronic scour. 16.4 Calf in extremis. 16.5 Abomasum at necropsy. 16.6 Chronic peri-weaning calf diarrhoea. 23.1 Lumen and keratinized lining in teat duct. 23.2 Signs of clinical mastitis. 27.1 Early stages of bovine herpes mammillitis. 27.2 Bovine herpes mammillitis (two days). 27.3 Bovine herpes mammillitis (four days). 27.4 Bovine herpes mammillitis and scab formation. 27.5 Bovine herpes mammillitis (about seven days). 27.6 Bovine herpes mammillitis (about two weeks). 27.7 Bovine herpes mammillitis (two to three weeks). 27.8 Bovine herpes mammillitis – teat after shedding necrotic tissue. 27.9 Pseudocowpox. 27.10 Pseudocowpox lesion (seven days). 27.11 Pseudocowpox (10–12 days). 27.12 Pseudocowpox scab. 27.13–16 Atypical Pseudocowpox lesions. 27.17 Cowpox showing vesicle development. 27.18 Cowpox following vesicle rupture. 27.19 Cowpox with scab formation. 27.20 Severe cowpox. 27.21 Staphylococcus aureus infection of teat. 27.22 Teat chaps. 27.23 Photosensitization of the teat. 27.24 Foot-and-mouth disease – vesiculation of the teat. 27.25 Pseudocowpox infection with cowpox infection. 27.26 Pseudocowpox infection with bovine herpes mammillitis. 27.27 Blackspot of a teat orifice. 27.28 Mud abrasion of the teat. 27.29 Ringworm lesions. 27.30 Thelitis and serous exudate in peractute mastitis. 27.31 Filamentous papillomatosis of the teat. 27.32 Nodular papillomatosis of the teat. 31.1 Hoof with corium removed. 31.2 Cross-section of white line. 31.3 Gross claw overgrowth. 31.4 Overgrowth from the sole. 31.5 White line across a square-ended toe. vi

31.6

Haemorrhage at the sole ulcer site and in white line. 31.7 Typical sole ulcer. 31.8 Heel ulcer and early sole ulcer haemorrhage. 31.9 Typical white line separation with impacted stone. 31.10 Rings on a cow’s horns demonstrate disruption of horn formation in the periparturient animal. 31.11 Cows prefer to walk on the soft surface of a rubber mat. 31.12 Cows walking along the grass verge to avoid the stony track. 31.13 Digital dermatitis and slurry heel. 31.14 A vertical fissure. 31.15 Axial wall fissure. 31.16 Interdigital necrobacillosis. 31.17 The chronic ‘hairy wart’ form of digital dermatitis. 31.18–19 Necrosis of the apex of the pedal bone. 31.20 Insertion of a tube to flush and drain deep pedal infections. 40.1 Classification and grading of embryos. 44.1 Anthrax bacillium. 44.2 Blackleg due to Clostridium chauveoi. 44.3 Endocarditis. 50.1 Generalized Trichophyton verrucosum infection. 50.2 Trichophyton verrucosum infection on calf’s head. 50.3 Linognathus vituli lice and ova on calf. 50.4 Sarcoptes scabiei infection. 50.5–6 Generalized sarcoptic scabies. 50.7 Nodular lesions of demodicosis. 50.8–9 Viral papillomatosis. 50.10 Pruritis/pyrexia/haemorrhagic syndrome. 50.11–12 Severe photodermatitis. 50.13–14 Dermatophilosis. 52.1 Cyclopia. 52.2 Esotropia: (a) early; (b) marked. 52.3 Epibulbar dermoid. 52.4 Infectious bovine keratoconjunctivitis. 52.5 Squamous cell carcinoma. 52.6 Anterior uveitis secondary to septicaemia of undetermined aetiology. 52.7 Congenital cataract. 52.8 Lens discision. 52.9 Papillary coloboma. 52.10 Normal bovine fundus. 52.11 Severe papilloedema with disc haemorrhages. 65.1 Acupuncture to treat anoestrus. 65.2 Stomach 36 acupuncture point.

List of Contributors

James G. Allcock BVM&S CertCHP MRCVS, Intervet UK Ltd, Milton Keynes, UK David M. Allen BSc PhD MBIAC, Beef Industry Consultant, formerly Head of Beef Improvement Services, Meat and Livestock Commission, Milton Keynes, UK

George L. Caldow BVM&S MSc CertCHP MRCVS, Scottish Agricultural College, Veterinary Science Division, Melrose, UK Neil Craven BVSc BSc PhD MRCVS, Pfizer Ltd, Sandwich, UK

Euan C. Anderson BVM&S PhD MRCVS, formerly Veterinary Research Laboratory, Harare, Zimbabwe

W. Mark Crawshaw BVetMed DCHP MRCVS, Scottish Agricultural College,Veterinary Science Division,Ayr, UK

Anthony H. Andrews BVetMed PhD MBIAC MRCVS, Independent Veterinary Consultant, formerly Senior Lecturer, Royal Veterinary College, UK

Christopher E. I. Day MA VetMB MRCVS Chinham House, Stanford in the Vale, UK

J. Desmond Baggot BSc MVM PhD DSc FACVPT DipECVPT FRCVS, School of Veterinary Medicine, St George’s University, Grenada, West Indies Ian D. Baker BVSc MRCVS, Hampden Veterinary Hospital, Aylesbury, UK David C. Barrett BSc(Hons) BVSc(Hons) DBR DCHP MRCVS, Senior Lecturer, Division of Farm Animal Medicine and Production, Department of Veterinary Clinical Studies, University of Glasgow, UK Felix D. Bastida-Corcuera DVM, PhD, University of California, Los Angeles, USA E. Hamish Batten BSc PhD, formerly School of Veterinary Sciences, University of Bristol, UK Peter G. C. Bedford BVetMed PhD DipECVO DVOphthal MRCVS, Small Animal Medicine and Surgery Group, Department of Clinical Sciences, Royal Veterinary College, UK Roger W. Blowey BSc BVSc FRCVS, Wood Veterinary Group, Gloucester, UK Steve Borsberry BVSc CertCHP DBR MRCVS, 608 Veterinary Clinic, Solihull, UK Hugh Boyd VMD MRCVS, formerly Senior Lecturer, Veterinary School, University of Glasgow, UK A. John Bramley BSc PhD, Department of Animal Sciences, College of Agriculture and Life Sciences, Vermont, USA Donald M. Broom MA PhD Hon DSc, Department of Clinical Veterinary Medicine, University of Cambridge, UK

Bridget Drew BSc PhD, Royal Agricultural College, Cirencester, UK W. Philip H. Duffus BVSc MA PhD MRCVS, School of Veterinary Science, University of Bristol, UK Roger G. Eddy BVetMed FRCVS, formerly at Shepton Veterinary Group, Shepton Mallet, UK Peter W. Edmondson MVB CertCHP FRCVS, Shepton Veterinary Group, Shepton Mallet, UK R. Denis Fielding BSc MSc PhD, Faculty of Veterinary Medicine, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, UK John Fishwick MA VetMB DCHP MRCVS, Department of Veterinary Clinical Science, Royal Veterinary College, Hatfield, UK Julie L. Fitzpatrick BVMS PhD MRCVS, Division of Farm Animal Medicine, University of Glasgow, UK E. Paul J. Gibbs BVSc PhD MRCVS, Department of Pathobiology, University of Florida, Gainsville, USA Colin J. Giles BVetMed PhD MRCVS, Vice President Medicine Pharmaceuticals R&D, Pfizer Inc., Kalamazoo, Michigan, USA Thomas W. Graham BSc DVM MPVM PhD,Veterinary Consulting Services, Davis, USA Douglas Gray BVM&S MSc MRCVS, Scottish Agricultural College, Veterinary Services, Bucksburn, Aberdeen, UK Graham A. Hall BVSc PhD FRCPath DipECVP MRCVS, CAMR, Porton Down, UK vii

viii

•

List of Contributors

Pat J. Hartigan BSc MA MVM PhD MRCVS, Honorary Fellow, Department of Physiology, Trinity College, Dublin, Ireland

Monika Mihm PhD MRCVS, Division of Veterinary Physiology and Pharmacology, Department of Veterinary Preclinical Studies, University of Glasgow, UK

Ken G. Hibbitt BVSc PhD MRCVS, formerly Head of Division, Institute for Animal Health, Compton, UK

Jeremy H. Morgan MA VetMB PhD MRCVS, formerly of the Institute for Animal Health, Compton, UK

J. Eric Hillerton BSc PhD FRES, Division of Environmental Microbiology, Institute for Animal Health, Compton, UK Archibald G. Hunter BVM&S DTVM MRCVS, Centre for Tropical Veterinary Medicine, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, UK

Andrea M. Nolan MVB PhD DVA DipECVA DipECVPT MRCVS, Dean of Veterinary Faculty, Department of Veterinary Preclinical Studies, University of Glasgow, UK Declan J. O’Rourke MVB FRCVS, Pfizer Ltd, Sandwich, UK

The late Peter S. Jarvis BSc, formerly of the Milk Marketing Board and Senior Adviser, Genus

Andrew R. Peters BA PhD BVetMed DVetMed FRCVS, formerly Professor of Animal Health and Production, Royal Veterinary College, University of London, UK

Philip W. Jones BSc PhD CBiol MIBiol, Department of Environmental Microbiology, Institute for Animal Health, Compton, UK

P. Jim N. Pinsent BVSc FRCVS, formerly Senior Lecturer, School of Veterinary Science, University of Bristol, UK

Kevin P. Kenny MVB PhD MRCVS, Department of Agriculture, Dublin, Ireland

Anthony Poole NDA CDA, formerly of Farm Management Services Information Unit, Milk Marketing Board, UK

R. Paul Kitching BVetMed PhD MRCVS, National Centre for Foreign Animal Disease, Winnipeg, Canada Aart de Kruif DVM PhD DipECAR, Clinic of Obstetrics, Ghent University, Belgium Richard A. Laven BVetMed PhD MRCVS, Scottish Agricultural College, Veterinary Science Division, Dumfries, UK Keith Lawrence BVSc PhD FRCVS, Elanco Animal Health, Basingstoke, UK Peter Lees CBE BPharm PhD CBiol FIBiol Dr(hc)Ghent Hon Assoc. RCVS Hon Dip ECVPT, Department of Veterinary Basic Studies, Royal Veterinary College, Hatfield, UK David N. Logue BVM&S PhD FRCVS, Scottish Agricultural College, Veterinary Science Division, Ayr Margaret H. Lucas BVSc BSc DipBact MRCVS, formerly of the Central Veterinary Laboratory, Weybridge, UK Richard W. Matthewman BSc MAgSc PhD, formerly of the Centre for Tropical Veterinary Medicine, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, UK Stephen A. May MA VetMB PhD DEO DipECVS DVR MRCVS, Department of Veterinary Clinical Studies, Royal Veterinary College, Hatfield, UK

John H. Pratt BVM&S DVSM MRCVS, formerly Head of Veterinary Services, Meat and Livestock Commission, Milton Keynes, UK David W. B. Sainsbury BSc MA PhD MRCVS FRSH CBiol FIBiol, formerly Lecturer, Animal Science Division, Department of Clinical Veterinary Medicine, University of Cambridge, UK Neil D. Sargison BA VetMB DSHP MRCVS, Faculty of Veterinary Medicine, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, UK Philip R. Scott DVM&S DSHP CertCHP FRCVS, Faculty of Veterinary Medicine, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, UK Jan K. Shearer DVM MS, College of Veterinary Medicine, University of Florida, Gainesville, USA I. Martin Sheldon BVSc DCHP DBR DipECAR PhD ILTM MRCVS, Unit of Veterinary Reproduction, Royal Veterinary College, Hatfield, UK David Sjeklocha DVM, Curtis, Nebraska, USA Alistair K. Smith BVM&S DBR MRCVS, Ovaflo Bovine Embryo Transfer, Skene, Aberdeen, UK Neville F. Suttle BSc PhD, formerly of the Moredun Research Institute, Penicuik, UK

List of Contributors

Shaun Sweiger DVM MS, Edmond, Oklahoma, USA Mike Tame BSc PhD Principle Associate, Abacus Organic Associates, East Stour, Dorset, UK Andrew J. Taylor MA VetMB MRCVS, formerly Senior Veterinary Surgeon, Genus Breeding Limited, Chippenham, UK Mike A. Taylor BVMS PhD MRCVS, VLA Veterinary Surveillance Unit, Central Science Laboratory, York, UK Stuart M. Taylor BVM&S MRCVS, formerly Senior Veterinary Research Officer, Stormont, Northern Ireland Lovell R. Thomsett DVD FRCVS, formerly Senior Lecturer, Royal Veterinary College, Hatfield, UK Tore Tollersrud DVM PhD, National Veterinary Institute, Oslo, Norway J. R. Townsend DVM, College of Veterinary Medicine, University of Florida, Gainsville, USA

•

ix

Patricia R. Watson BSc PhD, Division of Environmental Microbiology, Institute for Animal Health, Compton, UK A. David Weaver BSc DrVetMed PhD Dr(hc) FRCVS, Emeritus Professor, University of Missouri, Columbia, USA G. Henk Wentink DVM PhD, Research Institute of Animal Husbandry, Lelystad, The Netherlands David A. Whitaker MA VetMB MVSc MRCVS, Department of Veterinary Clinical Studies, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, UK J. Mike Wilkinson BSc PhD CBiol MIBiol, Chalcombe Publications, Welton, Lincoln, UK The late Bernard M. Williams DVSM PhD MRCVS, formerly Head of the Veterinary Investigation Service, Ministry of Agriculture, Fisheries and Food (now DEFRA), Tolworth, UK

Chris Venables BSc MIBiol CBiol, Veterinary Laboratories Agency, Addlestone, UK

Roger S. Windsor MBE BVM&S BSc MA MRCVS, formerly Veterinary Centre Manager, Scottish Agricultural College, Veterinary Science Division, Dumfries

Jos J. Vermunt Institute of Veterinary, Animal & Biomedical Sciences, Massey University, New Zealand

Geraint Wyn-Jones BVSc Hons DVR MRCVS, Meadowbank Veterinary Centre, Northop, UK

Timothy S. Wallis BSc PhD, Division of Environmental Microbiology, Institute for Animal Health, Compton, UK

Gilbert B. Young PhD MRCVS, formerly Director, Animal Breeding Research Organisation, Edinburgh, UK

Preface

It is now about ten years since the first edition of Bovine Medicine was published. While it was originally anticipated that it would be used mainly in Britain and Europe, it is pleasing to note that a good proportion of the sales have been in other parts of the world. In recognition of this, more emphasis has been placed on conditions and their treatment in areas other than temperate regions. Additionally, a new section gives an insight to the differences in bovine medicine as practised in various parts of the world. Almost all parts of the book have been updated or completely rewritten. There are some new chapters, including one which integrates the various problems which occur in cattle, another on basic surgical techniques and others on artificial insemination and embryo transfer. An effort has been made to encompass all the main subjects which occur in the husbandry and diseases of cattle. I wish to thank all the authors and co-editors for their hard work. Roger Blowey, Hugh Boyd and Roger Eddy have provided advice and assistance despite their many commitments. I would also like to thank John Sproat for supplying the photographs of cattle used on the end papers. Every effort has been made to identify copyright holders of material reproduced in this book. Any inad-

vertent omissions will be rectified in any future reprint or edition of this work. I hope that everyone reading the new edition will find it to be an interesting source of information.

Readers’ note Inevitably, when it comes to therapies, medicines and vaccines, each country has different needs and requirements. The laws concerning the use of particular therapeutic and preventative agents may vary and the reader is reminded that it is his or her duty to ensure that any preparation prescribed conforms with all relevant national legislation where the preparation is to be used. It is also essential to ensure that dosages and routes of administration are determined according to any national or local directions and other product information which has been provided with the medicine. While every effort has been made to ensure that the uses suggested and doses recommended are correct they should always be checked with currently available information. It must also be remembered that any meat withdrawal time or milk witholding time for drugs should follow the guidelines of the country in which a drug is used. A.H. Andrews

xi

Preface to the First Edition

Bovine Medicine aims to provide, within the covers of one book, much of the practical information available on cattle disease and production. Such an objective is admirable in sentiment but very difficult to achieve in practice. It involves the concentration of effort by a large number of different, and often very busy, experts into one volume. For the present part it is hoped that what we have produced will not only be a source of information but, in many areas, it will be an enjoyable, educational read. It is hoped that it will be used as a working guide rather than a reference book and that it will be of particular help to those at the ‘sharp end’ of the veterinary profession, i.e. in practice. Bearing this in mind, this work does not contain every detail concerning each disease, organism or clinical entity. Inevitably there are some areas of subject overlap as might be expected with skin conditions and ectoparasites and ‘downer cow’, etc. Where possible each author has provided his or her own perspective on the subject. In addition, references have been kept to a minimum to ensure a less disjointed read. In consequence, we

xii

would be pleased to receive comments from readers on any deficiencies or difficulties encountered in presentation or content. It has taken approximately 2 years to complete a work of this magnitude. The continual expansion in veterinary knowledge and expertise may well mean that in certain areas some recent developments have been omitted. Again, we would be pleased for any such deficiencies to be pointed out to us. There has been considerable recent interest in alternative medicine for animals. Mindful of this, a section is included on the subject to help readers make up their own minds on its relevance to cattle therapy. I must thank Blackwell Science, and particularly Peter Saugman for his patience during the production of this book. Much work has also fallen on my coeditors Hugh Boyd, Roger Blowey and Roger Eddy. However, the book would not have been completed but for the dedicated secretarial and managerial help of Mrs Rosemary Forster. A.H. Andrews

Part 1

MANAGEMENT

Chapter 1

Calf Rearing D.M. Allen

Introduction Calf reception Rearing systems Early weaning: bucket feeding Early weaning: machine feeding Follow-on rearing Performance targets Veal production Calf identification

3 3 3 4 5 5 5 5 6

Introduction Whether calves from the dairy herd are being reared as dairy herd replacements or for beef production, a good start in life is essential. Calves of subnormal weight at three months of age tend to lag behind throughout the growing period. The starting point for good calf rearing is the consumption of at least 2 litres of colostrum by suckling or bucket feeding within the first six hours of life and a further 2 litres within 12 hours. The passive immunity conferred on the calves by the immune lactoglobulin in colostrum is vital to disease resistance, especially if calves are transferred to another farm for rearing, probably via a collection centre or auction. Mortality among calves deprived of colostrum is high. Therefore, it is advisable to keep some colostrum in a freezer in case of emergencies. Colostrum is a rich feed and a good source of the fat soluble vitamins A, D and E. Therefore it is sensible to feed all available colostrum even to calves that are beyond the stage when they can gain passive immunity.

Calf reception Dairy-bred calves for beef rearing are usually purchased at about two weeks of age, often from a calf group or dealer. When they arrive at the farm, calves should be inspected individually and any showing signs of ill health returned to the supplier or isolated. Navels should be dipped in a concentrated iodine or phenol solution to guard against navel ill and joint ill. Any

calves with signs of lice should be treated with an approved ectoparasite product. A multivitamin injection containing vitamins A, D and E is good value for money. The calves should be housed in pens bedded liberally with dry straw and clean, fresh water should be made available. Milk is best withheld for a few hours after arrival but any calves that appear stressed may be given a warm drink of 1 litre of a proprietary electrolyte solution. If calves are housed individually, which is permissible up to eight weeks of age, pens should be at least 1.8 ¥ 1.0 metres and should permit visual and physical contact with at least one other calf. Group-housed calves up to 150 kg liveweight need a minimum space allowance of 1.5 m2, rising to 2.0 m2 at 150–200 kg. Pen floors should have a slope from back to front of at least 1 in 20 to permit good drainage. Calves do not mind cold weather but need good ventilation without drafts. The modern trend in temperate climates is to erect simple monopitch buildings in which calves can be housed until they are 12 weeks or older. In the coldest weather straw bales or wooden sheets can be placed above the rear half of pens to provide more insulation. Where calves are single-penned, the pens are dismantled at weaning and the calves left where they are as a rearing group. If buildings and pens are used continuously for calf rearing, after each batch they should be power washed or steam cleaned, disinfected and left empty for at least two weeks before restocking.

Rearing systems In high yielding dairy herds, calves are weaned off their dams as soon as possible after they have received colostrum and are reared by the early weaning system pioneered in the UK but also applicable worldwide. Calves can be weaned off milk replacer after five to seven weeks, which makes the system convenient and saves money compared to weaning at an older age. The secret of success is to ensure that individual calves are eating at least 1 kg per day of a palatable early weaning concentrate before they are weaned. 3

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Chapter 1

The commonest rearing system is a twice daily bucket feed of milk replacer, but some rearers use computercontrolled machines that mix milk replacer and provide it to the calves via teats from which they suckle. In the EU, where milk production is subject to milk quotas, milk produced over the quota has no market value so it is sensible to feed it to calves rather than purchase a milk replacer. However, if milk production is at or under quota, a milk replacer should be used. Feeding whole milk needs just the same attention to temperature and feeding level as milk replacer. The high cost of dried skimmed milk on which milk replacers used to be based has led to the development of so-called ‘zero’ milk replacers. These are based on dried whey supplemented with fats and lactose to equate as closely as possible to cow’s milk. Whey-based replacers are up to 25 per cent cheaper than skimmed milk products but can give equally good results. For bucket feeding, replacers are mixed at 125– 150 g/l, according to the manufacturer’s recommendation. The mix is made up with water at 45–50°C so that the temperature at feeding is 42°C. Automatic feeding machines mix replacer at 100–125 g/l but can be set to vary reconstitution rates according to the stage of rearing. It is essential to keep all feeding equipment scrupulously clean. Scouring and pneumonia are the twin scourges of calf rearing. Typically, calf mortality is 5 per cent, mainly due to these two causes, but it can rise to 10 per cent. The target in a well-managed calf rearing unit should be to keep mortality below 3 per cent. Scouring is most likely in the first two weeks following removal from the dam and may be simply because the calf has been overfed or the milk replacer is at the wrong temperature. However, it may also be caused by pathogenic organisms. E. coli is the classic cause but a survey of calf units by practising veterinarians identified a number of other pathogens responsible for scouring. The immediate reaction to scouring is to take the calf off milk and feed a warm electrolyte solution. If the scouring does not start to clear up within 24 hours veterinary advice should be sought. Antibiotics should only be used on veterinary prescription. If salmonella infection is suspected, veterinary advice should be sought straight away and rectal swabs taken for laboratory analysis so that the appropriate antibiotic can be prescribed. Infected calves should be isolated. Many Salmonella species are transmissible to humans so during an outbreak special attention needs to be paid to personal hygiene. Salmonellosis usually occurs in the first two or three weeks of life but can occur later, even beyond the milk feeding period (Chapter 15). Pneumonia can occur at any time but is most prevalent in still, damp winter weather and is exacerbated if

calves are moved at this time. Frequent observation is needed to identify the early symptoms of pneumonia – listlessness, holding back at feeding time, a runny nose, rapid breathing or coughing. Veterinary advice should be sought straight away. Not only is pneumonia a major cause of calf mortality but also infected calves that recover often fail to thrive due to lung damage. Dehorning and castration are stressful and so should not be done together, nor should they coincide with the stress of weaning. Healthy calves can be dehorned three weeks into the rearing period using a hot air or hot iron disbudder, with castration at four weeks.

Early weaning: bucket feeding The commonest early weaning rearing method is twice daily bucket feeding with weaning at five to seven weeks. With milk replacer mixed at 125 g/l, the first full feed for a purchased calf is 1 litre. Home-bred calves are fed this level twice daily until they are about five days old, then the feeding level per feed is increased by 0.25 litres every other day up to a maximum of 2 litres per feed, that is 4 litres per day. Some expert calf rearers have found a useful saving in labour, without detriment to calf performance, by feeding the calves milk replacer once daily after the first seven to ten days. In this case the feeding level is built up gradually to 3 litres per day. However, the saving in labour should not compromise calf inspection, which should continue frequently to detect health problems. From the start calves are fed an early weaning concentrate containing 18 per cent crude protein and with a good amino acid profile, since the calf needs some of its protein intake to escape fermentation and degradation in the forestomachs. The energy value should be at least 12.5 MJ ME/kg DM. Even the youngest calves crave some roughage in their diet and, rather than letting them pick up straw from the bedding, it is better to feed hay or straw from a rack. Hay is rarely of good enough quality for calves and, even if it is, they eat too much of it at the expense of concentrates and become pot-bellied. Instead, feed bright, dry barley or oat straw. As previously mentioned, calves must be eating at least 1 kg concentrate per day before they can be weaned. Weaning may be abrupt after about 35 days, or a gradual weaning procedure may be used in which the level of milk replacer is reduced gradually over an additional 5–10 days to encourage concentrate consumption. Gradual weaning avoids the check to growth that accompanies abrupt weaning. The early weaning concentrate should be fed ad libitum until it is replaced by a cheaper follow-on concentrate, or until it is rationed as forage feeds are introduced (p. 5).

Calf Rearing

The consumption of milk powder is 15–20 kg and the target daily gain to weaning is 0.5–0.6 kg/day, depending on breed type and sex.

Early weaning: machine feeding Feeding milk ad libitum to group-housed calves can be the preferred choice where the buildings used for calf rearing do not lend themselves to the erection of individual pens or, as in dairy herds, where calves are born over a long period. The saving in labour is not as great as might be supposed because, although mixing is automatic and cleaning is quicker, handling the calves is more time consuming, especially teaching them to suckle. The most sophisticated machines are computer controlled and recognize individual calves fitted with an electronic tag. So mixing rates and feeding levels can be varied from calf to calf, including a gradual weaning procedure. Some machines can feed whole milk as well as milk replacer and even dispense a small quantity of concentrates to encourage calves to eat dry feed immediately after suckling. Of course these machines are expensive but the cost is spread over up to 80 calves that can be reared at a time, so the annual depreciation per calf may be reasonable. A cheaper approach to ad libitum feeding held sway for a time but is little used now. This was to feed cold acidified milk which stays fresh for two to three days stored in a simple plastic bin and is led to a teat through a tube fitted with a non-return valve. The equipment is cheap but lacks the sophisticated control of individual calves achieved by computer-controlled feeders. Calves are trained to suckle about 1 litre of milk replacer and then the milk supply is removed until the next feed. The procedure is repeated twice in the next 24 hours and then calves are allowed to suckle ad libitum, with not more than six calves per teat. Intake may be depressed in the coldest winter weather and then it is advisable to use an immersion heater to take the chill off the milk replacer. The feeding equipment should be cleaned thoroughly between mixes. A trough containing early weaning concentrates should be placed near the teats, but far enough away to avoid spoilage by saliva or spilt milk. Calves fed ad libitum consume more milk replacer than restricted bucket-fed calves. This manifests itself as rather loose faeces that must be differentiated from scouring. The high replacer intake inhibits early concentrate consumption and may delay weaning. Therefore, it is important to employ a gradual weaning programme to allow weaning at five to seven weeks. Even at these high intakes of milk replacer, it is essential that fresh water should always be available.

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5

Consumption of milk replacer powder is 25–30 kg and the target daily gain to weaning is 0.6–0.7 kg/day, depending on breed type and sex.

Follow-on rearing When calves are weaned at five to seven weeks the early weaning concentrate must continue to be fed ad libitum. In the case of calves going into intensive beef systems, concentrate feeding continues to appetite through to 12 weeks, although the finishing diet is introduced gradually from eight to ten weeks. Where calves are designated for forage-based beef systems, forage is introduced by the tenth week and the early weaning concentrate is replaced by a cheaper mix. When calves reared through the winter are to be grazed in the next summer, it is important to hold gains at 0.6–0.8 kg/day until turnout in the spring or the ability of the calves to exhibit extra rapid compensatory growth on high quality grazed grass will be inhibited. To achieve this the follow-on concentrate needs to be rationed at about 21/2 kg/day with forage fed to appetite.

Performance targets Performance targets for early weaned bull calves fed concentrates ad libitum to three months are shown in Table 1.1.

Veal production Veal production is a specialized system of calf rearing designed to produce a white meat that is especially popular in Italy and Germany. Traditionally, calves were housed in narrow crates and fed milk only until slaughter at 14–16 weeks, producing a carcass of 100–110 kg. Subsequently the feeding period was extended to 22 weeks or more to produce a carcass of 160+ kg. Consumer revulsion at the unnatural production method has brought about considerable changes in the way veal is produced, sanctioned by EU and national legislation. For example, veal crates have been banned in Britain since 1990, although EU legislation does not ban existing crated housing in continental Europe until 2006. Similarly, legislation stipulates a minimum iron content for calf milks and insists that calves over two weeks of age have access to digestible solid food. The effect has been to promote the production of veal that is pink in colour rather than white. A welfare-friendly veal production system has been demonstrated experimentally in Britain with grouphoused calves fed milk replacer from a machine and

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Chapter 1

Table 1.1 Calf rearing targets to three months of age for bull calves fed concentrates ad libitum. Source: Meat and Livestock Commission (MLC). Bucket feeding

Machine feeding

Holstein–Friesian Hereford ¥ F

Charolais ¥ F Simmental ¥ F

Holstein–Friesian Hereford ¥ F

Charolais ¥ F Simmental ¥ F

15–20 170

15–20 185

25–30 160

25–30 180

Liveweight (kg) Purchase Weaning 3 months

50 68 110

55 76 120

50 71 115

55 80 130

Daily gain (kg) Preweaning Post weaning

0.5 0.9

0.6 1.0

0.6 0.9

0.7 1.0

Feeds (kg) Milk powder Concentrates

F = Holstein–Friesian.

supplemented with barley straw as a source of roughage. Carcasses were acceptable to the veal trade but variability of performance was an unsolved problem. In the Netherlands, the main EU veal producer, there are now two approaches to veal production. First there is a white veal system in which group-housed calves are fed largely on milk replacer but with limited access to maize silage (which does not affect meat colour). The calves are slaughtered at about six months of age at around 285 kg liveweight. A pink veal system is also employed by some producers in which calves are fed about 40 kg milk replacer powder plus 500 kg concentrates and 500 kg maize silage. The calves are slaughtered at about 32 weeks at a weight of around 320 kg.

Calf identification A beneficial consequence of the BSE crisis and subsequent foot-and-mouth disease epidemic is a realization

that being able to trace the whereabouts of cattle throughout their lives is an essential requirement of food safety for people and disease control in cattle. Traceability is subject to EU legislation. The British Cattle Tracing System (CTS) is administered by the British Cattle Movement Service (BCMS) that commenced operations in September 1998. This fully computerized system was preceded by a paper passport system that started in July 1996. A one-off survey was undertaken of all cattle in 2000, including older cows and bulls which did not have passports, so that all cattle could be included in the BCMS database. Calves must be double tagged within 36 hours of birth unless they are being sent for immediate slaughter. An application for a passport must normally be made within seven days of tagging but calves can be moved twice during the first 28 days of life, using the reverse of the cattle passport application form as a temporary passport. An all-numeric numbering system has replaced the former alpha numeric identity.

Chapter 2

Suckler Herds D.M. Allen

Introduction Planning the suckler herd Choice of bull Choice of cow breed type Rearing replacement heifers Suckler herd management Suckled calf management Grassland management Targets of performance

7 7 7 8 9 10 11 12 13

Introduction The key indicator of profitability and technical efficiency in suckler herds is the calf output produced annually from each cow that is bulled. The most profitable herds owe their success to producing a large number of live calves per 100 cows bulled, with low calf mortality, rapid growth to weaning and a high sale value per kg for well-reared calves. This is as true under dry range conditions as it is on productive temperate grassland. Suckler herd management is not the simple matter it may seem at first sight, with a cow suckling a single calf. The linked components are reproductive efficiency, milk production and growth. However, in practice the body condition of cows is a simple and sensitive barometer of their nutritional status and potential performance. Controlling body condition through the year is the key to high herd output at low cost. Most beef suckler cows are kept on marginal land in upland or range areas where winter (or dry season) feeds are scarce. So it is common for calves to be sold at weaning, or after a period of further feeding, to finishers on better land. However, increasingly in UK upland herds where suitable buildings are available, male calves are finished as bull beef on purchased concentrates.

Planning the suckler herd Fitting a suckler enterprise into farm resources is as important to profitable production as herd manage-

ment. Can the herd be integrated with a sheep flock? Are there arable crop residues that can be used to cheapen cow feeding? Are buildings and feeds available to add value to calves by feeding them beyond weaning? The answers to these and other relevant questions provide the framework on which a profitable enterprise can be built. Particularly important is the choice of season of calving. Most herds calve in the spring or at the start of the rainy season because this minimizes cow feeding costs. The cow is working hardest suckling her calf on low cost, high quality grazed forage. On productive grassland autumn calving is an option, the extra cost of winter feeding cows suckling calves being offset by greater calf weaning weight. Autumn calving usually achieves the highest financial gross margin per cow, but spring calving rivals its gross margin per hectare. The need to reduce production costs has forced many former autumn-calving herds to change to spring calving. The decision on calving season may be forced by the availability of housing and labour, regardless of feed availability. Housing allows a choice of calving season and avoids poaching of land by outwintered stock. However, the provision of housing increases fixed costs on the farm.

Choice of bull The bull contributes half the genes of all the calves sired by him and so choice of breed and individual bull are both critical to herd performance. Even at weaning, when maternal effects are expressed at their maximum, sire breed has a greater effect on weaning weight than dam type. Heavy breeds such as Charolais and Simmental are generally used as terminal sires, that is to produce the slaughter generation. They sire calves with the highest weaning weights (Table 2.1) and the rapid gains are carried through into the post-weaning period. However, the cost of this extra growth performance is a higher proportion of assisted calvings and greater neonatal calf mortality (Table 2.2). Overall, nevertheless, calves sired 7

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Chapter 2

by heavier breeds produce the greatest annual output of weaning weight per cow. It is several years since these survey data were collected and there may have been subsequent changes in the relative performance of breeds. Also, breeds such as the double-muscled Belgian Blue are now available to commercial producers in the UK. This breed is just below the Charolais in growth performance but has greater dystokia. Belgian Blue crosses have exceptional carcass characteristics with high killing out and meat yield percentages. Limousin crosses are also outstanding for these characteristics. Most commercial suckler herds in Britain have opted for continental terminal sire breeds, especially Charolais, Limousin and Simmental. However, some producers prefer local breeds or use Angus bulls to gain quality premiums that offset poorer growth performance. Easy care Angus and Herefords are often selected in pastoral and range countries where large numbers of cattle are managed by a single stockworker. Breed choice would

Table 2.1 Effects of sire breed on calf 200-day weights. Source: Meat and Livestock Commission (MLC). Sire breed

Hereford 200-day weight (kg) Difference from Hereford (+/- kg) Charolais Simmental South Devon (North) Devon Lincoln Red Sussex Limousin Aberdeen Angus

Type of farm Lowland

Upland

Hill

208

194

184

+32 +24 +23 +17 +14 +7 +7 -14

+33 +28 +27 +21 +20 +13 +10 -12

+21 +14 +16 +7 +5 +2 +2 -8

also be affected if herd replacements are home bred. Then easy calving breeds with good maternal abilities would be preferred (see p. 9). The selection of an individual bull within a breed is just as important as breed choice. In recent years bull selection has been transformed by the development of a sophisticated statistical method of analysing breeding records from pedigree herds, known by its acronym BLUP (best linear unbiased predictor). The analysis of records from all related cattle, whatever herd they are in, effectively disentangles management and genetic effects on performance to calculate estimated breeding values (EBVs) that can be used with confidence to select bulls of above average genetic merit. In Britain the recording agency Signet combines EBVs for selected performance characters into selection indices of overall genetic merit. There are two such indices. The calving value is used where ease of calving is paramount, for example for heifer matings and in the selection of bulls to breed female replacements. The beef index is used for bull selection when growth rate and carcass quality are the objectives, for example for terminal sires in suckler herds. Signet publishes EBVs and selection indices for participating breeds. A maternal index is under development.

Choice of cow breed type In range countries the tradition was to keep purebred herds of Angus, Hereford, Shorthorn or local breed cattle. To some extent that tradition still exists. For example, French suckler cows are still largely purebred. However, crossbred cows have a considerable advantage over purebreds due to hybrid vigour (or heterosis), which is most pronounced for improved reproductive efficiency. The outcome is that the weaning weight of calves from crossbred cows is 15–25 per cent above the average of the parent breeds. Add to this an

Table 2.2 Effects of sire breed on calving ease and annual productivity. Source: Meat and Livestock Commission (MLC). Sire breed

Charolais Simmental South Devon (North) Devon Limousin Lincoln Red Sussex Hereford Aberdeen Angus

Assisted calvings (%)

Calf mortality (%)

Calving interval (days)

Calf weaning weight per cow per year (kg)

9.0 8.9 8.7 6.4 7.4 6.7 4.5 4.0 2.4

4.8 4.2 4.0 2.6 3.8 2.0 1.5 1.6 1.3

374 374 375 373 375 373 372 372 370

208 203 203 200 199 198 196 189 179

Suckler Herds

improvement in longevity and the lifetime advantage to crossbreds is considerable. Recognition of the benefits of crossbreeding in Britain is as old as the development of breeds themselves. Traditional crossbreds include the celebrated Blue Grey (White Shorthorn bull ¥ Galloway cow), Shorthorn ¥ Highland and Irish-bred Blue Grey (Angus ¥ Dairy Shorthorn). As supplies of these traditional crosses started to become scarce some 30 years ago, beef breed ¥ dairy cows started to be used as suckler cows, notably Hereford ¥ Friesian and Angus ¥ Friesian. It was later still that US ranchers discovered the heterosis advantage of Hereford ¥ Angus and the reciprocal cross over either of the pure breeds. The Hereford ¥ Friesian was, and still is, widely used as a suckler cow. It produces more milk than the Blue Grey and weans a heavier calf; however, the Blue Grey has better reproductive efficiency and, overall, performance of the two crosses is similar. Both crosses share the advantage of medium body size. Heavy cows such as Charolais ¥ Friesian need more feed but are unable to translate enough of their greater weight into heavier calf weaning weight to rival the efficiency of a lighter breed type. Nonetheless, many British suckled calf producers use these heavier cows and are prepared to trade a theoretical reduction in efficiency (that may not be apparent at farm level) for the improved conformation of calves which commands a premium at the calf sales and later in carcass value. The penetration of the Friesian breed by extreme dairy Holstein genes from North America has caused such a deterioration in beef breed ¥ Friesian cow conformation that it shows through in the calf. This has sparked off a search for alternative suckler herd replacements that are crossbred with good maternal qualities and have acceptable conformation. Moreover, in the wake of the BSE crisis many herd owners wish to breed their own replacements so that they can maintain a closed cow herd. Merely saving heifer calves from terminal sire breeds such as Charolais increases cow size progressively and reduces maternal performance – the worst of all worlds. The simplest planned approach to breeding replacements is to breed about half the herd to a sire breed of medium size with good maternal qualities, for example Angus or Salers. In smaller herds this is best done by artificial insemination (AI). In the next generation, Angus cross females, for example, might be mated to Salers whose female progeny are in turn mated back to Angus. This two-breed rotation is known as crisscrossing. The other half of the herd would usually be mated to terminal sire breeds. Bulls for breeding herd replacements should be selected to have a good calving value index (which incorporates EBVs for calf birth weight, ease of calving

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9

score and gestation length) and a high EBV for 200-day milk (an estimate of the genetic merit for milk production that the sire passes to his female offspring). In some parts of the world, notably the US, sophisticated breeding programmes have been used to create composite breeds combining the best features of three or four foundation breeds. A composite may be bred to feature maternal qualities, terminal sire qualities, heat tolerance and so on. A four-breed composite is effectively a purpose-bred pure breeding population that retains up to 75 per cent of the hybrid vigour of the initial first (F1) crosses between the original four breeds. The creation of composite breeds needs very large numbers of cattle. However, commercial suckled calf producers with relatively small herds will have access to composites from international genetics companies with large-scale breeding operations involving thousands of cattle. The main demand will be for purposebred suckler herd replacements of good maternal ability.

Rearing replacement heifers The replacement policy in a suckler herd should involve culling cows that are persistently barren, calve unacceptably late or are on the verge of the emaciation commonly associated with old age. A typical replacement rate is 16 per cent which indicates an average herd life of seven years. In the UK, culling policies have been disrupted in the wake of the BSE crisis by the Over Thirty Month Scheme (OTMS) in which the carcasses of cattle over 30 months old are removed from human consumption. Compensation payments for culls are much lower than cull cow values before the BSE crisis and this will continue to inhibit planned culling until the scheme is eventually wound down. Replacements may be purchased as calves from dairy herds, as bulling heifers or, less frequently nowadays, as heifers on the point of calving. With calves and bulling heifers it is prudent to purchase a surplus of 15–20 per cent to allow selection. Heifers that prove unsuitable as replacements are slaughtered for beef. In most situations heifers should be calved for the first time at two years of age to optimise lifetime performance. However, autumn-born calves from the dairy herd would usually be calved at 21/2 years in a springcalving suckler herd. In either case, good management is necessary to achieve target mating and post calving weights (Table 2.3). Heifers are best calved at the start of the herd calving period to allow for an almost inevitable slippage in time to the second calving. Also, since dystokia is worst in

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Chapter 2

Table 2.3 Rearing targets for replacement heifers. Mating weight (kg)

Post calving weight (kg)

Two-year calving British breed crosses Continental breed crosses

325 350

510 550

Calving at 21/2 years British breed crosses Continental breed crosses

400 435

540 575

Fig. 2.1

heifers, it is desirable to mate them to an easy calving breed such as Angus or Hereford. Difficult calving is a cause of delayed rebreeding.

Suckler herd management Suckler herd management aims for a high proportion of cows producing live calves in a calving period of 12 weeks or less. The advantages of a compact calving period are, firstly, that herd rationing matches closely the nutritional needs of individual cows, saving feed costs. Secondly, calvings can be supervised closely to provide assistance when needed, reducing calf mortality. Finally, calf performance is uniform with few of the late-born calves that are so difficult to utilize profitably. Generally, a long drawn out calving period is a sure sign of low herd conception rate. Late calvers have too little time to rebreed by the end of the mating season and get later and later, eventually failing to get in calf altogether. The only solutions to an over-long calving period are to cull late calvers or switch them between spring- and autumn-calving herds so that they calve on time. The danger of the latter strategy is that cows shuttle from one herd to the other without the underlying causes of low conception rate being tackled. The main reason why cows fail to conceive is that they are too thin. Under UK conditions, body condition at mating, scored on a scale from 0 (emaciated) to 5 (grossly overfat), needs to be 21/2 in winter but can be as low as 2 if cows are grazing high quality forage and current nutrient intake is high. The key targets that achieve the necessary body condition at mating are a score of 3 in the autumn and 2 at turnout to grazing in the spring. The time to carry out condition scoring is in mid pregnancy, while there is still time to adjust feeding management before calving. The method of condition scoring (Fig. 2.1) is to grip the loin between the thumb and forefinger mid-way between the hip (hook) bone and the last rib on the left

Technique for condition scoring.

side of the cow. The thumb curls over the ledge formed by the transverse processes of the spine to feel the overlying fat cover. It is best to handle cows until experience of the technique has been gained but, thereafter, a skilled stockworker can use close visual inspection to obtain a working guide to condition. Descriptions of condition score classes are presented in Table 2.4. One possible confusion is with continental crosses of good conformation. Their thick muscling may overhang the transverse processes of the spine and confuse handling or visual assessments. If this is the case, condition should also be assessed by handling the ribs with the flat of the hand. If the score is above 3 in the autumn, autumn-calving cows are put at the risk of a difficult calving. If spring calvers score less than 3 in the autumn, the permissible winter weight loss is reduced and feed costs increase. Feeding spring-calving cows through the winter that are at target condition score 3 in the autumn allows the loss of one unit of condition score, which equates to about 100 kg liveweight or 0.5 kg daily. Autumn calvers, on the other hand, must be fed through the winter for the additional strain of lactation and must be at condition score 21/2 when mated in mid-winter. Therefore, in cows at condition score 3 in the autumn a weight loss of only 0.25 kg/day is permissible until they are safely in calf. If there is a time to feed suckler cows generously, this is it. Thereafter, the rate of weight loss can increase to 0.5 kg/day. Autumn-calved heifers are still growing as well as milking and should not be allowed to lose weight through the winter. These guidelines are translated into daily metabolizable energy (ME) allowances expressed as megajoules (MJ) for cows fed a typical moderate quality ration in Table 2.5. It is all too easy during the grazing season to concentrate on calf performance and forget that cows at target condition score 2 in the spring need to gain

Suckler Herds

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11

Table 2.4 Condition scoring of suckler cows. Condition score

Description

0 1 2 3 4 5

Spine very prominent with no detectable fat cover over the sharp transverse processes of the spine Spine still prominent but transverse processes no longer sharp Transverse processes can still be felt, but now rounded with a thin covering of fat Individual transverse processes can now only be felt with firm pressure by the thumb Transverse processes can hardly be felt, even with firm pressure Transverse processes completely obscured with a thick layer of soft fat and puffy fat deposits around the tail head

Table 2.5 Metabolizable energy (ME) allowances for winter feeding suckler cows. Reproduced from Allen (2001) with permission of Chalcombe Publications. Liveweight (kg) Spring calver (a) Precalvinga 500 600 700 (b) Post calvinga 500 600 700 Autumn calver (a) Prematingb 500 600 700 (b) Post matingb 500 600 700 a b

Daily weight loss (kg)

Milk yield (kg)

ME (MJ/day)

-0.5

0

55 62 69

-0.5

10

89 97 105

-0.25

10

99 107 115

-0.5

7

74 81 88

If no weight loss is permissible add 20 MJ ME per day. If no weight loss is permissible add 10 MJ ME per day.

100 kg liveweight by the autumn. If by mid-season there is any doubt that the whole herd or individual cows may not attain the required total gain, action must be taken to rectify the situation. The provision of more selective grazing of fresh pasture may suffice. Alternatively, it may be necessary to take more drastic action with autumn calvers and wean calves early to remove the strain of lactation.

Suckled calf management If cow performance is good, calf performance is usually also good. This is not to say that calf performance looks

after itself. Nevertheless, a compact calving means fewer of the late-born calves have subnormal weaning weights. In addition, achieving target body condition scores in cows is conducive to high milk yield. In most situations the cow is capable of producing as much milk as the calf can suckle. This can lead to problems early in the suckling period, especially with springcalving beef ¥ dairy cows of high milk potential, when calves consume too much milk and scour. If the cause of scouring is viral or bacterial it is worth considering an appropriate scour vaccine. Milk consumption increases quickly during the first month of suckling and, although calves pick at solid food early in life, milk intake dominates calf performance in the first three months. With a cow type of moderate yield potential, milk still accounts for half the calf gain in the third month and in higher yielding beef breed ¥ Friesians this balance is not reached until the fourth month. Nevertheless, by this time the intake of solid food by the calf is increasing rapidly. Milk intake is especially important to the spring-born calf that has a relatively short suckling period of six to seven months. The nutritional requirements of the calf and seasonal grass growth are well matched, although supplementary feeding helps to sustain daily gain from late summer onwards as grass growth and quality decline. Management of the autumn-born calf is more complicated because the suckling period is longer and peak milk yield must be supported on winter rations. The most cost-effective approach over the winter is to feed the cow well in the early months until she is safely in calf and then to rely increasingly on creep feeding calves concentrates and the highest quality conserved forage available. It is energetically much more efficient to feed the calf directly than to increase cow feeding to stimulate milk yield. When autumn-calved cows are turned out to grass in the spring there is a boost to milk yield, but by late summer calves require creep feeding to sustain daily gains. It is wise to wean the calves sooner rather than

12

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Chapter 2

Table 2.6 Performance targets for lowland and upland suckler herds. Continental breed sirea

Calves reared/cow Calf gain (kg/day) Weaning (months) Calf autumn weight (kg) Cow concentrate (tonnes) Calf concentrate (tonnes) Silage (tonnes @ 22% DM) Feeding straw (tonnes) a

British breed sirea

Autumn

Spring (silage)

Spring (straw)

Autumn

Spring (silage)

Spring (straw)

0.92 1.0 10 350 0.25 0.25 6.5 0.5

0.92 1.1 7 280 0.12 0.08 5.0 1.0

0.92 1.1 7 280 0.3 0.08 — 2.5

0.95 0.9 10 320 0.25 0.1 6.5 0.5

0.95 1.0 7 260 0.12 0.05 5.0 1.0

0.95 1.0 7 260 0.3 0.05 — 2.5

Mated to suckler cows of average weight 550–600 kg.

later so that they can be managed separately and the cows left to gain condition before housing. The least stressful way of breaking the bond between calf and dam at weaning is to house the calves. An alternative approach is to put the cows and calves in wellfenced adjacent fields within sight and sound of each other. In most ranching and pastoral countries bull calves are castrated for the convenience of herd management and a preference for steer beef over bull beef. However, in France, Italy and Spain it has become the custom to rear male calves entire because they grow faster and leaner than steers and are more profitable. In the UK, suckler bull beef is increasing and finds a ready market. The most common approach is to wean spring-born bulls in late summer and transfer them gradually over a period of about three weeks to an all-concentrate diet (Chapter 3). For the system to be successful it is a considerable advantage to have a compact calving period so that older bull calves do not pester late-calving cows when they are in oestrus. In any case, cows with bull calves need to be separated from those with heifers by six months of age or there is a risk of premature pregnancy in the heifer calves. For this reason the system works best in spring-calving herds because there is no need to split the herd.

Grassland management Grazed grass is the cheapest and one of the most nutritious feeds available on the farm. With financial margins under pressure, the key to profitable production is to utilize grazing to the full. This involves good grazing management and extending the grazing season where practicable.

Grassland management for suckler herds does not necessarily mean using the levels of nitrogen fertilizer employed by dairy farmers, although this may be the right policy on some productive lowland farms. In practice, especially on the upland farms where most suckler cows are kept in the UK, farmers use only moderate levels of nitrogen fertilizer and rely more on clover to increase sward productivity. Moreover, extensive grassland management is encouraged in the EU by the payment of extensification premiums for stocking lightly. Whatever the type of sward, grazing management should aim to control the average sward height of grazed and ungrazed areas. Cows gain most weight early in the grazing season when average sward height is maintained at 8–10 cm. However, they graze selectively leaving patches that go to seed and are of poor nutritional quality when they have to be grazed later on. So until mid season it is necessary to graze swards more tightly at an average sward height of 6–8 cm to inhibit seed heading. Thereafter, when the risk of seed heading is less and there is an inevitable build-up of dead herbage in the base of the sward, average sward height can be relaxed to 8–10 cm to allow selective grazing. In the period of peak grass growth in early summer, high stocking rates of three autumn calving cows per hectare or four spring calvers are needed to exert the necessary control of sward height. At these relatively high stocking rates it is important to have a reserve grazing buffer in case of reduced grass growth in dry weather. This can be achieved by setting aside an additional 25 per cent of grassland that is conserved as silage if possible, but grazed if necessary. As the season progresses beyond mid season the grazing area needs to increase and this is achieved by grazing aftermaths on fields cut previously for silage or hay.

Suckler Herds

Parasitic worms causing gastroenteritis and bronchitis are less of a problem in suckled calves than in young dairy-bred calves in their first grazing season. Nevertheless, it is advisable to treat autumn-born calves at weaning. In any case, both autumn- and spring-born calves should be treated at yarding to guard against winter scour (Chapter 19). With silage making the priority is a feed with high intake characteristics rather than the highest possible ME per kg dry matter (DM). Cutting can be delayed for a week or so to await dry sunny weather that allows an effective 24-hour wilt for clamp silage, longer for big bales, and produces silage with the best fermentation quality.

Targets of performance The objectives of suckler herd management outlined in this chapter have been compiled into suckler herd

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13

targets appropriate to lowland and upland herds in the UK and other European countries with similar climatic conditions (Table 2.6). For the predominant springcalving herds targets are shown for herds both on grass farms, where silage is the basic winter feed, and on arable farms, where winter diets are based on straw and concentrates. Achieving the physical targets is a prerequisite of profitable production.

Reference Allen, D. (2001) Rationing Beef Cattle, 2nd edn. Chalcombe Publications, Lincoln.

Chapter 3

Beef Finishing Systems D.M. Allen Introduction Planning and budgeting Finishing suckled calves and stores Winter finishing Grass finishing Dairy beef systems Cereal (barley) beef Grass and maize silage beef Eighteen-month beef Grass beef

14 14 15 15 17 18 19 19 20 20

Introduction A whole range of overlapping beef finishing systems is applicable to cattle bred in suckler and dairy herds. The higher the lifetime daily gain of the beef system, the younger is the slaughter age and the lighter the slaughter weight at a stated carcass fat cover. Also, within a given beef system, bulls grow faster and are leaner than steers which, in turn, grow faster and are leaner than heifers. These characteristics of beef systems make it possible to chart average relationships between slaughter age and slaughter weight, illustrated in Fig. 3.1 for Charolais crosses. It is possible to construct similar graphs for other breed types and to predict the likely slaughter weight of cattle slaughtered at a particular age and vice versa. Note that as long as the Over Thirty Month Scheme (OTMS) is in place as a BSE control measure in the UK, beef from cattle over 30 months old at slaughter is destroyed, although this will change from 2004 onwards. Cattle remain in an EU fat class for several weeks. The main EU fat class for bull carcasses is 3 on a five-point scale from 1 (ultra lean) to 5 (grossly overfat) and 4L for steers and heifers, which is the average fat class for all carcasses in Britain. Calves from beef suckler herds on marginal land usually have to be sold in the autumn for finishing on farms with more productive land. However, springborn calves may be overwintered for sale in spring, if buildings and feed are available, and bull calves may be finished on purchased concentrates as suckler bull beef. The heaviest yearling steer calves purchased by fin14

ishers in the autumn may be finished through the ensuing winter for sale at 16–18 months old. Heifers and lighter steer calves are fed a store ration over the winter in preparation for grazing the following summer. Any that fail to finish off grass are yarded for a further winter finishing period. Still, all too many cattle are managed aimlessly with no particular finishing system in mind and are sold finished or in store condition when prices seem favourable. This approach leads to a good deal of trading in suckled calves and stores, some of which may change ownership three or four times in their lifetime. Farm assurance schemes now limit the number of times an animal can be traded within the scheme. Under range conditions in the USA, the growth rate of suckled calves is poorer than on European grass farms. However, feed grains are cheap and a special approach to finishing has been adopted in beef feed lots. Weaned calves from range herds are sold to ‘back grounding’ farms where they are grown on forage at moderate store rates of gain as feeder cattle. They then enter feed lots at 12–18 months of age for rapid finishing over a five-month period on a ‘hot’ high-grain ration. In the case of dairy-bred calves, several distinctive beef systems have been developed. At one extreme is cereal (barley) beef in which bulls fed an allconcentrate diet grow rapidly to slaughter at 11–13 months of age. At the other extreme are forage-based systems in which steers and heifers are either winter finished off silage supplemented with concentrates for slaughter at 16–20 months of age or grass finished in summer at 20–24 months old. In reality, cattle passport statistics indicate that more than a third of steers do not follow any of the production systems described here and are slaughtered at 24–30 months of age. The reason is thought to be that farmers delay slaughter until after they have obtained the second beef subsidy (p. 15), paid from 22 months of age. It demonstrates how subsidy rules manipulate production and marketing decisions.

Planning and budgeting The fall in market prices for beef cattle in the aftermath of the BSE crisis has focused attention on beef system

Beef Finishing Systems

Slaughter liveweight (kg)

700 650 600 550 500 450 400 350 12

14

16 18 20 22 Slaughter age (months)

24

28

Fig. 3.1 Average relationships between slaughter age and slaughter weight for Charolais cross cattle. (Bulls were slaughtered at EU fat class 3, steers and heifers at EU fat class 4L.) 䊉 = Bulls; 䊏 = steers; 䉱 = heifers.

plans and budgets. Formerly, too many beef farmers were preoccupied by the margin between buying and selling prices, or even just the sale price achieved regardless of cost. Now controlling costs, whilst achieving performance targets, is very important. Also essential is maximizing eligibility for EU subsidies, without which profitable production is difficult. The EU beef regime that came into effect in January 2000 is more complex than previous schemes. As before, bulls may qualify for a single Bull Premium and steers for one or both Beef Special Premiums (BSP), the first of which is paid at 9–20 months of age and the second at over 22 months. There is no upper limit on the number of claims provided the stocking rate does not exceed 1.8 Livestock Units (LU) per forage hectare, otherwise claims are scaled back. If a national ceiling of claims is exceeded, payments are also scaled back. Cattle must be retained for at least 2 months after the claim is made. All slaughter cattle, including cull cows, qualify for a slaughter premium provided they have been on the farm for at least two months. Suckler Cow Premiums are paid up to a farm quota and a minimum of 5 per cent and maximum of 40 per cent of claims can be made on heifers over 8 months of age. Complex rules apply to Extensification Premiums paid on farms practising extensive production methods. Detailed rules and rates of payment can be found in official publications. In 2003 discussions were in progress to alter fundamentally the basis of subsidy payments with headage subsidies replaced by area payments. The starting point for planning is a decision on which beef system fits farm resources best, setting performance targets and drawing up a budget to evaluate margin potential. Figure 3.2 presents a budget format that can be used to evaluate finishing systems and shows as an example cereal bull beef from purebred Holstein–Friesian bulls.

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15

If production is based on borrowed capital, it is important to calculate the interest on working capital that must be paid. The conventional method of calculation is the cost of the calf or store plus half the variable costs multiplied by the monthly bank interest rate for the number of months cattle are fed. Sale returns are highly dependent on the quality of cattle produced, especially their conformation. Figure 3.3 illustrates differentials for steer carcasses classified by the EU method, in a conformation range from E (excellent), U+, -U, R (average), O+, -O and P (very poor). Note the severe discount for poor -O conformation, especially for carcasses that stray into what is regarded by most buyers as overfat class 4H. Holstein–Friesian carcasses fall into the poorest conformation classes -O and P and a high proportion of the beef is used for manufacturing. Good conformation classes -U and better contain mainly continental breed crosses. Generally, young bulls sell for the same price per kg carcass or slightly less than steers in deadweight sales, but command a premium at selected live auction markets. Heifers usually sell at a small discount. There is a steady move towards deadweight selling under pressure from supermarket buying specifications.

Finishing suckled calves and stores At the start of a winter feeding period there are two options for steers and heifers. Either the cattle are fed to gain at least 0.9 kg/day, often higher, for finishing that winter. Or they are fed a store ration to gain 0.6– 0.8 kg/day in preparation for grazing the following summer. It is generally held that the profitability of finishing depends mainly on buying and selling skills. It is perfectly true that the feeder’s margin – the difference between the purchase and sale price – determines the average gross margin. However, finishers with the best margins owe much of their success to achieving high standards of cattle performance.

Winter finishing Winter finishing has a feeding period of four to eight months, depending on breed, sex category and individual performance. At the start of the winter the cattle may be yearling suckled calves or older store cattle. Commonly, they are fed rationed concentrates with silage to appetite, but on arable farms arable byproducts may partly or wholly replace grass silage. Steers of all breed types are well suited to winter finishing. Early maturing heifers are less suitable because they finish too quickly at light weights. Nevertheless, continental cross heifers can be winter finished at around 0.9 kg/day on a high forage diet.

16

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Chapter 3

Budget (£/head) A B C D E

Calf or store cost Calf rearing to 3 months: dairy-bred calf Forage costs . . . cattle/ha @ . . . £/hab Concentrate costs 1.9 tonnes @ £100/t Other feeds: straw 0.3 tonnes @ £30/t straights . . . tonnes @ . . . /t by-products . . . tonnes @ . . . /t F Other variable costs: veterinary bedding marketing Miscellaneous Total G Total calf + variable costs (A + B + C + D + E + F) H Sale weight (kg liveweight or carcass) I Forecast sale price (£/kg) J Returns: weight H ¥ sale price I K Gross margin (excluding premiums) L Premiums: 1st beef special premium 2nd beef special premium bull premium slaughter premium extensification premium Total Overall gross margin (including premiums) K + L

a b

Example: cereal beefa (£/head @ 2003 prices) 40 58 0 190 9

10 20 8 10 48 345 475 kg 0.8 £/kg 380 35 0 0 130 50 0 180 215

Holstein–Friesian bull beef. Guidelines on forage costs at 2003 prices: intensive (350 kg N fertilizer/ha) £210/ha semi-intensive (250 kg N/ha) £150/ha extensive (75 kg N or less/ha) £70/ha.

Fig. 3.2

Budget format for beef finishing systems.

185 180 170 165 160

O+

140 –O 4L

4H

Be tte

3

fo rm

145

on

R

at

–U

150

ion

155

rc

Carcass p/kg

175

Fatter Fig. 3.3 Price differentials for steer carcasses of different EU conformation and fat classes. Source: Meat and Livestock Commission price report 1999.

Standards for winter finishing suckled calves and stores are shown in Table 3.1. Continental cross steers slaughtered at two years old or more may be too heavy for some buyers. Suckler bull beef is still relatively new to the UK, but has been commonplace in France for many years. Production is expanding in the UK but demand is limited and it is important to secure a market before commencing production. The system is simplest for springborn calves which are weaned in the autumn and transferred gradually over about three weeks to an allconcentrate diet containing 16 per cent crude protein. However, autumn-born calves weaned in the spring can also be used. The British safety code for bull beef production recommends no more than 20 bulls to a pen but much larger groups are housed in continental Europe. Maize silage is short of protein but has good feed intake characteristics and is an excellent source of energy. In continental Europe maize silage is widely

Beef Finishing Systems

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17

Table 3.1 Standards for winter finishing. Yearling suckled calf British

Feeding period (months) Start weight (kg) Daily gain (kg) Silage (tonnes, 22% DM) Concentrates (kg) Slaughter weight (kg) Carcass (kg)

18-month store

Continental

British

Continental

Steer

Steer

Heifer

Steer

Steer

Heifer

5 320 0.9 3.6 300 455 250

6 350 1.0 3.6 450 525 295

5 310 0.8 4 220 430 235

5 420 0.8 5.7 135 540 300

5 475 0.9 5.9 265 610 340

5 400 0.8 5.5 200 525 290

Table 3.2 Standards for suckler bull beef using continental crosses. Spring-born

Start age (months) Feeding period (months) Start weight (kg) Daily gain (kg) Concentrates (tonnes) Maize silage (tonnes)a Slaughter weight (kg) Carcass (kg) a

Autumn-born

Concentrates

Maize silage

Concentrates

Maize silage

6 6 245 1.4 1.4 — 500 280

6 7 245 1.3 1.0 3.3 525 295

6 6 230 1.4 1.4 — 485 270

6 7 230 1.3 1.0 3.1 510 285

Maize silage at 30% DM.

used as the forage base for intensive bull beef production. The medium-sized feed lots of the Po valley in northern Italy with a few hundred to a few thousand cattle are a good example. In these maize silage comprises 30–50 per cent of ration DM. Maize silage has not been used much for bull beef production in Britain but there is potential for systems in which maize silage forms up to 30 per cent of the dry matter of the diet, producing daily gains not far short of all-concentrate diets. Where suckled calf producers on marginal land have suitable buildings available, bull beef fed purchased concentrates can be a useful way of adding value to herd output. Standards for suckler bull beef are shown in Table 3.2. Achieving the target daily gains is a prerequisite of profitable production. In practice many producers extend the feeding period and take bulls to slaughter weights in excess of 600 kg. At these high slaughter weights there is a danger of feed cost exceeding the

value of daily gain and carcasses being too heavy for buyers.

Grass finishing Grazed grass is the cheapest and potentially the highest quality home grown feed. There is a growing realization of the need to exploit grass better by managing swards to maximize daily gains and, where practicable, to extend the grazing season. In grass finishing systems, achieving high daily gains is especially important so that marketing begins in midseason and reduces cattle numbers in step with declining grass production and quality. Two aspects of management are crucial. Firstly, in the winter preceding grass finishing, gains are held down at a store level so that cattle exhibit rapid compensatory growth when they are turned out onto spring grass. Secondly, grazing should be managed to get the best

18

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Chapter 3

Table 3.3 Specimen winter store rations. Weight (kg)

British cross steer/heifer @ 0.6 kg/day Silage (kg/day)

200 250 300 350 400

18 21 23 26 28

Straw + concentrate (kg/day) 3.5 4.0 4.5 5.0 5.0

+ + + + +

2.0 2.5 3.0 3.5 4.0

combination of daily gains in cattle and regrowth of high quality grass. Grass finishing may commence with stores purchased in the spring or with suckled calves or stores purchased in the autumn that are overwintered before grass finishing. Specimen low cost rations for overwintering cattle are shown in Table 3.3. The lower gain of 0.6 kg/ day is optimum for British cross steers and heifers of all breed types. The higher gain of 0.8 kg/day is suitable for continental cross steers. During the grazing season on set stocked pastures, the provision of a continuous supply of nutritious grass is achieved by controlling sward height (the average of grazed and ungrazed grass). In the first half of the season sward height is controlled at 6–8 cm to inhibit seed heading. Then in the second half of the season, when there is less risk of seed heading and dead herbage begins to accumulate in the base of the sward, grazing height is relaxed to 8–10 cm to allow more selective grazing. The confidence to manage cattle at the high early summer stocking rates needed to achieve this degree of control is helped by adding 25 per cent to the main grazing area as a buffer that can be grazed if grass runs short but is conserved if not needed. From mid-season grazing needs to expand onto aftermath regrowths on areas previously cut for silage or hay. Grazing performance is undermined if cattle, especially those in their first season of independent grazing, become infected with parasitic worms that cause gastroenteritis and bronchitis. Effective control programmes include early season treatment to inhibit the build-up of infective larvae on the sward, mid-season treatment accompanied by a move to fresh aftermaths on fields previously conserved or mid-season treatment with a long-acting bolus to control infection even though pastures carry infective larvae. The choice depends on farm circumstances (Chapter 19). Standards for an overwintering and grass finishing system are presented in Table 3.4. Because the second

Continental cross steer @ 0.8 kg/day Silage + concentrate (kg/day) 16 19 22 20 23

+ + + + +

Straw + concentrate (kg/day)

1 1 1 2 2

3.5 4.5 4.5 5.0 5.0

+ + + + +

3.0 3.0 3.5 4.0 4.5

Table 3.4 Standards for overwintering and grass finishing suckler-bred steers and heifers.

British cross

Continental cross

Steer

Heifer

Steer

Heifer

Winter store period Feeding period (months) Start weight (kg) Daily gain (kg) Concentrates (kg) Silage (tonnes)

6 270 0.6 90 4.5

6 235 0.6 90 4.3

6 300 0.8 500 5.2

6 260 0.6 90 4.5

Grass finishing Turnout weight (kg) Feeding period (months) Daily gain (kg) Concentrates (kg) Slaughter weight (kg) Carcass (kg)

375 5 0.8 50 500 275

345 5 0.7 0 450 245

445 6 0.9 150 600 335

370 5 0.8 50 490 270

BSP is paid from 22 months of age, steers that are close to this age at the end of the grazing season are often yarded for winter finishing just to claim the subsidy. It is a strategy that needs to be costed carefully.

Dairy beef systems In the UK the main dairy herd calving season is in late summer and autumn, which contrasts with many other countries where cows calve in the spring. It reflects the high proportion of milk produced used for year-round liquid consumption. Intensive indoor dairy beef systems can utilize calves born at any time of year. However, grass-based systems work best utilizing calves from the main calving season. At turn-out in the spring these calves are old enough to make effective use of grazed grass.

Beef Finishing Systems

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19

Cereal (barley) beef

Grass and maize silage beef

Cereal beef is a housed bull beef system feeding an all-concentrate diet to slaughter at 11–13 months of age. Carcasses have a creamy white fat which is popular with some supermarkets and independent butchers. However, it is advisable to secure market outlets before commencing production, especially if poor conformation Holstein–Friesians are reared. The system is at its most profitable when it adds value to home-grown grain or home-bred calves. Profitable production is heavily dependent on achieving high target daily gains. The protein content of the diet is reduced progressively from 18 per cent crude protein in the calf ration to 14 per cent in the final finishing ration. From six months of age part of the protein can be supplied by urea. Rumen enhancers such as monensin sodium improve feed conversion efficiency by about 10 per cent, but their continued use in the EU is controversial. Standards for cereal beef are shown in Table 3.5.

Grass silage bull beef was popular in the 1980s as a beef system that made very intensive use of grass, all of which was made into silage. Its flaw was that it was a system designed for its production capabilities rather than market demand. In the original system bulls were 16–18 months old at slaughter, by which time the carcasses were too heavy for many buyers and the fat was coloured by carotene. There are also question marks over the eating quality of beef from bulls over 14 months of age. There is still a place for grass silage bull beef up to 14 months of age and the standards in Table 3.6 are for slaughter at this age. The system could also be used for steers and heifers but, for reasons that have been enumerated already, grass-based systems now place emphasis on the utilization of grazed grass. The section on winter finishing (see p. 15) has already discussed the potential for maize silage in beef production. With up to 30 per cent of the ration DM as maize

Table 3.5 Standards for cereal bull beef. Breed type Holstein–Friesian

Limousin ¥ Friesian

Belgian Blue ¥ Friesian

Charolais ¥ Friesian/ Simmental ¥ Friesian

11.5 1.3 1.8 460 250

12.5 1.3 1.9 500 285

12.5 1.35 1.9 510 290

12.5 1.4 2.0 530 295

Slaughter age (months) Daily gain (kg)a Concentrates (tonnes)a Slaughter weight (kg) Carcass (kg) a

From 3 months of age.

Table 3.6 Standards for grass silage bull beef. Breed type

Daily gain (kg)a Slaughter age (months) Concentrates (tonnes)a Silage (tonnes @ 22% DM)a Cattle/ha Slaughter weight (kg) Carcass (kg) a

From 3 months of age.

Holstein– Friesian

Hereford ¥ Friesian

Limousin ¥ Friesian

Belgian Blue ¥ Friesian

Charolais ¥ Friesian/ Simmental ¥ Friesian

1.15 14 1.1 5.7 7.9 495 270

1.05 14 0.63 6.8 6.6 465 255

1.3 14 0.63 6.7 6.7 513 290

1.25 14 0.94 6.1 7.4 535 300

1.3 14 1.3 5.4 8.3 555 305

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Chapter 3

Table 3.7 Standards for maize silage bull beef production. Breed type

Daily gain (kg)a Slaughter age (months) Protein concentrate (tonnes)a Cereal (tonnes)a Silage (tonnes @ 30% DM)a Cattle/hectare Slaughter weight (kg) Carcass (kg) a

Holstein– Friesian

Hereford ¥ Friesian

Limousin ¥ Friesian

Belgian Blue ¥ Friesian

Charolais ¥ Friesian/ Simmental ¥ Friesian

1.25 13 0.50 1.0 3.8 8.7 490 265

1.2 12.5 0.47 0.7 4.0 8.3 455 245

1.25 13.5 0.52 0.7 4.4 7.5 510 285

1.3 13.5 0.52 0.7 4.4 7.5 530 300

1.3 13.5 0.52 0.75 4.4 7.5 535 300

From 3 months of age.

silage there is little decline in daily gain from cereal beef levels. Experience of the system is limited and so the bull beef system presented in Table 3.7 is somewhat speculative. It is based on 25 per cent of the ration DM as maize silage supplemented with a protein concentrate and cereal. Profitable production is heavily dependent on a high yield of good quality maize silage and achieving target daily gains. Continental ¥ Friesian heifers may be suitable for maize silage beef fed to gain about 1.0 kg/day and slaughtered at 435–450 kg liveweight.

Eighteen-month beef Eighteen-month beef is a grass-based system that utilizes dairy-bred steers born in the autumn. It is the original planned system of production in the UK. Calves are reared through their first winter, grazed from six to twelve months of age and then finished in their second winter on rationed concentrates with silage to appetite. Heifers may be used for eighteen-month beef, but are better suited to grass finishing. Profitability depends heavily on achieving good grazing performance. In farm practice this has taken second priority to making a large tonnage of first-cut silage. This partly explains the poor financial margins achieved in recent years. In addition, the system has a relatively high concentrate requirement, a high silage requirement and, at best, steers only qualify for a single BSP payment. The principles of good grazing management described for grass finishing (see p. 17) apply equally to eighteen-month beef. The cattle graze for the full season and so, from mid-season, there is a need to expand onto fresh aftermath grazing on areas previously cut for silage as the cattle grow heavier, but grass

production and quality decline. In addition, there is a strong case for supplementing calves with about 1 kg concentrate daily for two or three weeks after turn-out in the spring until they become accustomed to grazing. Also, supplementation should be reintroduced in late summer to counter rapidly declining grass quality, starting at 1 kg daily and building up to 2 kg daily for a month before housing. Standards for the system are shown in Table 3.8. The overall daily gain of 0.9 kg for Limousin ¥ Friesian steers is made up of 0.8 kg/day through the rearing winter, 0.8 kg/day during grazing and 1.1 kg/day in the finishing winter. The finishing gain would be achieved at an average concentrate consumption of about 2.5 kg cereal or concentrate with good quality grass silage to appetite. Limousin ¥ Friesian heifers would be managed at an overall daily gain of 0.8 kg/day to a slaughter weight of 450 kg.

Grass beef Grass beef is the most extensive of the planned dairy beef systems. Farmers see it as a low cost system that maximizes subsidy income. At best, steers qualify for both BSP payments, an extensification premium and the slaughter premium. Carcasses from continental cross steers may be too heavy for some buyers. Heifers are well suited to the system and can be more profitable than unsubsidized steers. Good grazing gains are essential for profitable production. If first season gains are below target, winter store feeding costs are increased to catch up lost ground. Ideally, winter gains should be 0.5– 0.6 kg/day for heifers and early maturing Hereford ¥ Friesian steers and 0.7–0.8 kg/day for continental cross steers.

Beef Finishing Systems

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21

Table 3.8 Standards for steers in eighteen-month beef. Breed type

Daily gain (kg) Slaughter age (months) Concentrates (tonnes)a Silage (tonnes @ 22% DM)a Cattle/hectare Slaughter weight (kg) Carcass (kg) a

Holstein– Friesian

Hereford ¥ Friesian

Limousin ¥ Friesian

Belgian Blue ¥ Friesian

Charolais ¥ Friesian/ Simmental ¥ Friesian

0.85 18 1.3 5.8 3.4 500 270

0.85 17 0.9 5.1 3.9 460 250

0.9 18 1.0 6.0 3.3 520 290

0.95 18 1.1 5.7 3.5 525 295

0.95 18 1.2 5.5 3.6 540 300

From 3 months.

Table 3.9 Standards for steers in grass beef production. Breed type

Daily gain (kg) Slaughter age (months) Concentrates (tonnes)a Silage (tonnes @ 22% DM)a Cattle/ha Slaughter weight (kg) Carcass (kg) a

Holstein– Friesian

Hereford ¥ Friesian

Limousin ¥ Friesian

Belgian Blue ¥ Friesian

Charolais ¥ Friesian/ Simmental ¥ Friesian

0.73 22+ 0.4 7.0 1.6 555 300

0.68 22+ 0.3 5.7 1.7 515 280

0.75 22+ 0.5 6.7 1.6 585 330

0.80 22+ 0.5 6.7 1.6 595 335

0.83 22+ 0.6 6.7 1.6 610 340

From 3 months of age.

In the second grazing season steers need to be marketed as soon as possible after they qualify for the second BSP to reduce stocking rate as the season progresses. Marketing of heifers should start in mid-season. This need to reduce stock numbers from mid-season in step with declining grass production favours early maturing types of cattle. So early maturing Hereford ¥ Friesian steers fit the system better than late maturing Holstein–Friesians or Charolais ¥ Friesians that may fail to finish off grass and have to be housed for a period of winter finishing. Similarly, early maturing heifers have advantages over later maturing steers. Nonetheless, all the breed types, steers and heifers can be utilized in the system provided their performance characteristics are understood and managed accordingly. Grazing management is complicated by the fact that there are two age groups of cattle on the farm. A

complex leader–follower grazing system was developed in which the younger cattle graze selectively ahead of the older age group. Despite its merits, it is rarely adopted by farmers who prefer to keep the two age groups separate. The principles of good grazing management described for grass finishing (see p. 17) are applicable to grass beef. As with eighteen-month beef there is a strong case for supplementing calves with about 1 kg concentrate daily for two or three weeks after turn-out in the spring and reintroducing supplementation in late summer to counter declining grass production and quality. Standards for steers in the system are presented in Table 3.9. As an example of standards for heifers, Limousin ¥ Friesians would have a lifetime gain of around 0.6 kg/day to slaughter at 20 months of age weighing 500 kg.

Chapter 4

Dairy Farming A.H. Andrews and A. Poole

Structure in Europe and the world Trends of structure in the United Kingdom Milk utilization Dairy breeds Feeding dairy cows Dry matter intake Energy Protein Feeding strategies Minerals and vitamins Grassland farming Grassland production Grassland utilization Winter feeding systems Dairy farm buildings Parlour and dairy Cow housing and feeding barn Feed storage area Calving and isolation boxes Slurry Herd records Physical records Breeding records Milk records Financial records Management Labour Breeding Culling Age at first calving Breed of sire used Genetic worth of the sire Health Economics of dairy farming Measures of efficiency Farm assurance and herd health schemes Organic farming The future

22 24 26 27 30 30 31 31 32 33 33 33 35 37 38 39 40 41 42 42 44 44 45 45 47 47 47 47 47 48 48 48 49 50 50 52 52 52

Structure in Europe and the world Dairy farming in Europe and elsewhere is a very diverse industry and ranges from high-yielding cows in Israel, the USA and Canada as well as within European countries such as the Netherlands, Denmark and the UK to the small, low-yielding herds of Greece, Portugal, Spain and Italy. In many parts of the world milking 22

herds consist of a single cow, often with a calf at foot, or very small numbers of low-yielding cows. This occurs in many parts of Africa and Asia, and in Europe smallish herds are seen in countries such as Greece, Portugal, Spain and Italy. While there have been very gradual changes in the last half-century in Europe and the United Kingdom, the introduction of milk quotas in 1984 accelerated these. In the last decade since the first edition of Bovine Medicine was published the changes have been faster and at the start of the new twenty-first century they have become very rapid indeed. There are increasing trends towards a so-called ‘global market’ with a lowering of tariff barriers. If this continues this will mean that many areas where milk price is directly or indirectly subsidized will have to deal with lowered price for the product. Many areas with low labour costs and good weather to grow crops are starting to gear themselves up to the challenge of producing low cost milk for export to other parts of the world. This is at present particularly occurring in North and South America. Over the past few years much thought has been invested by the World Trade Organization, among others, about increasing the flow of milk and dairy products across the globe. However, the dairy markets are some of the most protected of agricultural products and the Organization for Economic Co-operation and Development estimated in the late 1990s that member states producer support arrangements were, in absolute terms, higher than for all other commodities. It is this background which is causing international trade organizations to find ways to reduce export subsidies paid by countries and to alter tariff quotas for imported products. The introduction of milk production quotas had a very profound effect on the European milk industry. Its aim was to reduce overall European milk production and the changes undertaken by producers to accommodate this altered many milk parameters. The structure in 1983 prior to the change is given in Table 4.1a and the present situation within the enlarged EU is shown in Table 4.1b. The position presented in Table 4.1a was reached over the previous 23 years by each country expanding its milk production through an expanded herd size and increased yield per cow. Total

Dairy Farming

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23

Table 4.1a EEC dairy structure (pre milk quotas). Cows (’000)

Germany France Italy Netherlands Belgium Luxembourg UK Irish Republic Denmark Greece Portugal Spain

Herds (’000)

5451 6506 3120 2333 946 70 3257 1528 913 219 369 1885

Average herd size

363 367 424 58 45 2 54 77 35 77 115 –

Yield (l/cow)

15.3 19.8 7.3 40.8 21.7 29.7 58.2 19.9 28.2 3.1 3.2 –

Total production (’000 t)

4650 3950 3540 5330 3930 4274 4906 3910 5585 3200 3021 3382

26 007 33 337 11 030 12 550 4145 320 17 680 6 480 5 205 770 1 115 6 375

}

Self-sufficiency BF (%)

SNF (%)

116 122 66 256

136 128 63 116

104

116

86 298 212 – – –

104 175 142 – – –

Source: Milk Marketing Board (1986).

Table 4.1b EU dairy structure in 2000 (post milk quotas). Country

Germany France Italy Netherlands Belgium Luxembourg United Kingdom Irish Republic Denmark Greece Spain Portugal Austria Finland Sweden EU Fifteen

Cows (2000) (’000)

Herds (1997) (’000)

Average herd size (1997)

Yield (2000) (kg/cow)

Total production (2000) (’000 t)

Butterfat content (2000) (% by weight)

Protein content (2000) (% by weight)

4 539 4 413 2 172 1 532 629 44 2 339

186 146 102 37 20 1 36

27.9 30.7 20.5 44.0 32.3 36.5 68.8

6157 5844 5113 7302 5420 6030 6133

28 332 24 775 10 774 11 155 3 383 265 14 489

4.22 4.08 3.66 4.40 4.09 4.19 4.01

3.41 3.19 3.26 3.46 3.34 3.34 3.30

1 238

39

32.4

4191

5 280

3.70

3.23

644 173 1 141 355 621 358 426 20 624

13 24 106 70 86 29 16 911

50.8 7.7 11.9 5.2 8.4 13.3 29.6 24.0

7272 4756 5007 5819 4977 6916 7748 5885

4 720 805 5 900 2 057 3 340 2 524 3 348 121 146

4.28 3.67 3.75 3.84 4.13 4.22 4.18 4.07

3.44 3.22 3.09 3.19 3.33 3.29 3.31 3.31

Sources: various including mainly National Dairy Council (2001).

cow population did not increase to the same extent as the number of dairy producers gradually declined. The reasons for this were due to both individual national policies and the then EC requirements.

The Common Agricultural Policy (CAP) set out to increase food production, maintain farm incomes and prevent rural depopulation. This encouraged the very small farms of much of Europe to survive and expand,

24

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Chapter 4

Table 4.2 Production and milk quota (’000 tonnes) for EU Member States. Production

Germany France Italy Netherlands Belgium Luxembourg UK Irish Republic Denmark Greece Spain Portugal Austria Finland Sweden EU Fifteen

Milk quota

1983

1983–84

1991–92

2000–2001

26 429 33 230 11 310 12 782 4 149 319 17 878 6 380 5 361 765

23 792 26 768 9 914 12 197 3 643 294 15 950 5 599 4 933 588

22 927 24 613 9 221 11 213 3 364 272 14 789 5 301 4 525 581

27 865 24 236 10 314 11 075 3 310 269 14 602 5 342 4 455 675 5 917 1 872 2 749 2 407 3 303 118 391

Sources: Milk Marketing Board (1990); National Dairy Council (2001).

while for the larger producers, financial help made dairy farming relatively profitable compared with other sectors of agriculture. Thus total milk production for the 10 members of the EC at that time rose from 87.5 million tonnes in 1965 to 120.7 million tonnes in 1983. The success of the EU milk quota in controlling production is demonstrated by the fact that even in the expanded Union total milk production was 120.9 million tonnes in 1998. While the CAP was proving very satisfactory for dairy farmers, the financial support they were receiving was increasingly threatening the whole EU budget. Most of this aid was provided through intervention buying of surplus products. In fact, sale into intervention became the accepted market rather than the market of last resort. Thus by 1983, self-sufficiency levels rose within the EC to 125 per cent for butterfat (BF) and 166 per cent for solids-not-fats (SNF) (Table 4.1a) and the cost of dairy support made up one quarter of the whole EC agricultural budget. Thus at this stage, milk quotas were imposed to control milk production and each member country had to take a cut of varying proportions (Table 4.2). If national production exceeded the allocated quota then a super-levy was imposed. This super-levy was to be calculated either on a dairy basis or on an on-farm basis. On a dairy basis, if national production and the supplying dairy were over quota, then levy was imposed on the dairy and hence back to the individual over-

quota producers at a rate of 100 per cent of the target price for milk. On an on-farm basis, provided national production exceeded quota, each farm paid super-levy on excess production above its individual quota at a rate of 75 per cent of the target price for milk. In 1987–88 further changes to the means of determining super-levy liability were made so that those producers most over quota paid the highest proportion of the levy, again provided the national quota was exceeded. Quota has been transferable between individual farmers within a member state, either on a sale (attached to land or without, but both are complex) or lease basis (a much simpler procedure) or else on an administratively based system where unused quota reverts to an authority and is re-allocated. Further regulation in 1987 imposed a butterfat ceiling on quotas, thereby giving a reduction in national quota if the average butterfat of 1985–86 was exceeded. Also in 1987 further quota cuts were announced, resulting in a further fall by 1989 of 8 per cent. The calculation of any liability for excess production for a farmer is extremely complex. It depends on the amount of milk over quota and on the average butterfat content of the milk. Each producer has a butterfat reference figure. If a levy is to be charged then the farmer’s production volume will be adjusted up or down by the amount that the butterfat average differs from his/her reference figure. Again levies only arise when national production is too high. The objective of reducing milk production has been achieved. Initially it was envisaged that milk quotas would be phased out in the early 2000s. However, this has not been the case and the CAP reform has extended milk quota until 2006. Special increases in quota were allocated to Italy, Spain, Greece, Ireland and Northern Ireland in 2000 and 2001 in addition to the increase of 1.5 per cent given to all countries in three stages from 2005. The intervention price will be gradually cut from 2005 and it is expected that the system will have been re-examined in detail by then.

Trends of structure in the United Kingdom Changes to the structure in dairy farming in the United Kingdom have mirrored the trends over the last 25 years in Europe. Thus there are fewer producers and slightly fewer cows, but in larger herds and with a higher yield per cow (Table 4.3). This has been brought about by the virtual elimination of the small herd. In 1972, 20 per cent of cows were in herds of less than 30 cows, but by 1997 it was about 5 per cent. This acceleration has increased at the beginning of the new century as milk prices dropped, causing most farms either just to break even or to lose money. The foot and mouth disease outbreak of 2001 has caused more producers to cease milk

Dairy Farming

production, and present numbers of herds are likely to decrease sharply. The December 2001 census showed UK dairy cows down to 2.203 million with in-calf heifers down to 0.442 million. While beef cows were down to 1.673 million, incalf beef heifer numbers rose. The changes to larger herds have been facilitated by new technology and mechanization and a consequent loss of labour. In 1972, 67 per cent of farms milked through a cowshed, with only 28 per cent in 1990.

Table 4.3 The structure of dairying in England and Wales, 1965 to 2001. Year

Producers (’000)

Cows (millions)

Average herd size

Yield (l/cow)

1965 1970 1975 1980 1984 1988 1990 1995 1998 1999 2000 2001

100.5 80.3 60.3 43.4 39.3 31.7 31.5 28.1 24.7 23.3 21.8 20.2

2.65 2.71 2.70 2.67 2.70 2.38 2.33 2.10 1.92 1.94 1.84 1.76

26 33 46 58 67 69 70 74 77 82 85

3545 3755 4070 4715 4950 4870 5020 5380a 5770a 5955a 5940a

a

United Kingdom figures. Source: Milk Marketing Board, 1990; National Dairy Council, 2001.

Fig. 4.1 parlour.

Milking

in

the

herringbone

•

25

Herringbone parlours accounted for only 11 per cent of milking installations in 1972, but made up over 45 per cent in 1990 (Fig. 4.1), and are the main system today. The increased yields have been realized by improved feeding (see Chapter 9), breeding and management techniques. The breed of cow in the UK has altered, 64 per cent Friesian in 1965 moving to over 91 per cent Holstein–Friesian by 1990, which has also made a major contribution. Milk purchase has also undergone some very fundamental changes in the last century. Initially farmers sold direct to dairy companies. However, as the latter became larger the individual farmer had problems in obtaining a fair price. This resulted in Agricultural Marketing Acts in 1931 and 1933, which set up a framework whereby all the milk produced was taken by the Milk Marketing Boards who then had to sell it on the producer’s behalf. The Agricultural Act of 1993 allowed the abolition of the Milk Marketing Boards in Great Britain and from 1 November 1994 the Milk Marketing Scheme was revoked (Northern Ireland from 1 March 1995). In the deregulated market, producers are free to sell their milk wherever they choose including direct to dairy companies, or via intermediary organizations managed jointly by the dairy company and producers, or independent producer groups, usually co-operatives, who either then sell to the dairy companies or process the milk themselves. Many sold milk via Milk Marque, which was considered in 1999 to be a monopoly, resulting in its division into three new regionally based cooperatives, namely Axis, Milklink and Zenith, which

26

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Chapter 4

Table 4.4 Utilization of milk in England and Wales (%) to 1989–90 and in the United Kingdom (%) to 2000.

1964–65 1969–70 1974–75 1979–80 1982–83 1983–84 1984–85 1987–88 1989–90 1993–94a 2000a

Liquid milk

Butter

Cheese

Condensed milk

Cream

Others

73 66 62 50 45 45 48 49 51 86 50

3 10 8 23 31 30 27 23 20 2 2

11 10 16 15 14 14 15 19 18 4 22

5 4 4 3 2 2 2 2 2 2 4

5 7 8 7 6 6 5 3 4 3 2

3 3 2 2 2 3 3 4 4 3 20

Source: Milk Marketing Board (1986); National Dairy Council (2001). a Figures on a different basis to previously.

began to operate as fully independent businesses from 1 April 2000. There has since been more rationalization and mergers, with one group involved in milk purchase in Scotland, England and Wales becoming known as British Milk. Some milk purchasers now have their headquarters outside the UK. The last few years have seen many milk purchasers buying milk from individual farmers or small groups or farmer clubs. In the early part of the twenty-first century the number of purchasers has been reducing and farmers are starting to combine in co-operatives to provide more negotiating power with the purchasers. Milk is now purchased in varying ways, but is usually paid for according to its composition, cell count and bacterial count (undertaken in the UK by a Bactoscan, see Chapter 25). There are also seasonality payments.

Milk utilization While milk production has increased over the last 25 years, milk consumption has slightly reduced. The amount used as liquid milk has declined from 73 to 45 per cent. However, because of quotas this percentage has increased again (Table 4.4). Self-sufficiency in 1999 compared with 1996 in the UK was 74 per cent (68 per cent) for butter, 64 per cent (69 per cent) for cheese, 128 per cent (129 per cent) for condensed milk, 147 per cent (147 per cent) for cream and 187 per cent (112 per cent) for skim milk powder. Prior to the EU, the UK was mainly concerned with supplying the liquid market, with Commonwealth countries supplying butter and cheese requirements.

Fig. 4.2 A modern butter-making creamery produces and packs 5 tonnes of butter an hour.

This changed with increasing amounts of milk being used for manufacturing. At one stage (Table 4.4) butter manufacture increased (Fig. 4.2) with much intervention producing the so-called ‘butter mountain’. With liquid milk sales realizing the highest return to the producer, the producers in England and Wales should be in a more favourable position than the rest of the EU, as shown in Table 4.5. The large quantities of other uses constitute mainly milk powder and milk fed to livestock, which is common practice in some countries.

Dairy Farming

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27

Table 4.5 Utilization of whole milk, 1984–1989 (%). Liquid Milk

Germany France Italy Netherlands Belgium Luxembourg UK Irish Republic Denmark Greece

Butter

Cheese

Condensed milk

Cream

Others

’84

’89

’84

’89

’84

’89

’84

’89

’84

’89

’84

’89

13 9 29 6 15 11 41 10 8 29

14 17 28 6 16 13 48 11 6 30

46 38 14 42 55 56 26 62 38 3

34 36 14 36 51 53 20 58 37 2

13 22 44 27 5 3 14 9 30 47

17 28 43 32 7 4 19 13 32 53

4 1 – 8 – – 2 2 – –

3 1 – 6 1 – 3 2 – –

9 4 4 3 5 9 4 3 5 2

13 5 5 4 8 13 3 4 8 3

15 26 9 14 20 21 13 14 19 19

19 13 10 16 17 17 7 12 17 12

Source: Milk Marketing Board (1986, 1990).

Table 4.6 Dairy herd breed distribution.

Ayrshire Holstein/Friesian Guernsey Jersey Dairy Shorthorn Others and crosses

Approximate percentage of national herd

Yield (kg/cow)

Butterfat (%)

Protein (%)

2.0 90.0 1.8 1.6 0.3 4.3

5887 6960 4899 4708 5589 –

4.04 3.98 4.76 5.40 3.88 –

3.34 3.27 3.58 3.29 3.30 –

Sources: various, including National Dairy Council (2001).

While this table relates to the 1980s, proportions are relatively similar today. The surplus situation in Europe was at one time exacerbated by much of the liquid milk consumed being skimmed milk, or semi-skimmed milk, allowing the release of milk for butter production. The last 20 years have also seen a similar trend in the UK, with about 20 per cent of liquid milk consumed as skim or semi-skim in the 1980s, 55 per cent in 1994 and 62 per cent in 1998. The further quota restrictions have taken this into account.

Dairy breeds The principal dairy breeds of the United Kingdom are given in Table 4.6. These breeds or their local variations

are now becoming very similar in many other parts of the world. While every breed has its enthusiasts, the vast majority of herds are mainly Holstein–Friesian type (Fig. 4.3). These black and white cows are renowned for their high yields of average quality milk. As they become more extreme, the surplus males are of less use for beef. Recently the input costs have been examined by some farmers and there is a slight tendency for those who wish low input production to favour animals of a less extreme Holstein type. These animals are also often favoured by the organic milk producers. However, those aiming at the very high yielding herd are still pursuing a Holstein type of animal. The main drawback of such animals is that any surplus calves produced are of limited use in beef production. Such problems in the future may be overcome by the use of sexed semen and then possibly by the one of embryo transfer in those

28

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Chapter 4

Fig. 4.3

(a) A Friesian cow, (b) a Guernsey cow, (c) a Jersey cow, (d) an Ayrshire cow.

cows not required to produce dairy herd replacements. The increased interest in organic farming and sustainable agriculture is likely to be reflected in an increase in usage of Friesian-type animals, which are more adjusted to such production systems than the Holstein. The Channel Island breeds, Guernseys and Jerseys, are still popular with a minority of breeders. They are docile cows producing lower yields of very high quality ‘gold top’ milk. This sells at a premium to the liquid milk or cream markets. The milk is now often sold homogenized. The breed does produce very efficiently on the basis of weight of milk constituents produced. The beefing qualities are low and the fat tends to be yellow, but the meat can be acceptable when crossed with one of the continental beef breeds such as Charolais, Limousin, Simmental or Belgian Blue. Dystokia problems in the Channel Island breeds are few because of a broad and pliable pelvis that allows delivery of viable live calves when crossed with the large beef breeds. The Ayrshire is still regionally very popular in a few parts of its native Scotland. While its numbers have

decreased, the breed has currently been given a boost as its milk is being specifically retailed by some chain food stores. A smaller cow than the Friesian, it produces lower milk yields but of higher quality. It is a breed renowned for the dairy type and so is not very suitable for beef. The Dairy Shorthorn has suffered from the demise of being the major breed pre World War II, now slipping to almost insignificance. With good beefing qualities, it tended to fall between two stools, with neither the milk quantity of the Friesian nor the quality of the Channel Island breeds. Types of the breed are used in some countries. Its use may also increase on farms practising sustainable or organic agriculture. The beefing characteristics of the dairy breeds are of importance in England and Wales as the majority of the beef produced originates from the dairy herd. Until March 1996, the origin of British beef was as in Fig. 4.4. The Over Thirty Month Scheme (OTMS), which prevented the sale of older animals for human consumption, plus the Calf Processing Aid Scheme (CPAS), which paid a premium for calves slaughtered before 20

Dairy Farming

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29

Fig. 4.4 Sources of beef in the UK. Source: Meat and Livestock Commission.

Table 4.7 Sources of home-produced beef. Reproduced with permission from Meat and Livestock Commission (1999). 1993 (%)

1995 (%)

1996 (%)

1998 (%)

UK-bred steers, heifers and young bulls beef herd dairy herd

78

76

92

100

34 44

35 41

43 49

52 48

Cull cows beef herd dairy herd Adult bulls Irish cattle

19 8 11 1 1

22 6 16 1 1

8 3 5 0 0

0 0 0 0 0

days of age, payable from May 1996 until 31 July 1999, altered these proportions so that in the early twentyfirst century the origins are as in Table 4.7. These are likely to alter with an increase in the amount of beef

derived from the dairy herd. Recent BSE problems in other parts of Europe are also altering the types of animal which are entering the meat industry for use both directly and in manufacturing. In Britain, should the OTMS be removed, it will cause another alteration in the constituents of beef which is consumed. At present, increased proportions of total beef production are being used for manufacturing and catering and so if human consumption of over thirty-month-old beef is again allowed, there should be a market for the product. The Friesian breed has played an important part in beef production with most farmers producing sufficient of their cows pure to provide the heifer replacements for the dairy herd, with the remainder being bred to a beef bull to maximize calf returns. Figure 4.5 shows that, in most years, 60–70 per cent of inseminations have been to a dairy bull, with the remainder to beef breeds. These data cannot at present be updated, but the most numerous breeds of bull used for artificial insemination (AI) in 1986 are shown in Table 4.8. While the dairy inseminations follow the pattern of breed distribution,

30

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Chapter 4

Fig. 4.6

Food components.

dependent on the price and the quality of the bulls offered. Fig. 4.5 Dairy, dual purpose and beef inseminations as percentages of total inseminations. Source: Report of Breeding and Production Organization, MMB (1986).

Table 4.8 AI breed demand in MMB areas, 1986 (%). Ayrshire Friesian/Holstein Guernsey Jersey Shorthorn Total dairy breeds Aberdeen Angus Belgian Blue Charolais Hereford Limousin Simmental Others Total beef breeds

0.7 57.8 0.8 1.2 0.2 60.7 2.8 1.1 7.4 12.0 12.7 1.7 1.6 39.3

Source: Report of the Breeding and Production Organization, MMB (1986).

with beef the continental breeds are replacing the traditional British beef breeds, especially the Hereford. The Belgian Blue is more widely used in the UK than shown in Table 4.8, but again recent figures are unobtainable. The Aberdeen Angus continues to enjoy some support because of the ease of calving, particularly when used on maiden heifers or small cows. It also has some marketing advantages in that Angus beef can demand a premium. While there is an increasing amount of embryo transfer occurring and costs have reduced, it is still an uncommon procedure. However, the possible use of sexed semen does appear to offer considerable possibilities over the next few years. Its uptake will be very

Feeding dairy cows

(see also Chapter 9)

A vital feature of dairy cow management is correct feeding. Food, either purchased or home produced, amounts to 60 per cent of the variable costs of production so the efficiency of feed use is extremely important. In the past, most high-energy feeds were purchased as concentrates from feed manufacturing companies. The onset of bigger herds, access to machinery to mix up feeds and the ability to buy feed constituents at competitive prices have meant that many dairy and beef farmers now produce their own rations, often feeding them as complete feeds or total mixed rations (TMR). The main components of feed are shown in Fig. 4.6. All feeds contain water in varying amounts. Dry feeds such as cereals will only have about 14 per cent water, while other feeds such as mangels and other root crops will be up to 90 per cent water. While all cows require water it is the dry matter proportion of the total food that supplies the nutrients for maintenance and production. In general, the higher the dry matter of the overall diet, the higher will be the dry matter intake (DMI). Apart from the need for minerals and vitamins, the main aspects to consider in dairy cow feeding are DMI and energy and protein levels.

Dry matter intake Dry matter intake (DMI) is affected by the liveweight of the cow, stage of lactation, milk yield, type of feed and frequency of feeding. As a guide for estimating DMI the following equation is used: DMI (kg/day) = 0.025 ¥ liveweight (kg) + 0.1 ¥ milk yield (kg/day)

At calving DMI will be 2–3 kg/day lower than calculated, but it will then increase to peak at three to five

Dairy Farming

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31

Table 4.9 Energy requirements of dairy cows. Breed

Ayrshire Friesian Guernsey Jersey Shorthorn

Liveweight (kg)

Maintenance (MJ/day)

Production (MJ/kg milk)

Liveweight gain (MJ/kg gain)

Pregnancy (MJ/day)

500 600 450 350 550

54 63 49 40 59

5.3 5.2 5.8 5.9 5.1

34 34 34 34 34

23 23 23 23 23

Table 4.10 Digestible crude protein requirements of dairy cows. Breed

Ayrshire Friesian Guernsey Jersey Shorthorn

Liveweight (kg)

Maintenance (g/day)

Production (g/kg milk)

Pregnancy (g/day)

500 600 450 350 550

300 350 275 225 325

60 55 70 70 55

150 150 150 150 150

months after calving. After peak milk production, intake decreases slowly through lactation and is lower during the dry period. DMI can be increased by feeding highly or more digestible feeds such as maize silage. Thus cows will eat greater quantities of a 70 per cent digestibility (D) silage then one of 64 D. Also succulent feeds such as brewers’ grains, kale and roots considerably enhance intakes in an otherwise dry diet of hay or silage with concentrates. When feeding large quantities of concentrates, splitting the feed into three or four feeds rather than the conventional two in the parlour will also increase intake and reduce rumen acidity. This is also why TMR can work well and again it will increase feed intake.

Energy (see Chapter 9) The energy requirements of a dairy cow depend on her needs for maintenance, lactation, pregnancy and whether she is increasing or decreasing weight (Table 4.9). Energy in diets in Britain is measured as metabolizable energy (ME) and the units are megajoules (MJ) per kilogramme dry matter (DM). If dairy cows are in energy deficit then body fat will be mobilized, causing liveweight loss to make up for some or all of the deficit. This will contribute about 28 MJ of ME per kg liveweight loss. Estimated energy requirements are shown in Table 4.9. Thus, for example, a 600 kg Friesian cow producing 20 kg/day of milk, in calf and gaining 0.5 kg/ day liveweight would require:

Maintenance Production (20 ¥ 5.2) Liveweight gain (0.5 ¥ 34) Pregnancy Total energy required

63 MJ 104 MJ 17 MJ 23 MJ 207 MJ/day

Protein (see Chapter 9) Protein is required for both maintenance and production. In contrast to the case for energy, body tissues cannot be used to make up a shortfall in protein and so milk yields will suffer if protein is in deficit, especially in early lactation. Protein is often measured as crude protein (CP) and is given as percentage of dry matter. In rations it used to be measured in grammes of digestible crude protein (DCP) per kilogram DM. Requirements for maintenance and production are shown in Table 4.10. A refinement of the DCP system is the division of rumen degradable protein (RDP) and rumen undegradable protein (UDP). A dairy cow has a need for both types of protein. The system has been further refined into the metabolizable protein (MP) system. This looks at the rate at which protein becomes available within the rumen and is given as quickly degradable protein (QDP) and slowly degradable protein (SDP). These two (QDP + SDP) form what is known as the effective rumen degradable protein (ERDP). A cow has a need for both rumen degradable protein (both quick and slow) and rumen undegradable protein.

32

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Chapter 4

Different feeds contain different proportions or ratings of these. Thus silage is about 80 per cent degradable and soya is about 60 per cent degradable. Also, degradability does depend on the form of the feed, thus heating or formalin treatment reduces rumen degradability. The rate of passage out of the rumen also has an effect, with higher passage rates increasing the UDP. In many instances, although the protein supplied may be sufficient in terms of its CP or DCP basis, it may still be deficient in either RDP or UDP. In early lactation on a predominantly grass silage diet, any shortfall is likely to be in UDP; this explains the observed good response when fishmeal or soya was added. Meat and bone meal are also a good source of UDP but were banned in Great Britain in 1988 for ruminants and in the rest of the EU finally in 2001. The EU also decided to ban the use of fishmeal in ruminant diets from 1 January 2001, resulting in the loss of a major practical source of UDP. However, it may return.

for the first 120 days of lactation. As yield declines and appetite increases then balance should be reached and then any liveweight loss in early lactation can be replaced in mid to late lactation (see Fig. 4.7 and Chapter 9). As will be discussed later, a compromise has to be achieved between biological efficiency and economic efficiency. Very approximately, the most common feeds for dairy cows (grazing grass, grass silage and concentrates) have a relative cost of 1 : 2 : 3. Therefore, greater profits will be shown as the proportion of grass and silage in the total diet increases provided performance does not suffer (see Fig. 4.8). While flat rate feeding of concentrates is popular, particularly with total mixed rations (TMR), most farmers feed at least partly to yield. In most instances

Feeding strategies Many textbooks have been written on strategies for feeding dairy cows. The main principles are (i) to maximize DMI and (ii) to provide the cow’s requirements as cheaply as possible. These two requirements are associated as the higher the DMI then the lower the energy concentration in the diet and hence the cheaper the production of the ration. In early lactation of high-yielding cows, it will be difficult to satisfy their requirements within appetite. This will result in a loss of bodyweight, perhaps 0.5 kg/day,

Fig. 4.7

Nutrient gap.

Fig. 4.8

Feeding silage at a barrier.

Dairy Farming

Table 4.11 Examples of possible cow diets.

33

Table 4.12 Main mineral requirement of dairy cows.

Stage of lactation

Concentrates (kg DM/day) Silage (kg DM/day) Total DMI (kg/day) Energy supplied (MJ/day) Energy required (MJ/day)

•

Early

Mid

Late

8 8 16 180 195

6 12 18 195 186

2 12 14 145 133

this is important as dairy cows are not similar enough in their genetic make-up to allow feeding as if a single animal. It also cannot work unless cows are all at the same stage of lactation rather than calving over widespread periods or all the year round. Thus most farmers do to a certain extent ‘feed to yield’ or requirements, whereby concentrates are allocated on an individual basis depending on the yield attained and/or condition loss. In consequence, more concentrates are fed early on in lactation and are reduced as lactation progresses. Appetite is dependent on DMI so as concentrate consumption increases, forage intake reduces. This has the effect of limiting forage intake in early lactation as concentrates are normally eaten in preference to forages. Table 4.11 shows the effect of this on the cow’s diet. For correct digestion the dry matter ratio between concentrates and forage should be in the range 70 : 30 to 30 : 70 in early to mid lactation. Any lower and performance will suffer, any higher and digestion will suffer (see pages 829–32).

Minerals and vitamins The daily requirements for these must be adequately met if the dairy cow is to remain healthy and produce effectively. The major essential elements are calcium, phosphorus, magnesium, sodium, potassium, chlorine and sulphur. Table 4.12 gives the daily requirements for four minerals. The main vitamins required are A, D and E. As milk yields increase the mineral and vitamin requirements become more critical. They should always form an integral part of the ration. When proprietary concentrates are fed these will usually produce sufficient of these nutrients for the productive cow. However, where rations are all or nearly all TMR then addition of adequate amounts of vitamins and minerals is essential.

Grassland farming Grass and its derivatives, hay and silage, form an important part of dairy farming. The two major aspects to

Ca

P

Mg

Na

Maintenance (g/day) Liveweight (kg) 400 500 600

14 18 21

19 26 32

6 8 9

7 9 10

Production (g/10 kg milk) Fat content of milk (%) 4.0 5.0

28 30

17 17

6 6

6 6

consider are grassland production and grassland utilization.

Grassland production To get optimum production from grassland the basics must be correct. These include climate and soil type about which little can be done. Grass grows best on a medium loam soil with adequate summer rainfall. These conditions are most often found in the west of England and Wales. Where soil is heavy and waterlogged, then drainage can give good results. Conversely, in dry areas, irrigation has a part to play, although the economics of grassland irrigation in Britain are questionable on all except the driest farms. Soil acidity should be corrected to a pH of 5.5–6.5. Having achieved as near optimum as possible with the basics the next area to consider is grass varieties. For grazing, most seed mixtures are based on varieties of perennial ryegrass (Fig. 4.9). There are many recommended varieties in the National Institute of Agricultural Botany (NIAB) lists. Timothy is often sown, which adds some palatability and midsummer growth. Older grass varieties such as meadow fescue and cocks-foot are not often sown now. Most mixtures will also include some white clover. This provides nutrients by fixing atmospheric nitrogen and also increases intake by improving the palatability of the sward. But clover is difficult to establish and maintain in grassland receiving high levels of fertilizer nitrogen. Once established, and with good management, a grazing sward should remain highly productive for 10 years or more. The main enemy to this is grazing in too wet conditions, when treading and poaching will quickly destroy a sward and allow weed grasses to establish. Swards mainly for cutting are usually based on a shorter term perennial ryegrass or Italian ryegrass. These have a more erect growth habit and are easier to cut but are

34

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Chapter 4

Fig. 4.9 Cow set stocking, grazing a ryegrass sward.

Fig. 4.10 A good response is shown from nitrogen fertilizer.

not so persistent. They are often grown as a grass break in an arable rotation for two to three years. Often the species are sown pure. If clover is required then red clover is more suited to a cutting regimen than white clover. In between these extremes are many dual purpose mixtures that are both grazed and cut during a season. The best time to sow grass is in August–September. This gives it a chance to establish before winter and to be in full production the following spring. A spring reseed in April–May will lose much of the first year’s production and can be vulnerable to summer drought.

Having established the grass the fertilizer requirement must be satisfied. Normal recommendations for grazing would be an annual application of 300 kg/ha nitrogen, 40 kg/ha phosphate and 40 kg/ha potash. Under a cutting regimen the nitrogen and potash would be increased to 350 and 150 kg respectively. Whilst phosphate and potash are essential for grass growth the main response is shown to nitrogen. Much trial work has been undertaken showing a good response up to 400 kg/ha, but the average nitrogen use is still under 200 kg/ha (Fig. 4.10). Researchers have defined a target nitrogen use as being the point in the response curve where 10 kg of grass dry

Dairy Farming

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35

Fig. 4.12 Seasonal pattern of grass growth. Source: Milk from Grass (GRI and ICI). Fig. 4.11 Target nitrogen on five site classes. Source: Milk from Grass (GRI and ICI).

matter are produced for each 1 kg of fertilizer nitrogen. Nitrogen use is now controlled in many areas. Figure 4.11 shows the target point for five site classes, class 1 being the most suited to grass growth and class 5 the least suitable.

Grassland utilization Grass growth is uneven through the year with a peak in the spring and then falling away through the growing season (Fig. 4.12). Grass growth will also vary greatly between seasons depending mainly on the summer rainfall. Nor are the animal requirements even over the season. For all these reasons any system of grassland utilization must be flexible and adaptable to cover any situation. The overall aim is to provide the cow with her maintenance requirement and as much of her production as possible for each day of the year. This will be achieved with an integrated grazing and cutting system whereby in early season about one-third of the grass area is grazed and two-thirds is cut. This is reversed in mid season and then the whole farm is grazed in the autumn. The most common systems of grazing management are either continuous grazing or rotational grazing with paddocks or strip grazing. There is little to choose between systems in terms of output so choice is down to personal preference and ease of management. Under any system, cows should be stocked at a heavy density (6–8/ha) in the spring, which will allow a

maximum area to be cut without affecting milk production. Maintenance plus 20–25 l/day of milk can easily be obtained from spring grass. For an autumncalving cow, as grass declines so milk yield declines and there should be no need to introduce supplementary feeding. Spring-calving cows may need supplementary feeding to sustain yields in the summer. This may be concentrates or forage crops such as rape or stubble turnips. Efficient conservation is a vital part of grassland management. It both provides a feed for winter use by the cows and aids grassland management by utilizing grass surplus to the grazing requirement. The main options for conservation are either hay or silage. There is a continuing move away from hay towards silage on dairy farms because:

• • • •

it is more flexible and integrates better with grazing; silage is a better feed for dairy cows; silage can be made in poorer (not poor) weather conditions; and silage can respond to higher levels of fertilizer nitrogen use.

However, silage making does require a higher capital investment in both machinery and storage areas (Fig. 4.13). Much of this criticism has now been overcome by the use of contractors and with the advent of big bale silage. These have given even the smallest dairy farm the opportunity to improve grassland utilization and profitability by changing to silage making. Whilst grass is the most important forage crop, reference must be made to other forage crops that may have

36

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Chapter 4

Fig. 4.13 Silage making with a precision chop forage harvester.

a place on dairy farms by producing heavier yields than grass or producing feed in a season when grass is not available. The most popular forage crops are maize, fodder beet, kale, lucerne, and stubble turnips and rape.

Maize This is increasing in popularity in southern England and is normally made into silage but can be fed green. To be successful it requires high summer temperatures so even in southern England a sheltered field should be used. It produces a similar or heavier yield per hectare than grass and has the advantage of being harvested in one cut. The resultant silage is a very palatable, high energy, low protein feed that improves a winter ration. It is often mixed with grass silage in the proportion 1 : 1 to 1 : 4 maize: grass but can successfully be fed on its own.

Kale This is a high protein green feed grown mainly for grazing in the autumn and early winter. It produces a high yield of succulent feed that stimulates milk production. It can be cut and fed to dairy cows in the yards but is more commonly grazed, which means that it should be grown in dry fields with good access. Mud, dirty cows and bad feet can be a problem. However, some have successfully made silage.

Lucerne This is a drought-resistant legume that grows well on light chalky soils. Being a legume it fixes atmospheric nitrogen and hence is cheap to grow once established. Cut four or five times during the season it provides good yields of high protein silage, but it can be difficult to get a good fermentation in the silage. A useful crop for organic farms with suitable soils.

Fodder beet This has about the highest yield of dry matter per unit area of any fodder crop. It can be grown successfully anywhere but prefers a heavier soil. It is an arable crop and the farmer needs arable techniques to grow it successfully, especially for establishment, weed control and harvesting. It is harvested in October/November and stored for winter use. It provides a palatable high energy feed, which helps butterfat percentages.

Stubble turnips and rape Although these are not the same they are used for the same purpose – to provide a succulent green feed either in the summer or autumn. For summer use they need sowing in the spring but autumn grazing can be achieved by drilling after harvesting an early cereal crop. They both provide grazing when feed might otherwise be short.

Dairy Farming

Fig. 4.14

•

37

Self-feeding silage.

Winter feeding systems A winter feeding system will be partially dictated by the objectives, high or low milk yields, and by the facilities available. In all cases the first requirement is to know the quantity of bulk feeds available. Over a 200-day winter a Friesian cow may well consume about 3.5 t of dry matter. If there are 2.2 t of silage dry matter per cow then this will leave 1.3 t to be made up with concentrates or other purchased feed. Provided there are about 1.8 t of forage dry matter for a 200-day winter then a reasonable feeding system can be devised. This equates to about 7 t/cow of fresh weight silage. Anything much less than this will create problems, not so much from the cow’s point of view but from the economic side as it will tend to be an unprofitable winter. Anything more than this will be a bonus and an asset to the farm especially if of a high D value. All feed changes should be done gradually to prevent digestive upsets. Thus silage should be gradually introduced on a limited access basis from calving or by midSeptember, whichever is the earlier. The herd should be housed at night by some time in October depending on conditions and then housed continually from midOctober onwards, again depending on weather conditions. Over this period silage consumption will increase and other feeds can be gradually introduced. The same principle applies in the spring, when ideally the herd should be kept inside at night on silage for seven to ten days after turning out with grazing time gradually increased. Silage will either be self-fed (Fig. 4.14) or fed mechanically behind a barrier or in a trough. Selffeeding works well for low yields, provided that the

silage quality is even throughout the clamp, that the face is not more than 2 m high and that there is enough space at the face, 24 hour access of at least 40 cm/cow. To avoid secondary fermentation the silage face needs to move back by at least 150 cm/day. Self-feeding is labour saving and requires no machinery. It is better but not essential to have a roof over the silo and intakes will improve if a light is left on at night. Keep cows back from the silage face with a barrier, either a solid rail or an electric wire. The latter, however, can often reduce intake. To prevent waste the face must be kept tidy and waste silage removed. Mechanical feeding of silage will either involve putting the silage in a trough or behind a barrier with a tractor and fore-loader/blockcutter or else loading the silage into a forage wagon that will spread it behind the barrier. Many people claim that this will increase intake compared with self-feeding by 10 per cent or more. Two simple barrier designs are shown in Fig. 4.15. For 24-hour access the herd will need a minimum feed space of 40 cm/cow, but space of up to 75 cm is now often recommended for best intakes. Again cleanliness is important and waste silage should be removed on a regular basis, preferably at least once daily. It is important to ensure that silage is always available ad libitum. Leaving the trough empty for two to three hours before feeding will suppress intake and can cause digestive problems. It is a tremendous advantage to a winter feeding system to have a trough or barrier available as almost any feed can be fed behind it, from silage to hay, roots, brewers grains, sugar beet pulp or concentrates. This gives a great flexibility. When feeds such as dried beet pulp or concentrates are fed it is essential to have at least 60 cm/cow of trough space to ensure a reasonably even intake among cows.

38

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Chapter 4

Fig. 4.16 Fig. 4.15

Cows at a computerized out-of-parlour feed station.

Two types of feed barrier.

A sophistication of this system is complete diet feeding or total mixed rations (TMR). Here all the feeds are placed in a mixer wagon, which mixes them together and delivers the diet behind a feeding barrier. Because of the degree of mixing the cow is unable to separate out, say, barley from silage and so eats the whole mixture uniformly. Ideally the wagon has weigh cells so giving a very accurate measurement of feeds. Use of a mixer wagon allows the feeding of a wide range of feeds that may represent a very economical buy, but which are normally either difficult to feed or unpalatable, e.g. molasses and rapeseed meal. It also allows much more satisfactory feed digestion within the rumen and further down the alimentary tract. Some farmers are now buying straights and producing their own complete diets, usually with the help of a nutritionist. Attention is being focused on straights and ensuring that they are stored in satisfactory containers which allow the feed to be kept dry, vermin and bird proof. The introduction of herd health and quality assurance schemes has drawn attention to how feeds are stored. On some farms forage boxes are used instead of mixer wagons, but these do not really mix up the feed. Most milking parlours have facilities to feed concentrates and it is usual to feed these twice per day at milking time. A limit to be fed during each milking would be 4–5 kg. If anything above this is needed then an out-of-parlour feed at the barrier is beneficial. This not only splits the feeds, which helps digestion, but also allows a proportion of the concentrate to be replaced

with alternative feeds such as cereals, maize gluten or sugar beet pulp. A sophistication of this system is with computerized out-of-parlour feeders (Fig. 4.16). Each cow has a transponder identifying her to a feeder station. This is then programmed to allow a specified amount of feed per day in a number of feeds. The cow can then eat up to her allowance but no more. Although the capital cost of these installations is high they make for very accurate feeding, based on the sound principle of ‘little and often’. They perhaps demonstrate the way dairying will go in the future. Printouts can be obtained for cows not consuming their allocated amounts. In all feeding systems water must not be overlooked. With milk being 86 per cent water any shortage of water will quickly limit milk production. A dairy cow will need 60–100 kg of water per day and being creatures of habit tend to all want to drink at the same time, especially late afternoon. This makes a large reservoir and fast flow of water essential. The volume drunk will increase as milk yield increases and in dry hot weather, so that 120 litres or more is not uncommon.

Dairy farm buildings Because of the diverse nature of dairy farming there are almost as many different designs of dairy building units as there are dairy farmers. However, if starting from scratch the main needs are for a milking parlour and dairy, winter housing and

Dairy Farming

Fig. 4.17

Typical layout of a dairy unit.

feeding barn, food storage area, calving and isolation boxes, slurry handling area and various collecting yards and access concrete. A typical set of dairy buildings is shown in Fig. 4.17. Important considerations when designing a dairy unit include the following.

• • • • • • • •

Cow-free access for the milk tanker so that collection can be made at any time. Good cow flow so that cows come from the bedded area through the parlour and back with a minimum of narrow passages and sharp corners. Good feeding access so that cows can be fed without having to work amongst them. Access to silage storage areas away from the cows so that silage making can take place while the cows are in the yards or in for milking. Good handling arrangements for veterinary treatment and AI. Adequate slurry storage as spreading may be restricted in nitrogen vulnerable zones. Thought should be given to the way the buildings blend in with the surroundings. Choice of materials and site are important. Adequate loose boxes for calving, sick animals, etc.

Parlour and dairy This is the key to the whole dairy unit, being used twice (or three times) a day 365 days of the year. Cowsheds are very labour intensive and outdated while rotary parlours in the past have proved unreliable, with no benefits over a static parlour but are now becoming more common again. Automatic (robotic) parlours are also now being introduced. Figure 4.18 shows the most common parlours used, an abreast and a herringbone parlour.

Fig. 4.18

An abreast and a herringbone parlour.

•

39

40

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Chapter 4

The most simple parlour is the abreast, which is particularly suitable for herds of up to 80 cows with one man milking either with three milking units and six standings or six units and six standings. The cows enter and leave one at a time so a degree of individual treatment for a slow milker or slow eater is possible. The parlour should have a loft above to hold the concentrates, which fall by gravity to the feeder situated between each pair of cows. Milking rate will be about 30–40 cows/hour. In a herringbone parlour, by far the most common, the milker stands in a pit, which removes most of the bending required. The cows come in and out of the parlour in batches and stand at an angle to the pit on either side. A herringbone parlour is suitable for any sized herd and one man could comfortably milk 100 cows in two hours with a 10 : 10 herringbone, i.e. 10 milking units, 10 standings. For 300 cows or more larger herringbones with two or three milkers are common. A loft above the parlour will hold the concentrates and each standing will have a feeder. In some parlours feeding has been discontinued. Automatic cluster removers (ACRs) are now available that make it possible for one man to handle more machines without the danger of overmilking. In any parlour the work routine is to let the cow or group of cows in, feed them, dry wipe the udder or wash and dry if dirty, wash the udder, test the foremilk, attach the cluster, remove the cluster, teat dip or spray, transfer the milk and let the cows out. Pre-milking teat dipping is practised in some herds, especially those with high levels of environmental mastitis. The dairy should be adjacent to the parlour and will contain some dairy equipment such as the vacuum regulator, milk pump, water heater and washing equipment. The bulk milk tank will also be situated here. The capacity of the bulk tank is important and must be sufficient to hold the likely peak milk production. Except in a herd with a very compact calving pattern about 30–35 litres/cow capacity is normally sufficient. Both the parlour and dairy must be kept scrupulously clean and in Britain will be inspected regularly by the authorities. The motors and refrigeration unit should be housed separately in an engine house. It is also useful to have a small area near the parlour where the cowman can keep the records necessary for herd management.

Cow housing and feeding barn (Chapter 56) The choice for cow housing will rest between housing in straw yards and cubicles. Cows often appear more comfortable in a straw yard but if they are to keep clean they need about 6 m2/cow. They also use a lot of straw over a winter (about 2.5–

Fig. 4.19

A feed/sleep arrangement with metal cubicles.

3 tonnes per cow), which creates work to cart in and take out each day. But straw yards do help to alleviate a problem by reducing the volume of slurry produced. Cubicles (see p. 422) have gained in popularity and, well designed, can be a very trouble-free system with a low demand on labour (Fig. 4.19). The main requirement for comfort is to make the cubicle large enough, about 1.2 m wide and 2.2 m long, with a good lying surface. They can be made of metal or timber and a typical design is shown in Fig. 4.20. This design is for Friesian cows and does not offer sufficient flexibility for many high-yielding cows and so ones such as in Figs 4.21 and 4.22 are used. Other new models are also available. The measurements of an ideal cubicle are given in Table 4.13. The cubicle should slope from the head to tail end and the best surface is concrete with mattresses, mats or sand as a bed. A strategically placed headrail is essential to ensure the cow dungs in the scraper passageway. Passageways should be at least 2.4 m (8 ft) wide to allow for good cow flow and sufficient width for the scraper. The whole cubicle and scraper passageway can either be situated within an open span building or be part of a purpose-built cubicle building. For all situations it is important to have a draught-free environment with plenty of ventilation. This is normally achieved by the use of Yorkshire boarding (vertical boarding with gaps

Dairy Farming

to allow free movement of air) or with an open ridge to the building or kennel. With either straw yards or cubicle beds, the feeding areas can be either inside or outside the building. An inside area is preferable but will add to the cost. An example of an arrangement with a centre feed passage is shown in Fig. 4.23. The advantages of this type of arrangement are that the cows can be shut in the feed area while the cubicles are scraped and vice versa. Feed can be put out without driving through the cows and it is also possible to split

•

41

the whole herd into groups, by milk yield or calving date, which can assist management. There has been increasing emphasis on cow comfort, particularly from the point of view of preventing lameness and providing suitable conditions to ensure that cows lie down for similar lengths of time as they do when at grass. This is difficult or impossible to achieve with cubicles and so some farms have altered accommodation to straw yards (see Figs 4.24, 4.25 and 4.26). Such alterations do require sufficient space for each cow (see Table 4.14). They can result in rapid improvement of locomotion scores, and considerably reduce lameness due to white line disease and solar ulceration (Hughes, 2000). However, mastitis levels can rapidly increase, particularly due to Strep. uberis and E. coli, unless great care is taken in producing a satisfactory straw bed. The keys to success include making available a large quantity of straw for each cow (about 2.5–3 tonnes) and ensuring that it is kept dry when stored and the bed remains dry. Regular cleaning out every 4–6 weeks may help prevent mastitis problems, but this is possibly less important than the quality of the straw used. Good ventilation is also required to help keep the straw bed dry.

Feed storage area Fig. 4.20

A metal cubicle division.

Fig. 4.21 A cubicle suitable for a Holstein cow (courtesy of J. Hughes).

Fig. 4.22 A double fronted cubicle suitable for Holstein cows (courtesy of J. Hughes).

The major item here is the silage storage facility. This can range from a tower silo to a simple hardcore pad. Construction of a simple silo is worthwhile to make handling easier and to prevent waste. Clamp silos are the most common and are usually constructed with a concrete base and walls of earth, sleepers or concrete. Safety is essential and in Britain walls must be up to DEFRA (Department for the Environment, Food and Rural Affairs) standards bearing in mind the walls have to contain not only the weight of the silage but also pressure from the tractor when consolidating the clamp. For open silos, guide rails must be provided 900 mm above the wall and for roofed silos sufficient height (5.5 m) must be allowed for tractor clearance. All effluent must be contained in a sealed tank that can be pumped out. For self-feeding of silage the height of clamp must not be more than 2 m and capacity will need to be about 12–15 m3 per cow for a winter’s storage. If other feeds

42

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Chapter 4

Table 4.13 Measurements of cubicles suitable for high yielding Holstein cattle as determined in Britain (adapted from Hughes, 2000). Measurement

Metric (Imperial)

Length 2.4 m (8 ft) If double fronted cubicles with concrete fillet so maximum forward lungeing space length can be reduced to 2.28 m (7 ft 6 inches) Width 1.2 m (4 ft) If width 1.14 m (3 ft 9 in) there must be a flexible lower barrier Rear step 50 000 adult O. ostertagi Severe abomasal reaction

pH abomasal contents >5.0 >50 000 adult O. ostertagi plus large numbers of immature fourth stages Severe abomasal reaction

PCV, packed cell volume; RBC, red blood cell; Hb, haemoglobin.

quently the most severely affected. There will be a history that indicates grazing on potentially infected pasture during the preceding four to eight weeks in the case of type I ostertagiosis or during the previous late summer and autumn for type II ostertagiosis. Specific diagnosis (see Table 19.1) can be assisted by the following tests. (1) Faecal egg counts. Despite the dilution of faeces caused by diarrhoea, the nematode egg counts will be in excess of 1000 eggs/g. Counts may be higher in less severely affected calves that have not yet become severely diarrhoeic. In older animals and in some individuals in type II cases the faecal egg counts may be low enough to be misleading, and if suspected the results of other tests should be borne in mind. (2) Plasma pepsinogen. In healthy calves the normal level of plasma pepsinogen is less than 1 international unit (iu) of tyrosine. In affected calves the level will normally be greater than 3 iu, and in very severely diseased individuals up to 4.5 iu. It should be pointed out that in adult cattle the normal pepsinogen level can be 1.5– 2 iu, almost that found in calves in the prepatent period of type II ostertagiasis. Plasma pepsinogen levels in adults therefore should be carefully evaluated.

(3) Plasma gastrin. The plasma concentration of the hormone gastrin has been shown to rise at the time of patency in experimental infections and to peak at levels between 500 and 1000 pg/ml. Although still under investigation it may be used as a substitute for plasma pepsinogen in the future. (4) Post mortem findings. In both type I and type II ostertagiasis the abomasum (providing the animal has remained untreated) will contain large numbers of adult O. ostertagi. The number can vary from 50 000 to 1 000 000 in extreme cases. In type II disease pepsin digest of the abomasal mucosa or incubation in lukewarm normal saline will reveal large numbers of inhibited fourth stage worms. The pH of the abomasal contents will be raised to pH 4.5.

Treatment (see Chapter 60) Type I disease can be treated with almost any of the anthelmintics currently available such as levamisole, benzimidazoles or avermectins. Type II disease requires the use of some of the modern longer acting benzimidazoles or pro-benzimidazoles or avermectins such as ivermectin, doramectin, abamectin, eprinomectin or moxidectin. The avermectins and moxidectin are much

Endoparasites

the most effective in removing both adult and inhibited fourth stage parasites as a result of their persistence and slow excretion. Levamisole is much less effective for type II disease, as it has a poor efficiency against inhibited worms due to its rapid excretion (see p. 1021), and the benzimidazoles can vary in efficacy depending on the time of treatment in relation to the onset of inhibition of the worms, i.e. in the early and late stages of inhibition the larvae are thought to have a more active metabolism, and therefore absorb more anthelmintic; in the middle of the inhibition period they absorb less, and it is then that the benzimidazoles do not have the persistence necessary to kill the worms.

Prevention As for most parasitic diseases, prevention is more costeffective than treatment. Since there are no vaccines yet available for gastrointestinal nematodes, numerous schemes that combine grazing management and anthelmintic therapy have been developed. The methods fall into three types: (i) evasive; (ii) suppressive; and (iii) dilution. Evasive strategies: The basis of this category (also called the ‘Weybridge’ system) was first enunciated by Michel (1968) at the laboratory of the same name. Using the knowledge of the epidemiology of parasitic gastroenteritis that had then become available, Michel pointed out that if susceptible cattle were removed from infected to uninfected grazing just before the summer increase in infective larval numbers, serious parasitism could be avoided. When combined with anthelmintic treatment at the time of movement the system reduces the level of nematode worm egg contamination on the clean grazing. In essence, therefore, the system involves taking no prophylactic action until early July. At that time, pasture which has not been previously used for cattle grazing that year is available, after grass has been taken for silage making or some other form of conservation. The calves are given anthelmintic treatment before being moved to it. The timing of the treatment can vary with the pharmacokinetics of the anthelmintic used and its effect on nematode eggs if contamination of the aftergrass is to be avoided. For instance, the longer acting benzimidazole anthelmintics (e.g. oxfendazole, albendazole, fenbendazole) are ovicidal within a few hours after treatment and their slow rate of excretion means that cattle are protected from infection with susceptible parasites for approximately 30 hours after treatment. They can therefore be put back safely onto the contaminated grazing for 24 hours after treatment before transfer to the aftergrass. The same technique can be applied with avermectins and moxidectin, which

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although not ovicidal have an even longer half-life and will inhibit further infections for at least two weeks. On the other hand, levamisole has a rapid excretion rate and is also not ovicidal. If reduction of contamination as well as nematode removal is intended, cattle treated with levamisole require to be yarded after treatment at least overnight, if not for 24 hours. After this first treatment in early to mid July, and depending on the availability of grass and its previous grazing history, the calves may require no further treatment until housed in late autumn, although in practice many are treated four to six weeks after the first movement. Although highly effective and the most economical method of prophylaxis when carried out carefully, it should be pointed out that although excellent for control of gastrointestinal nematodes it is not completely effective in the prevention of lungworm infection caused by Dictyocaulus viviparus. Suppressive strategies: These have been introduced gradually since the mid 1970s and are also based on knowledge of the epidemiology of the infections. Unlike the evasive systems, which allow natural infection and pasture contamination to take place in spring and early summer, the basis of these methods is to suppress egg production during that period (Fig. 19.2). If pasture contamination is prevented or reduced, the summer increase of infective larvae is of such proportions as to cause a negligible risk of severe parasitism. Suppression is carried out by two different methods: (i) repeated anthelmintic treatments with standard preparations, the interval between which is determined by the pharmacokinetic properties of the chemical used; currently most of the anthelmintics used are avermectins or moxidectin: or (ii) the use of a device, usually an intraruminal bolus, which has a continuous slow release of the active anthelmintic for periods from 60 to 140 days. Such boluses are usually administered by balling-

Fig. 19.2

Rationale for anthelmintic suppression.

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gun at or just before susceptible calves are put out to grass in the spring, although recent experiments have shown that they can also be effective when given in midsummer to prevent infection in calves grazing previously contaminated fields. The length of prophylactic activity varies between different climatic areas and nematode species, e.g. in south-eastern areas of the UK suppression for eight weeks after being put to pasture in spring may be sufficient, but in wetter western areas it may require to be prolonged for a further five weeks and if lungworm infections are present on the farm for up to 15 weeks. Dilution strategies: Originally described in New Zealand as the Ruakura method (McMeekin, 1954) and further amended by Leaver (1970), the methods consist of the grazing of paddocks in relays by groups of calves followed by groups of older cattle. The basis of the technique is that the greater consumption of infective larvae by the immune or partially immune adults will delay and reduce the build-up of infective larvae on the paddocks. Initially, no anthelmintic treatments were given, but in modern practice the method is frequently combined with either of the evasive or suppressive techniques. The advantages and disadvantages of each of the three preventive methods are summarized in Table 19.2.

Parasitic bronchitis (husk, hoose) Dictyocaulus viviparus is almost the sole cause of severe pulmonary helminth infections in cattle. Occasionally other parasites are found, but rarely in numbers

sufficiently large to cause disease. In general, calves at grass from midsummer to autumn are those most frequently clinically affected, but heavy infections in animals of any age previously uninfected will produce signs. It is most prevalent in dairy-type calves, but is also common in weaned beef calves. The range of signs can vary from occasional coughing to severe respiratory distress, and is a reflection of the number of infective larvae ingested during a relatively short period.

Aetiology and epidemiology The immediate cause of clinical symptoms is the ingestion two to four weeks previously of large numbers of infective larvae of D. viviparus by non-immune cattle. Experimentally, severe infections can be induced by a single administration of larvae at a rate of between 25 and 50 larvae/kg body weight. Typically, an affected calf weighing 300 kg will have ingested between 7500 and 15 000 L3 (third stage larvae). This is a much smaller infection than is required to cause parasitic gastroenteritis by O. ostertagi, and is an indication of lesser margin for error involved in ensuring adequate prophylaxis. The epidemiology is more complex and infections are also much less predictable than are those of gastrointestinal nematodes, principally because at present not all details of larval survival and transmission are known. Infections are more prevalent in wetter areas, especially those in the west of the British Isles. One of the major differences between D. viviparus and gastrointestinal nematodes that has an influence on the unpredictability of infections is that the female worm produces eggs

Table 19.2 Advantages and disadvantages of the prophylactic methods for gastrointestinal parasites. Method

Advantages

Disadvantages

Evasive

Low labour cost Low anthelmintic cost Not likely to lead to anthelmintic resistance in nematodes

Does not protect against lungworm Reduces the flexibility of pasture usage in the late summer

Suppressive

If carried out for long enough will reduce the chances of lungworm infection More likely to lead to anthelmintic resistance in target nematodes

Higher labour or anthelmintic costs especially in the case of slow-release boluses Allows more flexible use of grazing

Dilution

Lower anthelmintic costs

Requires excellent fencing and high labour costs and is generally used only in well organized dairy farms Is not effective for prevention of lungworm infection

Endoparasites

containing fully developed larvae, which are passed in the faeces. These become infective within a much shorter time than the eggs of Ostertagia species and hence in optimal conditions can produce a rapid increase in their numbers. In addition to rapidity of maturation to infectivity, larvae are also dispersed from faecal pats by some of the following means: (i) ascending the common faecal fungus Pilobolus and being propelled into the air on discharge of the sporangium, to be carried by wind to adjacent areas; (ii) although unverified, there is evidence that earthworms or coprophagous beetles may act as transport hosts; (iii) also unverified, it has been reported that the European hare (Lepus europaeus) can be infected, although experiments have shown that the smaller blue hare (L. timidus), common in Ireland, is refractory to infection. In addition to these means of dispersal it has been shown that infective larvae can remain viable in soil as well as on pasture over the winter, and that small numbers of adult worms and hypobiotic larvae can survive and overwinter in infected animals despite their hosts having some immunity to further infection, only to mature and propagate larvae during the following spring.

Pathogenesis After ingestion, infective larvae penetrate the intestinal mucosa, moult to the L4 stage of their life cycle and migrate via bloodstream and lymphatic channels to the lungs. This takes place approximately one week after being consumed, and up to this point no clinical effects are observed in the host. After that period, larvae break out of blood vessels into alveoli and small bronchioles, after which they moult to become young adults, and as they increase in size they ascend the bronchiolar tree towards the large bronchioles and bronchi. Larvae are first found in faeces from the 25th day after infection.

Signs Clinical signs appear during the second week after infection and their severity depends on the number of developing worms. The signs range from occasional to repeated coughing, with a noticeably increased respiration rate in the worst affected. By the third week, severely affected cattle do little else except stand in a characteristic head extended position with rapid shallow breathing and frequent coughing. Although most calves, if not severely affected, will recover after treatment, a small percentage will suffer a relapse of clinical signs in the absence of fresh infection. The precise aetiology of this is uncertain, but autopsy reveals an oedematous rubbery lung with alveolar epithelialization observed microscopically.

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Necropsy The pathological progression during maturation progresses from alveolitis and bronchiolitis to bronchitis and severe emphysema, sometimes with superimposition of a secondary bacterial pneumonia. If left untreated after patency even moderate infections can progress in severity due to aspiration of eggs and hatched larvae back into previously unaffected alveoli and smaller bronchioles, resulting in bronchitis and pneumonia.

Diagnosis Affected cattle invariably present with varying degrees of respiratory abnormality, and since similar signs can occur as a result of infection by a variety of pathogens, careful differential diagnosis is advisable. The grazing history and time of the year in northern temperate areas invariably involve cattle grazing established pasture previously used by other cattle plus the appearance of clinical signs between July and October. Since the caudal lobes of the lung are more frequently affected, adventitious lung sounds are usually more apparent from these areas, in contrast to those from viral pneumonias, which usually affect the cranial and medial lobes. Confirmation of the diagnosis by identification of larvae in faeces or sputum samples can only take place after patency, which takes place approximately 25 days after infection, although it should be noted that in adults that are suffering from a reinfection the infection usually does not reach patency.

Treatment (see p. 1027) In order to kill the worms and larvae present in the lung tissues, anthelmintic treatment is essential. The most effective are the avermectins and moxidectin; levamisole and some of the more recently developed benzimidazoles or pro-benzimidazoles, such as oxfendazole, fenbendazole, albendazole and netobimin, are also effective, but the incidence of alveolar epithelialization is more common after their use, since they have little persistent efficacy and reinfection can occur if the same grazing is used before and after treatment. Severely affected animals may also require antibiotic therapy to control secondary bacterial pneumonia, and if anorexia has been present rehydration with electrolytes may also be helpful. In most outbreaks a range of severity is observed and it is frequently advisable to house the worst affected cattle, especially if climatic conditions would be stressful even to healthy calves. In addition, because treatment of severe cases can exacerbate signs farmers should be warned of the possibility. In outbreaks involving adult dairy cows care should be

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taken that the anthelmintic used does not prevent sale of milk products for a prolonged period until a withholding time long enough to allow excretion of the drug has passed. The most appropriate drug currently available is eprinomectin, the use of which requires no period of milk withdrawal from sale.

Prevention There are two major methods available, the first relying on inducing immunity and the second on suppression of infections.

time of turn-out to grass, and intraruminal boluses designed to release anthelmintic either intermittently or continuously for periods up to 140 days. The level of immunity stimulated depends on the number of larvae ingested from pasture and, since this can be highly variable, some cattle in a group may have inadequate resistance to future infection should they be exposed to it. As a result, careful monitoring is necessary after cessation of anthelmintic treatment and some thought required to plan cattle husbandry during the subsequent year and then as adults.

Stephanurosis (kidney worm) Vaccination (see p. 1011): Immunity can be stimulated by the use of a live vaccine, which takes the form of two doses of 1000 infective larvae irradiated by gamma irradiation. Calves should be two months old before vaccination and the doses separated by four weeks and preferably both doses given before going to grass in the spring or before the time of earliest challenge in outdoor calves. Although the vaccine induces excellent protection against clinical disease it does not completely prevent all worms from natural infections completing their life cycle, so that the parasite can be maintained at a very low level on pasture grazed by vaccinated cattle. If the farmer neglects to vaccinate, parasite numbers can quickly increase sufficiently, if weather conditions are favourable, to affect non-immune cattle within their first grazing season. Suppression: On farms where calves have suffered lung damage due to viral pneumonia, vaccination may be inadvisable because of the possibility of exacerbation of the existing lesions. Under these circumstances it has been found that regular anthelmintic treatments throughout the grazing season can suppress infection sufficiently to minimize the danger of clinical disease and at the same time allow some immunity to be induced by the natural ingestion of infective larvae from pasture which are subsequently killed before completion of their life cycle (see p. 1027). The method has also been successfully applied to normal healthy calves, but it requires to be carried out and monitored carefully, since there are potential problems in its use. Firstly, the length of time during which anthelmintic suppression is required may vary between areas with different climatic patterns and farming practices. In general in the British Isles it is necessary to provide anthelmintic cover until mid August. The methods of application require that the anthelmintic must be extremely effective against all stages of the parasitic life cycle of the nematode. Those anthelmintics used fairly successfully have been avermectins, either as injections or pour-ons administered at intervals after going to grass that are dependent on the particular pharmacokinetics of the drug used and the

Aetiology and epidemiology This is mainly an infestation of pigs but it can infect calves and is due to Stephanurus dentatus. The adult is up to 45 mm in length. The condition is found in the tropical and subtropical countries of Africa, East and West Indies, Brazil, Hawaii, Philippines, Australia and southern Europe where pigs are kept, but in calves adult worms do not develop. The larvae cause damage to the liver parenchyma during migration and produce thrombosis of the abdominal blood vessels, which may be fatal. Aberrant larvae can encapsulate anywhere in the host but the majority are found in all parts of the kidney. The eggs produced in the pig form hatch to produce first stage larvae. These develop to third stage infective larvae if there is warmth and moisture. The larvae are often ingested by earthworms and these act as a vector for infection. The infective larvae are otherwise susceptible to cold or drying. Transmission is either by ingestion, which may include earthworms, or by skin penetration. In the host they pass to the liver where they remain for a considerable time before going to other parts of the body.

Signs They are mostly of anaemia, ill thrift and ascites. Many infestations are without signs.

Necropsy Necrotic lesions with thrombosis in the mesenteric blood vessels and hypertrophy of the mesenteric lymph nodes are likely to be found. In a few cases there may be haemorrhages and abscesses in the lungs and kidneys.

Diagnosis This will depend on the presence of calves grazing areas with infected pigs. An immunodiffusion test can be used. There is a marked eosinophilia.

Endoparasites

Treatment and control Fenbendazole at high doses may be effective. Calves should not graze pastures recently used by pigs.

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suck blood and cause haemorrhagic anaemia and hypoalbuminaemia, and small numbers (about 2000) in comparison to other gastrointestinal nematodes, other than Haemonchus placei, will cause very severe disease and death.

Bunostomosis Bunostomosis in cattle is caused by the hookworm Bunostomum phlebotomum. It mainly affects cattle up to one year old and causes a range of signs from unrest and mild abdominal pain to diarrhoea and eventually anaemia depending on the stage of the infection and the number of worms present. It is more prevalent in subtropical and tropical regions than in temperate; this distribution has become especially marked during the last decade as the worm, which does not occur in large numbers, seems especially sensitive to some of the modern anthelmintics and may now be absent from those areas where frequent suppressive anthelmintic treatments have been applied.

Aetiology and epidemiology Bunostomum phlebotomum parasitizes the small intestine of cattle. Adults can reach 3.0 cm in length and are characterized by a large buccal capsule with lateral cutting teeth and a tooth-like structure in its base, which is the duct of an oesophageal gland. The worms suck blood, which can induce anaemia and in large numbers cause diarrhoea. The eggs from adult females pass out with faeces. Depending on climatic conditions, a parasitic infective larva, which is susceptible to desiccation, will develop under optimal conditions of adequate moisture and warmth within one week. The infective larvae can infect susceptible cattle in either of two ways.

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By penetration of the skin after which it enters the bloodstream and passes to the lung, emerging into the alveoli and after further moulting up the bronchial tree to the pharynx, where it is then swallowed and passes to the intestine to mature. By direct ingestion after which it burrows into the intestinal wall during development to emerge as an adult.

The prepatent period is eight weeks. The worm flourishes in conditions of adequate moisture and warmth and thus is generally a subtropical problem, but disease has been recorded in countries as far north as Scotland, where it has been seen in cattle maintained indoors on damp straw bedding.

Signs Heavy percutaneous larval infections cause restlessness, stamping and itching. Once in the intestine adults

Diagnosis It is difficult to diagnose when prepatent and mild anaemia is the main sign. When patent it should be differentiated from other parasites that cause haemorrhagic anaemia, e.g. H. placei and F. hepatica, and those deficiencies such as cobalt or copper (Chapter 21) that adversely affect erythropoiesis.

Treatment and control The parasite is sensitive to modern anthelmintics and can be controlled by their suppressive or strategic use. Other measures in housed cattle should be the provision of dry bedding and its replacement when soiled. Once infected and treated, cattle normally develop a strong immunity to the parasite.

Haemonchosis Haemonchosis is manifested by haemorrhagic anaemia and diarrhoea, and is caused by the presence in the abomasum of Haemonchus placei (synonym H. similis). As with bunostomosis it is mainly pathogenic in immature cattle, since infection in the first three years of life usually produces a strong immunity to reinfection. It also has a similar distribution, being commonest in subtropical and tropical countries, but present in most temperate countries and able to cause disease during any unusually warm periods of weather.

Aetiology and epidemiology Adults of H. placei suck blood from the surface of the abomasum. They are fairly large in comparison to other abomasal nematodes and measure 3 cm in length when fully grown. In the female the ovaries and intestine are spirally intertwined to give the worm its ‘barber-pole’ appearance and nickname. The male has large barbed spicules, and both sexes a small lancet in the buccal capsule. Female H. placei are very prolific egg producers and can lay up to 10 000 eggs daily. The eggs are passed in faeces and undergo a typical trichostrongyline development to infective larvae. The time taken to reach this stage varies considerably between temperate and subtropical climatic areas. In the former, it may take several weeks in contrast to four days under suitable conditions. The conditions for development of

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Haemonchus spp. have been studied in some detail, and it has been concluded that they require a temperature in excess of 18°C and rainfall of 5.3 cm/month for maximum translation, but can develop provided the mean minimum temperature is not less than 10°C. As a result of the combination of fecundity and rapid infective development in favourable conditions, pasture can become quickly contaminated with huge numbers of infective larvae. In the subtropics acute infections can therefore be found in susceptible young cattle, whereas in temperate areas infections are more likely to be chronic. Under adverse conditions in the tropics, e.g. dry seasons, infective larvae can undergo hypobiosis in a similar manner to Ostertagia spp., and resume development shortly before the rainy season commences. Once ingested, larvae undergo two moults before becoming adult in 26–28 days, when infections become patent. After the first moult, the L4 larvae and subsequent adults suck blood, leaving haemorrhagic spots on the abomasal epithelium, and the resultant blood loss is the major pathogenic sequelae. However, in large infections the pH of the abomasal contents may be increased in the same way as in ostertagiosis, with the resultant digestive disturbance, raised plasma pepsinogen, possible bacterial overgrowth and diarrhoea. Once patent, peak egg production from females is normally reached between six and seven weeks after infection and may continue for a further six to eight weeks. Cattle, unlike sheep, develop resistance to the worm and unless immunologically compromised by intercurrent illness or malnutrition the population decreases rapidly thereafter and the animal remains fairly resistant for the remainder of its life.

Signs There are two types of clinical picture. The first occurs in severe primary infections and presents severely anaemic, weak and sometimes diarrhoeic young cattle. The second is found in chronic lesser infections and typically causes weakness, lethargy, weight loss, a less acute anaemia, hypoproteinaemia, submandibular oedema and anasarca.

Diagnosis Diagnosis can be confirmed if the infection is patent by the examination of faeces samples, which may reveal very high faecal egg counts. The plasma pepsinogen level may be raised. The grazing and past parasitic history may be helpful in differentiating from other causes of anaemia or diarrhoea such as fasciolosis, bunostomosis, copper or cobalt deficiencies, babesiosis, coccidiosis, bacillary haemoglobinuria and malnutrition.

Treatment and control Anthelmintic treatment is the primary consideration and H. placei is susceptible to levamisole, avermectins, moxidectin and modern benzimidazoles as well as the flukicides rafoxanide, clorsulon and nitroxynil. This should be coupled with movement to uninfected pasture. Prevention can be achieved using similar methods as those described for ostertagiosis.

Trematodes Fasciolosis Fasciolosis in cattle is a chronic wasting disease caused by the presence in the liver and bile ducts respectively of immature and adult trematodes of the genus Fasciola. The disease is found in vast areas of the world, with the smaller F. hepatica (3.5 ¥ 1 cm) in temperate countries and the larger F. gigantica (7.5 ¥ 1 cm) in tropical regions the commonest species. Calves and yearlings are most commonly affected but any age of animal may be susceptible. Although it may take place at any time of the year, infection is most prevalent during autumn in temperate areas, with the resultant effects of disease becoming apparent in winter and spring.

Aetiology and epidemiology F. hepatica: Multiplication of the parasite is partially climatically regulated, since its life cycle involves an intermediate host that requires adequate moisture and a suitable ambient temperature. The intermediate hosts are various species of snail of the genus Lymnaea, which are found on wet mud surfaces. In the British Isles, L. truncatula is the species involved. It prefers a neutral or slightly alkaline habitat, but can survive in fairly acid conditions such as peaty hills, although under such conditions individual snails remain small and the population low. At its maximum it can have a shell length of 1 cm. The snail population fluctuates, being least in winter and greatest in June and July, especially in years when late spring rainfall has been above average, when large numbers accumulate and are therefore available for transmission of F. hepatica. Briefly summarized the life cycle of F. hepatica is as follows. The adult parasite in the bile ducts is a hermaphrodite and can be self- or cross-fertilized. Large numbers of eggs are produced by each parasite, which pass from the ducts to the gall-bladder and are subsequently passed into the intestine on contraction of that organ. Eggs are then passed in the faeces, but will not hatch unless moist and until an ambient temperature of 10°C is reached. Hatching at temperatures between 22 and 26°C takes nine days, but under normal

Endoparasites

temperatures in the months of May and June in the British Isles, it can take four weeks. On hatching, the released miracidium must locate and penetrate the foot of L. truncatula within three hours. Once in the snail, the parasite undergoes multiplication through stages of sporocyst and rediae and reaches the cercarial stage after a minimum of two months, although in colder temperatures it may take up to 16 weeks or should winter intervene complete development may cease until the following spring. Under natural conditions within the British Isles, cercariae from summer infections are released from snails between late August and October, and in some areas from overwintered infections in April or May. On release from the snail, which must take place in conditions of wetness, the cercariae swim to the nearest plant, encyst on its leaves and become the infective stage, termed metacercariae, several hundred of which can arise from one miracidium. Metacercariae on herbage can survive for several months and therefore maintain the infection from one year to the next. Cattle become infected by ingestion of grass on which metacercariae are encysted. The metacercariae excyst in the small intestine, the wall of which they penetrate to reach the peritoneal cavity where they move to the liver and invade its capsule. At this point the flukes are very small (about 1 mm) but as they burrow through the liver parenchyma they gradually increase in size and in primary infections in cattle will reach the bile ducts after six to eight weeks, when they mature and become egg-laying adults 10–12 weeks after ingestion. In response to the presence of fluke in the liver parenchyma, the liver of cattle produces a more intense fibrous reaction than that of sheep, and the resultant cirrhosis is much more severe and is longer lasting. The liver cells of cattle do not regenerate as do those of sheep, and the result of even moderate infection in cattle is a more fibrous liver parenchyma than in most other species. Within the bile ducts, the adult flukes suck blood and the spines on their cuticle cause multiple small haemorrhagic lesions. In cattle, the resultant fibrous reaction within the bile ducts is also more severe than in sheep and the bile duct walls thicken and become gradually calcified thereafter (Fig. 19.3). The result of the fibrous reaction during a primary infection in both bile ducts and parenchyma of cattle shortens the life span of adult flukes in the ducts to a maximum of 1.5 years and reduces the chances of flukes from subsequent infections being able to complete their life cycle. Cattle therefore become largely resistant to further infections, most of which do not become patent, and the few flukes that do so may take much longer than normal to reach patency and survive in bile ducts for a relatively short time.

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F. gigantica: Although similar in many respects to F. hepatica it is not found in western Europe, but is widespread within tropical and subtropical climatic regions. The intermediate hosts are also snails of the genus Lymnaea, but the species are more aquatic than those transmitting F. hepatica and thrive in swamps, drainage channels and artificially flooded areas. As a result the epidemiology is closely tied to the periods of maximum rainfall, the snails being infected and development in the snail completed within these periods. Cercariae are shed towards the end of the wet season and encyst on herbage and even on the water surface at the start of the dry season. The parasitic life cycle is similar to that of F. hepatica but each phase takes slightly longer with the result that patency of primary infections take three or four weeks longer than F. hepatica, eggs being found in faeces from 13 to 16 weeks after ingestion of metacercariae.

Signs In severe infections there is a progressive loss of weight with anaemia and occasionally oedema. Subclinical infections cause a reduction in milk yield and reduction in the growth rate of young cattle. Diagnosis: The disease is characterized by a gradual loss of condition that is exacerbated if the quantity and quality of feeding are suboptimal. A chronic anaemia develops and the packed cell volume (PCV) drops to approximately 20 per cent. Erythrocytes are hypochromic but normocytic, and while the leucocyte count may be slightly raised, the percentage of eosinophils in a differential count is greatly increased and may consist of up to 20 per cent of the total white cell count. In cows the total milk yield and the non-fat solids proportions may be reduced. Diagnosis can be confirmed by the presence of fluke eggs in faeces samples, but detection is not always as simple as in sheep, especially in adults, since even in patent infections excretion of eggs is intermittent. Examination of plasma shows a hypoalbuminaemia, and during the migration phase the plasma glutamate dehydrogenase (GLDH) is raised. Once the epithelium of the bile duct walls becomes diseased, the plasma concentration of gamma-glutamyl transpeptidase (GT) rises and this is a useful diagnostic indicator.

Treatment (see pp. 1026, 1028) Affected cattle are treated by administration of a fasciolicide. Of those currently used for cattle the commonest are triclabendazole, oxyclozanide, rafoxanide,

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Fig. 19.3 (A) Normal and (B) liver fluke infected bovine liver. (C, D) Microscopic sections of the same stained to show fibrous tissue.

nitroxynil, albendazole, netobimin and clorsulon. All will remove more than 90 per cent of adult flukes from the bile ducts, but they have variable efficiencies against the immature stages migrating through the liver. The most effective is triclabendazole, which will remove developing flukes from a few days after ingestion. Rafoxanide, nitroxynil and clorsulon are effective against six-week-old flukes at normal dose rates and at increased dose levels affect those four weeks old. Albendazole, netobimin and oxyclozanide at normal dose rates remove only adult flukes from the bile ducts and are ineffective against immature flukes. All require withholding of meat and milk for human consumption for variable periods dependent on their pharmacokinetics (see p. 1026).

Prevention There are four methods available that are used individually in suitable circumstances or can be combined

in an attempt to give a more rapid reduction in the prevalence of the parasite.

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Prophylactic use of anthelmintics to reduce both the number of flukes in cattle and the number of eggs excreted. This is by far the commonest practice and involves treatment of cattle once or twice annually. In the British Isles such treatments take place in the autumn and late spring. If the areas of snail habitat are delineated and small and they can be drained. This is usually not costeffective for fluke control alone if the sites are extensive. Small snail habitats can be fenced off during the time of greatest infection. Snail habitats can be treated with molluscicide. There can be environmental objections since many which were formerly in use were toxic to many species in addition to snails. The most satisfactory is N-tritylmorpholine, which although not available in the UK is used in many tropical countries.

Endoparasites

Paramphistomosis (stomach fluke disease, intestinal amphistomiosis) Aetiology and epidemiology The cause of acute paramphistomosis in Africa is Paramphistomum microbothrium. Other Paramphistomum spp. and Cotylophoron spp. are found in ruminants in Africa and tropical and subtropical regions. In Asia, Calicophoron spp. are found and one species occurs in Africa. Carmyerius spp. are seen in Africa, India, Pakistan and the Middle East. It has been recorded in a severe form in Australia, India and the USA. The life cycle is indirect and similar to that of Fasciola. It involves aquatic snails that are adapted to a variety of locations. Disease occurs only where there is a massive concentration of the infected planorbid snails. The metacercariae are ingested and the immature flukes develop in the duodenum, where they may be seen in the mucosa. The flukes are 3–4 mm long and 1–2 mm wide. They also develop in the abomasum but are less common. They then migrate through the abomasum to the rumen and reticulum, where again few are found. The prepatent period is very variable, being between one and a half to four months. Most outbreaks occur in the late summer, autumn or early winter when pastures are being contaminated with cercariae. Although all ages of cattle are susceptible, infestation is most commonly seen in yearlings. Fewer infestations occur in the adult, suggesting some degree of immunity.

Most disease occurs with immature flukes and so it is not easy to detect in the live animal but it can be missed at post mortem. Often other parasitic infestations are present, which again causes paramphistomiosis to be overlooked. However, the history and area where the cattle are grazing can give some indications. There is a reduction in the red and white blood cells and a hypoalbuminaemia. Differential diagnoses include copper and cobalt deficiencies, liver fluke, parasitic gastroenteritis, Johne’s disease in the adult and poisoning.

Treatment (see p. 1028) Few of the modern trematocides have been found to be effective against paramphistomosis. Oxyclozanide at 18.7 mg/kg has variable efficacy from approximately 50 to 90 per cent. Niclosamide at 100 mg/kg is highly effective against intestinal paramphistomes but ineffective for adults. Brotianide at 55 mg/kg is effective against adult flukes but less so against the immature stages.

Control Drainage of low-lying areas and destruction of the soil will considerably reduce infestation. The most susceptible animals, i.e. calves and immature cattle, should be kept away from likely snail habitats. Routine treatment against Paramphistomum before they mature and can infect snails is of use.

Schistosomosis (bilharziosis)

Acute paramphistomosis is due to a massive infestation in calves. There is a persistent fetid diarrhoea without blood or mucus, anorexia, weakness, marked loss of condition and then recumbency. In some cases there is submaxillary oedema and a pallor of the mucosa. Death occurs in about one to two weeks after signs develop.

Aetiology and epidemiology

Necropsy In the acute case there is severe inflammation of the duodenum and abomasum as the parasite penetrates deeply into the mucosa and sometimes the muscularis layer, and there is haemorrhage. There is muscular atrophy, subcutaneous oedema and fluid accumulation in the body cavities. Large numbers of small, immature, flesh-coloured flukes are present in the lumen. In less acute cases the duodenum is thickened and congested. There is fluid in the abdominal cavity.

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Diagnosis

Signs

Chronic: In heavy infestations of adult flukes there is a chronic loss of weight, a dry coat and anaemia.

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There are several parasites in the genus Schistosoma. Schistosoma bovis is found in African, Asian and southern European cattle. Schistosoma mattheei occurs in cattle in central and southern Africa and can infect man. Schistosoma indicum is found in India and Pakistan as is also S. spindale, which can also occur in south-east Asia and Indonesia. Schistosoma japonicum occurs in the Far East. Schistosoma nasale is again found in India and Pakistan and is unusual in that the adult occurs in the mucosal veins of the nose. Several minor species occur involving S. curassoni. Various species of the parasite are widespread and the adults live in veins. Unlike most flukes, Schistosoma spp. are not hermaphroditic and the longer male carries the long slender female, which is up to 25 mm long, in a gyroectoplasmic canal. Infection can be via the skin or gut. After penetrating the skin the schistosomulae (young flukes) pass via the lymphatic system to the right side of the heart. They then go via the lungs into the circulation and then to the liver. They mature in the portal

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Table 19.3 Intermediate snail hosts of Schistosoma spp. Species

Intermediate snail host genus

S. S. S. S. S.

Bulinus and Physopsis Indoplanorbis Oncomelonia Bulinus Lymnaea and Indoplanorbis

bovis indicum japonicum mattheei nasale

veins before migrating to their final area, usually the mesenteric veins, but they are also found in the urinary bladder veins in the case of S. mattheei and in the nasal mucosal veins in S. nasale. When infection is oral the gut is penetrated and the immature stages pass to the liver via the blood. Once mature, eggs are produced that can hatch within minutes if conditions are right. The freeswimming miracidiae penetrate snail hosts producing sporocysts, daughter sporocyst and cercariae but there are no redia. The cercariae must infect the final host within one or two days or they die off as there is no metacercarial stage. There are various genera of snails involved depending on the species of Schistosoma (Table 19.3). All the snails like mud except for Oncomelonia spp., which are aquatic. In many areas of Africa most of the cattle are infected but there are very few signs. Young cattle are more likely to be ill.

cally spiral. As the eggs hatch quickly they need to be fixed in 10 per cent formalin. Differential diagnosis involves coccidiosis, trypanosomosis, poisoning and Johne’s disease.

Treatment (see p. 1028) Trichlorophan, an organophosphorus compound, can be used parenterally, or niridazole or thioxanthane derivatives such as becanthane or hycanthane may be used. Treatment must be performed carefully otherwise a large number of dead schistosomes will produce emboli and lead to hepatic infarction or portal occlusion.

Control Immunity to the disease occurs but varies with the Schistosoma species. Control involves keeping cattle away from areas frequented by the intermediate host. Molluscicides can be of some benefit. Some vaccines are under development, e.g. a recombinant glutathione S-transferase derived from Schistosoma bovis has been shown to reduce both egg output and parasitic establishment. Such vaccines can be expected to be available in the next year or two.

Cestodes Taenia saginata

In severe infestation there are small grey-white granules in the gastrointestinal tract with petechial haemorrhages and ecchymosis. The ileocaecal body may be enlarged and haemorrhagic. Granulomas may also be scattered through the liver parenchyma as well as the lungs and bladder. In S. nasale infestation there may be nasal granulomas.

Taenia saginata is a cyclophyllidean tapeworm, for which man is the final host. It is transmitted to man by the ingestion of the intermediate larval stage in undercooked beef. Although the larval stage can be found in any age of cattle, viable cysts are found mainly in cattle up to two years of age. The presence of the parasite in the muscles of cattle does not cause clinical signs unless the animal is very heavily infected and the myocardium is involved, but because it is a zoonotic infection its presence can cause significant losses to the beef industry, especially in developing countries. In countries where sanitation standards are high it is a decreasing problem that on average is found in 0.5 per cent of bovine carcasses, with occasional heavy infections occurring under unusual circumstances. In those areas of Africa, Asia and parts of Latin America where human sanitation methods are poor or non-existent and local customs favour ingestion of raw or undercooked beef, the prevalence may be up to 20 per cent.

Diagnosis

Epidemiology

The signs and grazing history help but it is difficult to diagnose unless faeces are taken or nasal discharge if S. nasale is present. The eggs are large and characteristi-

The adult tapeworm inhabits the intestines of man. Its scolex has no hooks, and apparently moves up or down the intestine depending on whether the host has eaten

Signs The main signs are of diarrhoea, which may contain blood and mucus and is intermittent. There is a loss of condition and reduced resistance to other diseases. Death occasionally occurs. Infestation with S. nasale causes a mucopurulent nasal discharge with dyspnoea. Chronic cases develop nasal granuloma.

Necropsy

Endoparasites

recently or not. When the host’s stomach is empty the scolex moves back up the intestine towards the duodenum, and these movements produce hunger pains and vague intestinal discomfort. Fully grown the tapeworm may reach a length of 8 m. Mature egg-filled (about 25 000) proglottids are shed from its posterior end and are passed in faeces or wriggle out of the host’s anus nocturnally. Anal pruritis and occasional diarrhoea are usually the only signs apart from the aesthetic and hygienic conditions involved. The eggs are resistant to external conditions. They are inactivated within two weeks if desiccated, but are known to survive for 16 days in raw sewage, 71 days in liquid manure, 159 days on pasture and 200 days in sewage sludge. No normal method of handling sewage can inactivate them other than total incineration or extensive heat treatment. Extended periods of sludge digestion with or without heat may affect viability but technical proof is lacking. Chemical disinfectants other than some containing copper at very high pH (11.5) are not ovicidal. Two-thirds of outbreaks in developed countries have been shown to be associated with the spreading of sewage sludge on agricultural land. The remainder have been presumed to be caused by spread of seagulls feeding at sewage plants and passing viable eggs through them on to grazing land, or by accidental flooding of pasture by contaminated effluent streams from sewage plants. Migrant labour from less developed countries and infected stockmen have been implicated in some isolated local multiple infections. Once ingested, the egg hatches and the liberated oncosphere travels via the bloodstream to striated muscular tissue, including the myocardium. It develops in the muscle and reaches infectivity three months after ingestion, when it is recognizable as a whitish fluidfilled cyst with a diameter of approximately 1 cm, known as a cysticercus. It becomes enclosed in a thin fibrous capsule. Cellular immune reaction around it gradually increases and the capsule becomes thickened, eventually leading to the death of a high proportion of the cysticerci within 18 months and resistance to further infection, although some may survive for several years. After death the contents of the cysts become caseous and finally calcified. The masseter, tongue and heart muscles were generally considered preferential sites and are still examined carefully during meat inspection at abattoirs, in preference to damaging more expensive cuts of meat by the multiple incisions that would otherwise be necessary.

Control (see p. 1028) There are no drugs suitable for ante-mortem treatment. Carcasses that are found to be infected are normally treated in one of two ways:

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If lightly infected they are frozen to a temperature of -10° for a minimum of 10 days, after which any previously viable cysticerci will have been killed. Heavily infected carcasses are usually condemned as unfit for human consumption and rendered after heat treatment into animal feedstuffs in some countries. The thermal death-point of cysticerci is 57°C and meat for human consumption should be raised to at least that temperature if the possibility of infection is to be avoided.

Echinococcus granulosus and hydatid cysts There are two species of the taeniid tapeworm E. granulosus. The first is E. granulosus granulosus: the adult is found worldwide in the intestine of dogs and many wild Canidae but not the red fox. The intermediate form, the hydatid cyst, is found in domestic and wild ruminants, man and pigs, but not horses and donkeys. The second is E. granulosus equinus, which is almost exclusively found in Europe: adults parasitize the dog and the red fox, and horses and donkeys are the exclusive intermediate hosts. Cattle therefore are affected by hydatid cysts of E. granulosus granulosus. The majority of hydatid cysts cause little apparent disease as they are situated in the liver or lung, their presence only becoming disclosed at abattoirs. Occasionally, they develop in sites where their gradually increasing size causes pressure on vital organs., the resultant disease being dependent on the organ and system affected.

Aetiology and epidemiology The adult worms parasitize the small intestine of the dog. They are small worms, consisting of four segments of length 0.6 mm. Large numbers may be present in infected animals, each releasing one gravid segment daily containing many eggs, which are resistant to normal external climatic conditions and remain infective for up to two years. After ingestion by cattle or other hosts the oncosphere penetrates the wall of the intestine and is carried via the bloodstream to the liver or other organs where it lodges and starts to grow to become a hydatid cyst. Growth is relatively slow and may take at least one year to reach a diameter of 20 cm. In restricted sites the cyst assumes the shape of the space available, and daughter cysts may be formed and spread to other organs. If growth takes place in the omentum or mesentery, cysts can become very large. There is usually little cellular reaction around cysts in cattle. Since most cattle in developed countries are slaughtered in abattoirs there is little chance of further spread unless casualties are fed to farm dogs or packs

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of hounds. In underdeveloped countries or where carcasses are not disposed of, wild Canidae ingesting the offal become infected; the brood capsules from within the hydatid cyst evaginate, the scolex attaches to the intestinal wall and reaches adulthood and patency some six weeks later. Infection in dogs is usually symptomless.

Treatment and control (see p. 1028) Affected cattle are not treated specifically for hydatidosis, principally because of the difficulty of diagnosis, but also because anthelmintics are only now becoming available for treatment of infected human beings. Activity against larval forms has been claimed for praziquantel and albendazole, although most cysts are excised. Prevention is directed to ensuring that dogs do not become infected, either by regular treatment, the most effective anthelmintic being praziquantel, or by preventing the ingestion of infected offal.

Protozoa Coccidiosis Bovine coccidiosis almost invariably affects groups of cattle less than one year old, although it does occasionally occur in older animals. It is manifested by enteritis, diarrhoea and in severe cases dysentery. Not all members of the group are equally affected and light infections are self-limiting; severe infections can be fatal if untreated. The disease is caused by the ingestion over a short period of large numbers of oocysts of Eimeria species by non-immune cattle; the greater the infective dose, the more severe the signs produced. Eimeria are species-specific, and although 13 species have been isolated from cattle, E. zuernii, E. bovis and E. alabamensis are much the commonest and most pathogenic. They are found everywhere in the world where cattle are farmed. Cryposporidiosis is mentioned on pp. 204 and 286.

oocysts to survive and become infective, but frequently occurs three or four weeks after groups of purchased calves are mixed. In North America it has also been associated with the sudden stress of extreme temperature reductions in midwinter. After ingestion, the oocyst is disrupted, releasing eight sporozoites each of which penetrates an intestinal epithelial cell and develops into a trophozoite. Multiple fission within the trophozoite produces a schizont, which after a few days ruptures the cell to release a large number of merozoites, which in turn invade other epithelial cells. There are up to four generations of schizogony depending on the species involved. The location of the cells invaded is important for the pathogenicity of the species, e.g. E. zuernii and E. bovis both invade cells in the lower ileum and later schizogony and gametogony (the term used to describe the sexual stages) take place in the epithelial cells of the caecum and colon. The gametocytes are formed deep in the epithelium and their rupture causes severe disruption of the lining of the caecum with resultant haemorrhage into the lumen. After gametogony, oocysts are formed that subsequently are passed in faeces. They are not immediately infective but require to undergo sporulation, in which the sporocyts and sporozoites are formed ready for further infection. The last process requires adequate moisture and warmth and takes 24–72 hours. The total life cycle from ingestion to patency occupies 15–17 days for E. zuernii and 15–20 days for E. bovis. Oocyst production during infection with a single species lasts for five to twelve days, but may be prolonged in multiple species infections. The oocysts are very resistant to external conditions and will survive for up to two years in suitable environments with adequate moisture. They can resist moderate frosts down to -8°C for two months, but are susceptible to drought, high temperatures and the chemical action of ammonia.

Signs The presenting signs of diarrhoea or dysentery accompanied sometimes with severe straining in a group of calves leads to suspicion of coccidiosis.

Aetiology and epidemiology The presence of large enough accumulations of oocysts to cause disease is the result of farming practices that allow groups of cattle, which frequently have been stressed by transport and by mixing with others, to ingest food or water contaminated by faeces. It can happen either indoors on straw bedding, which is both damp and contaminated with faeces, or outdoors around drinking or feeding troughs. It can take place at any time of the year so long as conditions prevail that produce adequate moisture and temperature for

Diagnosis Examination of faeces samples for the presence of large numbers of oocysts can confirm the diagnosis. Care should be taken in interpretation of oocyst counts since small numbers are present in the faeces of many normal calves, and in severely affected diarrhoeic calves the main oocyst production phase may have passed or their numbers be misjudged due to the dilution factor of liquid faeces. Occasionally, calves may exhibit nervous signs, the reasons for which are as yet obscure, and viral

Endoparasites

diseases that considered.

have

cerebral

affects

should

be

Treatment (see p. 1029) Two considerations need to be borne in mind. Firstly, severely affected calves will require individual treatment with an anticoccidial and, if deemed advisable, fluid therapy with electrolytes and injections of antibiotics to control secondary bacterial infections. Anticoccidial treatments include injections of sulpha drugs or the oral administration of sulphadimidine at 140 mg/kg body weight daily for three days, or amprolium at 10 mg/kg for four or five days. Amprolium has been withdrawn from sale in many countries because of possible carcinogenesis, and it should be remembered that overdose with amprolium, which is a thiamine antagonist, has also been associated with production of cerebrocortical necrosis (CCN), so care should be taken to give the correct dose in those areas where it is available. Secondly, prophylactic treatment for other calves in the group should be assessed, depending on the numbers involved. Lasalocid at 1 mg/kg body weight per day, monensin included in the diet at 16.5 ppm of the diet or decoquinate at 100 ppm, either continuously to suppress all infection or for two cycles of medication for a week separated by a week when it is removed, can protect from the infection and allow sufficient immunity to be stimulated. A long-acting intraruminal bolus consisting of 1.6 g baquiloprim plus 14.4 g sulphadimidine is also effective, and sulphadimidine itself can also be used prophylactically at 35 mg/kg, but it should be borne in mind that as light infections are self-limiting such treatments may not be cost-effective. Other measures should be taken to reduce the chances of infection, i.e. removal of food contaminated with faeces and better siting of feeding and water troughs so that faecal deposition on food and in water is made less likely. If the problem is a recurring event with each batch of calves, thought should be given to a short period of anticoccidial treatment after two weeks of exposure to possible infection so that incipient infections are disrupted but sufficient stimulation of immunity has been allowed to take place. A potent anticoccidial of a novel chemical type, toltrazuril, has been used experimentally in this manner with great success and may constitute a significant future advance in the prophylaxis of the disease.

Neosporosis (see p. 584) Aetiology The cause is Neospora caninum, a coccidial protozoan discovered within the last decade, and now recognized

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as a ubiquitous parasite of cattle and dogs that also affects many other species of animals. Although it is the type species, recently, another species, N. hughesi, has been isolated from horses. Currently little is known of its development in animals that are naturally infected. The dog is the intermediate host, and is also a final host in prenatal infections. Infection can be both vertically transmitted from dam to calf in utero and lactogenically, naturally by ingestion of food and water contaminated with dog faeces containing Neospora caninum oocysts, or from cow to cow. The mechanisms of repeat congenital transmission are unknown at present.

Signs It is a major cause of abortion in both dairy and beef cattle, and has been observed in almost all countries in the world. Cows of any age can abort from three months of gestation to full term, although most abortions occur at 5–6 months. Foetuses can be born alive or may die in utero and be mummified or reabsorbed. Calves that are infected may be born underweight and with neurologic symptoms such as ataxia, decreased reflexes and exophthalmia.

Necropsy Tachyzoites and tissue cysts are found intracellularly in affected cattle. Tachyzoites measure 6 ¥ 2 microns. Tissue cysts are oval, 102 microns long, and are found in the central nervous system and retina. Although infection can be found in many organs, the commonest site is the brain. The characteristic lesion is a focal encephalitis with necrosis and non-suppurative inflammation. Hepatitis can also be found in epidemic abortions.

Diagnosis Ante-mortem diagnosis is by serologic methods. Several methods of assay of serum antibody are available, e.g. ELISA and indirect fluorescent antibody. A PCR (polymerase chain reaction) diagnosis of antigens is under development.

Treatment and control At present treatments are largely experimental. Sulphonamides, pyrimethamine and clindamycin have been used in infected dogs, and decoquinate has been shown to kill N. caninum tachyzoites in cultures. Dogs should not be allowed to eat aborted fetuses or fetal membranes, and their faeces should be prevented from contaminating bovine feedstuffs.

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Toxoplasmosis Toxoplasmosis is a protozoan zoonosis that can infect any species of vertebrate. It is mainly recognized as being most pathogenic for sheep, however it occasionally causes human illness, and it can cause significant disease in cattle, although abortion is not as common a result as in sheep (see p. 895).

Aetiology and epidemiology The parasite involved is Toxoplasma gondii. It has a two-host life cycle with both sexual and asexual stages. The definitive hosts are cats, both domestic and wild, which become infected by eating raw infected meat from the intermediate host, which can be any other species of vertebrate but is frequently a rodent. Once ingested the infective cysts are digested, each releasing large numbers of bradyzoites. They penetrate intestinal epithelial cells and undergo a coccidia-like series of schizogonies and finally gametogony in the small intestine to produce oocysts in faeces within one and a half weeks after ingestion of cysts. The cat then excretes oocysts for approximately two weeks. Oocysts remain viable for 17 months on pasture and if they contaminate animal feed any animal consuming it becomes infected. Within the intermediate host, development is asexual. The oocyst wall is disrupted, releasing eight sporozoites which reach the lymph and blood vessels after penetrating the intestinal epithelium. The tachyzoites, as they are now called, are spread throughout the body to muscles, heart, lungs, liver, uterus and central nervous system, where they penetrate cells and multiply asexually. It is during this phase that the intermediate host becomes ill. After each multiplication the infected cells rupture, releasing 8–16 tachyzoites for further spread. After some days of such divisions the host develops some resistance to the organism and the spread of tachyzoites ceases, but is replaced by the formation of slow-growing cysts, each of which eventually contains large numbers of bradyzoites. Normally these remain until ingested, but should the host’s immunity be reduced by other disease the invasive process can recommence. The tissue cysts are susceptible to freezing and cooking to 70°C for 30 seconds and therefore consumption of adequately cooked infected meat is harmless. The organism is ubiquitous. Blewett (1983) reviewed the serological surveys that have been carried out in domestic animals and came to the estimate that antibody was present in 6.5 per cent of horses, 12.5 per cent of cattle, 23.5 per cent of pigs, 30 per cent of sheep and 40 per cent of cats. He also postulated that different animals vary in susceptibility to infection and in the rate of loss of antibody, and concluded that cattle return to

a seronegative status much more rapidly than do sheep, which are as a result a more reliable indicator of the actual prevalence of the infection.

Diagnosis At autopsy or in abattoirs the most common findings are multiple necrotic granulomatous foci in internal organs. Histopathological examination is necessary for confirmation. In vivo, cattle are presented with vague pyrexic disorders sometimes affecting the central nervous system. If pregnant cows are affected, stillborn or weak calves that die within a few days of birth may result. Such calves frequently manifest nervous signs such as tremors of the head or neck, teeth grinding or convulsions. Serological diagnosis can be made using a variety of tests such as indirect immunofluorescence or enzymelinked immunosorbent assay (ELISA), or the SabinFeldman dye test. Because of its ease of use, an ELISA using both anti-IgM and anti-IgG for detection of both acute and chronic infection is currently being developed.

Treatment and control Treatment of acutely infected animals can be attempted by the use of pyrimethamine and sulpha compounds such as sulphadiazine or sulphadimidine. Results in animals have been disappointing compared with those in mice and humans. These drugs affect tachyzoites but not bradyzoites so that total elimination of the parasite is not possible. Recent experiments with the ionophore monensin have shown prophylactic activity in sheep, but there are no reports of its use in cattle (Buxton et al., 1987). Other preventative measures include prevention of cat faecal contamination of animal food and adequate destruction of infected carcasses.

Sarcosporidiosis (sarcocystosis) Aetiology The cause is Sarcocystis, a coccidial protozoan that has a predator–prey life cycle. The indirect hosts are dogs, cats and man and each may contain several species of sarcocyst, each one specific for a different intermediate host. Sarcocystis hirsuta is present in the ox and cat species, S. cruzi in the ox and dog and S. hominis in the ox and man. In the final host the Sarcocystis spp. undergo an enteric cycle with oocysts in the cells producing sporocysts in the faeces. On entry to some intermediate hosts those infected via the dog undergo schizogamy in blood vessel endothelial cells before

Endoparasites

passing to the muscle. Those of the cat are not pathogenic and are found in the oesophagus, and throughout the tissues of the intermediate host produce microscopic cysts. If cattle are grazing and ingesting a few oocysts this probably results in a strong immunity. Signs develop about 26 days after infection (see p. 895).

Signs Usually no signs occur but, following ingestion of massive doses, calves may develop anorexia, fever, emaciation and anaemia. Adults can suffer pyrexia, emaciation and abortion.

Necropsy There are usually petechial and ecchymotic haemorrhages throughout the body, especially in the heart, brain, liver, lungs, kidneys and muscle. Some animals show emaciation, lymphadenopathy, anaemia and ascites. Death is usually due to necrotizing endocarditis. Histologically, schizonts can be found in the endothelium throughout the body and haemorrhages, lymphatic infiltration and oedema occur in the tissues and organs.

Diagnosis This is usually based on post-mortem findings.

Treatment Pyrimethamine at 1 mg/ml and trimethoprim at 5.0 mg/ml alone or in combination with sulphonamides have been shown to inhibit the development of S. neurona in cell cultures. Sulphonamides alone were

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ineffective. The difficulty with any treatment is the maintenance of sufficient concentrations of the drugs in the cerebrospinal fluid, and relapses are usually ascribed to failure to do so.

Control This is difficult but involves keeping carnivores away from cattle. Infection in dogs and cats can be avoided by feeding them cooked meat.

References Armour, J., Jennings, F.W. & Urquhart, G.M. (1969) Inhibition of Ostertagia ostertagi at the early fourth larval stage. II. The influence of environment on host or parasite. Research in Veterinary Science, 10, 238–44. Blewett, D.A. (1983) The epidemiology of ovine toxoplasmosis. I. The interpretation of data for the prevalence of antibody in sheep and other host species. British Veterinary Journal, 139, 537–45. Buxton, D., Donald, K.M. & Finlayson, J. (1987) Monensin and the control of experimental ovine toxoplasmosis: a systemic effect. Veterinary Record, 120, 618–19. Leaver, J.D. (1970) A comparison of grazing systems for dairy herd replacements. Journal of Agricultural Science, Cambridge, 75, 265–72. McMeekin, C.P. (1954) Good rearing of dairy stock. Bulletin, Department of Agriculture, New Zealand, No. 228. Michel, J.F. (1968) The control of stomach worm infections in young cattle. Journal of British Grassland Society, 23, 165–73. Michel, J.F. (1969) The epidemiology and control of some nematode infections. Advances in Parasitology, 7, 211–82. Urquhart, G.M., Armour, J., Duncan, J.L., Dunn, A.N. & Jennings, F.W. (1987) Veterinary Parasitology. Longman Scientific, Harlow, pp. 1–286.

Chapter 20

Respiratory Diseases A.H. Andrews

Shipping fever (transit fever, pasteurellosis) Infectious bovine rhinotracheitis (IBR)

286 289

Shipping fever (transit fever, pasteurellosis) Epidemiology The condition is an important respiratory problem in groups of weaned suckled calves that have been sold, often via a market, hence the terms transit fever or shipping fever. They are usually over six months old and under two years. During part of the sale transactions they will probably have been mixed and grouped with other batches of animals of similar age during transport, at the market or following arrival at the finishing farm. Most cases occur within the first month of their entry to the fattening unit and most cases are seen at least 10 days after arrival (Andrews et al., 1981). The disease is characterized by an illness of sudden onset with dullness, pyrexia and anorexia. It is an acute exudative bronchopneumonia with toxaemia as well as much fibrin present in the exudate and often accompanied by fibrinous pleurisy (Blood & Radostits, 1989). The condition is common in North America, Europe and Britain. It is particularly prevalent in the American cattle feedlot industry and is the largest cause of mortality in that system. In a Colorado survey 75 per cent of all clinical disease in yearling cattle and 64 per cent of all post-mortem diagnoses were due to respiratory disease (Jensen et al., 1976). The morbidity and mortality rates vary considerably but a level of up to 35 per cent and a mortality of 5–10 per cent of those affected or 0.75–1 per cent of the susceptible population is often quoted (Blood & Radostits, 1989). More recently in Britain, morbidity rates of 73–100 per cent with a mortality of 0–8 per cent of those affected and an average mortality of 4 per cent have been reported (Andrews, 2000).

Aetiology The aetiology of the condition is still open to disagreement. It is considered to be stress or management 286

induced with the participation of infectious agents. The infection has been thought to be primarily viral, mainly due either to parainfluenza III (PI3) virus or infectious bovine rhinotracheitis (IBR) virus, followed by secondary infection with either Pasteurella multocida or Mannheimia haemolytica (Pirie, 1979). Mannheimia haemolytica biotype A serotype 1 is considered to be the most common isolate although biotype T strains have also been found. Mannheimia haemolytica biotype A produces a heat-labile cytotoxin that is ruminantspecific destroying leucocytes (Sherwen & Wilkie, 1982). Pasteurella multocida infection is only isolated occasionally. Recently, it has been proved experimentally that M. haemolytica biotype A1 can produce the disease as a primary agent in non-immune calves (Shoo, 1989). Disease does depend on administering the organisms into the lungs either intratracheally (Friend et al., 1977; Gibbs et al., 1983) or intrathoracically (Houghton & Gourlay, 1984; Panciera & Corstvet, 1984). However, the exact mechanism by which the organisms enter the lung and result in lesions is not yet known. Other evidence of M. haemolytica involvement is that calves previously exposed naturally to the infection are much more resistant to experimental and natural pneumonic pasteurellosis (Confer et al., 1984). Although M. haemolytica can be isolated from the nasal passages it is only in small numbers when calves are healthy and unstressed. The organisms can be present in low numbers in the tracheal air but are not considered to be normal inhabitants of the lungs (Grey & Thomson, 1971). However, as the calves are transported, move to market and then enter the feedlot, the number of M. haemolytica biotype A1 increases in the nasal tract, the tracheal air and then the lungs, where bronchopneumonia can result (Frank & Smith, 1983). Thus management factors are important. The effects of stress are extremely difficult to quantify and have not been successfully undertaken experimentally to produce transit fever. However, transportation of yearling cattle does result in a rise in plasma fibrinogen levels, which is indicative of stress (Phillips, 1984). Increased fibrinogen levels also occur following confinement in unfamiliar surroundings and deprivation of food and water. In addition, it seems that cattle sud-

Respiratory Diseases

denly introduced to a diet consisting of large amounts of cereal are more prone to respiratory problems (Wilson et al., 1985). The environment tends to be important in that disease seems to be related to the season of the year (Andrews, 1978), fluctuations in daily ambient temperature and increased concentration of airborne particles 2.0–3.3 mm in diameter (MacVean et al., 1986). Calves kept at a constant temperature of 16°C (60°F) showed minimum levels of nasopharyngeal bacteria at a relative humidity between 65 and 75 per cent. However, bacterial counts tend to rise at humidities on either side of this range (Jones & Webster, 1981). The interrelationship of different micro-organisms and transit fever still needs further elucidation. However, cattle entering feedlots with low serological titres to IBR, bovine respiratory syncytial virus (RSV) and Mycoplasma dispar were at greater risk of being treated for BRD (Rosendal & Martin, 1986). It has also been shown that IBR, PI3, bovine virus diarrhoea (BVD) and RSV are all associated with acute respiratory disease (Martin & Bohaz, 1986). In many outbreaks of transit fever it is likely that the stress of movement plus mixing with other calves, the introduction to housing and a new diet are sufficient to initiate disease. The main organism involved is usually a Mannheimia species, especially M. haemolytica biotype A1. Spread of infection is optimized by crowded conditions in transport and markets. It is also probable that as animals go down with disease and pass on the infection, the organism increases in virulence. This can be seen in some outbreaks in which disease can be traced from individual animals to other members of the same group and then to other groups (Andrews, 1976).

Signs (see p. 921) The peracute form is unusual but results in sudden death with no premonitory signs. In the acute form the animals are dull and inactive with excessive oculo-nasal discharges, which may be mucupurulent. There is usually anorexia although the cattle still drink, and a marked fever (40–41°C, 104–106°F). There is rapid (40+/minute), shallow breathing and a soft, productive cough, which tends to increase with exercise. On auscultation there are bronchial sounds over the anterior and ventral parts of the lungs, which become louder as the condition continues. In some cases squeaks and high-pitched sounds are heard, together with a pleuritic rub. Later signs can include dyspnoea with marked abdominal breathing and an expiratory grunt. Diarrhoea occurs in a few animals. There is usually a favourable response to therapy.

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Necropsy Death is usually the result of anoxia and toxaemia although occasionally in young cattle there is septicaemia. Usually, over one-third of the lung shows marked consolidation and the ventral parts of the apical and cardiac lobes are most involved. Initially, there is lung congestion and then hepatitis with exudate and, in some animals, emphysema. Bronchitis and bronchiolitis are usually catarrhal, often with serofibrinous pleurisy and a fibrinous pericarditis. There is usually much pleural effusion.

Diagnosis This depends on the history of age, recent movement, weaning or housing. The signs also help with severe respiratory signs involving the anteroventral parts of the lungs and pyrexia. Post-mortem findings of lung consolidation and pleurisy are present, and impression smears show bipolar staining organisms with methylene blue. Mannheimia haemolytica or P. multocida may be isolated from nasal swabs in live animals or lungs at post-mortem and their antibiotic sensitivity determined. Serology for antibody rise can be undertaken, as also can haematology but often the findings are variable.

Differential diagnosis Differential diagnosis includes enzootic pneumonia (see p. 242) but this usually occurs in younger calves with a different history. Infectious bovine rhinotracheitis (see p. 289) usually shows mainly upper respiratory signs and a conjunctivitis. Fog fever (see p. 866) is mainly apparent in older cattle at grass after a pasture move in the autumn. Parasitic bronchitis (see p. 272) is present in cattle following grazing. Acute bronchopneumonia would be almost identical except for bacteriological isolation. Contagious bovine pleuropneumonia is severe in all age groups of cattle and the affected animals suffer severe pain and toxaemia with a high mortality (see p. 868).

Treatment Therapy for shipping fever is given in Table 20.1. Treatment should begin early. Most cattle will usually show some improvement within one to three days of initiating treatment. Complete recovery may take four to seven days. Where severe outbreaks occur it may occasionally be necessary to use mass medication by water as most ill cattle still drink well. Anti-inflammatory agents are often useful in promoting a speedy recovery.

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Prevention and control Although the disease of transit fever is sporadic, many of the conditions that predispose to the problem can be defined. This should mean that methods of prevention should be relatively easy to institute. Ideally, the calves would be weaned at least two weeks prior to leaving the farm of birth (Andrews, 1976). They would be introduced to the type of feed to be provided on the rearing farm. In addition, they would be batched in groups that would go direct from the farm of birth to the rearing farm. In reality this does not happen as the farmer pro-

ducing the calves hopes that by selling them at market he will obtain a better price than by selling direct. In addition, the first farmer will be little concerned about the subsequent disease status of his calves once they have left his farm for sale. This makes the possibility of vaccination prior to movement difficult. As cattle go through markets, disease prevention tends not to be practised because many of the factors enhancing the likelihood of a disease outbreak are outside the control of the purchasing beef rearers. Thus they cannot control the time before moving, the transport of the animals from the farm of origin, their mixing

Table 20.1 Therapy for shipping fever. Drug

Amoxycillin trihydrate Ampicillin trihydrate Baquiloprim and sulphadimidine Cefquinome Ceftiofur Chloramphenicol (some countries) Danofloxacin Enrofloxacin

Method of administration

s.c., i.m. s.c., i.m. oral

Oxytetracycline Oxytetracycline (long-acting) Penicillin/dihydrostreptomycin

i.m. i.m. i.m. i.v., i.m. s.c. s.c. i.v., i.m. i.m. s.c. i.v., s.c., i.m. i.v., s.c., i.m. i.m. i.m.

Penicillin (long-acting) benzathine procaine Spectinomycin Spiramycin Sulphadimidine Tilmicosin Trimethoprim and sulphadiazine

i.m. i.m. i.v., i.m. i.m. i.v., s.c., oral s.c. i.m.

Trimethoprim and sulphadoxine

i.v., i.m.

Tylosin

i.m.

Mass medication Oxytetracycline Sulphamidine Trimethoprim and sulphadiazine Tylosin

oral oral oral oral

Erythromycin Florfenicol Marbofloxacin

Dose

Duration

(mg/kg)

(mg/lb)

7 5–10 4–8 36–72 1 1.1 10 1.25 2.5 7.5 5 20 40 2

3 2.5–5 2–4 18–36 0.5 0.5 5 0.6 1.25 3.75 2.5 10 20 1

10 20 (20–30 000 iu/kg) 20

5 10 (10–15 000 iu/lb) 10

5 6 10–20 20 150 10 4 20 3 12.5 4–10

2.5 3 5–10 10 75 5 2 10 1.5 6 2–5

Usually once Daily for 3–5 days Daily for 3–4 days Daily for 2–3 days Daily for 3 days Usually once Daily for 3–5 days

5 100 25

2.5 50 12.5

Daily Daily Daily Daily

Daily for 3–5 days Daily for 3 days Once or repeat after 48 hours Daily for 3–5 days Daily for 3–5 days 3–4 times daily for 3 days Daily for 3–5 days Daily for 3 days Once Daily for 3 days 2 (48 hours apart) Once Daily for 3–5 days Daily for 3 days Usually once Daily for 3 days

Daily for 3–5 days Daily for 3–5 days

for for for for

5 days 5–7 days 5–7 days 5 days

All animals should be provided with good-quality feed and adequate ventilation. Corticosteroids, e.g. betamethasone, dexamethasone, are often found to help in reducing the level of exudation. NSAIDs may be useful in reducing inflammation, and Mannheimia antisera may also be helpful.

Respiratory Diseases

with other cattle or the conditions present at market. Likewise they will probably have little direct say as to how the animals are transported or their mixing with other groups before their entry to the rearing farm. It is only once the cattle reach the rearers that control measures can be undertaken. Obviously, they can ensure that the animals are kept in as satisfactory an environment as possible and are only lightly stocked. This is best done by having the animals outside but this is resisted by most farmers because of the inconvenience and extra labour required. The new ration for the cattle can also be introduced slowly. The problem is worse in North America where calves often travel vast distances. Here various preconditioning programmes are undertaken. It is advised that calves should be fed prior to weaning and kept in the same place once the dams are removed. Following weaning, regular checking of the calves several times a day should be practised. When animals are travelling they should be given adequate periods of rest and offered feed and water. They should also be well bedded during transit. Some farmers inject multivitamin preparations before moving and vaccines can be used, including those against Mannheimia and PI3 virus. In many countries antibiotics are used following the move. These have given variable results mainly due to predicting when injections should be undertaken. This is because most problems occur about seven to ten days after entry to the feedlot or farm. When used, it is probably best to give long-acting preparations and initiate therapy when the first animals show disease. Use of antibiotic medication in the feed or water is a common practice in North America and while it appears to reduce mortality it has no effect on morbidity.

Vaccination If it is considered that M. haemolytica and at times P. multocida form an important part of the disease syndrome of transit fever then it might be possible to obtain some protection by vaccination. Various vaccines are present in Europe but currently only three are available in Britain. In North America various Pasteurella bacterins and viral vaccines have been used to assist with the control of transit fever. Their efficacy appears to be low and literature reviews suggest that at present there is little evidence to show the efficacy of such vaccines under feedlot conditions (Myers, 1984). Recently in North America several new vaccines have become available. One of these is a M. haemolytica vaccine/bacterial extract. This has been shown to be effective to controlled challenge provided two doses of vaccine have been administered prior to challenge (Sherwen & Wilkie, 1988). Response in a field trial has

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however shown only a slight decrease in morbidity of disease, with slight improvement in relapse rates and response to treatment (Bateman, 1988; Jim et al., 1988).

Infectious bovine rhinotracheitis (IBR) Aetiology Infectious bovine rhinotracheitis (IBR) is a highly infectious and contagious disease of cattle. It is caused by a virus known as bovine herpes virus 1 (BHV 1). It is generally considered that there are several strains of the virus, although often the differences between the strains are not easily shown in the laboratory. The disease is seen in North America, Europe and Africa. It is considered that the outbreak of severe respiratory disease that occurred in Great Britain in the mid1970s was due to a new strain being imported. Several European countries are undertaking eradication campaigns, many of which are progressing satisfactorily. They often involve initial vaccination with marker vaccines and then blood testing, and movement restrictions until the disease is no larger present. While the disease is primarily one of cattle, it can also infect deer, goats and pigs. The main sources of infection between animals are nasal discharge (or eye discharge), when it is affecting the respiratory system, and vaginal or preputial discharges, semen, or the fluids and tissues of the fetus when the infection involves the reproductive tract (see p. 579).

Epidemiology In most cases of respiratory infection disease is spread by aerosol. The genital form of the disease is contracted venereally. As respiratory infection is spread via the air, it can spread by direct contact between the animals or where the cattle are in the same air space, i.e. there is air contact. This can only be avoided by ensuring the walls extend from floor to ceiling and there is no contact with other animals either at the front of the pens or with other groups on either side. However, generally there is a need for close sustained contact between groups. This is why disease is often slow to spread within and between groups. It often takes two to five weeks to spread in a group. However, unexplained outbreaks of IBR do occur on isolated farms. Latent infection: There is a problem with BHV 1 in that it is able to become a latent infection. Thus once an animal is infected with a strain of the virus or vaccinated with a live viral vaccine, the virus may remain in the animal for the rest of its life without it showing any signs of illness. The site of latency is arguable but the virus

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can be found in the trigeminal nerve of clinically normal cattle. However, if the animal is stressed at all, such as when moved or calving, or becomes ill, the virus may be shed. Shedding can also occur in bulls when mating. This shedding may be, but is often not, accompanied by any signs of disease. Corticosteroid injections may promote virus shedding. The level of this latent infection is variable but can be up to 10 per cent of clinically normal animals. In addition, while most of these cattle will show antibody levels to the BHV 1 virus, some do not. Thus all cattle in herds where disease occurs have the capacity to spread disease even when there are no clinical signs of disease present in the herd. The only way of knowing whether or not disease is present is to look at the results of milk or blood tests. If a blood test shows an antibody titre (positive response) to BHV 1 in cattle other than calves it means that the animal(s) have been exposed to infection and could possibly be carriers. If a blood test from an animal is negative it generally means that the animal is unlikely to have been exposed to infection, but it does not completely rule out the possibility that the animal is a latent carrier of disease. Thus tests on individual animals are of limited significance; however, on a herd basis repeated negative tests indicate that it is highly unlikely infection is present. When tests show several animals with antibody levels in the herd then infection is present. The calf that receives colostrum from its infected mother will also show a positive antibody level to the test although not necessarily being infected. The antibody provided from the colostrum will usually remain for one to six months, depending on the amount received from the mother. Incubation period: The incubation period for the disease is very variable. Experimentally, it usually takes three to seven days. However, in most beef units disease occurs about 10–20 days after introduction of infected or susceptible animals. Longer incubation periods do occur. This is quite likely when it is considered that latent carriers may not be shedding virus at a particular time.

Signs Respiratory disease: This disease is the most common form. It is usually seen in cattle over six months old but can occur at a younger age. The signs vary considerably but typically they tend to be worst in animals from about six months to two years old. (1) Mild disease. This is just a conjunctivitis, i.e. slight reddening to the lining of the eye and eyelids with some discharge, usually watery and clear (see p. 921). This often occurs when the disease strain is mild or degree of infection is low, or the animal is resistant.

(2) Subacute disease. This is commonly seen in adult cattle and often is of only short duration. There is a marked rise in temperature lasting only a day or two (40°C, 104°F). Often there is a marked drop in milk yield. Again the lining of the eyes is reddened with discharge and this also involves reddening of the lining of the nose with nasal discharge. The animals will salivate and there may be a short, expressive cough. Breathing is rapid and shallow. The animals recover in 10 to 14 days. (3) Acute disease. The signs are as in the subacute form but the temperature tends to be higher (40–41°C, 104–106°F). These signs are particularly present in growing cattle between six months and two years old. The respiratory signs are more likely to include a cough and there is some respiratory distress. The discharge from eyes and nose tends to become profuse, yellow, thick and purulent. The lining of the nose may show grey areas, which consist of dead tissues that smell and are shed. The signs tend to last a lot longer before recovery occurs. (4) Peracute disease. The animals develop very high temperatures (42°C, 108°F) with eye and nasal discharge, respiratory distress, cough and then death in about 24 hours. Some cattle may die owing to complications and this is particularly so in the six month to two year age group. Here mortality may reach 10 per cent or more. However, it is usually only about 1 per cent. Some cattle keep a stertor (snoring breathing) for many months. Some become ‘puffers’ with bouts of respiratory signs including distress when breathing, loss of appetite and cough. These usually have a secondary bronchopneumonia and die in weeks or months after losing condition. Often they become recumbent before death. Characteristically, there is a sudden outbreak of disease involving the respiratory tract. This will initially involve the group of cattle to which infection has been introduced. It will then tend to spread round all the other groups and ages of cattle. This can often take a few weeks or many months, dependent on the strain of virus, the level of infection and the degree of exposure to infection of each group. Characteristically, an outbreak in a group reaches a peak at about two or three weeks after its start and is over between the fourth and sixth week. Reproductive form: In most cases the reproductive and respiratory forms are not seen together. (1) Infectious pustular vulvovaginitis. This is an infection of the vulva and vagina often lasting several weeks. It results in the discharge of pus from the vulva, usually in small quantities. There is reddening of the lining and

Respiratory Diseases

pustule presence. In some cases infection causes irritation in the vagina resulting in frequent urination and possibly increased straining (see p. 628). (2) Infectious bovine penoposthitis. Bulls show a small amount of purulent discharge from the prepuce. The surface of the penis and prepuce may be reddened with haemorrhages and small necrotic areas. (3) Endometritis. Infection of the uterus, with discharge, poor conception rates and short returns to oestrus, can occur if semen is infected. (4) Abortion (see p. 579). This is becoming increasingly common and occurs some weeks or months after the animal is infected. Abortion is usually at six to eight months of pregnancy and often the placenta is retained following abortion. In some cases of infection calves are born weak at the normal time. Generalized/alimentary form: This is seen in young newborn calves and is recorded mainly in America. It occurs when calves receive little or no immunity in the colostrum and are then subjected to infection. The animals show a severe temperature reaction, they do not eat and they salivate. The lining of the nose is red. The eyes may show a conjunctivitis. In addition, the lining of the mouth and the soft palate (at the back of the throat) are reddened with mucus present. The opening to the trachea, i.e. the pharynx, is also reddened with much discharge present. There is usually severe respiratory distress with a bronchopneumonia. Some calves show severe diarrhoea and dehydration. Central nervous system/encephalitic form: This is seen in calves under six months old and involves brain signs. The animals show incoordination with bouts of excitement and depression. In other cases there are convulsions, bellowing and blindness with salivation. This nervous form is rare. Other infections: Reports of infections of the udder and intestinal tract have been made. However, these are rarely the only systems affected.

Necropsy Respiratory form: In uncomplicated cases, lesions are restricted to the upper respiratory tract terminating at the upper bronchi. Inflammation of the muzzle and the nasal cavities varies from some congestion and petechiation with mucoid exudate, to a fibrinopurulent exudate with necrosis of the nasal mucous membranes. The submandibular and retropharyngeal lymph nodes tend to be swollen and oedematous. There is a laryngotracheobronchitis, which varies from a mild congestion of the

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mucous membranes with a mucoid discharge to large areas being covered by a necrotic layer of exudate (Pirie, 1979). In some cases there is pulmonary emphysema and secondary exudative bronchopneumonia, which may be purulent or necrotizing. Histologically, the mucous membranes show acute catarrhal inflammation and in some cases the epithelium and larynx tend to be infiltrated with neutrophils, lymphocytes, plasma cells and macrophages. In naturally occurring infections, inclusion bodies appear to be absent. Abortion: Aborted fetuses often show marked autolysis and focal necrotic hepatitis. Alimentary form: Epithelial necrosis of the turbinates, oesophagus, rumen and abomasum. Inclusion bodies are often evident in the surviving epithelium. Nervous form: A non-suppurative encephalitis occurs particularly affecting the cerebral cortex and internal capsule.

Diagnosis This will depend on the type but in the alimentary form it will depend on a history of IBR in the herd with virus present in the faeces or nasal swabs and possible necrotic areas on the turbinates. The nervous form is difficult to differentiate except that there is probably an IBR outbreak in the herd. At post-mortem examination the turbinates may show necrotic lesions. In the respiratory form the history is that a new animal or group has entered the herd. In most cases several animals will be affected and besides varying degrees of respiratory signs there will usually be a conjunctivitis with copious, initially serous, ocular discharge. There may be necrosis of the nasal mucosa but this is absent in the mouth. The virus can be isolated in upper nasal or ocular swabs and is detected by fluorescent antibody staining. Otherwise paired blood samples will show a rise in titre to the enzyme-linked immunosorbent assay (ELISA) test. Other tests used include the serum neutralization test, indirect haemagglutination test, complement fixation test and virus neutralization test. Bulk milk testing will indicate the status of a dairy herd.

Treatment There is a considerable divergence of opinion as to whether or not to use antibiotic treatment. If the disease appears to be uncomplicated, and this is unusual, then there would appear to be little point in therapy. If, however, as in most cases, there is secondary lung involvement, then therapy is justified. At the

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start of an outbreak all cases should be isolated as soon as possible because although it may not stop spread of the disease, the first animals are often clinically the worst affected. If antimicrobial agents are to be used, all ill calves should be treated for three to five days with any one of a number of drugs, including penicillin and streptomycin, oxytetracycline, ampicillin, trimethoprim and sulphadiazine, sulphadimidine, sulphamethoxypyridazine and sulphapyrazole. The animal should be given good, wholesome feed and it should be encouraged to eat and drink. Some farmers have vaccinated their calves with live vaccine after the start of an outbreak, with good results, but to be successful infection must not have become established. It should be remembered that for effective protection, vaccines should be introduced before the onset of infection. Several compounds have been found that are active against herpes viruses. However, many are toxic, but one drug, acyclovir, has been shown to be safe and may in the future be tried in animals.

Control Management: It is best to keep a closed herd. However, in America, and also Britain, infection has been found in closed herds. Any new animal entering a known uninfected herd should be blood tested prior to entry. If the test is negative the animal should be isolated for a month and then retested. The use of corticosteroids may allow detection of virus in swabs of carrier animals. If the tests are all negative the animal can be allowed to enter the herd. The risks then of the introduction of infection are small. If the animal suffers a respiratory problem while in isolation the second test should not be until two or three weeks after the end of the episode. Some farmers may need to go to these lengths to keep their pedigree herds free from disease, because many European countries will not accept exports unless they are shown to have a negative titre for IBR. The same conditions at present govern the entry of bulls to some artificial insemination (AI) centres. Vaccination (see p. 1010): An inactivated multicomponent vaccine has been available for a long time. The vaccine could be given as doses two to four weeks apart with a third injection at 10–12 weeks old. Its efficacy has at times been questioned. Subsequently, live IBR vaccines have become available. They are given by intranasal inoculation or injection and should be administered 24–48 hours after entry to the farm. Ideally, calves should be vaccinated 10 days prior to any movement. A gene-depleted live vaccine is available in some countries and allows control of disease. The immunity produced allows differentiation from that produced by the wild strain. This means the vaccination

can be used in an IBR eradication campaign. Live vaccines, as other vaccines, can present a possible danger if contaminated with other pathogens, such as BVDV. Beef calves can be vaccinated about two weeks or so before they are weaned. One vaccine is temperature sensitive and so only replicates in the upper parts of the respiratory tract. However, the vaccine can still produce circulating antibody levels in some cattle, which will preclude their export or their sale to AI centres. Another vaccine does replicate in organs other than the lungs and produces a good systemic immunity. The vaccines provide effective immunity but they do allow the replication and re-excretion of the IBR virus, which can thus spread infection to non-vaccinated animals. Several countries within the EU have successfully eradicated BHVI (IBR), including Denmark, Finland and Sweden. An EU-approved national compulsory eradication scheme is being undertaken in Austria. Control programmes are being pursued in the Netherlands, Belgium, France and Germany. A programme for the monitoring, screening, eradication and accreditation of freedom from IBR in being undertaken in the UK by Cattle Health Certification Standards (CHeCS).

References Andrews, A.H. (1976) Factors affecting the incidence of pneumonia in growing bulls. Veterinary Record, 98, 52–5. Andrews, A.H. (1978) Some factors influencing respiratory disease in growing bulls and the effect of treatment on liveweight. In Respiratory Diseases in Cattle. Seminar in CEC Programme of Coordination of Research in Beef Production, Edinburgh, 8–10 November 1977 (ed. by W.B. Martin), pp. 169–80. Martinus Nijhoff, The Hague. Andrews, A.H. (2000) Calf pneumonia costs! Cattle Practice, 8, 109–14. Andrews, A.H., Cook, G.L., Pritchard, D.G., Morzaria, S.P. & Gilmour, N.J.L. (1981) Observations on a respiratory disease outbreak in weaned suckled calves. Veterinary Record, 108, 139–42. Bateman, K.G. (1988) Efficacy of Pasteurella haemolytica vaccine/bacterial extract in the prevention of bovine respiratory disease in recently shipped feedlot calves. Canadian Veterinary Journal, 29, 838–9. Blood, D.C. & Radostits, O.M. (1989) Pneumonic pasteurellosis of cattle (shipping fever pneumonia). In Veterinary Medicine, 7th edn, pp. 663–73. Ballière Tindall, London. Confer, A.W., Panciera, R.J. & Fulton, R.W. (1984) Effect of prior exposure to Pasteurella haemolytica antiserum on experimental pneumonic pasteurellosis. American Journal of Veterinary Research, 45, 2622–4. Frank, G.H. & Smith, P.C. (1983) Prevalence of Pasteurella haemolytica in transported calves. American Journal of Veterinary Research, 44, 981–5. Friend, S.C., Thomson, R.G. & Wilkie, B.N. (1977) Pulmonary lesions induced by Pasteurella haemolytica in cattle. Canadian Journal of Comparative Medicine, 41, 219–23.

Respiratory Diseases

Gibbs, H.A., Allan, E.M., Selman, I.E. & Wiseman, A. (1983) Experimental bovine pneumonic pasteurellosis. Veterinary Record, 113, 144. Grey, C.L. & Thomson, R.G. (1971) Pasteurella haemolytica in the tracheal air of calves. Canadian Journal of Comparative Medicine, 35, 121–8. Houghton, S.B. & Gourlay, R.N. (1984) Bacteria associated with calf pneumonia and their effect on gnotobiotic calves. Research in Veterinary Science, 37, 194–8. Jensen, R., Pierson, R.E., Braddy, R.M., Saari, D.A., Lauerman, L.H., England, J.J., Keyvan, F.A.R., Collier, I.J.R., Horton, D.P., McChesney, A.E., Benitez, A. & Christie, R.M. (1976) Shipping fever pneumonia in yearling feedlot cattle. Journal of the American Veterinary Medical Association, 169, 500–506. Jim, K., Guichon, T. & Shaw, G. (1988) Protecting feedlot calves from pneumonic pasteurellosis. Veterinary Medicine, 83, 1084–7. Jones, C.R. & Webster, A.J.F. (1981) Weather induced changes in airborne bacteria within a calf house. Veterinary Record, 109, 493–4. MacVean, D., Franzen, D.K., Keefe, T.J. & Bennett, B.W. (1986) Airborne particle concentration and meteorological conditions associated with pneumonia incidence in feedlot calves. American Journal of Veterinary Research, 47, 2676–82. Martin, S.W. & Bohaz, J.G. (1986) The association between serological titres in infectious bovine rhinotracheitis virus, bovine viral diarrhoea virus, parainfluenza III virus, respiratory syncytial virus and treatment for respiratory disease

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in Ontario feedlot cattle. Canadian Journal of Veterinary Research, 50, 351–8. Myers, L.C. (1984) Questions on the efficacy of cattle vaccines. Journal of the American Veterinary Association, 184, 5–7. Panciera, R.J. & Corstvet, R.E. (1984) Bovine pneumonic pasteurellosis: model for Pasteurella haemolytica and Pasteurella multocida-induced pneumonia in cattle. American Journal of Veterinary Research, 45, 2532–7. Phillips, W.A. (1984) The effect of assembling and transit stresses on plasma fibrinogen concentration of beef calves. Canadian Journal of Comparative Medicine, 48, 35–41. Pirie, H.M. (1979) Respiratory Diseases of Animals, pp. 68–70, 71–4. Notes for a Postgraduate Course, Glasgow Veterinary School. Rosendal, S. & Martin, S.W. (1986) The association between serological evidence of Mycoplasma infection and respiratory disease in feedlot cattle. Canadian Journal of Veterinary Research, 50, 179–83. Sherwen, P.E. & Wilkie, B.W. (1982) Cytotoxin of Pasteurella haemolytica acting on bovine leucocytes. Infection and Immunity, 35, 91–4. Sherwen, P.E. & Wilkie, B.W. (1988) Vaccination of calves with leukotoxic culture supernatant from Pasteurella haemolytica. Canadian Journal of Veterinary Research, 52, 30–6. Shoo, M.K. (1989) Experimental bovine pneumonic pasteurellosis: A review. Veterinary Record, 124, 141–4. Wilson, S.H., Church, T.L. & Acres, S.D. (1985) The influence of feedlot management on an outbreak of bovine respiratory disease. Canadian Veterinary Journal, 26, 335–41.

Chapter 21

Trace Element Disorders N.F. Suttle

Introduction Differential diagnosis Definitions Cobalt disorders Copper disorders Iodine disorders Selenium disorders Manganese and zinc disorders

294 294 294 295 298 301 302 305

Introduction The full impact that trace element disorders can have on the health of cattle was seen when Europeans attempted to carry their methods of animal production to the New World and to the Antipodes. The geologically young soils bordering Australia, and forming the Florida peninsula and the interior of New Zealand’s North Island, were a graveyard for many an animal until the therapeutic effect of newly discovered essential trace elements became known. Crop and pasture growth was also limited by some of the deficiencies but these were the more easily diagnosed because they produced characteristic foliar abnormalities. The animal’s needs were more difficult to delineate because they lacked clinical definition and persisted where the more modest needs of the plant had been met. Since those pioneering days, trace element disorders have been described in many areas of the world and they continue to appear when new methods of production are introduced, but it is important to keep them in perspective.

most common being malnutrition, which is likely to be a whole herd problem. A preliminary check must be made of the quantity and quality of available feeds (Sinclair & Suttle, 2001). Trace element disorders usually afflict only a minority of the herd but a preliminary ‘audit’ of the likely mineral inputs and needs may narrow the range of possible culprits (Suttle & Sinclair, 2000). Responses to a broad mix of micronutrients would confirm this line of investigation. Depending on the history of the farm or area, it may be beneficial to attempt an earlier definitive diagnosis by using a specific trace element supplement, but proof of responsiveness amongst an affected minority may require unconventional statistical techniques which take into account initial variation in performance (Suttle, 2000). There may be cross-over between lines of investigation: correction of a gut parasite problem might improve trace element status, while improving the major nutrient supply of a herd (by improving ration digestibility) may lower status and increase the risk of trace element disorders. Seasonal and annual variations in incidence mean that it will always be necessary to review the need for any trace element intervention from time to time. Overall, following such a scheme should improve the precision of diagnoses.

Definitions Four terms will occur frequently in descriptions of the sequence of events that occur when cattle are deprived of essential trace elements, and these require definition:

• Differential diagnosis Trace element disorders carry more than their fair share of blame for poor cattle performance, due to the nonspecificity of most clinical signs, the pressures on practitioners to offer a quick diagnosis and the alacrity with which clients accept a diagnosis that may seem to exonerate them from blame. Figure 21.1 presents a scheme for differential diagnosis of some common problems. Of the three main lines of investigation shown, trace elements are only part of the least probable explanation, the

• • •

Depletion: the reduction of body stores of the element. Deficiency: the presence of subnormal concentrations of the element in blood or tissues. Disorder: the malfunction of trace elementdependent body processes (subclinical disorder). Disease: the presence of visible, clinical abnormalities.

They are particularly useful when describing the trace element status of cattle biochemically, and avoid the confusion caused by using the one word ‘deficiency’ to describe all four stages, and as a ‘tag’ for interpret294

Trace Element Disorders

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295

NON-SPECIFIC DISORDER (Ill-thrift, infertility, retained placenta)a

Possible cause

Fig. 21.1 Scheme for the differential diagnosis of trace element disorders with non-specific signs; proceed vertically with a given line of investigation only while test results are positive. WBC = white blood cell count; APR = acute phase proteins; FEC = faecal egg count.

INFECTION (Microbial or parasitic)

MALNUTRITION (Energy, E/protein, P)

MICRONUTRIENT DEPRIVATION (Mineral or vitamin)

Preliminary check

PATHOGEN AUDIT (WBC,APR, FEC, etc.)

FEED AUDITb

MINERAL/ VITAMIN AUDITc

Preliminary intervention

Broad spectrum antibiotic or anthelminthic

More feed and/or change E : P in feeds

Multi-mineral/vitamin mix (introduce, provide more or reformulate)e

Definitive test

Identify pathogen (s)

Metabolic profile

Mineral/vitamin profiled

Targeted intervention

Sustainable drug programme

Sustainable cropping, grazing & feed purchase policy

Specific trace element supplement

DIAGNOSIS a

Firstly, rule out ‘exotic’ (e.g. plant, agrochemical or industrial poisons) or common (poor oestrous detection, large calf) factors. b See Suttle (2002) for fuller details. c See Suttle & Sinclair (2000) for fuller details. d See Table 21.1 for best indices of trace element status. e Some untreated animals must be left to prove effecacy and allow specific follow-up tests to be made.

ing indices of mineral status which rarely reflect onset of disorder or disease. Throughout this chapter, use will be made of ‘marginal bands’ for diagnostic criteria (Table 21.1), which reflect the uncertainty of detecting the onset of health-limiting conditions. The following descriptions of specific disorders concentrate on the more commonly encountered deficiencies of cobalt (Co), copper (Cu), iodine (I) and selenium (Se).

Cobalt disorders Aetiology The only known functions of Co arise from its place at the centre of the corrin ring of two cobalamin (Cbl)

molecules, methyl-(Me) and adenosyl-(Ado) Cbl, which have contrasting functions in the body. MeCbl acts as a coenzyme to methionine synthetase and is linked to folate metabolism, through the use of methyltetrahydrofolate as the methyl group donor. Deficiencies of this coenzyme can theoretically impair methionine synthesis and the bioavailability of folate and cause formiminoglutamic acid (FIGLU) to appear in urine. AdoCbl enables propionate to be used for gluconeogenesis via succinate and the tricarboxylic acid (TCA) cycle, acting as coenzyme to methylmalonyl-CoA isomerase: insufficiency causes methylmalonic acid (MMA) to accumulate. The anorexia and anaemia that are successive debilitating consequences of deprivation may reflect the dysfunction of AdoCbl and/or MeCbl (Underwood

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Table 21.1 Marginal bands for commonly used biochemical indices of micronutrient status in the diet, serum or tissues of cattle: mean values falling within bands indicate a possibility of benefit from trace element supplementation; the more extreme the value and the more parameters affected, the greater the possibility becomes; values below (above for Fe:Cu and thyroid weight) bands indicate a probable benefit.

Dieta (mg/kg DM) Serumb (mmol/l) Tissuec (mmol/kg DM)

Cu

Co or vit B12

I

Mn

Se

Zn

5–15 3–8 150–300nL

0.04–0.06 0.25–0.5 ¥ 10-3M 0.2–0.4L

0.08–0.3 0.08–0.20 9.5–15.8 ¥ 103T

10–15 0.09–0.11 11–13H

0.03–0.06 0.13–0.26B 0.6–1.3nL

10–20 6–9 765–1070R

a Higher values are appropriate for: antagonist-containing diets (for Cu, Cu:Mo < 1–3, Fe:Cu > 50–100; Cu:sulphur < 0.0025); for I, with high goitrogen intake); for low agonist intake (e.g. for Se, low vitamin E intakes); for all elements when the digestibility of the ration is high. b The ranges are for adults; newborns often have different norms (e.g. 3–9 mmol/l then being adequate for serum Cu). c Superscript letters indicate sample origin: B = whole blood, H = heart, L = liver, M = milk, R = rib, T = thyroid; for the latter, an organ weight range of 0.3–0.8 g FW/kg LW is marginal; for the newborn (n), ranges may again differ, L Se being up to 3¥ that in the adult and L Cu 7–10¥ higher. Divide values by 3.3 (L) or 4.0 (H,T) for approximate fresh weight basis. Conversion from mmolar to mg units requires multiplication by: 63.5 for Cu, 58.9 for Co, 126.9 for I, 54.9 for Mn, 79.0 for Se, 65.4 for Zn and 1355 for B12; division by these factors converts mg to mmol units.

& Suttle, 1999). Loss of appetite was initially linked to Adocbl dysfunction and increased blood propionate concentrations, but disturbances of rumen fermentation (McDonald & Suttle, 1986; Kennedy et al., 1991) and the accumulation of other metabolites (e.g. MMA, Rice et al., 1989; succinate, Kennedy et al., 1991; homocysteine, Stangl et al., 2000) may also affect appetite. Loss of appetite would compound the effect of a diminishing supply of the glucose precursor, propionate. The anaemia of Co deficiency may reflect the role of MeCbl in DNA synthesis and red cell maturation. The basic cause of cobalt-responsive disorders is a simple nutritional deficit that can be traced to impoverished soils in which crops or pastures have grown. Interactions can occur in the soil that leave most of the Co adsorbed in unavailable forms onto manganese oxides, particularly at alkaline soil pH with soil Mn >1 g/kg (Suttle, 2000). If extraction with 0.43 m acetic acid yields 0.05 mg Co/kg dry matter (DM) (Underwood & Suttle, 1999). Interactions in the animal have been postulated because Co can be incorporated into various analogues of B12 by the rumen microbes. There is thus competition for Co in the rumen between different forms of the vitamin. Cobalamins are selectively absorbed in association with intrinsic factor but if analogues find their way into the bloodstream or tissues, they might complicate the assessment of vitamin B12 status and compromise functions of the vitamin. However, protective mechanisms would probably have evolved, if they are needed, against analogues so copiously produced in the rumen.

Clinical signs All ruminants require a dietary supply of Co for the synthesis of the essential vitamin B12 by rumen microorganisms. Cattle are less susceptible to a lack of Co than sheep, but when they succumb, they develop essentially the same clinical abnormalities in the same order: anorexia, loss of body condition, muscular wasting and finally an anaemia that is both normochromic and normocytic. In the early stages of the disease, the hair coat can become rough and discoloured (Judson et al., 1982) and may be repeatedly licked. Appetite may become depraved (pica). Eventually, the skin becomes thin and fragile and the mucous membranes pallid. The clinical picture is thus one of a ‘pining’ or ‘wasting’ disease, indistinguishable from many other causes of illthrift. Cobalt-deprived cattle may be more susceptible to infections than normal cattle (MacPherson et al., 1987a). There is a neurological disease that affects cattle in Australia when they graze Phalaris tuberosa pastures called ‘Phalaris staggers’; it can be prevented by Co dosage but not by administration of vitamin B12 and is, therefore, not a classical ‘deficiency’ syndrome. The response to Co may arise through the neutralization of fungal neurotoxins by the element (Underwood & Suttle, 1999).

Necropsy At necropsy, cattle suffering from Co deprivation show the hallmarks of starvation. There is little body fat except occasionally in the liver, which may be pale and friable due to fatty infiltration; this condition is,

Trace Element Disorders

however, far less common in cattle than in lambs or goat kids. In severely affected, anaemic individuals, bone marrow hypoplasia and splenic haemosiderosis will be found.

Diagnosis Cobalt-responsive disorders are best diagnosed through responses in growth or health to Co or B12 supplementation in controlled trials (e.g. Duncan et al., 1986). Biochemical confirmation of subclinical or clinical disease from the assay of plasma B12 is more difficult in cattle than in sheep. Plasma B12 concentrations appear to respond feebly to Co supplementation in cattle. Oral doses of Co ten times higher on a body weight basis than those that increase plasma B12 in sheep were apparently ineffective in cattle (N.F. Suttle & J. Brebner, unpublished data). High plasma B12 concentrations (>500 ng/l) are rarely found in cattle yet they are commonplace in sheep and values have often fallen to exceedingly low levels (140 pmol)/kg have been regarded as normal. There is a curvilinear relationship between Co and vitamin B12 concentrations in bovine liver which

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shows better fit at low than at high levels (Mitsioulis et al., 1995; Suttle, 1995); values between 0.06 and 0.08 mg Co/kg DM can be regarded as ‘marginal’ (Underwood & Suttle, 1999). The diagnosis of Co disorders from the presence of abnormal metabolites in the blood and urine was developed in sheep and non-ruminants and extended to cattle. Quirk & Norton (1988) found that heifers grazing pastures low in Co (0.036 mg/kg DM) remained healthy and excreted no MMA or FIGLU in urine, despite low plasma B12 concentrations (96 pg/ml). After calving, milk yield was unaffected but very low B12 concentrations in the milk (42–86 ng or 31–63 pmol/l) caused depletion of plasma B12 in their calves (59– 74 ng/l) and growth retardation, which was accompanied by increased urinary excretion of FIGLU. They concluded that MMA was less reliable than FIGLU as an index of dysfunction but their method for MMA was relatively insensitive (30 mmol/l). Assay of plasma MMA has been advanced as a measure of functional B12 status in sheep, with concentrations >5 mmol/l taken to be abnormal (Rice et al., 1987): as yet plasma MMA has not been tested for the confirmation of Co dysfunction in cattle but a marginal band of 5–15 mmol/l may well prove useful. Increases in plasma homocysteine are found after prolonged Co deprivation (Stangl et al., 2000).

Treatment or prevention Although there are clearly differences in B12 metabolism between cattle and sheep, there is no evidence that these affect the methods of treating and preventing disorders. The injection of B12 as cyano- or hydroxycobalamin, 2–6 mg/50 kg liveweight, provides protection for several weeks, even though responses in plasma B12 soon dissipate. Slow-release, injectable preparations of B12 are being developed in the Antipodes. Heavy cobalt oxide pellets given orally, in pairs or singly with a ‘grinder’, improve the B12 status of growing and adult cattle for several months (Judson et al., 1981; Quirk & Norton, 1988), even when a change in formulation halves their Co content (Judson et al., 1997b); the soluble glass bolus can also give sustained protection (Allen et al., 1985). The effectiveness of infrequent oral doses of Co in anthelmintics has not been tested but weekly doses of 35–70 mg Co without anthelmintic are said to be effective (Underwood & Suttle, 1999). Cobalt supplementation via the drinking water can be practised where there is a piped water supply (MacPherson, 1983). Use of ‘protected’ or chelated forms for oral use is contraindicated because Co must be given in forms which can be rapidly incorporated into vitamin B12 by rumen microbes. Evidence that volatile fatty acid (VFA) production by rumen microbes is influenced by

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Co deficiency (McDonald & Suttle, 1986; Rice et al., 1989; Kennedy et al., 1991) suggests a possible advantage for the oral route over the injection route, since only the former meets the needs of the microbes for B12. Comparisons between methods have rarely been conducted but one at least showed no advantage in calf growth for oral Co versus injected B12 (Judson et al., 1981). Administration of Co on a group basis via licks containing 0.1 per cent Co or mineral mixes containing up to 0.4 per cent Co may provide an inexpensive means of prevention but could not be guaranteed to protect all individuals. The best long-term strategy on certain soil types will be to apply Co salts, such as hydrated CoSO4, at 2–3 kg/ha, every three to four years. Responses may, however, be short-lived on sandy soils and negligible on calcareous or recently limed soils containing >1 g Mn/kg DM because most of the Co becomes ‘fixed’ in the soil. There is virtually no risk of overdosing with cobalt, but this should not be used as an excuse to overfeed Co to animals whose capacity to synthesize and absorb B12 is strictly limited.

Copper disorders

(see also Chapter 18)

Aetiology (see p. 254) Most Cu-responsive disorders in cattle are induced: they are induced in the rumen where the anaerobic degradation of sulphur(S)-rich, fibrous feeds leaves little of the ingested Cu in a soluble form. After weaning, less than 10 per cent of the total Cu input is absorbed during passage down the gastrointestinal tract and the percentage can be reduced to as little as 1–2 per cent by small increments in dietary Mo (Underwood & Suttle, 1999). Again it is transformations in the rumen that are pivotal: extrapolating from sheep, it appears that the progressive substitution of S2- for O2- in molybdate creates thiomolybdates, which complex Cu and bind it to the solid phase. Surplus trithiomolybdate (MoOS3) is absorbable and capable of changing the distribution of Cu in the blood and tissues (Underwood & Suttle, 1999). Just how important the systemic effects of thiomolybdates are under normal grazing conditions has yet to be determined. The ‘tell-tale’ appearance of abnormal plasma fractions, such as TCA-insoluble Cu, has been restricted to experimental situations, involving high levels of dietary Mo (35 mg/kg DM; Wang et al., 1988), and they may serve as slow release pools of Cu in the long term (Underwood & Suttle, 1999). Most cases of Cu-responsive growth retardation in cattle are associated with abnormally low ratios of Cu : Mo in the herbage (10 mg/kg DM), animals may develop diarrhoea immediately upon exposure to the antagonist (Suttle, 1988). Infertility has long been associated with Cu deprivation in cattle but there is little published evidence that deficiency leads to impaired reproduction unless Mo is involved (Phillippo et al., 1982, 1987a). Molybdenuminduced deficiency is associated with delays in the onset of oestrus, impaired conception rate and anoestrus: these abnormalities have yet to be induced experimentally by other antagonists of Cu, such as Fe (Phillippo et al., 1987a). Copper-responsive infertility in cattle given Mo, therefore, may result from the direct or indirect suppression of the release of luteinizing hormone (Phillippo et al., 1987a). Anaemia is a late sign of Cu dysfunction in growing calves (Suttle, 1988) and may be associated with Heinz body formation in the periparturient cow (Black, 1981). The in vitro viability and/or function of neutrophils from Cu-deficient cattle is poorer than that of cells from normal cattle (Suttle, 1988) but exposure to Mo can increase leucocyte counts (Gengelbach et al., 1997); there is no evidence yet for impaired resistance to infections in vivo (Arthington et al., 1996).

Necropsy The pathology of bovine hypocuprosis is largely unhelpful because the histological changes underlying

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the clinical signs, like the signs themselves, are nonspecific. The earliest and most dramatic lesions are likely to be those affecting the epiphyseal growth plates in the costochondral junctions and metatarsal/ metacarpal bones. These can become overgrown to the point that they spill over to leave islets of collagen distal to the plate in various states of irregular calcification and fibrotic replacement (Suttle, 1988). Gross degenerative changes are also seen in connective tissues such as the ligamentum nuchae. In severe cases showing diarrhoea, villous atrophy in the duodenal and jejunal regions is likely to be seen (Suttle, 1988) but is indistinguishable from that caused by gut parasites. The anaemia of Cu deficiency in the bovine is similar to that of Fe deficiency, i.e. macrocytic and hypochromic. Cardiac lesions including fibrosis of the myocardium have been reported in natural outbreaks only once, over 40 years ago, in Australia. While cardiac hypertrophy was seen in some experimentally depleted calves, which took a long time to develop clinical signs; it was not present in others that were depleted more rapidly (Suttle, 1988). Attention switched from the lesions that underlie the expected and familiar clinical signs to those which, though less spectacular, occur earlier and may underlie the debilitating effects of the disorder. Fell and his associates (Fell et al., 1985; Fell, 1987) found basement membrane defects in the pancreatic acinar cell, the duodenal enterocyte and kidney tubule, pointing to perhaps a common early failure of proteoglycan organization. It remains to be seen whether Mo can cause distinctive histological or ultrastructural changes at central sites such as the pineal body which may be crucial to the development of disorder (Phillippo et al., 1987a) and whether or not these are Cu-dependent.

Diagnosis Since none of the clinical signs of Cu deprivation given above is specific, diagnosis must be supported by biochemical tests showing subnormal tissue Cu status. Because availability has such a major effect on Cu uptake, herbage or dietary Cu concentrations alone are almost worthless and should be accompanied by measures of Mo and S and predictions of available Cu (Suttle, 1983a). In green swards, which contain enough sulphur to potentiate the Mo antagonism, Cu : Mo ratios 500 mg Cu/kg is likely to afford protection to the majority of the individuals that take to it in a given herd. If Cu proves to be useful as an antidote to Mo rather than an essential nutrient in some situations by rendering toxic thiomolybdates less available, the provision of Cu by slow rumenal release or steady dietary supplementation may have advantages over other forms of supplementation. The use of chelated forms of copper, such as ‘proteinates’ or copper lysine, as dietary supplements has given no consistent advantage over simple, cheap inorganic forms and cannot be relied upon to ‘protect’ copper from molybdenum or other antagonists (Underwood & Suttle, 1999).

Toxicity (see p. 948) Copper poisoning rarely occurs through the ingestion of excess Cu in weaned cattle because of poor absorption and a well-developed capacity to excrete surplus Cu via the bile. Tolerance of diets containing >250 mg Cu/kg DM for several months has been reported in Friesian steers (Felsman et al., 1973). Much higher absorptive efficiencies prior to weaning mean that calves reared on milk substitutes are relatively vulnerable, but they can tolerate up to 500 mg Cu/kg DM for brief periods (6 weeks; Jenkins & Hidiroglou, 1989). Oral drenching with CuSO4 solutions can cause haemolytic crises similar to those found in the more vulnerable sheep, but slower rates of exposure via the diet may sometimes cause or contribute to hepatic crises. Rapidly growing bull calves can die suddenly and show biochemical evidence of liver injury, in the form of raised AST activities, and Cu overload, in the form of raised kidney Cu levels, without evidence of haemolysis (no jaundice or increase in kidney iron) and only marginally raised liver Cu (C. Low, pers. comm.). Diagnosis of toxicity becomes possible when ‘liver enzyme’ values in serum are raised and values for indices of copper status enter the following ‘marginal’ ranges: serum, 0.018–0.020 mmol Cu/l; liver 6.4–16.0, kidney 0.6–0.8 and diet 1.57–3.14 mmol Cu/kg DM (multiply by 63.5 to obtain mg or ppm units). False ‘highs’ for plasma Cu during acute infections will be accompanied by Cu : Zn ratios >3–4. Acute Cu poisoning can be caused by overdosage via the parenteral route (Mylrea & Byrne, 1974) and is characterized by haemolytic crises and jaundice.

Trace Element Disorders

Iodine disorders

(see pp. 257, 586)

Aetiology Iodine has only one function in the body, as a constituent of the hormone tri-iodothyronine (T3), which regulates basal metabolic rate. The hormone is formed by the removal of iodine (deiodination) from thyroxine (tetra-iodothyronine, T4), the physiologically inactive form synthesized in the thyroid gland. Disorders can arise either from a simple lack of iodine in the diet or from the impairment of iodine metabolism by ingested goitrogens. Simple iodine deprivation rarely occurs in coastal regions or on small islands because of the large atmospheric inputs of iodine of marine origin. Diets containing 70 per cent of aseptically collected milk samples. Growth on blood agar may require incubation for 48 hours, preferably at 30°C, and stimulation by fatty acids supplied either by the milk or by additions to the media such as Tween 80.

Recommendations for control of mastitis In the USA, UK and Australasia and many other parts of the world there is a recommended mastitis control scheme based upon the ‘5-point plan’. The elements in the scheme are as follows: (1) (2) (3) (4) (5)

Apply an approved teat disinfectant after every milking. Treat clinical cases of mastitis. Infuse long-acting antibiotic into all quarters at drying-off. An annual milking machine test and appropriate maintenance. Cull cows showing repeated cases of clinical mastitis.

These measures were the basis of controlled experimentation in many countries and have been widely employed since the 1970s. Teat disinfection is to reduce

Coagulase-negative staphylococci and Corynebacterium bovis The incidence of coagulase-negative staphylococci has increased as herd cell counts have decreased. Several species of coagulase-negative staphylococci are commonly isolated from aseptically collected milk samples.

Fig. 23.4 Reduction in bulk milk cell count in England and Wales between 1979 and 1988.

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rates of new infection during lactation; the dry-cow therapy serves to eliminate a high proportion of subclinical infections present at the end of lactation and to prevent many new dry-period infections. Treatment of clinical mastitis assists the elimination of infection and in the resolution of clinical signs of disease and culling is employed to remove chronically affected cows. Finally, the milking machine maintenance is intended to ensure efficient milking and prevent machine-induced infections as described above (therapy for mastitis is dealt with in Chapter 30). A review of the progress in mastitis control following the introduction of these techniques has been described by Booth (1988). This shows major reductions in clinical mastitis incidence and in the reduction of bulk milk cell count (Fig. 23.4). The present status of improving mammary gland immunity is described in Chapter 29.

References Booth, J.M. (1988) 1. Control measures in England and Wales. How have they influenced incidence and aetiology? British Veterinary Journal, 144, 316–22. Boughton, E. (1979) Mycoplasma bovis mastitis. Veterinary Bulletin, 49, 377–87. Bramley, A.J. (1982) Sources of Streptococcus uberis in the dairy herd. I. Isolation from bovine faeces and from straw bedding of cattle. Journal of Dairy Research, 49, 369–73. Bramley, A.J. & McKinnon, C.H. (1990) The microbiology of raw milk. In Dairy Microbiology, Vol. 1 (ed. by R.K. Robinson). Academic Press, New York. Dairy Federation (1981) Laboratory methods for use in mastitis work. International Dairy Federation Bulletin 132, Brussels. Dairy Federation (1984) Recommended methods for somatic cell counting in milk. International Dairy Federation Document 168, Brussels. Dairy Federation (1987a) Bovine mastitis. Definition and guidelines for diagnosis. International Dairy Federation Bulletin 211, Brussels. Dairy Federation (1987b) Environmental influences on mastitis. International Dairy Federation Bulletin 217, Brussels. Dodd, F.H., Higgs, T.M. & Bramley, A.J. (1984) Cubicle management and coliform mastitis. Veterinary Record, 114, 522–3.

Erskine, R.J., Eberhart, R.J., Grasso, P.J. & Scholz, R.W. (1989) Induction of Escherichia coli mastitis in cows fed seleniumdeficient or selenium-supplemented diets. American Journal of Veterinary Research, 50, 2093–2100. Hill, A.W., Shears, A.L. & Hibbitt, K. (1979) The pathogenesis of experimental Escherichia coli mastitis in newly calved dairy cows. Research in Veterinary Science, 26, 97–101. Jackson, E.R. & Bramley, A.J. (1983) Coliform mastitis. Veterinary Record (In Practice Suppl., Vol. 5, No. 4) 135– 46. Jasper, D.E. (1982) The role of Mycoplasma in bovine mastitis. Journal of the American Veterinary Medical Association, 181, 158–73. Marshall, V.M.E., Cole, W.M. & Bramley. A.J. (1986) Influence of the lactoperoxidase system on susceptibility of the udder to Streptococcus uberis infection. Journal of Dairy Research, 53, 507–14. Schalm, O.W., Lasmanis, J. & Jain, N.C. (1976) Conversion of chronic staphylococcal mastitis to acute mastitis after neutropenia in blood and bone marrow produced by an equine anti-bovine leukocyte serum. American Journal of Veterinary Research, 37, 885–94. Schultze,W.D. (1985) Development in the identification of diseased udder quarters or cows. Proceedings International Dairy Federation Seminar Progress in the Control of Bovine Mastitis. Kieler Milchwirtschaftliche Forschungsberichte, 37, 319–28. Thomas, G., Over, H.J., Vecht, U. & Nansen, P. (eds) (1987) Summer Mastitis. Martinus Nijhoff, the Netherlands, 1–224. Williams, D.M. & Mein, G.A. (1985) The role of machine milking in the invasion of mastitis organisms and implications for maintaining low infection rates. Proceedings International Dairy Federation Seminar Progress in the Control of Bovine Mastitis. Kieler Milchwirtschafiliche Forschungsberichte, 37, 415–25.

Further reading Blowey, R.W. & Edmondson, P.W. (1995) Mastitis Control in Dairy Herds. Miller Freeman, Ipswich, UK, pp. 1– 196. Bramley, A.J. & Dodd, F.H. (1984) Mastitis control–progress and prospects. Journal of Dairy Research, 51, 481–512. Schalm, O.W., Carroll. E.J. & Jain, N.C. (1971) Bovine Mastitis. Lea & Febiger, Philadelphia, pp. 1–360.

Chapter 24

Summer Mastitis J.E. Hillerton

Aetiology Epidemiology Transmission Pathogenesis Clinical disease Treatment Control

337 337 337 338 338 339 339

Summer mastitis is an acute or peracute multifactorial infection of the non-lactating bovine mammary gland although clinical signs are often not obvious until parturition. The disease is reported from all four continents where dairy cattle are herded. It is, however, most prevalent in northern Europe and particularly common in some European cattle such as the Friesian/Holstein breeds, being rare in the Zebu.

Aetiology (see p. 334) Bateriological analysis of summer mastitis secretion shows a complex infection. Usually Arcanobacterium (Corynebacterium) pyogenes predominates and the severity of the infection is related to toxin production from synergistic growth with other bacteria that are anaerobic (see p. 338). Peptococcus indolicus is the most common anaerobe but Bacteriodes melaninogenicus and Fusobacterium necrophorum are often found. An undescribed microaerophilic coccus, the Stuart– Schwann coccus is also found. It rarely grows in pure subculture. Streptococcus dysgalactiae is also common and believed by some to be a primary agent predisposing to A. pyogenes infection. Much of the reported variation in bacterial culture, and especially isolation of anaerobes, probably results from suboptimal collection and transport of samples, allowing anaerobes to die out.

Epidemiology Summer mastitis is considered to be epidemiologically most severe in northern Europe. It is also prevalent in

Japan, and parts of the USA, as well as being reported from Greece, Australia, Zimbabwe and Brazil. The incidence varies greatly from country to country, as does the severity of the infection. Most cases in North America are recognized when heifers calve with a nonfunctional quarter from which the causative bacteria can be recovered, whilst in Japan systemic illness is more common. The incidence of summer mastitis varies locally. It is greater in the more intensive dairy areas but does not just depend on the density of cattle. It is only in the dairy industry that the importance of the disease is well recognized. It can be prevalent in beef cattle but loss of function of one-quarter is not so important economically in the suckler cow. The Dutch, Germans and Danes believe that summer mastitis is associated with sandy soils, but these correlate well with the best grassland. The high humus content, open structure and free-draining of sandy soils are particularly suitable for foraging, soil-dwelling insect larvae. The disease is most common in summer and early autumn but can also occur in spring. As well as season, it is particularly associated with calving pattern. In Ireland, with many spring-calving herds, the spring incidence is marked. The black and white dairy breeds seem most susceptible and in the absence of preventive measures the incidence is greatest in older cows.

Transmission It is a long and widely held belief that flies are involved in the transmission of summer mastitis. The peak incidence of disease in northern Europe occurs in July, August and September when flies are most abundant on cattle. The sheep headfly (or plantation fly), Hydrotaea irritans, is the most frequent visitor to the teats of dry cows and heifers. Flies around pastured cattle have been shown to carry the summer mastitis pathogens even in the absence of disease in the herd. The disease prevalence is coincident with the geographical distribution of the fly in most of Europe. Control of flies on cattle reduces the incidence of summer mastitis. Some 60 per cent of infections occur 337

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in the front quarters, which, it has been suggested, flies can reach more easily. Various studies using Hydrotaea irritans to transmit summer mastitis have given incomplete results. The flies have been shown to carry the various bacteria and to be able to regurgitate the bacteria on to teat skin several days after a previous meal. Contaminated teats have been demonstrated to be one precursor to disease. Recently a study in Sweden confirmed a much earlier, anecdotal, UK report that contaminated H. irritans could transmit summer mastitis experimentally. Summer mastitis also occurs frequently outside the fly season and in areas where the sheep headfly is not found. No other obvious vectors have been suggested in these situations. Cases of clinical mastitis, especially in newly calved cows, involving the same complex of bacteria, have been reported throughout the year. There are likely to be several risk factors to these infections including appropriate exposure to the bacteria and teat damage. Initial cases of summer mastitis in an outbreak probably occur by chance. Increased incidence will depend on the density of animals at risk; hence there is a peak incidence in late summer-calving herds simply because more animals are challenged when they are most susceptible. Probably the role of the fly is to increase the challenge. It therefore is involved in secondary transmission. The fly may also contribute by stressing animals. Fly pestering can reduce milk yields by inducing gross behavioural changes. Susceptibility to infection during late gestation when there are other environmental and husbandry stressors, especially poor forage and heat, may increase with fly challenge.

Pathogenesis Damage to secretory tissue is caused primarily by a toxin from A. pyogenes, with other virulence factors including a haemolysin, a coagulase and a hyaluronidase. The activity and quantity of these appears to be enhanced in mixed culture with P. indolicus. The route of invasion of the udder by a mixture of bacteria is unknown but it seems unlikely that simultaneous invasion by up to five species of bacteria occurs. It is possible to isolate one or more of these pathogens from the udder of the lactating or dry cow in the absence of overt clinical signs so it is likely that some predisposing factor(s) is needed to cause clinical disease. Evidence for the teat route of invasion in natural infections comes from the frequency of summer mastitis following teat-end damage. It has been possible to produce infections following surface contamination of

the teat with A. pyogenes alone. There is, however, no unequivocally accepted mechanism. Possibilities, each with proponents, include colonization of the teat skin or orifice spreading through the teat duct into the gland, bacteria entering the gland by draining via a supramammary lymph node from another site and invasion by haematogenous spread. All of the pathogens are ubiquitous on cattle, easily recoverable from mucous membranes and various lesions, and so a number of routes of invasion may occur naturally.

Clinical disease Diagnosis of the later pathogenic stages of summer mastitis is relatively easy and requires little experience. Early stages are more difficult to distinguish from other infections. The infection is most probably ascending so the primary sites are in the teat or in lactiferous tissue near the base of the teat. Initially, there is local inflammation and oedema. Expression of udder secretion may reveal a foul smell indicative of anaerobic bacteria. In summer months the teat may be attractive to flies and if the animal is housed the hind legs attract biting flies. Slightly later, behavioural changes in the animal related to toxaemia become apparent. The animal may be lethargic, inappetant, stop cudding and will become detached from the herd. These signs are easy to recognize at pasture. In newly calved and housed animals the first signs are often tenderness in the quarter, which can be confused with excessive intramammary pressure, and local temperature. The secretion will be discoloured, thick and creamy, rather than colostral, perhaps very clotted in a serous fluid, and frequently foul smelling. In addition to the extreme mastitis, in later stages pyrexia and lethargy develop. If the infection remains local there may be rupture of mammary abscesses to the exterior. More commonly, the animal becomes systemically ill with progressive lameness from the hind legs, swelling of joints and an elevated temperature. The bacteraemia/toxaemia may be fatal in a few per cent of cases; similarly there may be abortion. Perinatal death is substantially increased and many calves, often born prematurely, fail to thrive. The infection develops rapidly after the initial recognizable signs so confirmation of summer mastitis by bacteriology is rarely quick enough. Attempts have been made to develop cow-side diagnosis of anaerobic involvement based on specific metabolites but no practical technique is available. The time delay for confirmation is impractical. Evidence shows that 80 per cent of preliminary diagnoses of summer mastitis are correct (Hillerton et al., 1987). The other infections would also

Summer Mastitis

respond readily to the same therapy so unless drastic action, such as teat amputation or immediate culling, is indicated misdiagnosis in favour of summer mastitis has no economic or welfare disadvantages.

Treatment A number of different approaches to treatment can be taken. The one selected should depend on the anticipated outcome of the case, which in turn depends on the clinical severity of the infection. In a small number of cases the only recommendation is for immediate culling. Less drastic is to treat the infection purely as an abscess; to amputate the teat and drain. This is practised commonly in northern Europe with non-pregnant younger animals, which are often then reared for beef. In cows and heifers near to or at parturition the prognosis depends on the speed of diagnosis. In most cases in dry cows the infection is sufficiently well developed that destruction of secretory function is virtually complete. A clinical cure can sometimes be achieved but rarely a bacteriological cure. The prognosis is much better if the infection is diagnosed early, and therapy started immediately. The pathogens are susceptible to a wide range of antibiotics including penicillin/streptomycin preparations. However, there is a poor cure rate when the only therapy is infusion into the udder. This is because the tissue destruction is extensive locally and so diffusion of the antibiotic is limited. A greater success has been claimed for erythromycin, which diffuses more readily. Success has also been claimed for anti-anaerobe preparations containing metronidazole. Chlortetracycline can be useful in the lactating animal but should not be used in the dry gland as all secretory funtion will be destroyed. Claims have been made for a variety of other preparations including proteolytic enzymes mixed with antibiotics but controlled studies are rare. Usually, the most successful outcome follows a coordinated effort: frequent stripping of the quarter combined with parenteral intramuscular antibiotics and an intramammary infusion. This conventional approach, although labour intensive, affords the best prognosis for the udder. If systemic involvement is established then treatment of clinical signs to secure the health of the animal is all that can be achieved as the function of the infected quarter has been lost. The patient should be quarantined as it is a source of further infection.

Control Summer mastitis is so destructive and expensive that considerable investment in time and materials to

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control the disease is made by the 40–45 per cent of farmers who regularly experience losses. Preventive measures are neither simple nor foolproof and usually are damage-limiting rather than totally preventive. The basic aims are to limit exposure to infection from the herd, to prevent colonization of lesions and to prevent spread of bacteria to the mammary tissue. Assuming that summer mastitis infections will arise anyway it is important to recognize these early and segregate an infected animal to limit direct transfer of bacteria via, for example, bedding systems and indirect transfer by flies. Hydrotaea irritans do not pester housed cattle, so separate housing of infected animals is good practice. The epidemiological spread of infection is related to the density of susceptible animals and the abundance of vectors. Reducing the density of late gestation cattle by spreading the calving pattern and completely avoiding the fly season of July,August and September in northern Europe are likely to be highly effective strategies. Considerable effort is spent on fly control but this is the least effective method of disease control as persistent presence of insecticide on teats is hard to achieve. The synthetic pyrethroids now in common use are applied in ear-tags or as pour-ons to the back and probably spread by diffusion in sebum. However, the teats lack hair and sebaceous glands are sebum deficient, so limiting spread. Effective fly control on teats is only achieved by direct application or frequent reapplication of insecticide, or by the use of two ear-tags per animal. There has been a gradual decline in the proportion of dry cows suffering summer mastitis, and in the number of herds affected, in England and Wales since 1988. This has been coincident with the control of flies by use of ear tags and later by pour-on formulations. Frequently, summer mastitis follows infected lesions on or near the teats. These can be prevented or limited by use of surgical tapes, ensuring that the teats are cleaned first and not bandaged too tightly, or by frequent application of teat disinfectant. Many farmers teat-dip dry cows and heifers daily. This allows frequent inspection, trains the heifers to the milking parlour and ensures good teat condition. Prevention of teat lesions may reduce greatly the attractiveness for flies. The best tested and most effective means of reducing the incidence of summer mastitis is the general application of prophylactic antibiotic infused into the teat at drying-off. Following administration of synthetic penicillins in a long-acting base, summer mastitis rarely occurs within three weeks. Longer effects are achievable with some preparations. Where the incidence of disease warrants extra investment it is advisable to repeat the application of antibiotic after three weeks. The main problem is avoiding milk contamination after an early calving. All the evidence available

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shows a significant reduction of summer mastitis following use of dry-cow therapy. It can also be applied to heifers if the antibiotic is introduced gently into the teat duct. Attempts to produce a vaccine against summer mastitis have met with little success. This remains a long-term goal and will become more likely as multivalent vaccines are developed.

Reference Hillerton, J.E., Bramley, J.A. & Watson, C.A. (1987) The epidemiology of summer mastitis: a survey of clinical cases. British Veterinary Journal 142, 520–30.

Chapter 25

Bulk Milk Testing and Mastitis Monitoring D.J. O’Rourke and R.W. Blowey Cell counts What is a somatic cell count? Factors affecting the somatic cell count Determination of the cell content of milk Interpretation of somatic cell counts Total bacterial counts Sources of bacteria Bulk tank analysis Mastitis monitoring Introduction Recording systems Analysis of information Target figures Uses of mastitis monitoring

341 341 341 342 343 345 346 346 348 348 348 349 350 350

Cell counts What is a somatic cell count? The majority of somatic cells found in milk are white blood cells, with the remainder mainly epithelial cells shed by the secretory tissue of the udder. White blood cells are found throughout the body and their main function is to protect against disease. When large numbers accumulate they are visible as pus. The measurement of the number of somatic cells in milk is known as a somatic cell count.

Factors affecting the somatic cell count Mastitis Inflammation in the udder is in no way different from inflammation in other tissues. The cardinal signs of inflammation, namely swelling, redness, heat, pain and loss of function may not always be of recognizable intensity in mastitis. Signs of clinical mastitis are grossly visible but subclinical mastitis may go unnoticed. The majority of mastitis cases are bacterial in origin. One of the basic host responses to a bacterial infection is the infiltration of white blood cells from the blood into the udder. This is accomplished through the processes of diapedesis and chemotaxis. The degree and nature of the cellular response are likely to be proportional to the severity of the infection. In addition to bacterial

infections, there are certain other factors, some of which are physiological, that affect the cellular content of milk.

Stage of lactation The somatic cell count is high during the first week of lactation, then soon decreases and remains low for several weeks after which a gradual increase occurs until the end of lactation. As the milk volume decreases in the latter part of lactation, an apparent increase in cell numbers occurs from mere concentration of cells in a smaller volume of milk. The presence of high cell numbers in colostrum may be due to an excessive desquamation of epithelial cells in a small volume of milk in a gland resuming functional activity after a dormant period (Schalm et al., 1971).

Lactation age The somatic cell count increases with the lactation age of the cow (Fig. 25.1) (Blackburn, 1966). On the basis of histopathological examination of the udders, the increase in the average number of polymorphonuclear leucocytes with advancing lactation age was attributed to an increase in the extent of subacute inflammation of the ducts as well as an increase in the severity of lobular lesions.

Stress A sudden upset in the cows’ routine, for example a herd blood test or coming indoors in the autumn, can cause a raised cell count for a day or two.

Oestrus Bulling cows tend to have increased cell counts that are probably stress related.

Milking interval Irregular milking intervals will influence the somatic cell counts in milk. Comparisons of somatic cell counts in milk have generally shown higher counts for shorter 341

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Fig. 25.1 Average cell count for each of seven lactations. A, total cell count; B, polymorphonuclear leucocyte count; C, count of cells other than polymorphonuclear leucocytes. Source: Blackburn (1966), reproduced with permission of Cambridge University Press.

milking intervals. This variation in cell numbers is explained on the basis of total volume of milk secreted leading to a greater dilution of somatic cells during the longer milking interval (Schalm et al., 1971).

Fig. 25.2 Relationship between mean cell count of herd bulk milk (C) and vacuum reserve per unit (V). Source: Nyhan & Cowhig (1967).

(1)

Milking machine A significant correlation between cell counts and milking machine reserve air was observed by Nyhan and Cowhig (1967) in a survey of milking machine efficiency and mastitis in a random sample of 26 dairy farms (Fig. 25.2). Six of the herds were milked with machines that had a vacuum reserve of more than 0.11 m3/min free air (4 ft3/min free air) and these were the only herds with a mean bulk milk cell count of 7.0 cm

> 7.5 cm

2

Medium

4.5 to 7.0 cm

5.0 to 7.5 cm

1

Normal

< 4.5 cm

< 5.0 cm

0

Clinical assessment from total score Severe

8–10

Moderate

4–7

Mild

1–3

Normal

0

Fig. 34.4

Scoring system for the assessment of the severity of endometritis, suitable for use from 21 days postpartum.

ceutical industry continues to develop antibiotic products administered by this route, despite the widespread use of systemic antibiotics for treatment of other bacterial infections in cattle. Hormones: The hormonal treatment of endometritis is based upon observations that the genital tract is more susceptible to infection when under progesterone dominance and more resistant under the influence of oestrogens (Rowson et al., 1953). Oestrogens: Rowson et al. (1953) demonstrated that the bovine uterus was more resistant to infection with

A. pyogenes when either endogenous or exogenous oestrogen was present compared to during dioestrus, and suggested that exogenous oestrogen may be used therapeutically. Despite the potential of oestrogens for the treatment of endometritis, results have been equivocal and vary with the pharmaceutical preparation and dose administered. The treatment-to-conception interval was longer for cases of endometritis treated with a single intramuscular injection of 3 mg oestradiol benzoate per 500 kg body weight, compared with those treated using prostaglandin or intrauterine oxytetracycline (Sheldon & Noakes, 1998). Furthermore, regula-

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tory authorities have prohibited the use of oestrogens in several countries. Prostaglandins: The parenteral application of PGF2a, or its analogues, has been used widely for the treatment of endometritis. The majority of authors report that the presence of an active corpus luteum is required for optimal results when using prostaglandin to treat endometritis, which supports the hypothesis that the subsequent induced oestrus increases the uterine resistance to bacteria (Jackson, 1977; Sheldon & Noakes, 1998). Conversely, Pepper and Dobson (1987) reported that the efficacy of prostaglandin therapy for endometritis did not depend on the presence of an active CL, as determined by measuring milk progesterone concentrations. An alternative hypothesis for the mechanism of action of prostaglandin as a treatment for endometritis is a direct myometrial effect, with physical expulsion of uterine detritus. A number of clinical trials have studied the possibility of using the direct myometrial effect of prostaglandin therapy, to reduce the incidence of endometritis and improve subsequent fertility. A routine injection of prostaglandin shortened the calving-to-conception interval in normal cows compared with control animals (Etherington et al., 1988). However, a number of subsequent trials gave conflicting results. Meta-analysis of 24 trials where PGF2a was administered to cattle within 40 days of calving reported no beneficial effect on first-service pregnancy rate, although there was a small reduction in days open for treated cows (Burton & Lean, 1995). Other treatments: A variety of antiseptics have been administered by intrauterine infusion for the treatment of endometritis including solutions of Lugol’s iodine, polyvinyl pyrrolidine iodine, povidone-iodine, chlorhexidine and metakresol sulphonic acid. Many of these solutions cause a necrotic endometritis within 24 hours of infusion that may stimulate release of PGF2a in addition to possible direct effects on pathogenic organisms. However, despite clinical resolution of the endometritis using antiseptic solutions, the effect on fertility may not be beneficial. Nakao et al. (1988) administered a 2 per cent polyvinyl pyrrolidine iodine intrauterine infusion and reported that treated cows, particularly those with a purulent discharge, had an increased calving-to-conception interval compared with controls. In addition, some of these antiseptic products are not licensed for use in food producing animals.

Pyometra Pyometra is associated with the accumulation of pus in the uterus and by the persistence of functional luteal tissue on one or both ovaries. Affected cows do not

appear ill; however, they are anoestrus and may be presented to the veterinarian as ‘not-seen-bulling’ or for pregnancy diagnosis. Pyometra may be a sequel to the conditions discussed earlier in this chapter and therefore those factors that predispose a cow to RFM, metritis and endometritis can also be considered to predispose to pyometra. In addition pyometra may also be seen in cows after service (either natural or by AI). In most cases pyometra is a sequel to chronic endometritis as the uterus ceases to release the endogenous luteolysin PGF2a. Research has shown that the persistence of the CL in cows with pyometra is not due to an insufficiency in the synthesis of uterine PGF2a but is associated with inadequate secretion of luteal oxytocin (Vighio et al., 1991). The result is that the dioestrus CL persists and the genital tract remains under the influence of progesterone. The infection is thus not eliminated and the cervix remains closed, resulting in the accumulation of large quantities of purulent exudate in the uterine lumen. Occasionally there will be slight leakage through the cervix, resulting in a small amount of pus accumulating in the anterior vagina and an intermittent purulent vaginal discharge. In a small number of cases the persistent luteal tissue is a progesterone secreting (luteal) cyst rather than a persistent CL. In some instances the introduction of infection during dioestrus, such as occurs when a cow is artificially inseminated at an incorrect time, results in pyometra. Pyometra may also occur secondary to the death of a fetus, either caused by, or followed by, bacterial invasion by A. pyogenes and persistence of the CL of pregnancy. Infection with Tritrichomonas fetus also causes embryonic death and pyometra formation (Bon-Durant, 1997). When examined per rectum, cases of pyometra have enlarged uterine horns and must be accurately differentiated from a normal pregnancy before treatment can be administered. There are a number of distinguishing points:

• • • •

The uterus feels ‘doughy’ and the uterine wall is thicker than during pregnancy. It is not possible to palpate the amniotic vesicle or ‘slip’ the allantochorion membranes. Placentomes are not palpable or visible on ultrasound examination, although the caruncles of the previous pregnancy are occasionally detected. Ultrasonography will demonstrate the absence of a fetus and the presence of pus rather than normal fetal fluids.

The best and most appropriate treatment of pyometra is to bring about luteolysis with PGF2a or PGF2a analogues. However, this treatment should never be administered if there is any suspicion that the cow

The Postpartum Period

may be pregnant, as it will cause abortion in early pregnancy. The administration of PGF2a to cases of pyometra usually results in dilation of the cervix and expulsion of the purulent uterine contents, with oestrus occurring three to five days later. There is evidence to suggest that treatment of pyometra is improved by the administration of two doses of PGF2a 8 hours apart (Archbald et al., 1993). This is probably due to the fact that a single dose of exogenous PGF2a has only a very short duration of action, as the inadequate release of ovarian oxytocin from the CL in these cases is insufficient to maintain the normal positive feedback loop that brings about luteolysis by the release of further endogenous PGF2a. Many cases of pyometra go on to become pregnant, despite having a prolonged first luteal phase and a prolonged calving to pregnancy interval of 125 days compared to 74.8 days (Etherington et al., 1991). However, longstanding cases are associated with endometrial degeneration, which may increase the rate of late embryonic and early fetal losses. Comparison between pregnancy rates at first pregnancy diagnosis 33 to 70 days postservice and a subsequent diagnosis 120 to 150 days postservice have shown that attrition rates are 2.6 times higher in cows with previous pyometra than in cows without the condition (López-Gatius et al., 1996).

Postpartum anoestrus Introduction Postpartum anoestrus is a greater problem for beef cattle than dairy cows, and it is often evident in specific herds.

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>1.0 BCS points during the first 30 days after calving take longer to the first postpartum ovulation than those losing less than one unit (Beam & Butler, 1999). However, monitoring BCS over periods greater than 6 weeks postpartum often has a less clear association with the length of the anoestrus period. The pituitary secretion of FSH appears to be insensitive to NEB. Thus, successive waves of follicular growth start within 10 days of calving. However, in the anoestrus cows, dominant follicles fail to ovulate because of inadequate LH pulse frequency. Insulin-like growth factor-1 (IGF-1) is a likely hormonal mediator between nutrition and fertility. However, the precise mechanisms and how they may be modulated are not yet clear. Shortening the postpartum interval to the NEB nadir is a more tangible management objective to reduce the incidence of anoestrus in a herd. The suckling calf inhibits the release of GnRH from the dam’s hypothalamus, so suppressing LH pulse frequency. However, this inhibitory influence occurs as a consequence of the maternal bond between cow and calf, and it is not dependent upon sensory innervation of the udder (Williams & Griffith, 1995). The frequency and duration of suckling by a single calf are unrelated to the period of anoestrus, although suckling following adoption of an additional calf will delay the return of ovarian cyclicity. If the single calf is removed from its dam there is a corresponding increase in the frequency of LH pulses within two to six days. The inhibition of GnRH release is dependent on the cow being suckled by her ‘own’ calf, which she identifies by sight and smell. The mechanisms underlying this effect are unclear; in part, they may involve increased opioid tone within the brain.

Diagnosis Aetiology The two main predisposing factors are inadequate nutrition, specifically energy deficiency, and suckling or the maternal bond. Other associated factors are that it is more common during late winter, in the absence of a bull and following dystokia. Rarely, anoestrus may be associated with pituitary or ovarian damage. Negative energy balance (NEB) is common to most postpartum cows and is the difference between the dietary intake of metabolizable energy and the expenditure for maintenance and lactation (see p. 103). Consequentially, the balance between milk yield and feeding (including diet composition, feed supply and appetite) is an important determinant of the severity of NEB. However, in first lactation an animal’s metabolizable energy may also have to contribute to continued growth. The effect of NEB is most easily identified by monitoring body condition score (BCS). Cows that lose

At least two examinations, 10–14 days apart, are required to make a clinical diagnosis of anoestrus. Both ovaries are small and there is no CL detectable at either of the examinations; however, follicles up to 18 mm diameter may be identified. An alternative or additional method of diagnosis is to use milk progesterone analysis; two low values, at 10–14-day intervals, is indicative of anoestrus.

Treatment The most important consideration when presented with an anoestrus animal is to correct the underlying causes, in particular dietary deficiencies. The quantity and quality of feed supplied to the animal in relation to its milk yield should be determined. In addition, dry-cow management should be examined, paying particular attention to the transitional period. Monitoring BCS

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during the dry period and early lactation will help to quantify the severity of dietary energy deficiency. Two groups of pharmaceutical products may be used to treat anoestrus: GnRH and analogues, and progestagens. GnRH: The pituitary LH content and responsiveness to GnRH are complete by day 10 postpartum and so exogenous GnRH administered to the anoestrus cow will induce a transient LH and FSH release. However, the response to treatment depends on the stage of ovarian follicular wave. If there is a dominant follicle present, ovulation will occur. So, when daily ultrasound monitoring was used to identify a suitable dominant follicle, administration of GnRH consistently induced ovulation (Roche et al., 1992). However, the majority of animals did not express oestrous and had short luteal phases after ovulation. Gonadotrophin releasing hormone administered in the absence of a dominant follicle is ineffective, so overall blind-treatment success rates are variable. Progesterone: Administration of progesterone, using an intravaginal device or norgestamet by injection and implantation, is an alternative treatment for the anoestrus cow. In the absence of severe NEB, once the progesterone treatment is removed, there is an induced ovulation and such treatment overcomes the absence of behavioural oestrous that often occurs at the first postpartum ovulation. However, if the NEB is severe, progesterone treatment requires supplementation with 400–700 iu equine chorionic gonadotrophin (eCG) by intramuscular injection at the time of implant removal. An alternative to eCG is the administration of 1 mg oestradiol benzoate 24 hours after a seven-day progesterone treatment which increased oestrus expression and ovulation (MacMillan et al., 1995).

Control of these conditions is not simply a matter of good management at the time of calving.

Breeding decisions and the management of the pregnant and periparturient cow The most important way of reducing puerperal problems is to avoid dystokia. Where dystokia does occur it is essential that it is dealt with correctly at an early stage and that any developing problems observed after calving are also treated as soon as possible. Attention to all aspects of hygiene is also a basic requirement. If it were purely a veterinary matter it would be relatively simple to reduce the incidence of dystokia in the majority of herds. However, the measures required may not be acceptable to the farmer. Simple modifications such as improved supervision of calving and better housing may be judged to be too expensive. Selecting an easy calving breed of bull or individual bull within a breed may not produce calves with the desired conformation or genetic potential. The consequences of several synergistic adverse effects tend to be particularly serious. Therefore, if a client chooses to use a bull that is liable to produce a high rate of dystokia it is particularly important to avoid any other factor that predisposes to dystokia. Application of the following precautions will reduce the incidence of dystokia in a herd. (1)

(2)

Cystic ovarian disease Cystic ovarian disease can be a major problem in the postpartum dairy cow resulting in an increase of 6 to 11 days to first service and an increase in the calving-toconception interval of 20–30 days (Fourichon et al., 2000). However, this subject is dealt with elsewhere in this book in Chapters 35 and 36.

Prevention of postpartum disease problems The key to controlling postpartum disease problems is to recognize that they are interlinked (Peeler et al., 1994) and that their control is related to breeding management, nutrition, the management of the transition cow and management at and immediately after calving.

(3)

Selection of sires that produce calves of suitable size and conformation for the dams concerned. This refers to the breed and to the individual bull within the breed. Special care is needed for heifers (see Chapter 5). Induction of premature calving, if the fetus is likely to be too large at full term for a normal calving (see p. 687). Control of energy intake and avoidance of macromineral and trace element imbalances. (a) Do not let the dams get too fat, as the perirectal and perivaginal fat will narrow the birth canal, the dam may be less capable of forceful labour and the calf may also be larger. This is also an important way of avoiding necrotic vaginitis and other damage to the vagina. At calving a condition score of 2.5 (see p. 10) is advised. (b) Avoid undernutrition as cows in very poor condition also have problems of dystokia. (c) Regular body condition scoring and careful attention to the late lactation, dry period and particularly the transition period ration are required. This may be aided by the use of

The Postpartum Period

metabolic profiles (see Chapter 47). Specific dietary manipulations such as the use of salts to manipulate the dietary cation–anion balance (DCAB) of the transition cow ration may also be useful in reducing the incidence of periparturient problems (see p. 787). (4) Provision of a suitable environment, especially for cows that calve inside or in a restricted area. This should be clean, well bedded, with a good water supply, properly lit and with enough space to get at the cow if need be and to allow observation without disturbance. There also need to be facilities to safely restrain the cow. (5) Avoid stress and disturbance of the calving cow (Hindson, 1976). (6) Suitable supervision and timely intervention at calving will reduce the severity of those cases of dystokia that do occur (Hodge et al., 1982). (7) Proper training of the farmer and stockworkers in how to assist at calving should be supplied by the veterinarian. (8) When veterinary assistance is needed, the farmer and his staff must decide at an early stage to call for help. It is important that the veterinarian and the farmer should agree before the start of the calving season how these problems will be dealt with and at what stage the farmer will call for professional help.

Therapy immediately postpartum In addition to specific therapies such as those described above for uterine prolapse, cows that have had obstetrical interventions at calving may benefit from a course of systemic antibiotic. Metabolic diseases, such as milk fever, should be dealt with appropriately and if these cases are common, investigation into their causes is essential. This aspect of bovine medicine is dealt with elsewhere in this book (Chapter 46). The routine administration of agents such as PGF2a (see p. 524) and oxytocin (see p. 517) to postpartum cows is not justified by improvements in subsequent fertility; reports of the benefits in the published literature are inconsistent. Their use postpartum should therefore be restricted to animals where a specific indication exists, as described earlier in this chapter.

Conclusions The key to good fertility in multiparous cattle is to maintain a high level of stockmanship at all times, and to manage cattle in such a way as to minimize postpar-

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tum problems. The preparation of cattle for breeding begins well before the expected service date. Preparing the cow for parturition and particularly dry cow and transition cow management in the previous gestation period are crucial stages in this preparation. However, parturition is the key event, and it must be managed to minimize the development of abnormalities of the genital tract in the postpartum period, which may lead to problems of subsequent oestrous cyclicity, depression in conception rates, increased embryonic loss and subfertility.

References Adams, G.P., Matteri, R.L., Kastelic, J.P., Ko, J.C.H. & Ginther, O.J. (1992) Association between surges of folliclestimulating hormone and the emergence of follicular waves in heifers. Journal of Reproduction and Fertility, 94, 177–88. Amiridis, G.S., Leontides, L., Tassos, E., Kostoulas, P. & Fthenakis, G.C. (2001) Flunixin meglumine accelerates uterine involution and shortens the calving-to-first-oestrus interval in cows with puerperal metritis. Journal of Veterinary Pharmacology and Therapeutics, 24, 365–7. Archbald, L.F., Risco, C., Chavatte, P., Constant, S., Tran, T., Klapstein, E. & Elliot, J. (1993) Estrus and pregnancy rate of dairy cows given one or two doses of prostaglandin F2 alpha 8 or 24 hours apart. Theriogenology, 40, 873–84. Beam, S.W. & Butler, W.R. (1997) Energy balance and ovarian follicle development prior to the first ovulation postpartum in dairy cows receiving three levels of dietary fat. Biology of Reproduction, 56, 133–42. Beam, S.W. & Butler, W.R. (1999) Effects of energy balance on follicular development and first ovulation in postpartum dairy cows. Journal of Reproduction and Fertility Supplement, 54, 411–24. Bon-Durant, R. (1997) Pathogenesis, diagnosis and management of trichomoniasis in cattle. Veterinary Clinics of North America: Food Animal Practice, 13, 345–61. Borsberry, S. & Dobson, H. (1989) Periparturient diseases and their effect on reproductive performance in five dairy herds. Veterinary Record, 124, 217–19. Bretzlaff, K. (1987) Rationale for treatment of endometritis in the dairy cow. Veterinary Clinics of North America: Food Animal Practice, 3, 593–607. Brooks, G. (2001) Comparison of two treatments after retained fetal membranes on clinical signs in cattle. Veterinary Record, 148, 243–4. Bulman, D.C. & Lamming, G.E. (1978) Milk progesterone levels in relation to conception, repeat breeding and factors influencing acyclicity in dairy cows. Journal of Reproduction and Fertility, 54, 447–58. Burton, N.R. & Lean, I.J. (1995) Investigation by metaanalysis of the effect of prostaglandin F2a administered post partum on the reproductive performance of dairy cattle. Veterinary Record, 136, 90–4. Caron, J.P. & Le Blanc, P.H. (1989) Caudal epidural analgesia in cattle using xylazine. Canadian Journal of Veterinary Research, 53, 486–9.

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Cester, C.C., Ganiere, J.P. & Toutain, P.L. (1993) Effect of stage of oestrous cycle on tylosin disposition in genital tract secretions of cows. Research in Veterinary Science, 54, 32–9. Cook, N. (1998) Bovine herpes virus 1: clinical manifestations and an outbreak of infectious pustular vulvovaginitis in a UK dairy herd. Cattle Practice, 6, 341–4. Correa, M.T., Erb, H.N. & Scarlett, J.M. (1992) A nested casecontrol study of uterine prolapse. Theriogenology, 37, 939–45. Darwash, A.O., Lamming, G.E. & Woolliams, J.A. (1997) The phenotypic association between the interval to post-partum ovulation and traditional measures of fertility in dairy cattle. Animal Science, 65, 9–16. Eckersall, P.D. (2000) Acute phase proteins as markers of infection and inflammation: monitoring animal health, animal welfare and food safety. Irish Veterinary Journal, 53, 307–11. Eiler, H. & Hopkins, F.M. (1993) Successful treatment of retained placenta with umbilical cord injection of collagenase in cows. Journal of the American Veterinary Medical Association, 203, 436–43. Elliot, L., McMahon, K.J., Gier, H.T. & Marion, G.B. (1968) Uterus of the cow after parturition: bacterial content. American Journal of Veterinary Research, 29, 77–81. Etherington, W.G., Christie, K.A., Walton, J.S., Leslie, K.E., Wickstrom, S. & Johnson,W.H. (1991) Progesterone profiles in postpartum holstein dairy cows as an aid in the study of retained fetal membranes, pyometra and anestrus. Theriogenology, 35, 731–46. Etherington, W.G., Martin, S.W., Bonnett, B., Johnson, W.H., Miller, R.B., Savage, N.C., Walton, J.S. & Montgomery, M.E. (1988) Reproductive performance of dairy cows following treatment with cloprostenol 26 and/or 40 days postpartum: a field trial. Theriogenology, 29, 565–75. Fourichon, C., Seegers, H. & Malher, X. (2000) Effect of disease on reproduction in the dairy cow: a meta-analysis. Theriogenology, 53, 1729–59. Ginther, O.J., Wiltbank, M.C., Fricke, P.M., Gibbons, J.R. & Kot, K. (1996) Selection of the dominant follicle in cattle. Biology of Reproduction, 55, 1187–94. Gross, T.S., Williams, W.F. & Moreland, T.W. (1986) Prevention of the retained fetal membrane syndrome (retained placenta) during induced calving in dairy cattle. Theriogenology, 26, 365–70. Halpern, N.E., Erb, H.N. & Smith, R.D. (1985) Duration of retained fetal membranes and subsequent fertility in dairy cows. Theriogenology, 23, 807–13. Hernandez, J., Risco, C.A. & Elliott, J.B. (1999) Effect of oral administration of a calcium chloride gel on blood mineral concentrations, parturient disorders, reproductive performance, and milk production of dairy cows with retained fetal membranes. Journal of the American Veterinary Medical Association, 215, 72–6. Hindson, J.C. (1976) Retention of the fetal membranes in cattle. Veterinary Record, 99, 49–50. Hodge, P.B., Wood, S.J., Newman, R.D. & Shepherd, R.K. (1982) Effect of calving supervision upon the calving performance of Hereford heifers. Australian Veterinary Journal, 58, 97–100.

Holden, D. (1998) Local analgesia for surgery of the head, distal limbs and mammary gland. Cattle Practice, 6, 233–6. Hooper, R.N., Crabill, M.R., Taylor, T.S. & Roussel, A.J. (1999) Managing vaginal and cervical prolapses in cows. Veterinary Medicine, 94, 375–89. Jackson, P.S. (1977) Treatment of chronic post partum endometritis in cattle with cloprostenol. Veterinary Record, 101, 441–3. Joosten, I., Stelwagen, J. & Dijkhuizen, A.A. (1988) Economic and reproductive consequences of retained placenta in dairy cattle. Veterinary Record, 123, 53–7. Kaidi, R., Brown, P.J. & David, J.S.E. (1991) Uterine involution in cattle. In The Veterinary Annual (ed. by C.S.G. Grunsell & M.E. Raw), Vol. 31, pp. 38–50. Blackwell Scientific Publications, Oxford. Ko, J.C.H., Althouse, G.C., Hopkins, S.M., Jackson, L.L., Evans, L.E. & Smith, R.P. (1989) Effects of epidural administration of xylazine or lidocaine on bovine uterine motility and perineal analgesia. Theriogenology, 32, 779–86. Kossaibati, M.A. & Esslemont, R.J. (1995) Daisy. The DAIRY Information System Report No. 4 – Wastage in Dairy Herds. University of Reading. Kossaibati, M.A. & Esslemont, R.J. (1997) The cost of production diseases in dairy herds in England. The Veterinary Journal, 154, 41–51. Laven, R.A. (1995) The treatment of retained placenta: a survey of practitioners. Cattle Practice, 3, 267–79. Laven, R.A. & Peters, A.R. (1996) Bovine retained placenta: aetiology, pathogenesis and economic loss. Veterinary Record, 139, 465–71. Leslie, K.E., Doig, P.A., Bosu, W.T.K., Curtis, R.A. & Martin, S.W. (1984) Effects of gonadotrophin releasing hormone on reproductive performance of dairy cows with retained placenta. Canadian Journal of Comparative Medicine, 48, 354–9. López-Gatius, F., Labèrnia, J., Santolaria, P., López-Béjar, M. & Rutllant, J. (1996) Effect of reproductive disorders previous to conception on pregnancy attrition in dairy cows. Theriogenology, 46, 643–8. McDougall, S. (2001) Effects of periparturient diseases and conditions on the reproductive performance of New Zealand dairy cows. New Zealand Veterinary Journal, 49, 60–7. MacMillan, K.L., Taufa, V.K., Day, A.M. & McDougall, S. (1995) Some effects of using progesterone and oestradiol benzoate to stimulate oestrus and ovulation in dairy cows with anovulatory anoestrus. Proceedings of the New Zealand Society of Animal Production, 55, 239–41. Markusfeld, O. (1984) Factors responsible for post parturient metritis in dairy cattle. Veterinary Record, 114, 539–42. Mee, J.F. (1991) The incidence of retained fetal membranes on nine dairy research farms over a ten-year period (1978–1987). Irish Veterinary Journal, 44, 48–52. Moller, K., Newling, P.E., Robson, H.J., Jansen, G.J., Meursinge, J.A. & Cooper, M.G. (1967) Retained fetal membranes in dairy herds in the Huntly district. New Zealand Veterinary Journal, 15, 111–16. Nakao, T., Moriyoshi, M. & Kawata, K. (1988) Effect of postpartum intrauterine treatment with 2% polyvinylpyrroli-

The Postpartum Period

done–iodine solution on reproductive efficiency in cows. Theriogenology, 30, 1033–43. Noakes, D.E. (2001a) Injuries and diseases incidental to parturition. In Arthur’s Veterinary Reproduction and Obstetrics (ed. by D.E. Noakes, T.J. Parkinson, & G.C.W. England), 8th edn, pp. 319–32. W.B. Saunders, London. Noakes, D.E. (2001b) Postparturient prolapse of the uterus. In Arthur’s Veterinary Reproduction and Obstetrics (ed. by D.E. Noakes, T.J. Parkinson, & G.C.W. England), 8th edn, pp. 333–8. W.B. Saunders, London. Noakes, D.E., Wallace, L. & Smith, G.R. (1991) Bacterial flora of the uterus of cows after calving on two hygienically contrasting farms. Veterinary Record, 128, 440–2. Oakley, G.E. (1992) Survival and fertility of dairy cows following uterine prolapse. New Zealand Veterinary Journal, 40, 120–2. Olson, J.D., Ball, L., Mortimer, R.G., Farin, P.W., Adney, W.S. & Huffman, E.M. (1984) Aspects of bacteriology and endocrinology of cows with pyometra and retained fetal membranes. American Journal of Veterinary Research, 45, 2251–5. Parkinson, T.J. (2001) Infertility in the cow: structural and functional abnormalities, management deficiencies and non-specific infections. In Arthur’s Veterinary Reproduction and Obstetrics (ed. by D.E. Noakes, T.J. Parkinson, & G.C.W. England), 8th edn, pp. 383–472. W.B. Saunders, London. Peeler, E.J., Otte, M.J. & Esslemont, R.J. (1994) Interrelationships of periparturient disease in dairy cows. Veterinary Record, 134, 129–32. Pepper, R.T. & Dobson, H. (1987) Preliminary results of treatment and endocrinology of chronic endometritis in the dairy cow. Veterinary Record, 120, 53–6. Peters, A.R. & Laven, R.A. (1996) Treatment of bovine retained placenta and its effects. Veterinary Record, 139, 535–9. Peters, A.R. & Riley, G.M. (1982) Milk progesterone profiles and factors affecting post partum ovarian activity in beef cows. Animal Production, 34, 145–53. Plenderleith, B. (1986) Prolapse of the uterus in the cow. In Practice, 8, 14–15. Roche, J.F. & Boland, M.P. (1991) Turnover of dominant follicles in cattle of different reproductive states. Theriogenology, 35, 81–90. Roche, J.F., Crowe, M.A. & Boland, M.P. (1992) Postpartum anoestrus in dairy and beef cows. Animal Reproduction Science, 28, 371–8. Rowlands, G.A. & Lucey, S. (1986) Changes in milk yield in dairy cows associated with metabolic and reproductive diseases and lameness. Preventive Veterinary Medicine, 4, 205–21. Rowson, L.E.A., Lamming, G.E. & Fry, R.M. (1953) The relationship between ovarian hormones and uterine infection. Veterinary Record, 65, 335–40. Sandals, W.C.D., Curtis, R.A., Cote, J.F. & Martin, S.W. (1979) The effect of retained placenta and metritis complex on reproductive performance in dairy cattle – a case control study. Canadian Veterinary Journal, 20, 131–5.

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Savio, J.D., Boland, M.P., Hynes, N. & Roche, J.F. (1990) Resumption of follicular activity in the early postpartum period of dairy cows. Journal of Reproduction & Fertility, 88, 569–79. Savio, J.D., Keenan, L., Boland, M.P. & Roche, J.F. (1988) Pattern of growth of dominant follicles during the oestrous cycle of heifers. Journal of Reproduction and Fertility, 83, 663–71. Sheldon, I.M. (1999) Bovine endometritis: a review. Journal of Animal Breeding, 2, 2–14. Sheldon, I.M. & Noakes, D.E. (1998) Comparison of three treatments for bovine endometritis. Veterinary Record, 142, 575–9. Sheldon, I.M., Noakes, D.E. & Dobson, H. (2000) The influence of ovarian activity and uterine involution determined by ultrasonography on subsequent reproductive performance. Theriogenology, 54, 409–19. Sheldon, I.M., Noakes, D.E., Rycroft, A. & Dobson, H. (2001) Acute phase protein responses to uterine bacterial contamination in cattle after calving. Veterinary Record, 148, 172–5. Smith, M.C.A. & Wallace, J.M. (1998) Influence of early post partum ovulation on the re-establishment of pregnancy in multiparous and primiparous dairy cattle. Reproduction Fertility Development, 10, 207–16. Steffan, J., Adriamanga, S. & Thibier, M. (1984) Treatment of metritis with antibiotics or prostaglandin F2a and influence of ovarian cyclicity in dairy cows. American Journal of Veterinary Research, 45, 1090–94. Stevens, R.D. & Dinsmore, R.P. (1997) Treatment of dairy cows at parturition with prostaglandin F2a or oxytocin for prevention of retained fetal membranes. Journal of the American Veterinary Medical Association, 211, 1280–84. Stevens, R.D., Dinsmore, R.P. & Cattell, M.B. (1995) Evaluation of the use of intrauterine infusions of oxytetracycline, subcutaneous injections of fenprostalene, or a combination of both, for the treatment of retained fetal membranes in dairy cows. Journal of the American Veterinary Medical Association, 207, 1612–15. Stocker, H. & Waelchli, R.O. (1993) A clinical trial on the effect of prostaglandin F2a on placental expulsion in dairy cattle after a caesarean operation. Veterinary Record, 132, 507–508. Vighio, G.H., Liptrap, R.M. & Etherington, W.G. (1991) Oxytocin–prostaglandin interrelationships in the cow with pyometra. Theriogenology, 35, 1121–9. Waelchli, R.O., Thun, R. & Stocker, H. (1999) Effect of flunixin meglumine on placental expulsion in dairy cattle after a caesarean. Veterinary Record, 144, 702–703. Williams, G.L. & Griffith, M.K. (1995) Sensory and behavioural control of gonadotrophin secretion during sucklingmediated anovulation in cows. Journal of Reproduction and Fertility Supplement, 49, 463–75. Wischral, A., Verreschi, I.T.N., Lima, S.B., Hayashi, L.F. & Barnabe, R.C. (2001) Preparturition profile of steroids and prostaglandin in cows with or without fetal membrane retention. Animal Reproduction Science, 67, 181–8.

Chapter 35

Problems Associated with Oestrous Cyclicity H. Boyd, D.C. Barrett and M. Mihm

Manifestation Aetiology Diagnosis Treatment Prognosis Long interservice interval Prevention

530 532 535 541 542 544 544

Manifestation Normal oestrous cycles, clear oestrous expression and efficient and accurate detection of oestrus with a predictable interval to ovulation are still essential for the successful management of reproduction in cattle. Failure to observe oestrus or lack of oestrus adversely affects the efficiency of production and profitability by interfering with the reproductive markers shown in Box 35.1 (see also Chapter 41 (b) page 678). Inaccurate oestrous detection, i.e. identification of a cow as being in oestrus when she is not, leads to cows being inseminated when fertilization is not possible because there is no ovulation at the expected time after insemination, and to pregnancies being lost when already pregnant cows are inseminated using artificial insemination (AI). Missed heats that result in longer than planned intervals from calving to first service cause considerable economic loss. A missed oestrus will cause a delay of about 21 days until the next chance for service and this loss in milk production time and delay in producing a calf results in a loss of income. Assessment of the real loss (litres of milk/year; calves/100 cows per year) and the economic loss is complex. Where possible, herd-specific economic estimates should be undertaken to determine the cost–benefit of alterations in the various elements of herd fertility (Dijkhuizen et al., 1997). However, in herds with a conventional breeding strategy it may be useful to consider a rule-of-thumb value to estimate losses occasioned with every day the calving interval is extended beyond the target of 365 days. A figure that has remained remarkably constant over the last decade (to 2002) is £2.50 to £3.00/day for every day over the planned calving interval. In beef suckler cows, delay in achieving preg530

nancy causing very prolonged calving seasons results in a similar loss; this is partly due to management problems, such as loss of the seasonal calving pattern, but also because at weaning the calf is younger and therefore weighs less. The marketing advantage of being able to sell uniform batches of calves may also be lost if the calving season is extended much beyond nine weeks. Clients may present individual cases of cows that have not been seen in oestrus when due or overdue for service, but mostly the problem is seen on regular fertility visits when post service anoestrus is also detected in animals diagnosed not pregnant. It is important to differentiate as far as possible those cows that have not been in oestrus from those that have simply not been seen in oestrus either because of poor expression of heat or poor oestrous observation. This may require an assessment to be made of the efficiency of oestrous detection in the herd and careful examination of ‘anoestrus’ cows on more than one occasion. Regular milk progesterone assays may also be useful when attempting to determine whether an individual cow is undergoing oestrous cyclicity or is truly anoestrus. Suckler cows running with the bull may be presented as failure to conceive towards the end of the breeding season. The problem of abnormal oestrous cyclicity, which is most serious when it occurs on a herd or group basis, is often picked up retrospectively on herd record analysis.

Heifers Delayed puberty may affect targets for breeding age or date. It occurs mainly as a group problem because heifers are handled and fed in groups and the cause of anoestrus is nearly always related to the environment or to the management, particularly feeding (Webb et al., 1997). Occasionally, anoestrus is manifested in a group of heifers after natural service, which the farmer erroneously thought was successful because of lack of returns to service.

Cows after calving An extended interval between calving and first service, calculated on a herd basis, is the most important

Problems Associated with Oestrous Cyclicity

Box 35.1 Aspects of reproduction affected by failure to observe, or lack of, oestrus. Heifers Age at first calving Season of first calving Cows Interval from calving to first service (and thus calving to conception) Timely observation of returns to service

Table 35.1 Percentage of cows with various calving-to-firstservice intervals in days, based on 1595 cows in 15 herds. Calving-to-first-service interval (days)

Percentage of cows Cumulative percentage

0–55

Target 56–77

78–99

>100

15.9 15.9

32.2 48.1

24.7 72.8

27.1 99.9

manifestation of dysfunction of cyclicity and oestrus or oestrous detection. A farmer with a serious problem may not be aware of it because of poor records or good ones that are not used properly. In the example given in Table 35.1, in 15 herds that were not in fertility control programmes, the target for calving interval was 12 months and to achieve this target, cows should have had their first services 56–76 days after calving. The distribution of days from calving to first service for the 1595 cows served in these herds shows that about half of the cows were first served after the target date (Boyd & Munro, 1980). Recent data from the National Milk Records (NMR) representing approximately 1 million dairy cows shows that between January 1997 and September 2000 the mean calving to first service interval rose from 84 to 88 days (Barrett, 2001), therefore the majority of cows are probably now served after the target 56–76-day window (assuming a target calving index of 365 days). However, the voluntary waiting period, i.e. the number of days postpartum waited until first service, may be deliberately increased in highyielding cows, where the decision is taken to extend their lactation for economic and welfare reasons (Knight & Sorensen, 1998). On the best farm illustrated in Table 35.1, 67 per cent of the cows were served within 77 days of calving and on the worst farm only 21 per cent of cows reached that target. The situation in this group of herds is quite typical of the results obtained in many surveys carried out in

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different countries and demonstrates the seriousness of the problem. Within herds the incidence of the problem is quite variable at different times and there may be periods of four to six weeks during the year when a high proportion of cows appear to stop cycling or exhibit poor oestrous signs. This may be a direct seasonal effect in certain climates, but in temperate regions is probably largely a nutritional effect (Butler, 1999). The number of cows treated by veterinarians for anoestrus and suboestrus was reported to be low in the 1980s. Saloniemi et al. (1986) gave the incidence as 5.2 per cent of cows, falling from first calvers (6.3 per cent) to older cows (3.7 per cent). Markusfeld (1987) diagnosed inactive ovaries after two rectal examinations in 8.5 per cent of 7751 lactations. However, more recently 20 per cent of high-yielding cows have been shown to exhibit a delayed interval to first ovulation postpartum based on progesterone profiles (Opsomer et al., 1996). Another manifestation of absence of oestrus is the cow that starts cycling and then stops, a situation recorded in 5.2 per cent of cases in a survey based on progesterone assays by Bulman and Lamming (1978). In a similar study (Kassa et al., 1986), cyclicity started and then stopped in four (3.2 per cent) of 125 lactations. Once again this situation seems to have worsened over time; in a recent Dutch study, true return to anoestrus was seen in only 3 per cent of high-yielding cows, however, 20 per cent of cows showed a prolonged first luteal phase of more than 20 days based on their progesterone profiles (Opsomer et al., 1996). Royal et al. (2000) have shown an increase in the proportion of animals with one or more atypical ovarian hormone patterns from 32 per cent of cows in the period 1975–82 to 44 per cent in the period 1995–98. During the same period pregnancy rate to first service declined from 55.6 per cent to 39.7 per cent, again suggesting that fertility in dairy cattle has declined over time.

Cows after service Analysis of data from approximately 35 000 cows in 255 British herds (Warren, 1984) showed that 26 per cent of interservice intervals were greater than 48 days, i.e. more than two cycles (Table 35.2). These results are similar to the results obtained in other surveys. For example, in the 15 herds discussed above (Table 35.1), 25 per cent of the returns to service were after a delay greater than 48 days and in Boyd and Reed’s (1961) study in smaller herds at a time when management was less intensive, 23 per cent of returns were greater than 48 days. In Warren’s (1984) report the average interservice interval was 39 days, possibly due to a delay in the return to service of 39 - 21 days = 18 days. In some other surveys there were rather fewer very long intervals,

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Table 35.2 Percentage of cows with various intervals between services in days (Warren, 1984) Interservice interval (days)

Percentage of cows

1–17

18–24

25–35

36–48

49–90

91+

6

37

13

18

18

8

possibly due to different culling patterns or more efficient heat detection. In New Zealand, Moller et al. (1986) reported that only 8.6 per cent of return-toservice intervals were greater than 36 days. Nowadays in New Zealand and other locations where dairy farming is highly seasonal, repeats are often resynchronized which increases the submission rates for the first and second repeat cycles of the breeding season. While survey data do not explain why a cow has not been served, discussion with farmers makes it clear that in the majority of cases the reason is that the cow has not been seen in heat. In conclusion, failure to have cows served because they have not been seen in season is a widespread and important problem.

Aetiology The aetiology of anoestrus in the cow and heifer is complex because as presented to the veterinarian it includes several different conditions, as shown in Box 35.2. Because there is a wide range of types of anoestrus there is also a wide range of causes, some unknown. Moreover, a variety of management and environmental factors contribute to poor oestrous detection rates.

Physiological anoestrus It is important to bear in mind that during certain phases of the reproductive cycle, the absence of oestrus is physiological. These phases are prior to puberty, during pregnancy and for at least two weeks after calving. It is not uncommon for a cow that is pregnant to be presented to the veterinarian as a case of anoestrus. This occurs if there is unknown access to a bull, or unrecorded insemination or misidentification of the cow inseminated. In dairy cows, from which the calves are removed a day or so after birth, ovulation rarely occurs earlier than 15 days after calving; in general first postpartum ovulation occurs 17–21 days after calving in medium-yielding dairy cows calving in appropriate body condition and experiencing no major loss in body condition subsequently (Savio et al., 1990). This postpartum interval to

Box 35.2 Aetiology of anoestrus.

• • • • •

Physiological anoestrus: prepuberty, pregnancy, puerperium True anoestrus: no oestrous cycle and no ovulation or blocked cycle (prolonged luteal phase, such as with pyometra) Silent oestrus: better termed silent ovulation, i.e. ovarian cycles occur but no oestrous behaviour is detected Weak oestrus: poor oestrous expression (reduced length or intensity) Unobserved oestrus: oestrus normal, human error

first ovulation may be prolonged to 60 days in highyielding cows (Opsomer et al., 1996). In cows that are suckling, usually beef cows, the duration of noncyclicity may be extended from 25 to beyond 100 days, depending on body condition score at calving and postpartum nutrition (Stagg et al., 1995). The effect of suckling of one or more calves is to inhibit the return to cyclicity via neurohormonal routes, which can be modified by nutritional factors. This is demonstrated by the observation that some well-fed, well-managed beef suckler herds achieve a tight calving pattern at the same time each year, which requires an early return to cyclicity while the cows are still suckling their calves. For a list of factors that affect the onset of puberty, see Chapter 5.

True anoestrus The major causes of true anoestrus characterized by lack of ovulation are summarized in Box 35.3. (1) In heifers, bilateral gonadal aplasia, which causes permanent anoestrus and sterility, occurs in the common condition of freemartinism, found in the majority of female calves that are cotwins with males. It is also observed in bilateral ovarian hypoplasia, a rare inherited condition, in which the genes are passed on through fertile individuals with unilateral gonadal hypoplasia. Poor nutrition is important and discussed below.

Problems Associated with Oestrous Cyclicity

Box 35.3 Major causes of true anoestrus. Heifers Freemartinism Ovarian hypoplasia Inactive ovaries (poor nutrition) Cows Dystokia and postpartum problems Delayed involution (inactive ovaries) Pyometra (persistent corpus luteum) Cystic ovarian disease Poor nutrition prepartum, severe energy deficit postpartum, especially first calvers Age-related factors

(2) In cows a variety of abnormalities at or around calving, such as dystokia, retained fetal membranes, hypocalcaemia, metritis, endometritis and other postpartum abnormalities may result in delayed return to cyclicity (for a full discussion of this see also Chapter 34). (3) Ovarian cysts, traditionally defined as fluid-filled structures >25 mm in diameter and present for more than 10 days in the absence of a corpus luteum (CL), are quite commonly recorded in cases of anoestrus and in fact the majority of cows with cystic ovarian disease exhibit anoestrus. This traditional definition implied that cysts were static structures; however, this is now known not to be the case, and cysts should be considered dynamic both in structure and function (Cook et al., 1990). The likely hormonal mechanism of cystic ovarian disease is failure of the preovulatory luteinizing hormone (LH) surge. In some cases there may be failure of the ovary to respond to LH at the start of oestrus (Brown et al., 1986). Cystic ovarian disease is a very complex condition and in many cases the cyst produces a mixture of steroids, which are variably absorbed into the general circulation. In the postpartum period, particularly during the first six weeks, some cows (approximately 20–25 per cent) experience ovulation failure followed by the development of palpable but functionally transient cystic structures that may not interfere with subsequent cyclicity. Towards the end of this period many farmers become concerned about lack of oestrus and so the cow is presented for veterinary examination. Cystic ovaries were associated with 6 to 11 more days to first service and with 20 to 30 more days to conception in a metaanalysis of papers published between January 1987 and January 1999 (Fourichon et al., 2000). By about six weeks after calving an ovarian cystic structure should be regarded as pathological. Cysts are often classified as either follicular (about 70 per cent; single large cyst or multiple smaller cystic structures) or luteal and it is

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easy to understand why the cow with the luteal cyst, which is predominantly progesterone producing, does not exhibit oestrus, though it is less clear why she fails to cycle. However, follicular cysts with oestrogen production are also found in cases of anoestrus. This may be due to the low level of the steroid produced in some cases, while in other cases it may result from the negative effect on the behavioural centre of high levels of oestrogen circulating more or less continuously. Another explanation for the lack of oestrus in cows with follicular cysts is that the behavioural centres in the brain, which control the expression of oestrus, respond better to oestrogens if they have been primed by progesterone. Garverick (1997) in the USA and Dobson et al. (2001a) in the UK have both reviewed cystic ovarian disease. Factors associated with the occurrence of cystic ovarian disease are discussed further in Chapter 36. (4) The role of nutritional deficiencies in anoestrus is relatively straightforward in heifers but is complex in adult dairy cows. (a) In heifers it has been shown in many field trials that low energy intake that causes slow growth rate is associated with delayed puberty. Onset of puberty tends to be related to body weight rather than age. The mechanism is discussed in Chapter 5. (b) In adult lactating dairy cows it is not clear how feeding affects return to cyclicity after calving, even when only energy is considered; however, evidence is growing to suggest that the effect may, at least in part, be mediated by insulin-like growth factor-1 (IGF-1) levels (Taylor et al., 2001). It is clear that dairy cows experience a metabolic crisis early postpartum, as energy loss cannot be compensated for by energy intake and stored energy is utilized. Factors that exacerbate the negative energy balance including the feeding levels before and after calving, particularly the energy density of the ration, excessive energy loss due to high milk yield and increased body condition loss after calving (body condition score loss of more than 0.5) will prolong the interval to first ovulation, as will associated metabolic or other diseases postpartum. A clear relationship has been shown between the timing of the negative energy balance nadir (the lowest point of the negative energy balance postpartum) and the interval to first ovulation, the LH pulse frequency and the LH-dependent fate of the first dominant follicle selected postpartum (Canfield & Butler, 1990; Beam & Butler, 1997). First ovulation occurs 7–14 days after the energy balance nadir; thus, if the lowest point of the negative energy balance is reached between the first to second week postpartum, cows can be expected to ovulate by 21–30 days postpartum. However, in cows in

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which body condition score loss exceeds 1, the interval to first ovulation may be prolonged to 60 days and beyond. One method to try to take into account these many interacting factors is regularly to measure the body condition score of cows (Anon, 1984); particularly important times include drying off, calving and service times. (c) In the beef suckler cow, prepartum nutritional deficits leading to reduced body condition at calving delay the interval to first ovulation by more than 40 days to 90 days and beyond (Stagg et al., 1995, 1998). The delay in resumption of ovulatory activity is associated with continued atresia of recurrently selected dominant follicles; instead of ovulation of the 2nd to 4th dominant follicle postpartum, it is on average the 9th dominant follicle which eventually secretes sufficient oestradiol to induce the gonadotrophin surge and ovulation. As circulatory concentrations of FSH are not affected by pre- or postpartum diet, the detrimental effects of low body condition score at calving on the fate of dominant follicles selected early postpartum are attributed to reduced LH secretion, which reduces dominant follicle oestradiol production. The relationship between nutrition and fertility is a complex one which is still not fully understood. There is a vast body of literature on this subject which is too extensive to review here. However, the reader may find the following reviews of interest: Britt (1995); Webb et al. (1997, 1999); Wathes et al. (1998); O’Callaghan and Boland (1999); Garnsworthy and Webb (2000) and O’Callaghan et al. (2000). Several studies have shown that cows in their first lactation exhibit a disproportionately high incidence of true anoestrus, with lack of ovulation. A variety of explanations for this have been put forward, in particular the inhibitory effects of lactation and growth on the recovery of the LH pulse frequency early postpartum, preventing dominant follicle maturation and ovulation. Another suggestion is that this is mainly the result of the high incidence of dystokia that occurs in first calvers. However, the high incidence of anoestrus in first calvers is often attributed to nutritional and environmental factors. Excessive weight loss and very poor body condition result in cessation of ovulation and cyclicity, presumably through hypothalamic–pituitary dysfunction (see Chapter 67). Cows continue to grow until their second or third lactation and therefore young animals have to carry out the tasks of milk production, growth and reproduction simultaneously, at a time when adult dentition has not been fully developed. In dairy cows it is also the time when the young, smaller cow is introduced to the highly competitive environment of a herd, which, particularly during the housing period, makes it difficult for small animals to compete

for food. It is also presumably a stressful experience being low within the herd hierarchy. (d) In many cases first calvers may exhibit a high incidence of lameness. Lameness (see Chapters 31 and 32) is a cause of weight loss that can result in true anoestrus and also, because of the associated pain, can cause poor oestrous expression in animals that are cycling. Various other forms of stress such as surgery, changes in social grouping, transport and heat stress may all affect fertility, thus stress on breeding cattle should be minimized whenever possible (Dobson et al., 2001b). (5) Among miscellaneous causes of persistent corpus luteum is the rare condition of uterus unicornis, in which one horn of the uterus is absent. Ovulation on the side without a uterine horn results in a corpus luteum that is not exposed to locally produced prostaglandin and therefore does not regress after 16 or 17 days.

Silent ovulation and unobserved oestrus First ovulation postpartum is generally silent (80 per cent), but once cycles have been established, silent oestrus is not a common phenomenon, as was clearly demonstrated by Williamson et al. (1972), who carried out continuous observation of 107 cows for 21 days and concluded that four demonstrated silent oestrus. This has been confirmed by others in field trials in herds in which silent oestrus was thought to be a problem. Generally, when oestrous detection methods are improved, there is a corresponding reduction in the number of cases regarded as silent oestrus. Many cases previously diagnosed as silent oestrus are in fact unobserved oestrus. Incidence figures for silent ovulation are most reliable when based on serial progesterone assays, as in the study of 1400 cows by Ball and Jackson (1984) in which 21 per cent of the cows had ovulated but had not been seen in oestrus. This level of non-detected oestrus is in agreement with other studies. McLeod et al. (1991) reported 78 per cent of ovulations in their study were correctly identified by conventional oestrous detection, confirming that approximately 20 per cent of those cows ovulating are not seen in oestrus. To what extent delayed return to service is due to unobserved oestrus is not clear, but Humbolt (1982), using milk progesterone assays, calculated that only 29 per cent of delayed returns were due to embryonic death and that 73 per cent were due to anoestrus (including true, silent and unobserved oestrus). However, ovulation without the accompanying signs of oestrus (that is, silent oestrus) does occur. The best documented situation relates to the first ovulation after

Problems Associated with Oestrous Cyclicity

Box 35.4 Causes of silent and weakly expressed oestrus.

• • • • •

Social Pain and fear Weight loss Genetic factors Presence of calf and suckling

calving, particularly if it occurs within the first 20 days. Otherwise it is almost impossible to distinguish between silent and unobserved oestrus. Some instances of oestrus are so weak or last for such a short time that detection by conventional observation is a matter of chance. Standing oestrus lasts for about 8–12 hours in cows and 6–8 hours in maiden heifers. However, 20 per cent of heats last less than 6 hours (Esslemont et al., 1985). Increasing herd sizes and decreasing availability of skilled manpower on many farms is probably exacerbating the problem of poor oestrous detection. It may also be the case that high-genetic-merit, high-yielding modern dairy cattle exhibit oestrous behaviour either less intensely or for a shorter duration, making oestrous detection more difficult. The causes of silent oestrus, weak oestrus and short oestrus are not well understood, but those considered to be the main factors are presented in Box 35.4. (1) Social factors within the group of cows, the size of the group and the reproductive status of the rest of the group all play a role in oestrous behaviour and in the frequency of mounting (Britt, 1987). Mounting requires that there is both a cow in oestrus and a cow that is willing to mount. Cows that are usually bullied or are low in the pecking order are less likely to stand to be ridden when they are in oestrus than more dominant cows. A small group of cows, say fewer than four or five, may be less effective at stimulating mounting behaviour than a larger group of sexually active cows. Cows at different stages of the reproductive cycle vary in their likelihood of trying to mount a cow in oestrus. The most likely to jump are those in or near oestrus, followed by nonpregnant cows in the early luteal phase followed by pregnant cows. At the end of an intensive breeding season when most cows are pregnant the remaining cows to be served may be more difficult to detect because of the absence of cows willing to mount. In the main, oestrous detection is therefore easier in tight seasonally calving herds, where a large number of cows are eligible for service within a given time period, than in a herd with a wide calving spread and fewer non-pregnant cows in the herd at any one time. The presence of a bull inhibits cow-to-cow interaction, but this may be made up for by the bull’s own

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sexual monitoring of the herd. However, a bull may not choose to serve all cows in oestrus if several are in season at the same time. (2) Pain and fear. As oestrus is a behavioural phenomenon that is subject to psychological influences, it can be inhibited by discomfort, pain or fear. Severe adverse weather conditions such as driving rain and cold reduce cows’ interest in sexual behaviour. Slippery flooring produces fear of falling and may inhibit oestrous behaviour. The pain caused by lameness inhibits oestrous expression. (3) Weight loss. It has been suggested that weight loss is associated with an increase in silent heats. (4) Genetic factors are almost certainly involved. The subjective nature of the measurement of oestrous expression makes it difficult to gather enough reliable data to evaluate the hereditary influence. Reports from progeny testing stations, where large groups of daughters from bulls under test were kept, showed that different daughter groups exhibited oestrus in characteristic ways. There may also be differences between breeds in expression of oestrus. Currently, there is much anecdotal evidence to suggest that the modern high-genetic-merit Holstein exhibits oestrus less well than the traditional British Friesian, or some other dairy breeds. (5) Presence of calf and suckling. The presence of a suckling calf may reduce expression of oestrous behaviour in some cows as well as affect oestrous cyclicity.

Epidemiological data In a study of 70 775 lactations in Finnish Ayrshire cows in which only cases treated by veterinarians were analysed (Saloniemi et al., 1986) it was noted that the chance of a cow being presented to the veterinarian as anoestrus was affected by parity (highest risk in first calvers), calving season (highest risk in cows that calved from September to February), herd milk yield (highest incidence in high-yielding herds) and the occurrence of metritis (Chapter 34), mastitis (Chapter 23) and ketosis (Chapter 46).

Diagnosis A systematic approach to diagnosis is essential and the clinician should follow the steps outlined in Box 35.5. If the anoestrous cow is in a herd in which the veterinarian is running a fertility control programme involving regular visits, diagnosis will be both easier and more reliable because there will be historical informa-

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Box 35.5 The diagnosis of anoestrus.

• • • • • •

History (including records) General clinical examination (including condition score) Special examination of the reproductive system Rectal palpation and transrectal ultrasound examination Vaginal specular examination Laboratory tests, e.g. progesterone assays

Fig. 35.1

•

Cyclic solid CL.

Fig. 35.3

Dominant follicle on right ovary bordering the CL.

Fig. 35.4

Two corpora lutea in a 6-week pregnancy.

Cyclic CL with lacunae on right ovary.

tion available and it will be simpler to introduce routine sampling where this is indicated. There are two separate but overlapping aspects of diagnosis:

•

Fig. 35.2

Stage 1: assessment of ovarian status to determine whether the case is true anoestrus, in which there is no ovulatory activity, or in which cyclicity is prevented by a persistent corpus luteum or other progesterone producing structure; or silent or unobserved oestrus, in which ovarian cycles are taking place. Stage 2: assessment of the causes of the condition.

Stage 1: assessment of ovarian status Since the word ‘cycle’ implies repetition, theory would dictate that assessment of whether or not a cow is cycling necessitates repeated examinations over an interval that should allow the observation of two oestrous periods. Under practical conditions it is usually assumed that the animal is cycling if it is possible to prove that ovulation has recently taken place. Another common assumption concerns a group of animals. It is usually considered that the group as a whole is cycling if two-thirds of the cows are in the luteal phase, i.e. the same fraction of the oestrous cycle that the luteal phase occupies. Furthermore, the description of the ‘luteal phase’ given in Chapter 33 presents some difficulties in connection with diagnosis. This is because a corpus luteum is unlikely to be palpable until approximately seven days after oestrus, but

may be functional before that time. However, positive detection of a functional corpus luteum via ultrasound examination (size and echogenicity, Figs 35.1–35.4) is usually closely related to its progesterone secretion. Progesterone assay of milk or plasma will only produce a definite, recognizable rise after a similar delay; to confirm cyclicity a sequence of progesterone assays two or three days apart showing a pattern consistent with a luteal phase followed by a period of low progesterone level and another luteal phase should be seen. Accordingly, for clinical purposes ‘luteal phase’ is defined as from day 5 to day 17 and the normal ‘period

•

Problems Associated with Oestrous Cyclicity

Box 35.6 History taking for anoestrus cows.

• • • • • •

Date of calving Any abnormality at and after calving Has the cow been seen in oestrus since calving? Could the cow be pregnant? Oestrous detection methods in the herd Are there other cows in the herd with similar problems?

of low progesterone’ is expected to be from day 18 through oestrus (day 0) to day 4. This definition applies to the majority of cows in a normal population and is needed to form a basis for rational diagnosis, but its use should be tempered by the realization that no definition will fit all cases (Bloomfield et al., 1986). The first step is to take a history of the case. Relevant information, required for both stages of diagnosis, is shown in Box 35.6. The next step is to find out if there is functional luteal tissue present in the ovaries. The traditional way to do this is to palpate the ovaries per rectum, but there are now several choices. One is to carry out a single or a series of milk progesterone assays, which gives a quick, reliable result. Another is ultrasound scanning, which allows the user to observe functional luteal tissue in the ovary (Figs 35.1–35.4) (Omran et al., 1988; Boyd & Omran 1991). The choice of method will depend on circumstances as each method has advantages and disadvantages. Rectal palpation is immediate, simple, requires little restraint of the cow and, if part of a regular visit, is relatively cheap. It also allows other observations to be made on other parts of the reproductive tract and on the animal’s general condition. There is minimal risk of misidentification of the animal, a danger always present when samples are taken for analysis. On the other hand, it is a less accurate indicator of luteal function than a progesterone assay. Real-time ultrasound scanning is a valuable tool that, in experienced hands, is capable of giving a very accurate picture of ovaries and uterus (Figs 35.1–35.13). Rectal palpation alone, when undertaken by an experienced clinician, can be relatively accurate. For example, Dawson (1975) compared the findings made by rectal palpation shortly before slaughter with postmortem observations. He identified accurately 125 (89 per cent) of 141 ovaries with corpora lutea. The errors were mainly in cows with small corpora lutea and also some with cysts or follicles. However, others have suggested that rectal examinations alone are less accurate. On the basis of milk progesterone assays (which were assumed to be correct) Ott et al. (1986) summarized their own and other workers’ results, as shown in Table 35.3.

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Table 35.3 The accuracy of corpora lutea detection by rectal palpation based on comparison with milk progesterone assay. Corpus luteum Present

Absent

244 82

158 70

Number of cases Accuracy (%)

Fig. 35.5

Long-standing follicular cyst.

Fig. 35.6

Follicles on right ovary.

Fig. 35.7 phase.

Non-pregnant right uterine horn during the luteal

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Fig. 35.8 Non-pregnant left uterine horn during the luteal phase with bladder ventrally.

Fig. 35.11

Fig. 35.9

Fig. 35.12 Early PD 6 weeks.

Fig. 35.10

Pyometra.

Early PD 4.5 weeks.

The use of progesterone assays has the advantage that they can be incorporated into a fertility control programme and used prior to a visit, so that the clinician has information available before the examination of the animal. They can also be used after the visit to give extra information about the case. There may be slight problems in deciding the level of circulating progesterone that can be taken as indicative of luteal function and caution needs to be exercised in interpretation of absolute values, as these may change depending on time from milking (Waldmann et al., 1999).

Early PD 5.5 weeks.

Fig. 35.13 Male fetus (3 months).

The accuracy of ultrasound scanning was investigated by Pieterse et al. (1990), who examined the ovaries of 59 cows by rectal palpation, ultrasound scanning (5 MHz linear array transducer) and dissection on the day of slaughter, and concluded that for the detection of a mid-cycle corpus luteum the sensitivity of rectal palpation was 83 per cent and for ultrasonography the sensitivity was 80 per cent. For the detection of follicles, ultrasonography was considered to be significantly better than rectal palpation, with ultrasonography detecting 95 per cent of follicles over 10 mm in

Problems Associated with Oestrous Cyclicity

diameter whereas rectal palpation only detected 71 per cent. These results obviously reflect in part the quality of the ultrasound equipment used and the skill of the clinician palpating the ovaries and interpreting the ultrasound images. In another study comparing the use of ultrasound and rectal palpation (Fishwick, 1993), the accuracy of palpation and ultrasonography in detection of luteal tissue was compared to contemporaneous plasma progesterone concentrations. In this study the overall accuracy of manual palpation was 62 per cent compared with 83 per cent for ultrasound examination. In cows with high progesterone status, manual palpation (60 per cent) was significantly less accurate than ultrasound imaging (94 per cent), whilst in cows with a low progesterone status manual palpation (65 per cent) and ultrasound imaging (70 per cent) were both equally accurate. In general it would be expected that imaging of the ovaries using modern ultrasound equipment, for example using a 7.5 MHz transducer, would be more accurate than manual palpation. However, individuals highly skilled in rectal palpation may be able to detect luteal tissue with an accuracy comparable to ultrasound, but will not be able to palpate small follicles that are readily detected by ultrasound scanning. Reduced cost of equipment and improved image quality combined with practice and much increased use within veterinary medicine have made transrectal real-time ultrasound examination of the bovine reproductive organs the examination of choice in regular fertility visits. If there is evidence of functional luteal tissue, the possibilities shown in Box 35.7 exist. The simplest way to decide whether the animal is pregnant or has a pathological condition is to carry out rectal palpation or ultrasound examination of the ovaries and genital tract, plus in some cases a vaginal examination. This will, however, fail to reveal very early pregnancy before 25–28 days after service using ultrasound and below 35–40 days using manual palpation. Figures 35.10 to 35.12 show examples of ultrasound images of early pregnancy. Figure 35.13 shows an image of fetal sexing in a three-month-old fetus. The most common finding is that ovaries and uterus appear to be normal and these cases are usually regarded as normal cycling cows that have simply not been seen in oestrus. Box 35.7. Likely reasons for the presence of functional luteal tissue.

• • • •

Cycling (days 5–17 inclusive) Pregnancy Ovarian pathology (luteal cyst) Uterine pathology (pyometra with persisting corpus luteum)

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Box 35.8 Likely reasons for no luteal tissue being present.

• • •

True anoestrus Cycling (day 18 through oestrus to day 4) Ovarian pathology Freemartin: heifer Cystic ovarian disease

Booth (1988) has investigated the accuracy of diagnosis of luteal cysts using rectal palpation, and the clinical finding of luteal cysts was confirmed by progesterone assay in only 54 per cent of cases. This accuracy can be improved by transrectal ultrasound scanning. For example, Douthwaite and Dobson (2000) reported that diagnostic criteria for follicular cysts using ultrasound examination and plasma progesterone assays agreed in 92 per cent of cases; a similar comparison for luteal cyst diagnosis gave a 74 per cent agreement. The rapid on-farm diagnostic method of choice should thus be transrectal ultrasonography, supported by milk progesterone assay where required. If initial examination shows there is no functional luteal tissue, there are also the various possibilities shown in Box 35.8. When the initial examination reveals no luteal function and apparently normal ovaries and tract, and no evidence of mucus or mucohaemorrhagic discharge on the tail to indicate recent oestrus or ovulation, the cow’s ovarian status is unresolved. If she is cycling normally and in the low progesterone phase of the cycle, a corpus luteum will become palpable and visible by ultrasound examination in the ovary within approximately 7 days from the first examination. A second examination at 7–10 days after the first will detect this corpus luteum. This second examination must not be delayed too long, as some cows (those at day 5) will go into the low progesterone phase again in about 12 days after the first examination. These calculations can be upset by the considerable variations in cycle lengths and progesterone patterns that occur in a normal population of cows, as detailed by Bloomfield et al. (1986). It is also very useful to carry out a vaginal examination at the time of the first examination, as the presence of copious, clear mucus is strongly indicative of the peri-oestral stage of the cycle. In this way vaginal examination may allow a diagnosis to be made without the need for a second progesterone assay or a second rectal palpation. If a second examination or sampling is required it is best done 7–10 days after the first. It is even better if serial sampling for progesterone assays can be arranged. It is necessary to work out a satisfactory regimen of sampling. This involves making a compromise between the biological ideal, which might be daily

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samples, and what is acceptable to the farmer because of the cost, labour and interference with the milking routine. For example, a sampling regimen of two to three samples per week, which will give a useful picture of the oestrous cycle but is not frequent enough to time oestrus exactly, may be unacceptably frequent for a farmer. This situation may change in future if accurate and reliable automated systems to assess the cows’ physiological state using biosensors can be developed (Koelsch et al., 1994; Mottram, 1997; Scully et al., 2000). New developments in this area of technology may allow automatic milk progesterone assays, and other assays, to be performed while cows are being milked, allowing the timing of ovulation to be accurately predicted and removing the need for oestrous detection. Detection of antral follicles in the ovary, the observation of uterine tone and assays for oestrogens are all of limited value because they do not give clear indication of exact timing of oestrus to predict ovulation. There are a number of aids to detection of oestrus that can aid diagnosis (Boyd, 1984). The veterinarian now knows whether the cow or group of cows is exhibiting true anoestrus or is undergoing ovarian cycles. If a conclusion of anoestrus has been reached an important question is whether (i) the cow is in ‘deep’ anoestrus, which means that she is not likely to start cycling soon and may revert to an anoestrous state following treatment, or (ii) whether she is in ‘shallow’ anoestrus and liable to begin cycling soon and be responsive to therapy. Unfortunately, it is almost impossible to predict accurately the ‘depth’ of anoestrus. However, if the cow is in extremely poor condition and if she has small hard ovaries she is probably in deep anoestrus and may require a combination of treatments to induce first ovulation, with the possibility of subsequently reverting to an anoestrous state. Detection of the LH pulses that occur in the cow about to start cycling and are absent in those in deep anoestrus requires a series of samples taken at short intervals. At present (2003) LH assays cannot be done in a practice laboratory but are routinely carried out in affiliated research laboratories.

Stage 2: assessment of the cause of anoestrus or silent ovulation This section deals with the difficult question of how to find out what has caused the abnormal ovarian status or the problem of oestrous expression or detection. To some extent procedures followed for diagnosis of ovarian status also give the clinician an understanding of the causes of the ovarian dysfunction. Examples of these are listed in Box 35.9. Three of the causes of inactive ovaries: nutritional deficiency causing metabolic stress and severe negative energy balance, delayed

Box 35.9 Causes of dysfunction of the ovarian cycle.

• • • • • • • •

Freemartinism (congenital) Ovarian hypoplasia (inherited) Uterus unicornis (congenital) Pyometra (periparturient problems) Some cases of inactive ovaries Nutritional and metabolic stress Systemic disease Delayed involution

involution and concomitant disease, present some problems in diagnosis. In cases of delayed involution, the enlarged uterus and particularly the enlarged cervix, which involutes more slowly, usually make the diagnosis of the immediate cause easy. However, on some occasions, by the time the cow is examined the uterus may well have returned to normal size and the veterinarian will have to depend on a history of periparturient problems and possibly of abnormal vaginal discharges noted by the farmer (see Chapter 34 page 523 for details of an involution scoring system). The clinician should look for any other disease condition in the cow examined for anoestrus. Especially important is any disease that causes loss of body condition or pain. There is a complicated series of factors, such as actual and potential milk yield, feeding before and after calving and weight change after calving, which are very difficult to assess. Body condition of the cow should be noted at the time of examination for anoestrus, but this deals with only part of the problem (Anon., 1984). If body condition is poor or loss of body condition score has been extreme, or if there are many cases of inactive ovaries, feeding should be investigated. Feeding analysis and metabolic profiles are discussed elsewhere in this book (see Chapters 9 and 47). On occasion there is no clear reason for the occurrence of inactive ovaries, either in the individual cow or when the condition affects a group of animals. When investigating silent oestrus and unobserved oestrus, the veterinarian should find out about the following:

• • • • • • • •

Organization of oestrous detection. Ease of cow identification. Method of recording. Layout of the buildings. State of the floors and levels of lighting. The way the cows are handled, moved around and assigned to groups. Amount of knowledge of oestrus and the oestrous cycle among the people who are detecting oestrus. Motivation for oestrous detection.

Problems Associated with Oestrous Cyclicity

• •

Time made available for oestrous detection. Personalities of the people involved.

Treatment

(see also Chapter 42)

When using proprietary products, the clinician should consult the data sheets, produced by the manufacturers, for details of use, contraindications and other guidance. Successful treatment, leading to oestrus, service and pregnancy, depends not only on veterinary therapy but on husbandry and breeding management, some aspects of which are described in the data sheets and also on page 525. Different manufacturers of apparently similar products often give slightly different advice about their use and users should be aware of the major differences between some of these products. Some of the therapeutics, for example Prostaglandin F2a (PGF2a) are dangerous for humans and could cause return to service and abortion in cows, and therefore the veterinarian must handle them responsibly and with care. Where drugs that result in oestrus are used, efficiency of oestrous detection will be enhanced as the clients are told to concentrate on a specific time for oestrous detection; their attention is focused on the cows treated and aids to oestrous detection such as tail paint are often used.

True anoestrus: no functional luteal tissue Two points should be remembered when dealing with these cases:

• •

All healthy, suitably fed cows will start cycling in the first two months after calving. There must be an underlying reason for the occurrence of this type of true anoestrus and an attempt should always be made to find the cause and deal with it. Where the cause appears to be nutritional, improved feeding should be part of the treatment of the affected individual and should also be considered for other recently calved cows. Consideration should also be given to the body condition changes and feeding regimen of the dry cows as well as the management and nutrition of the transition cow. Particular care should be taken to ensure that high-genetic-merit dairy cows do not become too fat during the dry period (Rukkwamsuk et al., 1999).

At present there are two main hormonal treatments for inactive ovaries: (i) administration of gonadotrophin-releasing hormone (GnRH) or analogues with GnRH activity and (ii) insertion of a progesterone-releasing device (see p. 681).

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Administration of an adequate dose of GnRH results, in the majority of cases, in luteinization or ovulation of healthy dominant follicles present at the time followed by a transient period of progesterone production that can first be identified about five days after treatment. The duration of this progesterone phase is very variable, ranging from one or two days to the lifespan of a normal cyclic corpus luteum, and therefore the interval from treatment to oestrus is very variable, about 8–22 days. It is desirable to follow up these cases to ensure that luteinization or ovulation has taken place; this is best done by ultrasound scanning or by progesterone assay. If there is luteal tissue present at the follow-up examination 7 days later, it is useful to treat the animal with PGF2a or an analogue, as this will make the resulting oestrus more predictable. Regular fertility control visits at weekly intervals are ideal for this regimen; however, visits are often at fortnightly intervals and this may be a less suitable period between the initial and follow-up treatment when using the GnRH–PGF2a regimen. If, on the follow-up examination, there is no luteal tissue the cow should be dealt with as a new case. The use of a progesterone or synthetic progestagen slow release device also mimics the progesterone rise before first ovulation. This device is left in the vagina or implanted subcutaneously at the base of the ear for 8–12 days and the animal should be served at the oestrus that occurs in many cases about two or three days after withdrawal. Fixed-time insemination 48 and 72 hours (or a single insemination at 56 hours) after withdrawal may be carried out (follow data sheet recommendations for whichever product is selected). If oestrus is observed later another insemination should be carried out. Avoid stress and drastic change of diet during and after treatment (see p. 683). In those animals in which increased negative energy balance, poor body condition or very strong behavioural effects inhibit LH pulse frequency and thus dominant follicle maturation, final differentiation of the preovulatory dominant follicle or the preovulatory oestradiol rise may have to be enhanced. The addition of equine chorionic gonadotrophin (eCG) given at the end of the progesterone or synthetic progestagen treatment will induce oestrus 48 hours later. Similarly, treatment with a very low dose of oestradiol benzoate 24 hours after device withdrawal will induce oestrus 12–20 hours later, but consideration will have to be given to the national legislation relating to the use of these drugs in dairy or beef cattle. The treatment of follicular cysts involves either using intravaginal progesterone releasing devices (PRID or CIDR) or establishment of endogenous luteal tissue with chorionic gonadotrophin or GnRH (Dobson et al., 2001a). There is evidence to suggest that the success of

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treatment of follicular cysts depends on whether the cyst is producing oestradiol or not, as reflected by the presence or absence of other follicles >5 mm in diameter. Treated with either an intravaginal progesterone releasing device or GnRH, cystic follicles in the presence of other follicles had a pregnancy rate to all inseminations of 91 per cent compared with 69 per cent if no other follicles were present at the time of treatment (Tebble et al., 2001).

with a view to treating with PGF2a or an analogue, if appropriate. Conservative treatment is preferred in the first instance by some clients who would rather leave the animal untreated, are content to know that she is cycling and hope to observe the next oestrus. In these cases aids to heat detection should be used and the animal re-examined if she is not seen in season within the next two weeks.

True anoestrus: functional luteal tissue

Silent oestrus/unobserved oestrus: no corpus luteum present

The therapeutic approach is to cause luteolysis by parenteral administration of PGF2a, or an analogue, followed by intensive oestrous detection up to one week after injection and insemination at observed oestrus. In the case of pyometra (Fig. 35.9), the client should be advised to delay service until it appears that the infection has cleared up, as indicated by an oestrus at which the mucus from the vulva is free of pus. It is advisable that the veterinary surgeon should examine these cases at a follow-up visit to ensure the uterus has returned to normal (Figs 35.7 and 35.8). The treatment of cystic ovarian disease depends largely on whether the structure is progesterone producing or not. If considered a luteal cyst with functional luteal tissue, as judged by ultrasound examination or milk progesterone assay, the logical treatment is to administer PGF2a, although alternative therapies such as the use of intravaginal progesterone releasing devices may also be successful (Douthwaite & Dobson, 2000).

Silent oestrus/unobserved oestrus: corpus luteum present There are two standard approaches in these cases, the choice being between (i) the induction of luteolysis using PGF2a or an analogue and (ii) leaving the animal untreated to be observed when she comes in heat. The method chosen will depend on many variable factors, such as the season, the time since calving, the herd calving pattern and the inclination of the client, and therefore the decision has to be made individually for each case. Treatment with PGF2a or an analogue should, in the majority of adult cows, result in oestrus in 2 to 7 days, with the peak period being days 3 and 4 after treatment. Service should be at observed oestrus and aids to oestrous detection should be used. Enhanced oestrous expression may be observed when combining a progesterone or synthetic progestagen device with PGF2a. Cows that are not seen in oestrus after treatment should be re-examined after 14 days (Young, 1989)

These cases do not benefit from immediate drug therapy as animals are showing ovarian cycles but have either just regressed their CL or are in the early luteal stage following ovulation. Improvements in husbandry, i.e. oestrous detection, and, possibly, feeding may be required to enhance detection and oestrous expression, and it may be useful to enhance oestrous expression hormonally by using eCG or oestradiol benzoate following treatment with a progestagen device (see above). Because diagnosis is uncertain until the second examination (7 or 14 days later), it is questionable whether these cows should be treated at the first visit. If there is no corpus luteum on the second examination, the condition is to be regarded as true anoestrus and dealt with accordingly.

Prognosis In considering prognosis, primary attention has to be paid to the return to cyclicity, which can be measured either by observation of oestrus or, more reliably, by one or more progesterone assays at planned times after treatment. The outcome of treatment is influenced by both the veterinarian and the client (and perhaps also by the cow), as presented in Box 35.10. Factors influenced by the veterinarian, which affect the outcome of treatment for anoestrus, are as follows: Box 35.10 Contribution of farmer and veterinary surgeon to influencing prognosis. Prognosis influenced by veterinarian Accuracy of diagnosis Selection of cases Choice of therapeutic intervention Follow-up examination Prognosis influenced by farmer Oestrous detection Herd pregnancy rate Culling rate

Problems Associated with Oestrous Cyclicity

•

•

The accuracy of diagnosis is the basis for correct treatment. There is good evidence that identification of a corpus luteum by palpation by experienced veterinarians is over 80 per cent accurate (see p. 537) and that differentiation between follicular and luteal cysts is much less accurate (see p. 539); however, such a diagnosis can now be more specific due to the routine use of ultrasound scanning, and can be enhanced via using milk progesterone assays. Selection of cases for treatment has an important influence on the outcome. For example, the corpus luteum early in the cycle is less responsive to PGF2a or an analogue than is the mid-cycle corpus luteum. Accurate assessment of the stage of the cycle will aid in the correct selection of animals for treatment. Similarly, if treatment is confined to cases in which corpora lutea are positively diagnosed, better results may be obtained than if less critical selection of cases is undertaken. However, when PGF2a treatments based on the presence of a corpus luteum were compared with 14-day fixed treatments, the fixed treatments were still superior resulting in better reproductive performance (Heuwieser et al., 1997).

Other factors that influence the success of luteolysis and whether the cow comes in season after successful luteolysis are not well documented. However, it is possible that nutritional factors are involved in the subsequent expression of oestrus.

• •

None of the luteolytic products commercially available achieve 100 per cent luteolysis (Ball & Jackson, 1984; Martinez & Thibier, 1984). Re-examination and retreatment in good time of all cases that do not respond to the initial treatment will affect the time from initial treatment to oestrus, service and conception.

The farmer also affects the outcome of the treatment in important ways.

•

•

•

The efficiency of detection of oestrus in the herd is crucial to the effectiveness of treatment when measured by the number of cases that come into season within a certain number of days. The first-service pregnancy rate in the herd which is to some extent under the control of the farmer, not least because correctly timed insemination is essential for conception, will have a great effect on the success rate as measured in time to conception. High culling rate and willingness to cull may result in apparently good results because the failures are culled, but depending on the economic factors pertaining at the time this may be a false economy (Esslemont & Kossaibati, 1997; Whitaker et al., 2000).

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Heifers Freemartins and cases of bilateral ovarian hypoplasia are sterile and will never cycle or become pregnant. Groups of heifers with delayed puberty due to low energy intake will return to cyclicity after restoration of a suitable energy intake level and other correction of the feeding. How long this will take depends on many things. Under the best possible circumstances, i.e. where the animals are in not excessively poor condition and where there is no complicating disease factor, it will take approximately two months of good feeding before most of the group start cycling (Imakawa et al., 1986). Hormonal treatments to induce and thus advance first ovulation can be used if the management system is seasonally restricted; introduction of a bull may also aid in the induction and synchronization of first ovulation.

True anoestrus after calving in cows In cases of pyometra with a corpus luteum, the failure to cycle is very effectively dealt with by using PGF2a. Ott and Gustafsson (1981) reported that more than 80 per cent of treated cows emptied the uterus and came in season a few days after treatment. If one treatment fails to produce luteolysis, then a second injection almost certainly will be successful. There is evidence to suggest that treatment of pyometra is improved by the administration of two doses of PGF2a, 8 hours apart (Archbald et al., 1993) (see p. 524). Inactive ovaries are treated with either GnRH to cause ovulation and thus a progesterone rise, which then primes the animal to express heat at the next ovulation, or a progesterone or progestagen releasing device. Some indications of the results that can be obtained were shown in a field study involving 62 acyclic cows (Ball & Lamming, 1983). There were two main differences between the two methods. Firstly, ovarian response to the progesterone intravaginal releasing device (PRID) was better, as 89.7 per cent of cows ovulated compared to 73.9 per cent of those treated with GnRH. Secondly, after the PRID, fixedtime insemination resulted in 59 per cent conceptions (measured by milk progesterone) whereas after GnRH, a number of cows that responded successfully were not seen in heat so that only 26 per cent of the cows treated became pregnant at the ovulation after treatment. One problem with GnRH treatment is that the luteal tissue produced has a very variable lifespan with the result that the timing of heat and the next ovulation cannot be predicted and may occur from 8 to about 20 days after treatment. In order to cause more predictable onset of oestrus and next ovulation following GnRH treatment, a luteolytic dose of PGF2a can be given 6–7

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days after GnRH. Such a protocol can be further combined with a second injection of GnRH or an injection of human chorionic gonadotrophin (hCG) 48 hours after PGF2a to time the next ovulation in all animals and use fixed-time insemination (De Rensis & Peters, 1999). Occasionally, cows will come into oestrus quickly after GnRH treatment and this may be due to treating an animal that was just about to start cycling spontaneously. In all reports on treatment of inactive ovaries there are some animals that do not respond to conventional treatment. It is obvious that cows that are still under the influence of the original aetiological factors (such as poor condition) are unlikely to respond well. Similarly, cows in deep anoestrus may not respond satisfactorily to hormonal treatment. It appears that those cows with inactive ovaries, lacking any detectable structures, respond poorly to treatment and may revert to an anoestrous state. In considering the outcome of treatment of cows with cystic ovarian disease associated with anoestrus there are a number of relevant points to note:

•

• •

•

With the important exception of cases seen within six weeks of calving, spontaneous resolution of these cases is not to be relied upon (Garcia & Larsson, 1982). The condition tends to recur unless treatment results in ovulation of a healthy new dominant follicle and conception occurs. To the extent that there is a familial predisposition to cystic ovarian disease, the use of offspring from affected dams for breeding purposes is not advisable. Results have to be looked at in two stages. The first stage is the resolution of the cystic condition and the induction of normal oestrus and ovulation. The second is getting the affected cow pregnant.

Where diagnosis is correct and appropriate treatment is given the return to ovarian normality is good. The majority of luteal cysts respond to PGF2a or an analogue; in one study (Booth, 1988) 79 per cent of cows had low levels of circulating progesterone within 7 days. In the same field trial, 73 per cent of cases with follicular cysts that were treated with GnRH or hCG plus progesterone had functional luteal tissue by 14 days after treatment. The pregnancy rate achieved again depends very much on the ability of the farm staff to detect oestrus and have the cow served at the correct time. This, plus the difficulty in accurate diagnosis of the type of cyst present, means that on many farms an unacceptably high percentage of cows with cystic ovarian disease are eventually culled.

Silent and unobserved oestrus after calving in cows Prognosis for unobserved oestrus is good and pregnancy rate is not greatly different from that for cycling cows in the same herd that have been observed in oestrus. Seguin (1981) compiled results from six trials in which 886 cows were treated; 67 per cent were in oestrus after treatment and pregnancy rate to service at that oestrus was 54 per cent. Seguin (1981) also cited trials in which controls and treated cows had the same pregnancy rate, whereas O’Farrell and Hartigan (1984) obtained a statistically significantly poorer pregnancy rate in the suboestrus cows treated with an analogue of PGF2a than in controls. This latter finding is supported by an analysis of more than 10 000 cases of unobserved oestrus in Israel and 30 000 normal controls (Mayer et al., 1987). First-service pregnancy rate for unobserved oestrus cows was 35.2 per cent compared with 60.3 per cent for the controls. In an interesting study (Ball & Jackson, 1984) in which non-detected oestrus cows were treated with an analogue of PGF2a, and monitored by observation and progesterone assays, 84 per cent of the cows had complete luteolysis after a correctly timed injection. Of all the cows treated 42 per cent were seen in oestrus within 4 days of treatment and 60 per cent within 14 days. One factor that makes prognosis difficult is the effect of the age of the corpus luteum on the response to PGF2a or an analogue. Luteolysis is unlikely to occur in cows treated before day 5 of the cycle and it may be day 7 before maximum effect results. Even when luteolysis occurs, the time from treatment to ovulation varies greatly depending, in a complex manner, on the stage of dominant follicle development when the cow is treated (MacMillan, 1983; Kastelic et al., 1990). If there is a healthy dominant follicle present, oestrus will usually occur on the third day after treatment; should there be no dominant follicle present at the time of PGF2a injection, 5–7 days will pass until induction of oestrus occurs. Prognosis is improved if the veterinarian actively follows up all cases, both those treated and those left untreated, within two weeks.

Long interservice interval Prognosis in these cases is similar to preservice cases, but because of the longer time since calving the urgency to get the cow reserved is greater.

Prevention The economic importance of prevention of anoestrus in all its forms can hardly be overstated. The cost-effective

Problems Associated with Oestrous Cyclicity

application of preventive measures, however, calls for careful consideration, and a balance has to be achieved between undue intervention in cows that would resume normal cycles spontaneously and unnecessary loss of time due to leaving intervention too late. For example, the majority of cows that are not cycling by six weeks after calving will be coming in season by eight weeks, i.e. in time for service within the target period. On the other hand, cows that are left without examination and treatment until the end of the target period for first service, say 11 weeks after calving, will lose a great deal of production time. However, with the increase in milk yield and genetic merit of dairy cows, more prolonged voluntary waiting periods may be economically viable and of benefit to the individual animal.

Heifers Prevention of delay in the onset of puberty depends on good nutrition and the avoidance of diseases that interfere with growth rate (see also Chapter 5). The first step is establishment of clear targets. The farmer should decide at what age, or at what time of the year, the heifers should have their first calves. It is a simple calculation from that target to decide when the service period should start, so that the majority of the heifers calve within the planned period. The exact timing for the start of the service period will depend on how critical both the beginning and the end of the calving period are held to be. If conditions are good, such as a healthy, fertile young bull running with well-grown, healthy, cycling heifers, more than 80 per cent of heifers should be in calf after six weeks of the service period and practically all by nine weeks. To ensure that the majority of the heifers are cycling at the beginning of the service period it is necessary to aim for a growth rate that achieves the appropriate body weight, taking account of the breed involved. Puberty occurs around 280 kg in large Holsteins and Holstein/Friesians, around 260 kg for Friesians and around 230 kg for Jersey heifers; these weights equate to approximately 40–45 per cent of the expected adult weight. A rough rule-of-thumb for the rearing of heifers to calve at 2 years of age is to aim for prepubertal growth rates in g/day that equal the adult body weight in kg. For example, if the expected adult weight is 650 kg, rear at a rate of 650 g/day. Target growth rates and the key target weights for dairy heifers in the UK are given in Chapter 5. The veterinarian has a number of roles to play. Initially, it is necessary to make the farmer aware of the need to plan for a specific calving season or age and what this implies in terms of growth rates. Thereafter, the job is mainly to give advice and to make sure that the client monitors the growth rate of the heifers

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and onset of puberty. The farmer should consult the veterinarian at an early stage if it looks as though not enough animals are starting to cycle at the expected time, and hormonal treatments to induce first ovulation and synchronize oestrus and ovulation in a group of heifers may be considered. Avoidance of disease conditions that will interfere with growth is also the veterinarian’s responsibility and is described elsewhere in this book. This should not only assist the attainment of the target for age at puberty but should also help to reduce the high mortality rate that occurs between birth and puberty. Most farmers are aware that female calves born twin to a bull calf are very likely to be sterile freemartins. Few realize that measurement of the vagina in the very young calf and comparison with a normal calf can be used to decide if a suspect calf is a freemartin. Alternatively, in valuable animals blood sampling both twins for karyotyping will usually clarify the issue and allow early culling if desired. However, this procedure is too expensive for use in most commercial cattle.

Prevention of anoestrus in adult cows after calving The foundations for early return to normal cyclicity and getting cows served are listed in Box 35.11. All these factors are very much under the farmer’s control, although the veterinarian has an important part to play in ensuring that the husbandry is up to standard, that intervention, if required, at and after calving is timely and appropriate and that cyclicity is monitored and aberrations are treated.

• •

Prevention of dystokia and postpartum abnormalities is a basic requirement for optimal cyclicity and fertility and has been discussed on p. 526. Routine veterinary postpartum examination and treatment can effectively limit the adverse effect of abnormalities around calving and delayed involution. It is essential to examine all cows that experienced dystokia or postpartum problems by not later than 28 days after calving. Many veterinary practitioners incorporate routine examination of all cows two to four weeks after calving, as this allows them to deal with problems early (see also Chapter 34).

Box 35.11 Factors likely to prevent postpartum anoestrus.

• • • • •

Appropriate body condition and nutrition in the dry period Normal calving Disease-free puerperium, or adequate rapid treatment of diseases in the puerperium Suitable transition period feeding and regular checking of body condition score postpartum Efficient oestrous detection

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Table 35.4 Effect of various treatments on interval from calving to first service. Calving – service interval (days)

Reference

PGF2a

GnRH

Both

None

– – – – 92 61 73 81/51

81 88/89 72/74 – 108 67 – –

– – – 61 85 64 – –

77 83 73 63 84 58 69 91/58

There is an attractive concept that by routinely administering PGF2a or an analogue, GnRH or both in the early postpartum period it is possible to improve return to cyclicity and pregnancy rate. It is clear that GnRH given before day 20 after calving will initiate early cycles and PGF2a or an analogue given a little later increases the number of cycles in the first six weeks after calving (Benmrad & Stevenson, 1986). The effect of these treatments on overall fertility is less well defined; Table 35.4 shows results obtained in several field trials. Meta-analysis of data from 4052 cows in 24 trials published in 10 papers looking at the effect of injecting PGF2a in dairy cattle within 40 days of calving on the rate of pregnancy at first service and the number of days open came to the following conclusions. Treatment with PGF2a during this early postpartum period had no effect on the first service pregnancy rate of cows with a normal or abnormal puerperium. An analysis of those data for the number of days open showed that a significant percentage (54 per cent) of the treated cows had fewer days open than the untreated cows, and that this difference tended to be greater for cows with an abnormal puerperium. The weighted average reduction in days open between treated and control cows was 2.6 days for trials with abnormal cows and 3.3 days for trials including normal and abnormal cows (Burton & Lean, 1995). This effect is probably largely due to improvements in the submission rate; it is questionable whether any improvement in calving-to-first-service and calvingto-conception interval justifies the treatment costs and the cost of the extra semen that would be used if PGF2a were administered routinely to postpartum cows. Thus the routine administration of PGF2a (or other hormone preparations) to cattle without a specific therapeutic indication probably cannot be justified. In addition to the routine application of these treatments to normal cows not conferring any benefit in

Langley & O’Farrell (1979) Nash et al. (1980) Nash et al. (1980) Richardson et al. (1983) Etherington et al. (1984) Benmrad & Stevenson (1986) Young & Anderson (1986) Schofield et al. (1999)

terms of reproductive efficiency, there is the danger that induction of a corpus luteum with GnRH in a cow that still has an infected uterus after calving can lead to pyometra. Selected treatment of cows with uterine or ovarian pathology is on the other hand entirely justified.

•

Nutrition. For normal reproductive function it is vitally important that nutritional levels before and after calving are correct. It has been suggested that condition score at calving should not exceed 3.0 and 2.5–3.0 should be the target at service.

Oestrous detection Once the foundation for good fertility has been established it is essential to ensure that oestrous detection is as good as humanly possible. Before discussing how oestrous detection can be improved it is worth asking the question: why is oestrous detection inefficient? After all, many stockworkers who carry out this task have worked with cows for years and know the signs of oestrus well. However, in a recent study of stockworker’s attitudes, oestrous detection was recognized as being an important task, but was generally a task that was disliked (Seabrook & Wilkinson, 2000). This may be because it is time consuming and often requires the stockman to spend time watching cows at antisocial hours. The decreasing availability of labour on farms is resulting in reduced labour hours per cow per year and overworked staff often do not have the necessary time to dedicate to oestrous detection. Good oestrous detection requires regrouping and possibly moving animals as well as accurate observation and recording of behavioural events several times a day over months on end and is therefore a very demanding task. It is made more difficult because of the short dura-

Problems Associated with Oestrous Cyclicity

tion of oestrus exhibited by many cows, the time of the night or day when oestrus occurs, the weak and indefinite nature of signs shown by some cows when in season and the fact that some animals not in season exhibit some of the signs of oestrus. Veterinarians who wish to educate dairy workers on heat detection would be well advised to attempt to carry out heat detection themselves, so that they may understand the practical difficulties. If oestrous detection is not a priority for staff and is impossible to organize even with the assistance of oestrous detection aids, then the use of hormonal treatments to synchronize oestrus and ovulation should be contemplated and discussed (see p. 678). This will reduce oestrous detection periods to very specific times, or allow the use of fixed-time artificial insemination with no heat detection. However, pregnancy rates to single fixed-time insemination may be low, and this will also have to be discussed with the client. The details of the various oestrous synchronization regimens for cattle are discussed elsewhere in this book (see p. 684). The stockworker’s dilemma occurs when a cow exhibits signs of oestrus just short of actually standing to be ridden and the decision is taken to have the cow inseminated. If the cow is not in season this decision is criticised. However, if the cow is not inseminated, a cow in season may have been missed. In a large herd these critical decisions have to be made many times a year. Good heat detection is based on the following facts.

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• • • •

•

• •

The definitive sign of oestrus is standing freely to be ridden. It has been proposed that a cow that mounts onto another cow’s head is in pro-oestrus. Cows in oestrus, of course, also mount other cows. There may be an interval of as much as 30 minutes between bouts of riding. Oestrus rarely lasts for more than 18 hours and in many cases lasts for less than 6 hours. Oestrus often starts during the night. Oestrous expression is greatest during quiet times of the cow’s day and night. This means oestrus is seen less often around milking times and when cows are fed. As well as a willingness to stand on the part of the cow in oestrus, it is necessary to have a cow that wants to and can mount as discussed above (see aetiology, p. 532). This can cause particular problems when most cows in the herd are pregnant. When cows are loose housed there is often a particular area that cows prefer to use for oestrous expression. Stalled cows may have reduced physical expression of oestrus (Claus et al., 1983).

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A rational system of oestrous detection should be based on these facts and the following points are required for a good heat detection system: (1)

(2)

(3)

The cows should be observed three times per day for 30 minutes each time. The periods of observation should be when the herd is peaceful after milking and feeding. Often these times are: (a) briefly before collecting the cows for morning milking; (b) in mid-morning; (c) before the evening milking; and (d) late in the evening, a very good time for detection of oestrus. The housing conditions must be suitable for cows and observer. Good non-slippery floors on which the cows feel secure are essential. The observer must be able to see all the cows clearly, should be comfortable and should have a paper and pen to write down details of the cows’ behaviour. Good lighting is required. The cows must be clearly identifiable from a distance.

There are many aids to oestrous detection; however, there is at present no one substitute for close observation of the cows’ behaviour (review by Boyd, 1984; Stevenson, 2001). Aids to heat detection either detect unobserved standing to be ridden or depend on the fact that cows in oestrus are likely to behave in ways that, although not unique to oestrus, occur with greater frequency during oestrus. Increased frequency of bellowing, increased restlessness, reduced milk yield, change in routine behaviour such as order of coming into the milking parlour for milking, and increased body temperature are non-specific, oestrus-related events. There are also a number of physical changes in the genitalia related to oestrus that can be measured, such as change in electrical resistance and viscosity of the vaginal mucus. Marking systems fixed on the cow’s pelvic region to detect standing to be ridden when the cows are not being observed can be valuable in suitable circumstances. Examples are tail paint, tail flags and detectors that contain dye that is squeezed out under sustained pressure from another cow. All of these suffer from the defect that rubbing or pressure that is not caused by the cow standing freely to be ridden may trigger them. Television cameras with video recording have also been used to observe cows continuously and can be viewed later, at increased speed. There are problems of identity (very big numbers on shoulders and rumps are needed) and replaying the recordings is a tedious chore. Milk progesterone assays, which can be used either as an aid to or as a replacement for oestrous detection, are discussed later (see p. 548).

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Pedometers that automatically monitor and record the cow’s level of activity can also be used to detect behavioural changes that are consistent with oestrus in some management systems. It is probable that in future sophisticated decision support software integrated into computerized milking parlour systems will be developed to detect cows likely to be in oestrus and automatically shed them from the main herd for the attention of the stockman. These decision support tools will use various data automatically generated from a number of sources such as pedometers, milk yield, milk temperature, order of milking and milking frequency (fully automated milking systems only), and data detected by integrated biosensors such as in-line milk progesterone assays and assays of other milk constituents. Cows will be identified by implanted microchips. These may also advance beyond the current static data-specific microchip that simply holds the data it was implanted containing, to a new generation of smart chips that record the animal’s health and disease history along with other information such as its movement history. It may even be possible in future to develop integrated implanted biosensors that analyse and record the animal’s physiological state, including data related to reproduction.

Anoestrus after service In the majority of cases, delayed return to service is due to unobserved oestrus, as has been shown in the reduction in the number of long return-to-service intervals when oestrous detection is improved. One problem, in a case where the return-to-service heat signs are not clear, is that the result of inseminating by AI a cow that has been served, and could be pregnant, may be loss of the conceptus. Improved efficiency by the use of aids for heat detection is particularly useful in these cases because the service date can be taken as the start of the oestrous cycle. Clearly, in those cases where insemination takes place in the luteal phase this starting point is erroneous, a fact that will become clear to the stockworker as heat detection aids and substitutes are used. Use of a three-week calendar and the application of a marker such as tail paint shortly before expected return to service can help efficiency of observation. Systematic use of milk progesterone assays at about the expected time of return to service can help in overcoming problems of long interservice intervals. High progesterone followed by two successive days of low progesterone is an indication that service should be carried out on the next day. Eddy and Clark (1987) demonstrated, in four large dairy herds, that the efficiency of heat detection after service could be improved greatly by the use of milk progesterone assays. The pre-

ferred sampling regimen was every second day from days 18 to 24 after service. The financial benefit to cost ratio was 7.5:1. Some veterinarians report improvements based on a single progesterone assay on day 19 after service. For good results it is necessary for the stock personnel to understand the test and to be willing to carry out the extra work carefully and conscientiously. Very poor pregnancy rates have been reported to result if progesterone assays are used as the only basis for insemination without the active incorporation of oestrus detection (Foulkes & Goodey, 1988). However, the use of milk progesterone assays to confirm that cows are in oestrus before inseminating them can improve pregnancy rates and reduce the number of mis-timed inseminations (McLeod et al., 1991; Watson, 1996). Strategic milk progesterone monitoring as a diagnostic and management tool in dairy cattle is discussed by Darwash and Lamming (1997). Under experimental conditions milk progesterone monitoring has also been used in suckler cow fertility investigation and management (Mann et al., 1998); however, logistical problems will almost certainly prevent widespread use of this technology in the field. Resynchronization of repeats following an initial synchronizing treatment using a progesterone device is used successfully in New Zealand and other locations where the breeding period needs to be kept short; used progesterone devices are re-inserted on day 16 to days 21 or 22 following first service, and return oestrus detected on days 23 or 24 (Van Cleeff et al., 1996; McDougall, 2001). This increases submission rates in the first three weeks of the breeding season and focuses heat detection periods to a specific time following first service. A similar regimen has been successfully used in the UK in beef suckler herds (Penny et al., 2000).

Acknowledgement The ultrasound images were produced at the University of Glasgow Veterinary School using digital acquisitions from Toshiba Medical Systems.

References Anon. (1984) Dairy Herd Fertility. Ministry of Agriculture, Fisheries and Food, Reference Book 259, pp. 1–80. HMSO, London. Archbald, L.F., Risco, C., Chavatte, P., Constant, S., Tran, T., Klapstein, E. & Elliot, J. (1993) Estrus and pregnancy rate of dairy cows given one or two doses of prostaglandin F2 alpha 8 or 24 hours apart. Theriogenology, 40, 873– 84. Ball, P.J.H. & Jackson, P.S. (1984) The use of milk progesterone profiles for assessing the response to cloprostenol treatment

Problems Associated with Oestrous Cyclicity

of non-detected oestrus in dairy cattle. British Veterinary Journal, 140, 543–9. Ball, P.J.H. & Lamming, G.E. (1983) Diagnosis of ovarian acyclicity in lactating dairy cows and evaluation of treatment with gonadotrophin-releasing hormone or a progesterone releasing intravaginal device. British Veterinary Journal, 139, 522–7. Barrett, D.C. (2001) Cattle Fertility Management in the UK. Cattle Practice, 9, 59–68. Beam, S.W. & Butler, W.R. (1997) Energy balance and ovarian follicle development prior to the first ovulation postpartum in dairy cows receiving three levels of dietary fat. Biology of Reproduction, 56, 133–42. Benmrad, M. & Stevenson, J.S. (1986) Gonadotrophinreleasing hormone and prostaglandin F2a for postpartum dairy cows: estrous, ovulation and fertility traits. Journal of Dairy Science, 69, 800–11. Bloomfield, G.A., Morant, S.V. & Ducker, M.I. (1986) A survey of reproductive performance in dairy herds. Characteristics of the patterns of progesterone concentrations in milk. Animal Production, 42, 1–10. Booth, J.M. (1988) The milk progesterone test as an aid to diagnosis of cystic ovaries in dairy cows. Veterinary Record, 123, 437–9. Boyd, H. (1984) Aids to oestrus detection – a review. In Dairy Cow Fertility (ed. by R.G. Eddy & M.J. Ducker), pp. 60–7. British Veterinary Association, London. Boyd, H. & Munro, C.D. (1980) Experience and results of a herd health programme – rectal palpation and progesterone assays in fertility control. In IX International Congress on Animal Reproduction and AI, Vol. 2, pp. 373–80. Boyd, H. & Reed, H.C.B. (1961) Investigations into the incidence and causes of infertility in dairy cattle. Fertility variations. British Veterinary Journal, 117, 18–35. Boyd, J.S. & Omran, S.N. (1991) Diagnostic ultrasonography of the bovine female reproductive tract. In Practice, 3, 109–18. Britt, J.H. (1987) Detection of oestrus in cattle. Veterinary Annual, 27, 74–80. Britt, J.H. (1995) Relationship between postpartum nutrition, weight loss and fertility. Cattle Practice, 3, 79–83. Brown, J.L., Schoenemann, H.M. & Reeves, J.J. (1986) Effect of FSH treatment on LH and FSH receptors in chronic cysticovarian-diseased dairy cows. Journal of Animal Science, 62, 1063–71. Bulman, D.C. & Lamming, G.E. (1978) Milk progesterone levels in relation to conception, repeat breeding and factors influencing acyclicity in dairy cows. Journal of Reproduction and Fertility, 54, 447–58. Burton, N.R. & Lean, I.J. (1995) Investigation by metaanalysis of the effect of prostaglandin F2a administered post partum on the reproductive performance of dairy cattle. Veterinary Record, 136, 90–4. Butler, W.R. (1999) Nutritional effects on resumption of cyclicity and on conception rate. Fertility in the HighProducing Dairy Cow, BSAS Occasional Meeting, Galway, Ireland, September 1999, pp. 13–14. Canfield, R.W. & Butler, W.R. (1990) Energy balance and pulsatile LH secretion in early postpartum dairy cattle. Domestic Animal Endocrinology, 7, 323–30.

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Claus, R., Karg, H., Zwiauer, D., von Butler, L, Pirchner, F. & Rattenberger, E. (1983) Analysis of factors influencing reproductive performance of the dairy cow by progesterone assay in milk fat. British Veterinary Journal, 139, 29–37. Cook, D.L., Smith, C.A., Parfet, J.R., Youngquist, R.S., Brown, E.M. & Garverick, H.A. (1990) Fate and turnover rate of ovarian follicular cysts in dairy cattle. Journal of Reproduction and Fertility, 90, 37–46. Darwash, A.O. & Lamming, G.E. (1997) Strategic milk progesterone monitoring. Cattle Practice, 5, 353–5. Dawson, F.L.M. (1975) Accuracy of rectal palpation in the diagnosis of ovarian function in the cow. Veterinary Record, 96, 218–20. De Rensis F. & Peters A.R. (1999) The control of follicular dynamics by PGF2a, GnRH, hCG and oestrus synchronization in cattle. Reproduction in Domestic Animals, 34, 49–59. Dijkhuizen, A.A., Huirne, R.B.M., Jalvingh, A.W. & Stelwagen, J. (1997) Economic impact of common health and fertility problems. In Animal Health Economics – Principles and Applications. (ed. by A.A Dijkhuizen & R.S. Morris) pp. 41–58. Post Graduate Foundation in Veterinary Science, University of Sydney. Dobson, H., Douthwaite, R., Nobel, K.M., O’Donnell, M.J., Ribadu, A.Y., Tebble, J.E. & Ward, W.R. (2001a) Cystic ovaries in cattle. Cattle Practice, 9, 185–9. Dobson, H., Tebble, J.E., Smith, R.F. & Ward, W.R. (2001b) Is stress really all that important? Theriogenology, 55, 65–73. Douthwaite, R. & Dobson, H. (2000) Comparison of different methods of diagnosis of cystic ovarian disease in cattle and an assessment of its treatment with a progesteronereleasing intravaginal device. Veterinary Record, 147, 355–9. Eddy, R.G. & Clark, P.L (1987) Oestrus prediction in dairy cows using an ELISA progesterone test. Veterinary Record, 120, 31–4. Esslemont, R.J., Bailie, J.H. & Cooper, M.J. (1985) Fertility Management in Dairy Cattle, pp. 1–143. Collins, London. Esslemont, R.J. & Kossaibati, M.A. (1997) Culling in 50 dairy herds in England. Veterinary Record, 140, 36–9. Etherington, W.G., Bosu, W.T.K., Martin, S.W., Cote, J.F., Doig, P.A. & Leslie, K.E. (1984) Reproductive performance in dairy cows following postpartum treatment with gonadotrophin releasing hormone and/or prostaglandin: a field trial. Canadian Journal of Comparative Medicine, 48, 245–50. Fishwick, J.C. (1993) An assessment of the accuracy of manual rectal palpation as compared with ultrasound imaging of the genital system, milk and plasma progesterone concentrations, and the response to therapy in cows not observed in oestrus. RCVS Diploma in Cattle Health and Production Dissertation, pp. 1–47. Royal College of Veterinary Surgeons Library, London. Foulkes, L.A. & Goodey, R.G. (1988) Fertility of Friesian cows on the second, third and fourth days of low milk progesterone concentration. Veterinary Record, 122, 135. Fourichon, C., Seegers, H. & Malher, X. (2000) Effect of disease on reproduction in the dairy cow: a meta-analysis. Theriogenology, 53, 1729–59. Garcia, M. & Larsson, K. (1982) Clinical findings in post partum dairy cows. Nordisk Veterinaer Medicin, 34, 255– 63.

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Moller, K., Lapwood, K.R. & Marchant, R.M. (1986) Prolonged service intervals in cattle. New Zealand Veterinary Journal, 34, 128–32. Mottram, T. (1997) Automatic monitoring of the health and metabolic status of dairy cows. Livestock Production Science, 48, 209–17. Nash, J.G., Ball, L. & Olson, J.D. (1980) Effects on reproductive performance of administration of GnRH to early postpartum dairy cows. Journal of Animal Science, 50, 1017–21. O’Callaghan, D. & Boland, M.P. (1999) Nutritional effects on ovulation, embryo development and the establishment of pregnancy in ruminants. Animal Science, 68, 299–314. O’Callaghan, D., Lozanot, J.M., Fahey, J., Gath, V., Snijders, S. & Boland, M.P. (2000) Recent developments in the effect of nutrition on fertility in dairy cows. Irish Veterinary Journal, 53, 417–25. O’Farrell, K.J. & Hartigan, P.L (1984) The treatment of nondetected oestrus (NDO) in dairy cows with cloprostenol. Irish Veterinary Journal, 38, 23–8. Omran, S.N., Ayliffe, T.R. & Boyd, J.S. (1988) Preliminary observations of bovine ovarian structures using B-mode real time ultrasound. Veterinary Record, 122, 465–6. Opsomer G., Mijten P., Coryn M. & de Kruif A. (1996) Postpartum anoestrus in dairy cows: a review. Veterinary Quarterly, 18, 68–75. Ott, R.S., Breulaff, K.N. & Hixon, J.E. (1986) Comparison of palpable corpora lutea with serum progesterone concentrations in cows. Journal of the American Veterinary Medical Association, 188, 1417–19. Ott, R.S. & Gustaffson, B.K. (1981) Therapeutic application of prostaglandins for post partum infections. Acta Veterinaria Scandinavica (Suppl.), 77, 363–90. Penny C.D., Lowman, B.G., Scott, N.A. & Scott, P.R. (2000) Repeated oestrus synchronisation of beef cows with progesterone implants and the effects of a gonadotrophinreleasing hormone agonist at implant insertion. Veterinary Record, 146, 395–8. Pieterse, M.C., Taverne, M.A.M., Kruip, T.A.M. & Willemse, A.H. (1990) Detection of corpora lutea and follicles in cows: a comparison of transvaginal ultrasonography and rectal palpation. Veterinary Record, 126, 552–4. Richardson, G.F., Archbald, L.F., Galton, D.M. & Godke, R.A. (1983) Effect of gonadotropin-releasing hormone and prostaglandin F2a on reproduction in postpartum dairy cows. Theriogenology, 19, 763–70. Royal, M.D., Darwash,A.O., Flint,A.P.F.,Webb, R.,Woolliams, J.A. & Lamming, G.E. (2000) Declining fertility in dairy cattle: changes in traditional and endocrine parameters of fertility. Animal Science, 70, 487–501. Rukkwamsuk, T., Kruip, T.A.M. & Wensing, T. (1999) Relationship between overfeeding and overconditioning in the dry period and the problems of high producing dairy cows during the postparturient period. The Veterinary Quarterly, 21, 71–7. Saloniemi, H., Groelm, Y. & Syvaejaervi, J. (1986) An epidemiological and genetic study on registered diseases in Finnish Ayrshire cattle. II. Reproductive disorders. Acta Veterinaria Scandinavica, 27, 196–208. Savio, J.D., Boland, M.P., Hynes, N. & Roche J.F. (1990) Resumption of follicular activity in the early post-partum

Problems Associated with Oestrous Cyclicity

period of dairy cows. Journal of Reproduction and Fertility, 88, 569–79. Schofield, S.A., Kitwood, S.E. & Phillips, C.J.C. (1999) The effects of a post partum injection of prostaglandin F2a on return to oestrus and pregnancy rate in dairy cows. Veterinary Journal, 157, 172–7. Scully, A., Hunter, M., Gregson, K., Lamming, G.E. & Darwash, A.O. (2000) The use of on-farm software for automatic interpretation of milk progesterone data: an aid to dairy fertility management. Cattle Practice, 8, 407–10. Seabrook, M.F. & Wilkinson, J.M. (2000) Stockpersons’ attitudes to the husbandry of dairy cows. Veterinary Record, 147, 157–60. Seguin, B.E. (1981) Use of prostaglandins in cows with unobserved oestrus. Acta Veterinaria Scandinavica (Suppl.), 77, 343–53. Stagg, K., Diskin, M.G., Sreenan, J.M. & Roche, J.F. (1995) Follicular development in long-term anoestrous suckler beef cows fed 2 levels of energy postpartum. Animal Reproduction Science, 38, 49–61. Stagg, K., Spicer, L.J., Sreenan, J.M., Roche, J.F. & Diskin, M.G. (1998) Effect of calf isolation on follicular wave dynamics, gonadotropin and metabolic hormone changes, and interval to first ovulation in beef cows fed either of two energy levels postpartum. Biology of Reproduction, 59, 777–83. Stevenson J.S. (2001) A review of oestrous behaviour and detection in dairy cows. In Fertility in the High Producing Dairy Cow. Occasional Publication No. 26, pp. 43–62. British Society of Animal Science London. Taylor, V.J., Beever, D.E. & Wathes, D.C. (2001) Plasma IGF1 levels in relation to ovarian function in high producing dairy cows. Cattle Practice, 9, 197–201. Tebble, J.E., O’Donnell, M.J. & Dobson, H. (2001) Ultrasound diagnosis and treatment outcome of cystic ovaries in cattle. Veterinary Record, 148, 411–13. Van Cleeff, J., Macmillan, K.L., Drost, M., Lucy, M.C. & Thatcher, W.W. (1996) Effects of administering proges-

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terone at selected intervals after insemination of synchronized heifers on pregnancy rates and resynchronization of returns to service. Theriogenology, 46, 1117–30. Waldmann, A., Ropstad, E., Landsverk, K., Sørensen, K., Sølverød, L. & Dahl, E. (1999) Level and distribution of progesterone in bovine milk in relation to storage in the mammary gland. Animal Reproduction Science, 56, 79–91. Warren, M.E. (1984) Biological targets for fertility and their effects on herd economics. In Dairy Cow Fertility (ed. by R.G. Eddy & M.J. Ducker), British Veterinary Association, London. pp. 1–14. Wathes, D.C., Robinson, R.S., Pushpakumara, A., Cheng, Z. & Abayasekara, D.R.E. (1998) Nutritional effects on reproductive performance in dairy cows. Cattle Practice, 6, 371–7. Watson, C.L. (1996) Milk progesterone analysis – an underused asset in fertility control of the dairy cow. Cattle Practice, 4, 277–80. Webb, R., Garnsworthy, P.C., Gong, J.G., Gutierrez, C.G., Logue, D., Crawshaw, W.M. & Robinson, J.J. (1997) Nutritional influence on subfertility in cattle. Cattle Practice, 5, 361–7. Webb, R., Royal, M.D., Gong, J.G. & Garnsworthy, P.C. (1999) The influence of nutrition on fertility. Cattle Practice, 7, 227–34. Whitaker, D.A., Kelly, J.M. & Smith, S. (2000) Disposal and disease rates in 340 British dairy herds. Veterinary Record, 146, 363–7. Williamson, N.B., Morris, R.S., Blood, D.C. & Cannon, C.M. (1972) A study of oestrous behaviour and oestrus detection methods in a large commercial dairy herd. 1. The relative efficiency of methods of oestrus detection. Veterinary Record, 91, 50–8. Young, I.M. (1989) Dinoprost 14-day oestrus synchronisation schedule for dairy cows. Veterinary Record, 124, 587–8. Young, I.M. & Anderson, D.B. (1986) First service conception rate in dairy cows treated with dinoprost tromethamine early post partum. Veterinary Record, 118, 212–13.

Chapter 36

Failure to Conceive and Embryonic Loss D.C. Barrett, H. Boyd and M. Mihm Manifestation Aetiology Stage 1 Failure of ovulation after oestrus Stage 2 Fertilization failure Stage 3 Embryonic death Stage of failure not known Diagnosis Treatment Prognosis Prevention

552 554 554 557 559 562 563 566 569 572

Manifestation Return to service or detection of non-pregnancy up to six weeks after insemination/natural service are the ways in which poor pregnancy rate due to failure to conceive and embryonic losses are presented. This can have a major economic impact in any herd, but is particularly noticeable where a tight seasonal calving pattern is sought.

Interservice intervals The interval in days that has elapsed between the unsuccessful service and the next oestrus is part of the manifestation of the condition of return to service. The concept of normal and abnormal interservice intervals has been discussed in connection with postservice anoestrus (see p. 531). While the distribution of interservice intervals varies greatly between herds, reflecting in part the management efficiency in the herd, in many cattle populations fewer than 50 per cent have a normal interservice interval of 18–24 days.

Observable abnormality Another manifestation of return to service is the normality or otherwise of the cow at the return oestrus. The farmer can observe certain deviations from normality in these cows, in particular the presence of a purulent discharge from the vulva. The farmer may also report aberrant sexual behaviour. In relevant cases, the observant client may notice some of the changes associated with chronic cystic ovarian disease, such as slackening 552

of the pelvic ligaments and voice change. In general, however, the cow that returns to service presents an apparently normal oestrus as regards both behaviour and visible signs. The way in which the client presents return to service cases affects the clinician’s response to the problem. It is presented either as an individual cow problem or as a herd (or group) problem, and it is presented with or without evidence of past or present pathology.

Individual cows Individual cases are presented in two quite different ways, which influence how they are dealt with. In the first way, some cows are presented to the veterinarian that have been served two or three times and are still not pregnant. To understand these cases properly they have to be considered within the context of the entire population of cows and heifers in the herd. In any group of apparently normal cows served correctly by a fertile bull or inseminated properly with good semen, either for the first time after calving or at a repeat service, a considerable number will return to service depending on first-, second- and third-service pregnancy rates in each particular herd. Most of these animals are only temporarily infertile and the majority will become pregnant within an acceptable time. Although there is some understanding of the stage at which these losses occur, i.e. whether there is fertilization failure or early embryonic death, the aetiology is known to only a limited extent. For this reason these returns appear to happen at random. Field studies show that about 12 per cent of cows are still not pregnant after three services as is demonstrated in Table 36.1, which is taken from a population of 5744 cows with a first insemination pregnancy rate of 60.6 per cent (Boyd & Reed, 1961a). ‘Actual results’ are compared with the ‘expected results’ that would have occurred if all subsequent inseminations had had a pregnancy rate of 60.6 per cent. However, in recent years a drop in pregnancy rates of approximately one per cent per annum has occurred in high-genetic-merit dairy cattle populations (Royal et al., 2000; Barrett, 2001). This has resulted in expected pregnancy rates of

Failure to Conceive and Embryonic Loss

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Table 36.1 The percentage of cows that required various numbers of inseminations for pregnancy with a first insemination pregnancy rate of 60.6 per cent. Number of inseminations required for pregnancy 1 2 3 >3 or culled

Actual results

Expected results

Percentage

Cumulative percentage

Percentage

Cumulative percentage

60.6 20.4 7.2 11.8

60.6 81.0 88.2 100.0

60.6 23.9 9.4 6.1

60.6 84.5 93.9 100.0

50 per cent or less to a single service, thus increasing the proportion of animals within a herd not pregnant after three services. Farmers often wait until a cow has had three unsuccessful services before presenting her to the veterinarian and Table 36.1 shows that (with certain reservations) about half of these cows, 6.1% versus 11.8%, are not pregnant because of the same (unknown) factors that establish the level of the first insemination pregnancy rate. It is therefore to be expected that half of these cows will not exhibit any diagnosable cause of return to service and that their expectation of pregnancy at the next service is about the same as that for first insemination. However, pregnancy rates to three or more services are usually reduced due to an accumulation of animals with reproductive problems. Warren (1984) cited published data from four different cattle populations in which pregnancy rates to first service ranged from 47–57%. Within these populations, however, the herd pregnancy rates would vary widely. In the second instance, other cases, for which the term ‘chronic repeat breeder’ might be used, are presented because they have returned to service repeatedly over a long period of time. These cases have been differentiated into apparently normal repeat breeders and those with abnormalities on the basis of cycle length, sexual behaviour and detectable abnormality, a differentiation of limited clinical value. These chronic repeat breeders require a different approach from the cases discussed above because they are generally cows that the owners regard as particularly valuable and therefore the clinician can devote more time and money to their diagnosis and treatment. The prognosis in chronic repeat breeders is inevitably poor because they have been given so many opportunities to become pregnant without success. It is animals of this type that may be hospitalized in teaching and research institutions where they are given expensive diagnostic and therapeutic treatment, although this is becoming more and more uneconomic within the UK.

There is no realistic incidence figure for chronic repeat breeders because their retention in the breeding herd is dependent on extraneous factors but clearly is unlikely to be more than 6 per cent of the breeding population, although it may be higher in individual herds. The number in any given herd will be determined by various economic factors which dictate at what point it becomes more economic to cull a cow and replace her rather than persist in attempting to get her in calf. Overall culling rates in UK dairy herds are about 20–25 per cent per annum (Esslemont & Kossaibati, 1997; Whitaker et al., 2000). Poor fertility is the single most important reason for involuntary culling. With 30–40 per cent of cull cows being culled for infertility, this represents almost 10 per cent of dairy cows calving each year (Kossaibati & Esslemont, 1995). The exact cost to the farmer of an involuntary cull will vary from farm to farm and from time to time, depending on the cost of a replacement, the value of a cull cow, the milk price and availability (and cost) of milk quota, loss of genetic merit and many other factors. For this reason it is impossible to give an exact cost here, but on a typical commercial dairy farm it is probably between £600 and £800 per cull cow at the present time (2003).

Herd or group problems Return to service may affect many animals in the herd in which case the client is very worried about the extent of the problem and the serious effect it will have on production and profits. For an assessment of the condition it is necessary to analyse the breeding records to determine pregnancy rates to first, second and further inseminations (or other measure of the success rate of services) and interservice intervals (see also Chapter 41(b)). The range of incidence of return to service is very wide. In a population of herds with any given mean herd pregnancy rate there is a tendency for the herd averages to be distributed at random round this mean, as demonstrated in Table 36.2. Just over 40 years ago,

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Table 36.2 Distribution (%) of herd average first insemination pregnancy rates in 191 dairy herds (Boyd & Reed, 1961a). Herd first insemination pregnancy rate (herd average)

Total

80 5.2%

31–40 3.7%

41–50 16.2%

51–60 25.1%

the overall herd first insemination pregnancy rate in 191 herds was 59.9 per cent (Boyd & Reed, 1961a). Although not demonstrated here, it is usual for the distribution to be skewed towards the lower end of the scale. The skewed distribution of these data tends to be seen in all studies, however in more recent surveys the first insemination pregnancy rates are lower than those reported by Boyd and Reed (1961a). For example, the mean first service pregnancy rate in 90 herds in the UK was reported as 47.3 per cent in the 1992/1993 calving season (Kossaibati & Esslemont, 1995). National Milk Records (NMR) data from approximately one million dairy cattle in 9000 herds showed that the pregnancy rate to first service (based on available pregnancy diagnosis data and non-return rates at 48 days) was 52.5 per cent in September 2000 (Barrett, 2001). This will be an overestimate of the true pregnancy rate as a proportion of the data are based on non-return rates which will include some cows culled that were not rebred after failing to conceive. Royal et al. (2000) reported that 265 first services out of 667 resulted in pregnancy in their study of Holstein Friesian dairy cows between October 1995 and June 1998. This equates to a first service pregnancy rate of 39.7 per cent. Given these recent data it seems reasonable to accept a target first service pregnancy rate of 50 per cent in modern dairy herds, while accepting that in some high yielding herds this may be difficult to achieve. It is helpful to think of the pregnancy rate for any individual herd as dependent on the combined effects of the following factors:

• •

•

The random variation around the mean of the population of herds. The background effect, which is dependent on management and environmental factors that are liable to be constant over a long period. Examples, any of which individually would tend to result in low herd pregnancy rates, are inaccurate oestrous detection, unsatisfactory feeding, a high incidence of endometritis (see p. 521) or poor semen handling and insemination techniques (see Chapter 39). Specific pathogenic causes, such as a subfertile bull or venereal diseases such as campylobacteriosis, or other infectious conditions known to affect fertility

61–70 27.2%

71–80 19.4%

99.9%

Box 36.1 Reasons for unsuccessful services. Stage 1 Stage 2 Stage 3

Ovulation failure Fertilization failure Loss of the conceptus, due to early (3 week return intervals) or late embryonic death (3–6 week return intervals) or fetal death (>6 week return intervals) Stage of failure unknown

•

such as bovine virus diarrhoea virus infection (see p. 578) or leptospirosis (see pp. 580, 735). The incidence of chronic repeat breeders, which to some extent relates to the background effect.

Aetiology There are three main stages at which failure to achieve or maintain a pregnancy can occur. Although it is often not possible to assign an individual case to one of these stages this knowledge is useful in understanding the aetiology of return to service. The stages are shown in Box 36.1.

Stage 1 Failure of ovulation after oestrus The most important condition in which there is oestrus without ovulation is cystic ovarian disease. It is important to define ‘cystic ovarian disease’ because not all cases of ovarian cysts are pathological (see Box 36.2). This traditional definition implied that cysts were static structures; however, cysts should be considered dynamic both in structure and function (Cook et al., 1990). When studying the aetiology of ovulation failure the conclusions reached are affected by which animals are included as clinical cases. For example, cows identified as having cystic ovarian disease at routine preservice veterinary examination will form a different population from cystic ovarian disease cases detected in repeat breeder cows. Histological and biochemical examination of ovarian cysts demonstrates that cysts are complex structures. On clinical examination and gross anatomical inspec-

Failure to Conceive and Embryonic Loss

Box 36.2 Definition of cystic ovarian disease (see also Chapter 35).

• • • •

Persisting, steroid-secreting follicles >2.5 cm in diameter No functional corpus luteum present for more than 10 days Abnormal sexual cycle (anoestrus, nymphomania, virilism) More than six weeks after calving

Box 36.3 The possible pathogenesis of cystic ovarian disease.

• • •

Insufficient luteinizing hormone (LH) release: hypothalamic–pituitary dysfunction causing lack of GnRH release (commonest cause) Insufficient production of LH by the pituitary (rare) Failure of the dominant follicle to respond to LH

tion, however, there appear to be two main types of cysts: follicular cysts, which are like large follicles, and luteal cysts, in which obvious luteal tissue produces a thicker cyst wall. These may be difficult to differentiate from a corpus luteum with a central lacuna, which frequently occurs during the normal oestrous cycle (Okuda et al., 1988). It is well known that follicular cysts can occur and spontaneously resolve during the first few weeks after calving in some cows that then return to normal cyclic ovarian function, albeit later than normal counterparts (Savio et al., 1990). It is often suggested that cows with cystic follicles up to six weeks after calving should be regarded as normal and not be interfered with unless they are nymphomaniac or show other signs of abnormality. Box 36.3 is to some extent hypothetical but should act as a reminder that there are several possible routes that can result in cystic ovarian disease, among them long-term exposure to oestradiol or subnormal concentrations of progesterone (Dobson et al., 2001a) and cortisol release following stress (Dobson et al., 2001b). There have also been suggestions that energy imbalance due to high milk yields may be contributory, although this has not been substantiated by correlation with either b-hydroxybutyrate concentrations or body condition score (Dobson & Nanda, 1992; Tebble et al., 2001). There have been many studies of the causes of cystic ovarian disease and factors that predispose to the condition are listed in Box 36.4. There is lack of unanimity about causes, which may reflect differences between the populations of cattle selected for investigation as well as variations in the definition of cystic ovarian disease.

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Box 36.4 Factors that predispose to or cause cystic ovarian disease.

• • • • • •

Heredity High yield Age Exogenous oestrogens Nutrition and season of the year Dystokia and periparturient disease

Heredity: A familial predisposition to cystic ovarian disease through sire or dam has been recognized for many years (Bane, 1964). Other studies have produced less clearcut results or even failed to detect a hereditary effect at all (Dohoo & Martin, 1984a). It is possible that this difference is partly due to the stage at which diagnosis is carried out. If the incidence is assessed at routine preservice checks most of the detected cysts are likely to be attributed to environmental factors rather than heredity; on the other hand, one might expect considerably more evidence of hereditary predisposition if the assessment is made on a sample of repeat breeders. While most veterinarians are generally aware that there is a hereditary component in cystic ovarian disease, their clients want to know to what extent breeding a replacement heifer from a cow with cystic ovarian disease will increase the risk of that daughter having the disease. It is not easy to answer this because cystic ovarian disease may not occur in a daughter until she has had several calves and so field studies take many years and involve complex statistical analysis. Early studies carried out by Henricson (1957) helped to answer the question. He analysed data from two artificial insemination (AI) centres of cases presented at the time of insemination and classified cows as:

• • •

Having cystic ovarian disease on more than one occasion in a service period; Having only one observation of cystic ovarian disease; and Without cystic ovarian disease.

The effect of age was taken into account and the results expressed as an average frequency of the condition, where 1.00 is equivalent to an incidence of 100 per cent (Table 36.3). Henricson (1957) also studied the effect of the sire and noted that the average frequency of cystic ovarian disease in individual bulls’ daughters ranged from 0.00 to 0.258. Whether the low incidence of cystic ovarian disease in beef breeds is directly due to hereditary factors, to the lower milk production or to some other factor is not known. High milk yield: Cystic ovarian disease may be related to high milk yield. It occurs most frequently at the peak

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Table 36.3 Dam effect on incidence of cystic ovarian disease (COD) in daughters (Henricson, 1957). Number of times COD diagnosed in dam in one service period

>1 1 0

Average frequency of COD in daughters Centre 1

Centre 2

0.255 0.170 0.143

0.228 0.158 0.116

of lactation approximately six weeks postpartum and at the age when the cow has reached her full milking potential, which is why it is more common in pluriparous cows than in first calvers. There is a secondary peak of cases late in lactation; presumably these are cases that have been picked up on the examination of repeat breeders. Bartlett et al. (1986b) discussed, without coming to a conclusion, whether high milk yield causes cystic ovarian disease, cystic ovarian disease causes high yield or there is a common cause of both! Saloniemi et al. (1986) thought that the relationship between cystic ovarian disease and ketosis was due primarily to high milk yield, leading to greater energy demands that in turn resulted in both ketosis and interference with LH production or release. Some workers have been unable to find an adverse effect of high milk yield on the occurrence of cystic ovarian disease (Dohoo & Martin, 1984a). Age: It is widely accepted that cystic ovarian disease is rare in heifers before their first calving, not common in first-lactation cows and then increasingly observed in mature cows, with possibly some slight fall off in old animals. Exogenous oestrogens: Administration of oestrogens in the follicular phase will cause a premature LH peak. This will not cause ovulation if no dominant follicle is present at the time. If oestrogens are administered shortly before dominant follicle selection, the cow may not be able to produce a second LH peak due to down regulation of the hypothalamic response to oestradiol and consequently the dominant follicle will continue to grow and not ovulate. This may be one explanation why a single large dose of an oestrogen for therapeutic purposes may be followed later by cystic ovaries. Recent transitions to organic farming may involve grazing periods on pastures with a high component of oestrogenic plant material; however, a much increased incidence of cystic ovarian disease in such herds has not been reported to date. An analogous situation may

arise when oestrogenic substances, such as those found in mouldy brewers’ grains, are eaten. Seasonal effect: A very definite seasonal effect has been reported by many authors, with most reports indicating that the incidence is highest in winter (Dohoo et al., 1984a,b; Saloniemi et al., 1986). The effect can be so great that Bane (1964) stated that it is meaningless to talk of an incidence figure for cystic ovarian disease if details of season (and age) are excluded. The range in his data was from 2.23 per cent for cows that calved in May to 9.68 per cent for October calvers. The relative frequency of severe cases was higher in autumn calvers. Some authors (Bartlett et al., 1986b) reported high levels in summer and autumn. The causes of the seasonal effect are not clear but may be linked to nutritional effects, and could also include the hours of daylight, temperature extremes and stressors such as housing. Dystokia and periparturient disease: Some information suggests that dystokia and periparturient diseases may predispose to cystic ovarian disease. It is possible that preparturient factors that cause the postpartum conditions also affect the incidence of cystic ovarian disease, for example overfeeding leading to fatty liver (Reid et al., 1979). It has been demonstrated experimentally that damage to the endometrium can prolong the existence of cystic follicles and so inhibit spontaneous recovery (Fathalla et al., 1978) (see also Chapter 34). Other causes: It is possible that gross adhesions can bind the ovary so tightly that ovulation does not take place, but this must be a rare phenomenon. Of much greater importance is the concept that in cows which had other reproductive disorders there were possibly more than the expected cases of cystic ovarian disease (Jasko et al., 1984). Reviews of the literature show that incidence ranges from about 6 to nearly 20 per cent (Bartlett et al., 1986b; Garverick, 1997). However, diagnostic methods affect the reported incidence figure, for example Coleman et al. (1985) found that the single most important factor that influenced the incidence was the veterinarian who made the diagnosis! Selection of cases is also important, as has been discussed already. It is generally agreed that follicular cysts make up about two-thirds of recognized cases of cystic ovarian disease (Booth, 1988; Garverick, 1997) although again this figure depends a little on the diagnostic method and criterion used. While the most important reason for failure to ovulate is considered to be cystic ovarian disease, there are also a proportion of cows who have a delayed ovulation after oestrus, resulting in an extended period

Failure to Conceive and Embryonic Loss

Box 36.5 Causes of fertilization failure.

Box 36.6 Causes of ovarian and bursal adhesions.

•

• • •

• • • • • • • • • •

Rectal palpation just before ovulation (bursting preovulatory follicles, interference with egg flow into the uterine tubes) Interference with egg transport Interference with sperm transport Delayed ovulation Insemination at wrong time in relation to ovulation Service too soon after calving Poor quality spermatozoa Poor quality oocyte (e.g. from persistent follicles) Failure to serve the cow Metritis and salpingitis Vaginitis and cervicitis

from insemination to ovulation. The incidence of delayed ovulation can be as high as 11 to 13 per cent, as shown in one study by Lamming and Darwash (1998).

Stage 2 Fertilization failure To achieve fertilization a number of events in the cow (oestrus, ovulation, gamete transport) and in the bull (spermatozoa production, insemination) have to take place and must synchronize with each other. Failure of any one of these events to occur correctly or at the right time will almost certainly result in fertilization failure. The causes of fertilization failure will be discussed, mainly based on the headings shown in Box 36.5. The first two causes, interference with gamete transport, are relatively rare occurrences. Interference with egg transport: After ovulation the egg has to be transported to the site of fertilization in the uterine tube. Adhesions affecting the ovary and bursa and blockage of the uterine tube will prevent this happening. Factors that cause adhesions, which are fairly rare, are listed in Box 36.6. The ease with which fluids and small objects can be transported spontaneously up or down the uterine tube is demonstrated in two techniques used to investigate uterine tube patency. In one of these tests, phenolsulphonphthalein (PSP) dye is introduced into the uterus and ascends spontaneously through the uterine tube into the peritoneal cavity and becomes absorbed and secreted in urine. In the other test, starch granules deposited in the bursa descend through the uterine tube into the uterus and vagina (Kessy & Noakes, 1979). Transport in the uterine tube is under hormonal control and can be affected by abnormal variations in steroid hormone production and by oxytocin, but the role of these factors in field conditions is not known.

• • • •

•

557

Trauma Rectal palpation (Enucleation of corpus luteum – no longer indicated as a therapeutic practice in cattle) Caesarean section – inducing (localized) peritonitis Ascending infection Postpartum metritis Therapeutic infusion of uterus Descending infection from peritoneum Specific infections, e.g. Ureaplasma sp. Mycoplasma sp.

As transport of the egg depends on secretory and ciliary activity in the uterine tube, salpingitis will interfere with transport of both eggs and spermatozoa, even when the lumen remains patent. Interference with transport of spermatozoa: Adhesions in the female tract that block egg transport, and have been discussed above, will generally interfere with transport of spermatozoa. There are rare anatomical abnormalities such as white heifer disease (segmental aplasia of the paramesonephric ducts), which results in blockage of the tubular genitalia at various levels. Poor AI technique, such as insemination in the anterior vagina or caudal half of the cervix, will result in the majority of cases in the loss of much of the inseminate by reflux through the vulva. In contrast, in natural service the ejaculate is deposited in the anterior vagina and on the external os of the cervix, but the volume of the ejaculate and the enormous number of spermatozoa allow loss by reflux while sufficient spermatozoa are transported to the uterine tube. Returning to AI, a rough operator could damage the uterus with the insemination pipette. While it is unlikely that bad insemination technique is much of a problem with a technician inseminator service, it is very likely that the range of expertise among stockworkers who inseminate their own cows is so great that some gross technical errors may be made. Hunter (1999) discusses possible modifications of the technique used for AI involving deep intrauterine insemination and the effects this may have on the transport and storage of spermatozoa within the female reproductive tract. Delayed ovulation: Delayed ovulation is a condition in which the interval from the onset of oestrus to ovulation is so much longer than normal that service at the recommended time does not result in fertilization

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because of the ageing of the spermatozoa. While many authors are of the opinion that the condition is rare, there are a number of papers that suggest that it occurs quite commonly (Hancock, 1948; Nakao et al., 1984; Lamming & Darwash, 1998). Watson and MacDonald (1984) studied events around insemination using rectal palpation and assays for progesterone and oestradiol17b. They concluded that in cows with a follicle in the ovaries on the day after insemination (which may indicate delayed ovulation if onset of heat occurred more than 30 hours before) this was often due to erroneous timing of insemination in relation to the onset of oestrus and not to delayed ovulation. As the condition is so difficult to study, ideas about its aetiology must be theoretical. It is possible that there is an abnormality of the LH surge or response of the preovulatory dominant follicle to the LH surge. It has been hypothesized that deficiency of energy intake may be involved in the aetiology. The role of stress is also speculative, but it is interesting that corticosteroids can block LH release (Wagner & Li, 1982); also the fact that the adrenal cortex under the influence of adrenocorticotrophic hormone (ACTH) can produce some progesterone may be significant in suppressing the LH surge (Watson & Munro, 1984). The importance of stress in bovine reproduction is reviewed by Dobson et al. (2001b). A little understood condition called prolonged low or suprabasal progesterone was described by Jackson et al. (1979) as affecting 18 per cent of cows treated with an analogue of prostaglandin F2a (PGF2a) and also about 18 per cent of control cows. After oestrus there was an excessively long period of low progesterone, followed by a rise which seemed to indicate that ovulation took place eventually. The herd incidence ranged from 7 to 33 per cent and appeared to be low in herds with adequate nutrition. Other surveys have not revealed such a high incidence. Some workers think prolonged low progesterone is most commonly associated with treatment with PGF2a or an analogue causing incomplete luteolysis and subsequent recovery of some luteal function. Independent of its cause, it will lead to persistence of a dominant follicle resulting in lowered fertility following its ovulation. This does not appear to be due to poor fertilization rates, but to more losses during early embryonic development (Mihm et al., 1994). Insemination at the wrong time in relation to ovulation: Service during the luteal phase is only a minor problem with natural service but a major one with AI (Sturman et al., 2000). However, on farms using hand mated natural service, a cow restrained in a service crate may be mated when she is not in oestrus. Artificial insemination at the wrong time is an important cause of fertilization failure. Progesterone assays

of milk or blood taken on the day of insemination will detect insemination during the luteal phase of the cycle but will fail to pick up inseminations that are one or two days too early or too late. The reported incidence of luteal phase progesterone levels on the day of insemination is variable. The incidence of 5.2 per cent in wellrun herds reported by Claus et al. (1983), with over 20 per cent in problem herds, is typical of several other trials. Laitinen et al. (1985), in a large field study, reported that the lowest incidence of luteal phase inseminations occurred in the summer. Oltner and Edqvist (1981) observed that in herds with a high incidence of wrongly timed inseminations, even inseminations apparently at the correct time resulted in low pregnancy rates, presumably because of other aspects of poor management. The reasons are misidentification of a cow that actually is in season or misinterpretation of sexual behaviour, such as jumping another cow, which is thought incorrectly to indicate oestrus. The stockworkers are often under considerable pressure to get all cows served by a target date and are criticised by veterinarians and others, that cows in oestrus are missed too frequently. This can result in error through an overenthusiastic determination to increase the oestrous detection rate. The importance of inseminating only cows in oestrus was demonstrated by Sturman et al. (2000), who reported that in a herd they studied 19 per cent of inseminations were performed when progesterone levels were high in the oestrous cycle or while cows were pregnant. Insemination of pregnant cows led to an estimated 17 per cent induced embryonic death or abortion! Incorrect timing of insemination in relation to onset of oestrus also occurs. Watson et al. (1987) confirmed that insemination 24 hours or more after the cow is first seen in oestrus results in a marked reduction in pregnancy rate, possibly due to ageing of the oocyte before fertilization. It is likely that insemination very early in oestrus also causes reduced fertility, possibly due to reduced sperm survival rates before fertilization. There is a long-established, successful rule of thumb about the ideal time for insemination (Trimberger, 1948). Cows first seen in the morning should be inseminated late that afternoon. Cows first seen in the afternoon or evening should be inseminated next morning. Cows still in oestrus 24 hours after first being seen should receive a second insemination. This pragmatic recommendation takes account of the relatively short lifespan of both spermatozoa and ova within the female tubular tract (about 24 hours), the need for capacitation of bull spermatozoa (about 6 hours) and the interval from the onset of oestrus to ovulation (about 24–30 hours). Incorrect timing within oestrus is of little significance with natural service in which the service is usually early

Failure to Conceive and Embryonic Loss

in oestrus. The large quantity of the ejaculate and the great numbers of spermatozoa deposited in the anterior vagina ensure that there is a long-lasting supply of fertile spermatozoa in the uterine tube at the site of fertilization. Service too soon after calving: It has been known for many decades that service within six weeks of calving results in reduced pregnancy rates. The expected conception rate increases from approximately 20 per cent, at 20 days post partum, to reach normal rates (at the time the studies were carried out these were 50 per cent calving rates) from 50 days post partum. The reasons are likely to be both ovarian and uterine in origin so in some cases the cause is most probably fertilization failure and in others embryonic death. Elimination of infection and restoration of endometrial structure and function after a normal calving requires 5–6 weeks in most animals. Poor-quality semen or poor insemination technique: Poor semen quality may result in either low pregnancy rate or no pregnancies at all, mainly through fertilization failure but also to some extent through embryonic death. Again there are marked differences between natural service and AI. Because of laboratory control of the semen and follow-up of the results of insemination it is very unlikely that semen supplied by a reputable AI organization will give poor pregnancy rates. The exception to this is semen that has been poorly stored or incorrectly handled on farm for use in DIY AI systems. Schermerhorn et al. (1986) found that a technician inseminator service gave rather better results than farmer DIY insemination, although this may depend on the level of training received by DIY inseminators before they begin inseminating their own cows. Howells et al. (1999) showed that the amount of training received with live cows significantly affected future pregnancy rates; for those who spent up to three days training in an abattoir using live cows there was an increase of 5.9 per cent in the calving rate they achieved in their first year for every day they spent training. If AI technique is satisfactory, poor results with DIY inseminations could possibly be related to mishandling of the semen. By contrast a bull used for natural service may be of reduced or low fertility or even sterile and serve a number of cows before the owner realizes that something is wrong. Farmers are often not aware that a bull that has been fertile may become infertile or lose libido (see Chapter 38). Where fresh diluted semen is used, semen that is stored too long will give poor results. Failure to serve the cow: In certain circumstances when a bull is used to serve the cows, a cow in oestrus is not

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served. Bulls can develop abnormalities of the penis that prevent normal service, and lack of libido is not uncommon (see p. 610). When animals are running freely, such as heifers or beef cattle, it is essential to include an adequate number of bulls in the group. If there are too few bulls for the number of cows, some cows in oestrus may not be served. The required cow to bull ratio depends on the type of terrain, the age and libido of individual bulls (see p. 610). Metritis, salpingitis, vaginitis and cervicitis: Infection of the tubular genitalia may interfere with the survival of the spermatozoa in transit and so reduce the chance of fertilization. Endometritis and metritis are fairly common (see p. 524) but in addition a number of species of organisms have been recovered from the uterine tubes and may cause salpingitis or directly affect fertilization, as for example reported by Grahn et al. (1984), in connection with fertilization failure with BVDV infection (see pp. 578, 853). Infectious agents in the uterine tube include Leptospira hardjo (see p. 735), Ureaplasma spp. and Mycoplasma bovigenitalium.

Stage 3 Embryonic death The stage of the embryo lasts from fertilization of the egg until about day 42 after conception, by which time the organ systems have been laid down and placentation has been established. Failure of maternal recognition of pregnancy will cause early embryonic loss, and the animal returns to oestrus at normal intervals (70 000 lactation records. For the practitioner this means that evaluation of fertility in small herds is

Failure to Conceive and Embryonic Loss

difficult due to the large impact of small numbers of observations on overall herd results. While there are considerable differences between the findings certain concepts have emerged:

• •

• •

Reproductive diseases at and after calving tend to occur as an interrelated complex (see Chapter 34). Some diseases that are not specific infections of the reproductive tract have an adverse effect on reproduction, e.g. Leptospira hardjo, BVD virus (McGowan & Kirkland, 1995) and BHV-1. There is disagreement on the effect of high yield on fertility. There is disagreement on the effect of hereditary factors on fertility.

Although the relative importance of the factors listed above, along with other management factors, is still poorly understood, what does seem to be beyond doubt now is that fertility, at least in high producing dairy cows in the UK, is declining over time (Barrett, 2001). The relationship between nutrition and fertility is a complex one that is still not fully understood. The reader may find the following reviews of interest: Britt (1995); Webb et al. (1997); Wathes et al. (1998); Webb et al. (1999); O’Callaghan and Boland (1999); Garnsworthy and Webb (2000) and O’Callaghan et al. (2000). As an example of the complex interactions affecting fertility, data from the very large study by Saloniemi et al. (1986) showed the consequential effects of specific causes described in Table 36.5. For details of other complex interactions, the reader is referred to some original texts: Andersson et al. (1991) and Gustafsson and Emanuelson (1996): hyperketonaemia and fertility; Bartlett et al. (1986b) and Garverick (1997): cystic ovarian disease; Bartlett et al. (1986a) and Sheldon (1999): metritis/endometritis; Curtis et al. (1985): metabolic disease, mastitis; Dohoo and Martin (1984a): age, season and sire; Dohoo & Martin (1984b): mastitis and ketosis; Britt (1995): nutri-

•

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tion, weight loss and fertility; Loeffler et al. (1999): time of disease, milk yield and body condition; Dohoo et al. (1984): disease, production and culling; Rowlands et al. (1986) and Peeler et al. (1994): interrelationship of diseases; Saloniemi et al. (1986) and Fourichon et al. (2000): reproductive diseases.

Diagnosis Although a herd consists of many individuals, diagnosis of a return-to-service problem that affects a large part of a herd requires a different approach from that taken to investigate the cause in an individual animal. For this reason the individual will be dealt with first, followed by the herd fertility problem.

Diagnosis of the individual repeat breeder cow One problem with diagnosis is that by the time the cow is recognized as being a repeat breeder the situation that prevailed at the time of reproductive failure may well have changed. The clinician should take a history and carry out a systematic clinical examination to find out whether any of the factors that are likely to cause return to service are present. The fullness and, therefore, costs of the investigation will need to be discussed with the farmer in advance and a diagnosis may only be pursued in valuable animals. A systematic approach to diagnosis is essential and the following procedure is suggested (Box 36.8). History: The history should cover various points as shown in Box 36.9. General examination: The clinician should carry out a brief general examination looking at the following points:

Table 36.5 The consequential effects of management and disease on problems of fertility (reproduced from Saloniemi et al., 1986 with permission of the publisher). Cause

Consequential effect Retained fetal membranes

Winter calving Highest herd milk yield Parturient paresis Mastitis Ketosis Retained fetal membranes Metritis

No Yes Yes

Metritis

Anoestrus/suboestrus

Ovarian dysfunction

Yes Yes Yes Yes Yes Yes

Yes Yes

Yes Yes

Yes Yes

Yes

Yes

Yes

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Box 36.8 The systematic diagnosis of return to service.

• • • • •

History Analysis of records General clinical examination and body condition Examination of the reproductive tract (rectal, vaginal and suitable aids including ultrasound examination) Appropriate laboratory tests

Box 36.9 The main factors to be covered in history taking.

• • • • • • • •

• • • •

Date of calving. Dystokia and puerperal diseases Postpartum reproductive disease Other diseases (e.g. lameness, metabolic diseases) Service details Dates Bull used Natural or AI Inseminator service or DIY AI Major management or environmental changes Is this considered to be a herd or individual cow problem?

Body condition and conformation; Signs of non-reproductive disease; Signs of vaginal discharge or dried pus or mucus on the tail or hindquarters; and Other signs, for example a raised tailhead.

Rectal examination: The technique of rectal palpation of the genital tract is fully described in various textbooks, as are the characteristics of the various normal and abnormal structures in the ovaries and tract. The purpose of carrying out a rectal examination is to assess:

• • • • • • •

The state of the ovaries; The condition of the bursae and uterine tubes; Uterine abnormality or status (e.g. metritis, adhesions, pregnancy); Internal slackness of the pelvic ligaments; Absence of fat inside the pelvis (body condition); Vulval discharge (stimulated by palpation); Evidence of other conditions detectable on rectal examination (e.g. cystitis, pyelonephritis, fat necrosis).

Nowadays it is general practice to supplement, or even replace, the manual rectal examination with a transrectal ultrasound examination. This has the same aims as listed above, but will on the whole give more accurate results. The use of transrectal ultrasound examination as a diagnostic tool and the comparative levels of accuracy of rectal examination and ultrasound

are discussed more fully in Chapter 35 (see p. 536). The use of milk progesterone assays may also improve diagnostic accuracy (see p. 548). Accuracy of diagnosis of cystic ovarian disease by rectal examination: When undertaking rectal palpation there are obvious difficulties in trying to assess the nature of a cyst without rupturing it. A large, soft corpus luteum with no palpable ovulation papillum can be mistaken for a cyst. Some authors are very sceptical about the accuracy of diagnosis of cystic structures by rectal palpation alone, for example Stolla et al. (1980) and Guenzler and Schallenberger (1981). However, accuracy is immensely improved with transrectal ultrasound examination (Douthwaite & Dobson, 2000), and once again milk progesterone assays have their place in confirming whether functional luteal tissue is or is not present (Chapter 35). Accuracy of diagnosis of endometritis: Clinical diagnosis of endometritis is discussed in some detail in Chapter 34 (see p. 521). Vaginal examination: There is a choice of two methods of vaginal examination on the farm: manual or visual using a vaginal speculum. In both cases the perineal region and vulva are thoroughly cleaned and the veterinarian uses fresh plastic gloves. With manual examination mucus in the anterior vagina is gathered and on withdrawal of the hand examined visually and olfactorily. Minimum lubrication is used to avoid confusion between clear mucus and the lubricant. The cervix and vaginal wall are palpated for lesions and abnormalities. The vaginal speculum should be introduced with care and, when fully inserted, will give a clear view of the cervix. With both techniques the clinician may have difficulty in passing the vulvo–vaginal junction, which is the narrowest part of the tract at this level. When using a speculum great care should be taken to ensure that the speculum does not transfer infection between cows. This is best achieved by using disposable, single-use specula or autoclaving equipment between cows. If a single speculum is to be used on a number of cows at a single visit, it must be thoroughly disinfected between cows. Box 36.10 shows the factors that should be checked in a vaginal examination. Selection of samples for laboratory examination: Selection of the appropriate laboratory examinations and the frequency of sampling depend very much on circumstances, including the value of the cow. The items listed in Box 36.11 may be considered. To extend the physical examination beyond what is possible by palpation and transrectal ultrasound, the patency of the uterine tubes can be investigated using the phenosulphonphthalein (PSP) dye test and/or starch grain test as described by Kessy and Noakes (1979).

Failure to Conceive and Embryonic Loss

Box 36.10 Factors to be checked by vaginal examination.

• •

Anatomical abnormalities. Heifers Damage Caused by dystokia: Rectovaginal fistula Pneumovagina/urovagina (see p. 519) Damage to the cervix Serving injuries caused by the bull Sadistic human interference Other acquired conditions Vaginitis (see p. 519) Type and quantity of mucus Purulent Bloody Smelly Clear oestrous mucus

• • • • • •

•

• • • • • • • •

Single milk progesterone assay: an adjunct to rectal palpation and ultrasound examination Serial milk progesterone assays: monitor events around service, confirm diagnosis, monitor treatment Oestrone sulphate from milk, blood (specifically from the placenta: indicates live calf) Heparinized blood for cytogenetic analysis Clotted blood for serology (e.g. BHV-1, BVDV, Leptospira hardjo, Neospora caninum) Purulent material from the uterus: aerobic and anaerobic culture, antibiotic sensitivity Uterine biopsy for histology Samples from the cervix and uterus for serology and cytology Vaginal mucus for campylobacter diagnosis using the vaginal mucus agglutination test (VMAT)

New technological aids to diagnosis: In recent years advances in biochemistry, electronics and fibre optics, along with skills and materials developed for embryo transfer, have opened up new diagnostic possibilities. There is every reason to believe that new equipment and concepts will continue to be produced, which presents problems as well as opportunities for the veterinarian. Most of the new techniques do not require specifically veterinary skills and so may be used by a wide range of operators, although for best effect knowledgeable interpretation is needed. Choices have to be made about the lasting value of each new step forward as investing capital and training in inappropriate technology is unproductive. The relatively new aids to diagnosis can be classified as:

565

Box 36.12. Steps required to diagnose a herd fertility problem.

Box 36.11 Types of samples required for various laboratory tests.

•

•

•

History Analysis of records Breeding Health Production Selected clinical examinations and sampling Conclusion

Quick, cheap and, in some cases, automated hormone analysis; Non-invasive (or acceptably invasive) examination of internal organs: hysteroscopy, endoscopy (transrectal ultrasound is already routinely used during on farm fertility examinations); Automatic or semiautomatic recording of physical, behavioural and biochemical changes that are related to the animal’s reproductive status, such as body temperature, restlessness, changes in milk composition and hormone content; Computer analysis of data: compilation over time of various measurements in the individual and analysis of herd records (see Chapter 41b).

Diagnosis of a herd problem It is necessary to approach the diagnosis of a herd fertility problem systematically. It is not practical to lay out in any detail a series of steps to be followed because as the investigation develops the information obtained guides the continued course of the investigation. The four main causes of herd problems are poor fertility management, an infertile ‘male’, nutritional errors and deficiencies and infectious conditions. In general terms the steps required are shown in Box 36.12. History: The object of history taking is to acquire information on the factors shown in Box 36.13. Analysis of the records: It is useful, if possible, to examine the breeding records before visiting the herd. If there are no records then establish a recording system. The objectives of record analysis in connection with a herd fertility problem are the following: (1)

(2)

To assess the current level of fertility in the herd and to establish whether a problem exists, and if so to determine the seriousness of the situation. To look for clues to aetiology, by looking at the fertility of subgroups within the herd: • Bull, semen or inseminator; • Age (lactation) group; • Yield group;

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Box 36.13 History taking in determining herd fertility problems.

•

•

• • •

•

•

•

General aspects of the herd and farm Number of breeding stock (male and female) Stocking density Type of housing Details of grazing Targets for reproduction and production Other enterprises Information about the stockworkers Definition of the perceived problem Anoestrus Return to service Vaginal discharges Other manifestations Duration of problem Proportion of herd affected Reproductive management Calving management Service management: cows and heifers (heat detection, timing of AI, technician or DIY AI) Bulls Nutrition Ration formulation Feeding system Assessment of adequacy of nutrition e.g. yield, milk composition, condition score, metabolic profiles Details of ‘herd health plan’ Disease monitoring Intervention levels Preventive medicine initiatives Vaccination protocols Biosecurity Disease status of herd Details of herd status for infectious diseases known to affect fertility, e.g. BVDV, BHV-1, leptospirosis Incidence of conditions that have a direct effect on fertility, e.g. retained fetal membranes, endometritis Other diseases and conditions in the herd, e.g. lameness

• • •

Seasonal effect; Familial effect; Relevant infectious disease: e.g. non-specific endometritis after calving, Campylobacter fetus, Leptospira hardjo, Neospora caninum, BHV-1, BVDV, etc.

Analysis and interpretation of herd fertility records are discussed in much more detail in Chapter 41a,b. Once a cause of the infertility is suspected, a valuable technique is to group the records of all animals that are influenced by the suspect factor and compare these with the records from all other cows. It can be difficult to identify the cause of a problem where farmer insemination is associated with poor pregnancy rate. In these

cases there may be no comparative data on the bull’s fertility; the problem could be due to poor insemination technique or to improper semen handling. Examination of the animals: It is very useful to examine as many cows as possible to obtain a current picture of the herd, to observe the condition of the cows and to detect or confirm the incidence of obvious reproductive abnormalities. It also reveals the (in)accuracy of the information supplied by the farmer or farm staff. Advice should be given about culling of individuals that have a very poor prognosis. By this stage the clinician should have a good idea of the type of problem; how the investigation then develops is a matter of clinical judgement which cannot be detailed further.

Treatment

(see Chapter 42)

The veterinarian is faced with some difficulties when having to decide on appropriate and effective treatments for cows that are presented as infertile. This is partly because of the complex aetiology of return to service, but also because of the time that has passed since the factors that initiated the problem were present. When using pharmaceutical products the reader is advised to consult the manufacturers’ data sheets for details of treatment, withdrawal periods, dangers and contraindications. Wherever possible the treatment should be followed up to see whether it has been successful or not and, if need be, repeated or changed.

Ovulation failure The most important cause of ovulation failure is cystic ovarian disease. Treatment is based on whether the cyst has been diagnosed as follicular or luteal. In most cases the condition is probably caused by hypothalamic– pituitary dysfunction and it is, therefore, logical to treat the condition systemically. There is little or no benefit in rupturing the cyst manually, which also involves a risk of causing haemorrhage and ovarian adhesions. Nor does there appear to be any benefit from administration of drugs directly into the cyst. Many cystic structures found less than 42 days after calving are transient and benign, and in general these do not require to be treated. Only if abnormal behaviour indicates that they are pathological or if there is some pressing management need should they be treated. For follicular cysts the three therapeutics of choice are human chorionic gonadotrophin (hCG),

Failure to Conceive and Embryonic Loss

gonadotrophin-releasing hormone (GnRH) or GnRH analogues, such as buserelin, and progesteronereleasing intravaginal devices (PRIDs) and controlled internal drug release (CIDR) (Dobson et al., 2001a). They all work in different ways to achieve the same end, i.e. to put the animal under the influence of progesterone. One effect of this is to allow a build-up of LH in the pituitary so that enough endogenous LH is available after removal of the progesterone devices or regression of the (induced) corpus luteum. This leads to normal preovulatory follicle development and ovulation, and in all cases the cow should be served at the first heat after treatment. The duration of exposure to exogenous or endogenous progesterone is thought to be important in the non-recurrence of the cystic condition, with 14 days being preferable to seven (Nanda et al., 1989). There is also evidence to suggest that the success of treatment of follicular cysts depends on whether the cyst is producing oestradiol or not, as reflected by the presence or absence of other follicles >5 mm in diameter. Following treatment with an intravaginal progesterone releasing device or GnRH, animals had a pregnancy rate to all inseminations of 91 per cent when other large follicles were present in addition to the cyst, compared with 69 per cent if no other follicles were present at the time of treatment (Tebble et al., 2001). Human chorionic gonadotrophin has an LH-like direct action on the ovary to induce luteinization of the cyst or follicles. GnRH stimulates the release of LH from the pituitary to achieve the same result. In both cases the lifespan of the luteal tissue produced is variable, ranging from about six days to about 18 days, and oestrus can be expected about 8–22 days after treatment. It is desirable to examine the treated cows about seven days after treatment for the presence of luteal tissue. If luteal tissue is found, treatment with PGF2a or an analogue is a suitable way of increasing the predictability of the following oestrus. Service should be at that oestrus and aids to oestrous detection should be used. If there is no satisfactory response to the first treatment, the cow should be re-examined and treated again. For cysts containing functional luteal tissue as judged by ultrasound examination or milk progesterone assay, injection of PGF2a or an analogue followed by insemination at observed oestrus is the most suitable treatment. An alternative treatment, suitable for both types of cystic ovarian disease, is the insertion of a PRID/CIDR, which can be left in position for 12 days, and after withdrawal the cow should be served, either at a fixed time or preferably at observed oestrus (Douthwaite & Dobson, 2000). If the type of cyst cannot be diagnosed accurately, then administration of PGF2a or an analogue, either on the day of PRID/CIDR withdrawal or

•

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up to three days before, can improve predictability of the oestrous response. If fixed time insemination is used and oestrus is observed later the animal should be inseminated again.

Fertilization failure Delayed ovulation: For many years one of the standard ways of treating apparently normal repeat breeders on the farm has been to administer hCG or GnRH on the day of service. The theory behind this was that many of these cases were thought to be due to lack of an adequate gonadotrophin surge delaying ovulation, although controlled trials of this type of treatment are lacking and a better approach may be to inseminate the cow again 24 hours after the first insemination. Interference with transport of egg or spermatozoa: When this is due to bilateral blockage of the uterine tubes (or other parts of the female tract), there is no simple treatment. In some cases the diagnostic dye test may remove a minor blockage and attempts have been made to achieve this by adding antibiotics and corticosteroids to the dye, which is introduced into the uterine tube end of the uterus under gentle pressure using a cuffed catheter. In valuable animals the use of ovum pick-up techniques using transvaginal ultrasound-guided oocyte aspiration can be used to harvest oocytes for in vitro production of embryos. One or more of these embryos could then be implanted back into the uterus of the donor, although it is probably more advisable to implant valuable embryos derived in this way into other healthy heifers. In those animals that are not considered of high enough genetic merit to be used as oocyte donors, but which the farmer simply wishes to get back in calf so as to induce another lactation, the implanting of a low cost embryo may be used as a treatment. This has now become commercially feasible and technically achievable for repeat breeders with no uterine or endocrine abnormalities; single step (in straw) embryo thawing, using embryos frozen in ethylene glycol, is used, which allows embryo transfer with little more equipment and skill than that required for AI (May, 1996). Other factors that can cause failure of fertilization are:

• • • •

Service at the wrong time; Poor-quality semen; Infertile bull; Problems with artificial insemination.

These are dealt with elsewhere under Prevention, in Chapter 38 on the bull, or by common sense.

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Embryonic death Although the aetiology of early embryonic death is listed under nine headings (Box 36.7) only non-specific endometritis (already dealt with in Chapter 34), specific metritis caused by C. fetus (see p. 582) and a variety of other infections and possibly maternal endocrine environment are suitable for conventional treatment. All the other conditions should be corrected by management improvements or are dealt with in different chapters of this book. A number of different Campylobacter spp. are associated with infertility and abortion in cattle, the speciation and subspeciation of which is complex and currently under review using modern molecular techniques. However, it is clear that the most common isolates associated with fertility problems in the UK are C. fetus subsp. venerealis and C. fetus subsp. fetus (Newell et al., 2000). Infection with either of these subspecies should be thought of as a herd problem. In the case of C. fetus subsp. venerealis the natural habitat of the organism is the bovine reproductive tract and it does not multiply in the intestinal tract; it is thus transmitted only as a venereal disease (Taylor, 2002; see also p. 582). In the bull, in which infection with C. fetus subsp. venerealis is limited to the surface of the prepuce and penis, spontaneous cure does occur but is erratic and unreliable. Moreover, if the bull continues natural service of infected cows he will be re-infected as the superficial nature of the infection does not stimulate an immune response in the bull. The organism colonizes the crypts of the preputial epithelium which increase in both size and number as the bull ages. This means that the prepuce of the older bull provides favourable conditions for the persistence of the organism, giving a higher incidence of carrier bulls among those over 5 years of age. Diagnosis and treatment are also more difficult in the older bull (Taylor, 2002). The usual treatment of the bull involves preputial lavage with streptomycin in a viscous oily medium and parenteral treatment with the same antibiotic. Taylor (2002) recommends daily systemic (e.g. intramuscular) treatment with a combination of streptomycin and dihydrostreptomycin, each at 150 mg per ml as sulphates at a dose rate of 10 mg per kg body weight. Taylor (2002) gives a detailed description of the technique of preputial lavage. It is important that both systemic and local treatments are carried out thoroughly and are repeated daily for three consecutive days. This needs to be combined with further sampling for the organism not less that 30 days after treatment has finished to confirm success of treatment. In a confirmed outbreak of campylobacteriosis, the bulls should be sampled twice, not less than three days and not more than seven days apart, and this should be repeated a

further 30 days later. Taylor (2002) describes in some detail the technique for collecting samples by preputial washing. Although there is no natural immune response in the bull, one successful form of treatment depends on vaccination (Clark & Dufty, 1982). The vaccine is licensed for use in a number of countries but not in the UK, although one can be made under licence in the UK for specific herds. Treatment of cows with local or systemic antibiotics is unreliable and because cows develop resistance to the infection it is usually best to wait for this to develop. Whatever course is followed an infected cow should be regarded as potentially infective for at least two gestations after initial infection. Even after this time a few cows may remain infected. As it takes only one cow to infect a bull when natural service is practised, it is clear that it is hazardous to allow natural service of any cows that have ever been infected. Vaccination of cows (where permitted) is widely and fairly effectively practised in range conditions. On a herd basis, when campylobacteriosis is diagnosed the best advice is that natural service should stop and all services should be by AI using semen from noninfected bulls. Recently infected cows will continue to return to service for some time. In suckler herds where the use of AI to observed natural oestrus may be problematic this approach can be facilitated by the use of repeated oestrous synchronization and fixed-time artificial insemination as described by Penny et al. (2000). There is a management alternative, which is extremely difficult to carry out successfully over a long period and should be advocated only under special circumstances. This is to segregate the herd and use the infected bull(s) on infected cows and AI or noninfected bulls on non-infected cows and heifers. However, this depends on the accurate identification of the infection status of all animals. Manipulation of the maternal endocrine environment post insemination by the exogenous administration of progesterone or progestagens has been tried as a treatment of repeat breeder cows or where herd conception rates are particularly poor. However, the results of such studies are variable and seem to be affected by the time of progesterone administration and the initial fertility levels. A meta-analysis of 17 progesterone supplementation studies showed that treatment during the first week of pregnancy resulted in an increase in pregnancy rate, especially on farms with poor fertility, while treatment during the second and third weeks of pregnancy gave no overall significant increase (Mann & Lamming, 1999). At the present time treatments of this type cannot be recommended as a means of improving conception rates, and more research is needed to identify suitable hormonal treatment strategies.

Failure to Conceive and Embryonic Loss

An alternative post-insemination treatment involving the administration of GnRH (or GnRH analogues such as buserelin) to the cow around 11 days after insemination has become popular in recent years. In some studies this has been shown to give very good results. For example Sheldon and Dobson (1993) achieved an improved pregnancy rate to first service of approximately 10 per cent. A recent meta-analysis of studies of the effect of GnRH 11–14 days after insemination concluded that while results were not consistent across all studies, there was a significant improvement in pregnancy rate amongst 2541 cows across six studies (Peters et al., 2000). However, post insemination hormonal treatments remain an unpredictable means of improving pregnancy rate on any one given farm, and in most instances resources would probably be better targeted at improving the management of the herd rather than instigating such treatment regimens.

Stage of failure unknown: non-specific endometritis The two most common therapeutic approaches are (i) promotion of the cow’s normal resistance to infection by inducing oestrus and (ii) the use of antibiotics. There is a tendency for spontaneous elimination of the infectious agents from the uterus, most likely due to the cow going through successive periods of oestrus. The current practical approach to treatment is discussed in detail in Chapter 34 (see p. 521).

Prognosis From the client’s point of view successful treatment means that the cow becomes pregnant; this is a twostage process. Firstly, the cow has to return to normal reproductive function and secondly she has to conceive and remain pregnant. While the first stage is mainly the responsibility of the veterinarian, the second stage often depends on the farmer and farm staff. Where poor husbandry (i.e. feeding, housing or breeding management) is thought to be causing return to service, prognosis must be guarded because it is often a difficult and slow task for the veterinarian to effect a marked improvement.

191 141

569

Results of treatment reported by different workers are rarely comparable because different criteria for selection of cases and assessment of success may have been applied. In many cases self-cure is a phenomenon and because controlled studies are rare, interpretation of results is problematic. Accordingly it is suggested that, as well as reading published reports, clinicians should analyse their own practice records of diagnosis, treatment and outcome. The most common situation is the cow presented after a few unsuccessful inseminations (or services), which on examination appears to be normal. These apparently normal repeat breeders have an expected pregnancy rate at the first service after examination that is about the same as the first service pregnancy rate in the herd, as indicated in Table 36.6. This is not to say that the factors influencing fertility in first service and repeat breeder cows are the same. In the first service cows, fertility may be affected by closeness to calving and the stress of peak yield. The population returning to service will have overcome these problems, but will include a higher proportion of cows that will never become pregnant. Unfortunately before their ultimate disposal, cows in the last group will have had two or three different treatments and several examinations at regular visits. In most cases there is no reliable way of identifying these problem cows. Where economics allow the hospitalization and intensive investigation and therapy of repeat breeder cows in referral centres (now very uncommon in the UK), the owner should be given a definite prognosis as soon as possible to minimize the cost involved in keeping and treating cows over several weeks. Much of this cost is due to the fact that once an animal has been served there is little positive that can be done except to monitor changes until pregnancy or non-pregnancy is confirmed. With modern diagnostic methods such as ultrasound scanning it is now possible to reduce the waiting time from service to diagnosis of nonpregnancy to a minimum of 25–30 days, and milk progesterone analysis can be used to give an indication of pregnancy status as early as 19–20 days post service. Other methods of early pregnancy diagnosis such as assays for bovine pregnancy-associated glycoprotein

Table 36.6 Response of apparently normal repeat breeders served without treatment. Number of cows

•

Treatment

Percentage pregnant at first AI after examination

Reference

None None

59.7 60.0

de Kruif (1975) Refsdal (1979)

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(bPAG) may also be used to speed up pregnancy diagnosis (Skinner et al., 1996). If the prognosis is favourable, costs are reduced if the cow is returned to the owner’s farm where the local veterinarian can treat her. Accurate prognosis with long-term repeat breeder cows is also difficult. The prognosis for natural conception must always be regarded as poor, but particularly so in cases with blocked uterine tubes, persisting endometritis and anomalous steroid hormone production from the ovaries. For example, of 33 chronic repeat breeders treated by Boyd et al. (1984) only eight became pregnant. However, the use of embryo transfer techniques to maintain animals for subsequent lactations may offer some hope and has been shown in some studies to give reasonable results. May (1996) reports pregnancy rates in the region of 50 per cent using-single step (in straw) embryo thawing, with embryos frozen in ethylene glycol. Furthermore, nowadays it is also possible to harvest oocytes from valuable animals for in vitro production of embryos, and thus offspring, using transvaginal ultrasound-guided oocyte aspiration of ovarian follicles. The two most commonly diagnosed specific pathological causes of return to service are cystic ovarian disease and purulent endometritis.

Cystic ovarian disease (see p. 526) In data collected from a number of veterinary practices Bartlett et al. (1986b) recorded that culling rate for cows that had cystic ovarian disease was 26.6 per cent, compared with 21.6 per cent for other cows. Cows with cystic ovarian disease that conceived had an interval from calving to conception 33.5 days longer than cows without cystic ovarian disease. More recently cystic ovaries were associated with 6 to 11 more days to first service and with 20 to 30 more days to conception in a meta-analysis of papers published between January 1987 and January 1999 (Fourichon et al., 2000).

In general, three factors affect the outcome:

•

• •

The time that has elapsed since calving. Cases of cystic ovaries that occur up to six weeks after calving have a good chance of spontaneous recovery. Cases that are first seen six months after calving have a very poor prognosis. The accuracy of diagnosis. If the type of cyst is misdiagnosed, selection of inappropriate treatment may give poor results. The aetiology of the condition affects the outcome. If the cyst is caused by a temporary environmental influence such as poor nutrition, then the prognosis is good even without treatment, once this environmental influence is corrected. At the other extreme, if it is one of the minority of cases caused by deficiency of LH receptors in preovulatory dominant follicles, the prognosis may be poor in the short term as this may be the consequence of events occurring up to months previously.

The results presented in Table 36.7, in most of which diagnosis and outcome were checked by progesterone assays, are typical of earlier published field trials. However, these data do not illustrate the ultimate benefit of treatment, which should be measured in terms of calving or treatment to conception intervals and culling rates (see Table 36.8). Guenzler and Schallenberger (1981) treated 66 cows in which luteal cysts had been diagnosed by rectal palpation. After treatment with an analogue of PGF2a, complete luteolysis occurred in the 35 cows with mid-cycle levels of progesterone and all but three of these started normal cycles. The first service pregnancy rate for these cows was 40 per cent. The two groups of cows with lower levels of progesterone cycled erratically after treatment and had first service pregnancy rates of 20 and 24 per cent. Nanda et al. (1988) treated 77 luteal cyst cases with an analogue of PGF2a and 65 per cent of these exhibited initial recovery, i.e. the cyst regressed and a corpus luteum formed;

Table 36.7 The treatment of follicular cystic ovarian disease with GnRH. Number of cows

Type of cyst

Confirmed by progesterone assay

Treatment

Successful result: progesterone rose within 14 days

Reference

104 30 12 116 55 44

Follicular Follicular Follicular Follicular Follicular Follicular

Yes Yes Yes No Yes Yes

GnRH GnRH None GnRH GnRH hCG + progesterone

73 (70%) 25 (83%) 3 (25%) 61 (53%) 40 (73%) 32 (73%)

Nakao et al. (1983) Ax et al. (1986) Ax et al. (1986) Nanda et al. (1988) Booth (1988) Booth (1988)

Failure to Conceive and Embryonic Loss

•

571

Table 36.8 Fertility parameters of cows treated for follicular and luteal ovarian cysts (mean ± SE).

a b

Treatment (n cows)

Follicular cysts

Matched controls

Treatment (n cows)

Luteal cysts

Matched controls

Calving to conception (days)a

PRID (n = 22)

93 ± 27

90 ± 37

PRID (n = 14)

132 ± 49

93 ± 52

Treatment to conception (days)a

PRID (n = 22)

24 ± 19

PRID (n = 14)

60 ± 67

Culling rate (%)a

PRID (n = 22)

41

4

PRID (n = 14)

11

7

Calving to conception (days)b

GnRH (n = 16)

82 ± 7

70 ± 6

PGF2a (n = 22)

141 ± 15

68 ± 9

Treatment to conception (days)b

GnRH (n = 16)

48 ± 9

PGF2a (n = 22)

20 ± 5

Culling rate (%)b

GnRH (n = 16)

44

PGF2a (n = 22)

9

Calving to conception (days)b

PRID (n = 21)

125 ± 17

Treatment to conception (days)b

PRID (n = 21)

33 ± 8

Culling rate (%)b

PRID (n = 21)

29

70 ± 6

From Douthwaite and Dobson (2000). From Tebble et al. (2001).

not all became pregnant and in 18 per cent the cyst recurred. More recent results from Douthwaite and Dobson (2000) and Tebble et al. (2001) are summarized in Table 36.8. In these studies the overall interval from calving to conception was significantly greater than that of matched controls irrespective of cyst type or treatment. Cows treated for luteal cysts took significantly longer to get in calf than those treated for follicular cysts, again irrespective of treatment. Cows treated for follicular cysts had a higher culling rate than those with luteal cysts. It would seem that at least in the herds used in these studies, farmers and veterinarians were prepared to persevere with cows diagnosed with luteal cysts, even at the expense of an extended calving to conception interval, whereas cows with follicular cysts tended to be culled earlier.

Purulent endometritis/metritis (see pp. 519, 521) Ott and Gustafsson (1981) reviewed reports on over 600 cases and showed that in 85 per cent the uterus was emptied within a few days of treatment with PGF2a or an analogue. In most reports the authors stated that pregnancy rate after successful treatment was lower

than in normal cows. Time from treatment to conception was about 75 days. Factors that affect prognosis have been quantified by Anderson (1985) who modified a system proposed by Studer and Morrow (1978), which was based on a careful analysis of clinical and laboratory observations. Anderson took into account (i) the time since calving, (ii) whether oestrus had occurred since calving, (iii) the amount of pus, (iv) the size of the cervix and (v) the diameter of the larger affected horn. By giving points for these factors a cumulative score was calculated that gave a useful prediction about the eventual outcome of the case. Cows that had been in oestrus had a poor prognosis, presumably because they had not responded to the normal defence mechanism. Pepper and Dobson (1987) found that the relative amount of pus in the discharge gave a (non-significant) indication of the pregnancy rate after treatment and that time from calving to treatment was significantly related to pregnancy rate after treatment. Cows treated with PGF2a or oestrogen within 40 days of calving had a pregnancy rate of about 55 per cent compared with a significantly poorer result for cows treated later. From Anderson’s (1985) data it appeared that in successfully treated cows there was a high incidence of

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periparturient problems at the resultant calving and a very high culling rate in this group of animals in the year after treatment, observations that warrant further study. The treatment and control of endometritis and metritis are discussed in more detail in Chapter 34. As regards the outlook for herds with a return-toservice problem prognosis varies and obviously is related to the diagnosis. Some episodes of herd infertility are of short duration and normal fertility returns spontaneously. In cases where a definite infectious cause is identified, such as campylobacteriosis, the outcome can be completely satisfactory with the elimination of the infection and the return to a normal herd pregnancy rate. This depends on treatment being carried out carefully and the subsequent control of breeding management being optimized. Where the problem is related to poor husbandry caution should be expressed until clear signs of improved management are noted.

(5)

(6)

(7)

(8)

Prevention Improvement in pregnancy rates is achieved by encouraging good husbandry and avoiding factors that have an adverse effect on fertility. While it is possible to achieve a very high fertilization rate (up to 100 per cent), some embryonic death is inevitable, which is why it is rare for a herd to achieve a pregnancy rate of greater than 70 per cent. There are a number of items, listed below, which contribute to good fertility, but deficiency in any one of these is likely to produce poor pregnancy rates. (1) (2) (3)

(4)

Accurate heat detection. Proper nutrition and maintenance of suitable body condition before and after calving. Avoidance of dystokia and post partum abnormalities and timely veterinary intervention where indicated. This should reduce the incidence of delayed involution, non-specific endometritis (Chapter 34), blocked uterine tubes, cystic ovarian disease, etc. (see Chapter 34). The proper use of records can help to achieve a good pregnancy rate and to avoid long interservice intervals. This is done by: (a) not serving cows too soon after calving (not before 42 days); (b) being aware of the expected return-toservice date (for example, by using a threeweek calendar); (c) ensuring early pregnancy diagnosis via transrectal ultrasound and milk progesterone assays;

(9)

(d) checking the fertility of the bulls; (e) checking the efficiency of the inseminators, and the quality of the semen used; (f) understanding the causes of fertility variations in a specific herd. Avoidance of service contact outside the herd and ensuring veterinary examination, isolation and testing of bought-in breeding stock, especially bulls will reduce the risk of introducing venereal diseases and other diseases affecting fertility. (See also Chapter 57 for a more in-depth discussion of biosecurity.) Good housing environment and cattle handling will help to avoid stress, lameness, discomfort and fear in the herd. Consideration should be given to reproductive dysfunction with a hereditary component, e.g. cystic ovarian disease. Interventions that may cause embryonic death should be avoided, such as drastic changes in feeding and environment, herd medication and the administration of vaccines in the weeks after service. In the case of vaccines the manufacturer’s recommendations should always be followed. Drug therapy, using either antibiotics or hormones, in the post partum phase has been advocated as a way of improving pregnancy rates. The doubtful value of this is discussed below.

Where specific drug therapy is applied selectively in cows identified as likely to have poor fertility this is obviously a suitable approach. However, it has been proposed that routine treatments should be applied to all cows, normal and abnormal, and this is much more questionable. For example in one study post partum administration of PGF2a 21 days after calving reduced the interval to first oestrus and first service by about 10 days. Pregnancy rates to first service were increased and the number of services to conceptions was reduced from 2.0 to 1.3 (Schofield et al., 1999). However, a number of trials have given conflicting results. Metaanalysis of 24 trials where PGF2a was administered to cattle within 40 days of calving reported no beneficial effect on first service pregnancy rate, although there was a small reduction in days open for treated cows (Burton & Lean, 1995). It is now becoming socially unacceptable to administer hormonal products to cattle as ‘routine’ treatments, and some sectors of the industry such as organic milk producers and many consumers would rather that hormone preparations were not used at all, or that their use were restricted to individual cows with particular problems that cannot be treated by any other means. The routine use of antibiotics in both normal and abnormal cows after calving or at the time of

Failure to Conceive and Embryonic Loss

insemination should be strongly discouraged; results have shown no benefit to normal cows. Antibiotic usage should be restricted to those animals where there is a specific therapeutic indication, and where failure to treat may compromise the animal’s welfare. In order to overcome problems with oestrous detection, oestrous synchronization and fixed time AI may be employed; Lane et al. (2001) have reviewed methods of synchronization. The technique is best suited for dairy heifers and beef suckler cows. For best results the farmer, the veterinary surgeon and a member of the insemination organization should discuss the whole operation well beforehand. The best results are obtained when only reproductively normal cows at least six weeks after calving (preferably longer) or maiden heifers are included, although it is possible to synchronize cows that have had a shortened post partum period (Penny et al., 2000; Penny & Lowman, 2002). First calvers and animals in poor body condition tend to give poor results and may need additional hormones such as equine chorionic gonadotrophin and nutritional treatments. Results following synchronization of dairy cows can be satisfactory (Biggadike & Mawhinney, 1996; Jobst et al., 2000) and cost-effective (Esslemont & Mawhinney, 1996), but currently still need inseminations at observed oestrus for optimal results. Stress and any change in management and diet should be avoided during preparation and for three to four weeks after insemination. As far as possible other interventions such as vaccination should be avoided during the same period. Some of the oestrous synchronization regimens may be used for the repeat synchronization of cows not in calf to the first service (Penny et al., 2000; McDougall, 2001; Penny & Lowman, 2002); this allows repeated fixed time insemination. However, if repeat synchronization is not to be used it is essential that preparation is made to deal with the cows that return to oestrus, such as an intensive period of heat detection approximately 19–24 days after the initial service. If natural service is to be used on these returns it is essential that the ‘sweeper bull’ is not presented with an excessive number of cows in oestrus over a very short period of time (see Chapter 38).

References Anderson, D.B. (1985) A clinical study of chronic endometritis in dairy cows. MVM thesis, Glasgow University. Andersson, L., Gustafsson, A.H. & Emanuelson, U. (1991) Effect of hyperketonaemia and feeding on fertility in dairy cows. Theriogenology, 36, 521–36. Austin, E.J., Mihm, M., Ryan, M.P., Williams, D.H. & Roche, J.F. (1999) Effect of duration of dominance of the ovulatory follicle on onset of estrus and fertility in heifers. Journal of Animal Science, 77, 2219–26.

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Ax, R.L., Bellin, M.E., Scheinder, D.X. & Haase-Hardie, J.A. (1986) Reproductive performance of dairy cows with cystic ovaries following administration of Procystin TM1. Journal of Dairy Science, 69, 542–5. Ayalon, N. (1978) A review of embryonic mortality in cattle. Journal of Reproduction and Fertility, 54, 483–93. Bane, A. (1964) Fertility and reproductive disorders in Swedish cattle. British Veterinary Journal, 120, 430–41. Barrett, D.C. (2001) Cattle fertility management in the UK. Cattle Practice, 9, 59–68. Bartlett, P.C., Kirk, J.H.,Wilke, M.A., Kaneene, L.B. & Mather, E.C. (1986a) Metritis complex in Michigan Holstein– Friesian cattle: incidence, descriptive epidemiology and estimated economic impact. Preventive Veterinary Medicine, 4, 235–48. Bartlett, P.C., Ngategize, P.K., Kancene, J.B., Kirk, J.H., Anderson, S.M. & Mather, E.C. (1986b) Cystic follicular disease in Michigan Holstein–Friesian cattle: incidence, descriptive epidemiology and estimated economic impact. Preventive Veterinary Medicine, 4, 15–33. Beghelli, V., Boiti, C., Parmigiani, E. & Barbacini, S. (1986) Pregnancy diagnosis and embryonic mortality in the cow. In Embryonic Mortality in Farm Animals (ed. by L.M. Sreenan & M.G. Diskin), pp. 159–67. Nijhoff, Dordrecht/Boston/Lancaster. Biggadike, H. & Mawhinney, I. (1996) Planned breeding routine in dairy cows using a treatment regimen involving GnRH and PGF2a. A multi site study (interim report). Cattle Practice, 4, 289–91. Bon-Durant, R. (1997) Pathogenesis, diagnosis and management of trichomoniasis in cattle. Veterinary Clinics of North America: Food Animal Practice, 13, 345–61. Booth, J.M. (1988) The milk progesterone test as an aid to the diagnosis of cystic ovaries in dairy cows. Veterinary Record, 123, 437–9. Boyd, H. & Reed, H.C.B. (1961a) Investigations into the incidence and causes of infertility in dairy cattle – Fertility variations. British Veterinary Journal, 117, 18–35. Boyd, H. & Reed, H.C.B. (1961b) Investigations into the incidence and causes of infertility in dairy cattle – influence of some management factors affecting the semen and insemination conditions. British Veterinary Journal, 117, 74–86. Boyd, H., Renton, J., Munro, C., Harvey, M., Isbister, J. & Kelly, E. (1984) Clinical studies of a series of long (term) repeat breeder cows and heifers. Vlaams Diergeneeskundig Tijdschrift, 53, 165–9. Britt, J.H. (1995) Relationship between postpartum nutrition, weight loss and fertility. Cattle Practice, 3, 79–83. Burton, N.R. & Lean, I.J. (1995) Investigation by metaanalysis of the effect of prostaglandin F2a administered post partum on the reproductive performance of dairy cattle. Veterinary Record, 136, 90–4. Clark, B.L. & Dufty, J.H. (1982) The duration of protection against infection with Campylobacter fetus subsp. venerealis in immunised bulls. Australian Veterinary Journal, 58, 220. Clark, B.L., Dufty, J.H. & Parsonson, I.M. (1986) The frequency of infertility and abortion in cows infected with Trichomonas fetus var. brisbane. Australian Veterinary Journal, 63, 31–2.

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Claus, R., Karg, H., Zwiauer, D., von Butler, I., Pirchner, F. & Rattenberger, E. (1983) Analysis of factors influencing reproductive performance of the dairy cow by progesterone assay in milk fat. British Veterinary Journal, 139, 29–37. Coleman, D.A., Thayne, W.V. & Dailey, R.A. (1985) Factors affecting reproductive performance of dairy cows. Journal of Dairy Science, 68, 1793–803. Cook, D.L., Smith, C.A., Parfet, J.R., Youngquist, R.S., Brown, E.M. & Garverick, H.A. (1990) Fate and turnover rate of ovarian follicular cysts in dairy cattle. Journal of Reproduction and Fertility, 90, 37–46. Curtis, C.R., Erb, H.N., Sniffen, C.J., Smith, R.D. & Kronfield, D.S. (1985) Path analysis of dry period nutrition, postpartum metabolic and reproductive disorders, and mastitis in Holstein cows. Journal of Dairy Science, 68, 2347–60. Dobson, H., Douthwaite, R., Nobel, K.M., O’Donnell, M.J., Ribadu, A.Y., Tebble, J.E. & Ward, W.R. (2001a) Cystic ovaries in cattle. Cattle Practice, 9, 185–9. Dobson, H. & Nanda, A.S. (1992) Reliability of cyst diagnosis and effect of energy status on LH release by oestradiol or GnRH in cows with ovarian cysts. Theriogenology, 37, 465–72. Dobson, H., Tebble, J.E., Smith, R.F. & Ward, W.R. (2001b) Is stress really all that important? Theriogenology, 55, 65–73. Dohoo, I.R. & Martin, S.W. (1984a) Disease, production and culling in Holstein–Friesian cows. III. Disease and production as determinates of disease. Preventive Veterinary Medicine, 2, 671–90. Dohoo, I.R. & Martin, S.W. (1984b) Disease, production and culling in Holstein–Friesian cows. IV. Effects of disease on production. Preventive Veterinary Medicine, 2, 755–70. Dohoo, I.R., Martin, S.W., McMillan, I. & Kennedy, B.W. (1984) Disease, production and culling in Holstein–Friesian cows. II. Age, season and sire effects. Preventive Veterinary Medicine, 2, 655–70. Doig, P.A., Rulinke, H.L., Mackay, A.L. & Palmer, N.C. (1979) Bovine granular vulvitis associated with Ureaplasma infection. Canadian Veterinary Journal, 20, 89–94. Douthwaite, R. & Dobson, H. (2000) Comparison of different methods of diagnosis of cystic ovarian disease in cattle and an assessment of its treatment with a progesteronereleasing intravaginal device. Veterinary Record, 147, 355– 9. Esslemont, R.J. & Kossaibati, M.A. (1997) Culling in 50 dairy herds in England. Veterinary Record, 140, 36–9. Esslemont, R.J. & Mawhinney, I. (1996) The cost benefit of a planned breeding routine for dairy cows (Ovsync/Intercept). Cattle Practice, 4, 293–300. Fathalla, M.A., Geissinger, H.D. & Liptrap, R.M. (1978) Effect of endometrial damage and prostaglandin F2a on experimental cystic ovarian follicles in the cow. Research in Veterinary Science, 25, 269–79. Fourichon, C., Seegers, H. & Malher, X. (2000) Effect of disease on reproduction in the dairy cow: a meta-analysis. Theriogenology, 53, 1729–59. Franco, O.L., Drost, M., Thatcher, M.J., Shille, V.M. & Thatcher, W.W. (1987) Fetal survival in the cow after pregnancy diagnosis by palpation per rectum. Theriogenology, 27, 631–43.

Fredriksson, G. (1984) Some reproductive and clinical aspects of endotoxins in cows with special emphasis on the role of prostaglandins. Acta Veterinaria Scandinavica, 25, 365– 77. Garnsworthy, P.C. & Webb, R. (2000) Nutritional influences on fertility in dairy cows. Cattle Practice, 8, 401–405. Garverick, H.A. (1997) Ovarian follicular cysts in dairy cows. Journal of Dairy Science, 80, 995–1004. Grahn, T.C., Fahning, M.L. & Zeinjanis, R. (1984) Nature of early reproductive failure caused by bovine viral diarrhea virus. Journal of the American Veterinary Medical Association, 185, 429–32. Guenzler, O. & Schallenberger, E. (1981) The treatment of ovarian cysts in cattle with prostaglandins – possibilities and limitations. Acta Veterinaria Scandinavica, 77 (Suppl.), 327–41. Guerin, B., Nibart, M., Marquant-Le Guienne, B. & Humblot P. (1997) Sanitary risks related to embryo transfer in domestic species. Theriogenology, 47, 33–42. Gustafsson, A.H. & Emanuelson, U. (1996) Milk acetone concentrations as an indicator of hyperketonaemia in dairy cows: the critical value revised. Animal Science, 63, 183–8. Hancock, L.L. (1948) The clinical analysis of reproductive failure in cattle. Veterinary Record, 60, 513–17. Henricson, B. (1957) Genetical and statistical investigations into so-called cystic ovaries in cattle. Acta Agriculturae Scandinavica, 7, 3–93. Howells, H.M.J., Davies, D.A.R. & Dobson, H. (1999) Influence of the number of days spent training in an abattoir with access to live cows on the efficiency of do-it-yourself artificial insemination. Veterinary Record, 144, 310–14. Hunter, R.H.F. (1999) Pre-fertilisation events and the fate of bovine spermatozoa in the female genital tract. Cattle Practice, 7, 261–6. Jackson, P.S., Johnson, C.T., Bulman, D.C. & Holdsworth, R.J. (1979) A study of cloprostenol-induced oestrus and spontaneous oestrus by means of the milk progesterone assay. British Veterinary Journal, 135, 578–90. Jasko, D.J., Erb, H.N., White, M.E. & Smith, R.D. (1984) Prostaglandin treatment and subsequent cystic ovarian disease in Holstein cows. Journal of the American Veterinary Medical Association, 185, 212–13. Jobst, S.M., Nebel, R.L., McGilliard, M.L. & Pelzer, K.D. (2000) Evaluation of reproductive performance in lactating dairy cows with prostaglandin F2a, gonadotrophin-releasing hormone, and timed artificial insemination. Journal of Dairy Science, 83, 2366–72. Kastelic, J.P. (1994) Noninfectious embryonic loss in cattle. Veterinary Medicine, 89, 584–9. Kessy, B.M. & Noakes, D.E. (1979) Determination of patency of fallopian tubes in the cow by means of phenosulphonphthalein and starch grain tests. Veterinary Record, 105, 414–20. Kossaibati, M.A. & Esslemont, R.J. (1995) Wastage in Dairy Herds. Report No. 4 DAISY – The Dairy Information System. Department of Agriculture, University of Reading. Kruif A. de (1975) Fertiliteit en subfertiliteit Nj het vrouwelijk rand. Thesis, Utrecht. Laitinen, E.R., Tenhunen, M., Haenninen, O. & Alanko, M. (1985) Milk progesterone in Finnish dairy cows: a field study

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Newell, D.G., Duim, B., van Bergen, M.A.P., GrogonoThomas, R. & Wagenaar, J.A. (2000) Speciation, subspeciation and subtyping of Campylobacter spp. associated with bovine infection and abortion. Cattle Practice, 8, 421–5. O’Callaghan, D. & Boland, M.P. (1999) Nutritional effects on ovulation, embryo development and the establishment of pregnancy in ruminants. Animal Science, 68, 299–314. O’Callaghan, D., Lozanot, J.M., Fahey, J., Gath, V., Snijders, S. & Boland, M.P. (2000) Recent developments in the effect of nutrition on fertility in dairy cows. Irish Veterinary Journal, 53, 417–25. Okuda, K., Kito, S., Sumi, N. & Sato, K. (1988) A study of the central cavity in the bovine corpus luteum. Veterinary Record, 123, 180–3. Oltner, R. & Edqvist, L.E. (1981) Progesterone in defatted milk: its relation to insemination and pregnancy in normal cows as compared with cows on problem farms and individual problem animals. British Veterinary Journal, 137, 78–87. Ott, R.S. & Gustafsson, B.K. (1981) Therapeutic application of prostaglandins for post partum infections. Acta Veterinaria Scandinavica, 77 (Suppl), 363–9. Peeler, E.J., Otte, M.J. & Esslemont, R.J. (1994) Interrelationships of periparturient diseases in dairy cows. Veterinary Record, 134, 129–32. Penny, C.D. & Lowman, B.G. (2002) Mating beef cows without natural service – a triple synchronisation system. Cattle Practice, 10, 23–6. Penny, C.D., Lowman, B.G., Scott, N.A. & Scott, P.R. (2000) Repeated oestrus synchronisation of beef cows with progesterone implants and the effects of a gonadotrophinreleasing hormone agonist at implant insertion. Veterinary Record, 146, 395–8. Pepper, R.T. & Dobson, H. (1987) Preliminary results of treatment and endocrinology of chronic endometritis in the dairy cow. Veterinary Record, 120, 53–6. Peters, A.R., Martinez, T.A. & Cook, A.J.C. (2000) A metaanalysis of studies of the effect of GnRH 11–14 days after insemination on pregnancy rates in cattle. Theriogenology, 54, 1317–26. Refsdal, A.O. (1979) Undersoekelse av kviger og kyr utsjaltet paa grunn av ufruktbarhet. Thesis, Oslo. Reid, I.M., Roberts, C.J. & Manston, R. (1979) Fatty liver and infertility in high-yielding dairy cows. Veterinary Record, 104, 75–6. Robinson, R.S., Mann, G.E., Lamming, G.E. & Wathes, D.C. (1999) The effect of pregnancy on the expression of uterine oxytocin, oestrogen and progesterone receptors during early pregnancy in the cow. Journal of Endocrinology, 160, 21–33. Rowlands, G.J., Lucey, S. & Russell, A.M. (1986) Susceptibility to disease in the dairy cow and its relationship with occurrences of other diseases in the current or preceding lactation. Preventive Veterinary Medicine, 4, 223–34. Royal, M.D., Darwash,A.O., Flint,A.P.F.,Webb, R.,Woolliams, J.A. & Lamming, G.E. (2000) Declining fertility in dairy cattle: changes in traditional and endocrine parameters of fertility. Animal Science, 70, 487–501. Saloniemi, H., Groehn, Y. & Syvaejaervi, J. (1986) An epidemiological and genetic study on registered diseases in

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Taylor, A.J. (2002) Venereal Campylobacter infection in cattle. Cattle Practice, 10, 35–42. Tebble, J.E., O’Donnell, M.J. & Dobson, H. (2001) Ultrasound diagnosis and treatment outcome of cystic ovaries in cattle. Veterinary Record, 148, 411–13. Trimberger, G.W. (1948) Breeding efficiency in dairy cattle from artificial insemination at various intervals before and after ovulation. University of Nebraska College of Agriculture, Agricultural Experimental Station, Research Bulletin 153. Wagner, W.C. & Li, P.S. (1982) Influence of adrenal corticosteroids on postpartum pituitary and ovarian function. In Factors Influencing Fertility in the Postpartum Cow (ed. by H. Karg & E. Schallenberger), pp. 197–219. Nijhoff,The Hague. Warren, M.E. (1984) Biological targets for fertility and their effects on herd economics. In Dairy Cow Fertility (ed. by R.G. Eddy & MA. Ducker), pp. 1–14. British Veterinary Association, London. Wathes, D.C., Robinson, R.S., Pushpakumara, A., Cheng, Z. & Abayasekara, D.R.E. (1998) Nutritional effects on reproductive performance in dairy cows. Cattle Practice, 6, 371–7. Watson, E.D., Jones, P.C. & Saunders, R.W. (1987) Effect of factors associated with insemination on calving rate in dairy cows. Veterinary Record, 121, 256–8. Watson, E.D. & MacDonald, B.J. (1984) Failure of conception in dairy cattle: progesterone and oestradiol-17b concentrations and the presence of ovarian follicles in relation to the timing of artificial insemination. British Veterinary Journal, 140, 398–406. Watson, E.D. & Munro, C.D. (1984) Adrenal progesterone production in the cow. British Veterinary Journal, 140, 300–306. Webb, R., Garnsworthy, P.C., Gong, J.G., Gutierrez, C.G., Logue, D., Crawshaw, W.M. & Robinson, J.J. (1997) Nutritional influence on subfertility in cattle. Cattle Practice, 5, 361–7. Webb, R., Royal, M.D., Gong, J.G. & Garnsworthy, P.C. (1999) The influence of nutrition on fertility. Cattle Practice, 7, 227–34. Whitaker, D.A., Kelly, J.M. & Smith, S. (2000) Disposal and disease rates in 340 British dairy herds. Veterinary Record, 146, 363–7. Wolfenson, D., Roth, Z. & Meidan, R. (2000) Impaired reproduction in heat-stressed cattle: basic and applied aspects. Animal Reproduction Science, 60/61, 535–47. Wrathall, A.E. (1995) Embryo transfer and disease transmission in livestock: a review of recent research. Theriogenology, 43, 81–8.

Chapter 37

Fetal Loss G. Caldow and D. Gray

Introduction Pathophysiology Placentitis Causes of abortion Viral causes of abortion Bovine viral diarrhoea (BVDV) Bovine herpes virus 1 (BHV1) Other viruses Bacterial causes of abortion Brucellosis Leptospirosis Bacillus licheniformis Listeria monocytogenes Salmonellosis Campylobacter Miscellaneous bacteria Protozoal causes of abortion Trichomoniasis Neosporosis Other infectious agents causing abortion Chlamydia and rickettsia Mycotic abortion Non-infectious causes of abortion Investigation Conclusion

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Introduction The failure of the cow to carry a calf to full term or to produce a live calf causes financial loss through disruption of the normal pattern of milk production, the loss of genetic material or an absolute loss in output for the beef cow. These losses can have a profound effect at the herd level. For example, neosporosis has been reported to cause abortion rates of 26 per cent (Wouda et al., 1999). Losses on this scale may be relatively unusual, but annual losses of 10 per cent are not uncommon. Assessing the scale of these losses is made difficult by the definitions used and the differing clinical manifestations. In Britain abortion is described as the birth of a live or dead calf before 271 days’ gestation and stillbirth as the production of a dead calf after 272 days of gestation (Noakes, 1986). However, agents that infect the conceptus, such as bovine viral diarrhoea virus (McGowan & Kirkland, 1995) or leptospira organisms

(Bolin & Alt, 1998) can cause embryonic death or death that occurs shortly after birth. Such embryonic loss or early abortion is difficult to detect and increased neonatal mortality may not be immediately associated with disease processes that affect the fetus. It is also important to define what is normal or unavoidable loss. Spontaneous chromosomal abnormalities are commonly held to account for the bulk of unavoidable wastage and a loss of 20 per cent of embryos by day 45 of gestation has been estimated (Roche et al., 1981). After this period losses are far lower: an abortion rate of 6.5 per cent was calculated by Forar et al. (1995) who reviewed 26 published studies. Stillbirth losses of 4 to 6 per cent have been quoted (Miller, 1988) and a study of more than 2000 beef cow calvings found a mortality rate of 4.5 per cent within 24 hours of birth (Nix et al., 1998). In contrast, the target used in beef production in Britain for live calves born is 94 per cent (MLC, 1998) and the estimate of 1.9 to 2.0 per cent losses after day 42 of gestation (Sreenan & Diskin, 1986) may be a more realistic target for unavoidable fetal loss. This is further supported by a survey of Irish dairy cows that found an abortion rate of 1.7 per cent (Mee, 1992). From this it would seem justifiable to use an interference level of 3 per cent for abortions or losses after confirmation of pregnancy at around 6 weeks and one of 2 per cent for deaths at parturition and in the neonatal period.

Pathophysiology The clinical manifestation of disease of the conceptus is largely the consequence of the stage of development when exposure to the agent occurs (McGowan & Kirkland, 1995), the difference in virulence between strains of recognized fetal pathogens (Dubovi, 1992) and the degree and duration of exposure in the case of non-infectious causes. The corpus luteum is necessary for maintenance in the first half of gestation (Wendorf et al., 1983) and destruction of the corpus luteum during that time will usually result in the termination of pregnancy and the expulsion of a fresh fetus and membranes. However, fetal death may either cause lysis of 577

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the corpus luteum and the expulsion of an autolysed fetus some days later or the corpus luteum may persist and the fetus and membranes then undergo mummification. If bacterial infection is present maceration of the fetus is the result. As a consequence, early abortions are rarely observed and when they are the advanced autolysis limits the examinations that can be carried out. The fetus and placenta maintain the pregnancy in the later stages. Fetal death removes this support and abortion follows after a period of a few days. Autolytic change is a feature in these cases too, characterized by the presence of bloody fluid in the body cavities (Dillman & Dennis, 1976) and a loss of microscopic cell detail. However, fetal death is not the only consequence of disease processes affecting the fetus and placenta. Fetal stress primarily due to anoxia will trigger the steroid response necessary for normal parturition (Knickerbocker et al., 1986) and a relatively fresh fetus can be expelled in these circumstances; indeed, calves may be born alive and survive from day 260. Signs of prolonged fetal stress include staining of the perineum by meconium and inhalation or ingestion of meconium.

Placentitis Placentitis is the principal lesion in several infectious disease processes associated with fetal loss, and in cattle the placenta is often retained after abortion in the second half of gestation. The precise reasons for placental retention are not known, but this is a further factor limiting the investigation of many cases.

Causes of abortion A wide range of infectious and non-infectious causes of abortion have been reported, many of which are associated with only occasional or sporadic fetal loss. The following discussion concentrates on the more prevalent conditions in British herds, with only occasional reference to exotic causes.

Viral causes of abortion Bovine viral diarrhoea (BVDV) (see p. 853) Laboratory diagnostic rates of 5.4 per cent (Kirkbride, 1992a) and 6.5 per cent (Caldow et al., 1996) have been reported, but the widespread evidence of infection in English dairy herds (Paton et al., 1998) and the ability

of the virus to cause abortion in the early stages of gestation, at a time when both finding the fetus and achieving a diagnosis are more difficult, suggest that the true rate of fetal loss due to BVDV may be higher. Infection is most often introduced into the herd by the purchase of a persistently infected (PI) breeding replacement and can be maintained in the herd by the birth and survival to breeding age of further PI animals. In the beef herd infection can be maintained within successive calf crops as the calves are kept with the cows during the breeding period and beyond the first trimester of pregnancy. Persistently infected animals produce the largest amount of virus, particularly in their nasal secretions, while acutely infected animals are also infectious to others for at least 15 days (Duffell & Harkness, 1985). Both persistently infected bulls (Meyling & Mikel-Jensen, 1988) and bulls undergoing acute infection (Paton et al., 1989) can pass the virus in semen. Acute infection during the breeding season and in the first trimester of pregnancy can result in a range of outcomes from reduced conception rates or fetal death to the persistence of infection in the fetus (Kirkland et al., 1997). Infection in both the first and the second trimester can cause abortion or developmental abnormalities, particularly of the nervous system (Baker, 1987). The virus appears to be less pathogenic to the fetus in the third trimester and from 100 to 120 days of gestation the fetus can mount an immune response to the virus, a response that becomes more effective as the pregnancy progresses. Following acute infection, the virus multiplies in the placentome, but does not cause placentitis, before moving into the fetus. In the first trimester lesions in the fetus include meningitis with cerebellar cortical destruction and necrotizing bronchiolitis (Casaro et al., 1971), but these are rarely observed due to autolysis. Sublethal damage in the first trimester and beyond can result in the birth of calves with lesions such as retinal dysplasia and cerebellar hypoplasia. The difference in virulence between strains described for both type 1 and type 2 viruses (Dubovi, 1992), along with stage of gestation at which individual cows are exposed to infection and the variation in the level of herd immunity, explain the wide differences seen in the outcome of BVDV infection in breeding herds. The virus can be isolated from an aborted fetus although the success of this is limited by autolysis. It can also be demonstrated in fixed tissues using immunohistochemistry. This allows the agent to be associated with lesions observed on histological examination (Ellis et al., 1995). Nested reverse chain transcriptase polymerase chain reaction (PCR) techniques have been used to detect viral RNA in tissues and may, in future,

Fetal Loss

become the diagnostic technique of choice (Nettleton & Entrican, 1995). As maternal antibody cannot cross the bovine placenta, antibody detected in fetal fluids indicates fetal infection. However, when antibody is detected in late abortions without the presence of specific pathology BVDV may not have been responsible for fetal death (Brown et al., 1979). Maternal immunity to infection is not life-long. Infection with heterologous strains of the virus can also overcome natural immunity. Control should therefore be based on a programme that includes best practice biosecurity, identifying and removing persistently infected breeding animals from the herd and screening purchased replacements for the presence of PI animals. Vaccines (p. 1011) now available in Britain have been shown to prevent fetal infection (Brownlie et al., 1995), but vaccination should not be relied upon as the sole preventive strategy. The success of eradication and biosecurity as a means to control BVD can be measured by the progress made by the countries that have embarked on national or regional control programmes (Hult & Lindberg, 1998)

Bovine herpes virus 1 (BHV1) (see also p. 289) In Western Europe there is little to suggest that BHV1 is a significant cause of abortion. In contrast, in North America BHV1 has been shown to be the most frequently diagnosed viral cause of abortion (Kirkbride, 1992a; Anderson et al., 1997) and experimental challenge models to test vaccine efficacy have resulted in a high rate of fetal loss (Miller et al., 1995). This difference may be the consequence of a variation in virulence between the strains of the virus found on the two continents. BHV1 exists as two distinct subgroups and causes two clinical syndromes: infectious bovine rhinotracheitis (IBR) and infectious pustular vaginitis (IPV). Neither clinical syndrome is exclusively associated with a particular genotype of the virus and abortions have been observed with both subgroups (Barr & BonDurant, 1997). As with all herpes viruses the agent is maintained in a latent form in infected animals, but can be re-activated at times of stress (Kaashoek et al., 1996). In young animals epidemic IBR often follows the introduction of market purchased animals to the herd. Similar outbreaks of clinical disease may be seen in adults, but subclinical disease is more common in this age group. Infection in breeding herds tends to become endemic, with young cows infected as they enter the breeding herd (Pritchard, 1992). Experimental infection with the virus at 25 to 28 weeks of pregnancy resulted in abortions between 17 and 85 days later (Miller et al., 1991). In abortions

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attributed to natural infection with BHV1, fetuses show no typical gross lesion, but histological examination consistently reveals multifocal coagulative necrosis in the liver and less frequently in the lung, lymph nodes, kidney and placenta (Kirkbride, 1992b). These changes and the absence of fetal antibody suggest an acute infection and appear to conflict with the prolonged period between experimental infection and abortion. Virus can be isolated from up to 50 per cent of fetuses that show histological lesions typical of BHV1 infection with the placenta being the most useful tissue for culture (Kirkbride, 1992b). Other diagnostic techniques that have been described include fluorescent antibody staining on cryostat sections of fetal tissues, immunostaining of lesions observed in fixed tissues and PCR techniques (Rocha et al., 1999). It seems likely that active immunity ensures that reinfection does not result in significant clinical disease and the use of a live modified vaccine has been shown to prevent abortion following experimental challenge (Cravens et al., 1996). However, it remains unclear how long after infection cows are protected from the abortifacient effects of the virus. As BHV1 is an insignificant cause of fetal loss in Britain there is little financial incentive to control the disease in breeding herds for this reason alone. However, the virus may be found in the semen of infected bulls and it is illegal to sell semen from antibody-positive bulls to third countries within the European Union (EU). Several continental European countries have successfully eradicated the disease or have national control programmes in place and individual herds within these countries are unable to import seropositive animals. There is therefore a sound argument for pedigree and high genetic merit herds to eradicate the disease by a test and cull programme supplemented by biosecurity measures. Gene deleted vaccines offer an alternative to a test and cull programme and have been used in the Netherlands (Kaashoek et al., 1995). Even where breeding herds do not sell semen or pedigree animals, the apparent difference in virulence between European and North American strains of the virus makes it prudent to exclude exotic strains of BHV1 by implementing biosecurity measures.

Other viruses While a range of other viruses have been isolated from aborted fetuses there is little to support their role as important causes of fetal death. The exceptions are bovine herpes virus 4 (BHV4) and Akabane virus. There is epidemiological evidence of an association between BHV4 seropositivity and abortion in cows in

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Belgium (Czaplicki & Thiry, 1998) and in the USA the virus was the third most frequently isolated from fetal submissions to a diagnostic laboratory over a 10-year period (Kirkbride, 1992b). There is no published record of the agent’s involvement in British cattle and relevant diagnostic tests are rarely used. It may be of value to consider BHV4 when the usual investigative procedures in problem herds have been unsuccessful. Akabane virus is an arthropod borne virus that has been shown to cause a range of congenital abnormalities that include arthrogryposis and hydranencephaly as well as abortion. The virus occurs in Australia, Japan, South East Asia, Africa, Israel and Turkey and it would appear to be maintained in a range of mosquito and culicoides species (Charles, 1994). The significance of Akabane virus to British herds is limited, but the trade in live animals that would follow inclusion of countries such as Turkey to the European Union could render this virus something other than an exotic curiosity.

Bacterial causes of abortion Brucellosis (see also p. 461) According to EU criteria Britain is officially free of Brucella abortus infection, but animals from areas with a lower status for this disease are imported and as a consequence the government continues to carry out post import checks and routine serological monitoring of the herds in Britain. The organism is an intracellular pathogen that is spread in infected uterine discharges. After infection has occurred, usually by ingestion, an animal remains infected for life and the principal sign of this infection is abortion due to placentitis. This is characterized as a purulent intercotyledonary placentitis with necrosis of the cotyledons. Live calves are produced from subsequent pregnancies although the uterine discharges remain a source of infection. Apart from the severe effects on cattle production the disease is also an important zoonosis. In Britain there is a legal obligation for farmers to notify the government’s animal health service of any bovine abortion and it is then at their discretion to require the collection of diagnostic material by the farmer’s veterinary surgeon. Microscopic examination of smears made from vaginal swabs, bacteriological culture of milk and vaginal swab and a range of serological techniques can then be employed to screen for evidence of the disease. It is important for both farmers and their veterinary surgeons to recognize that these procedures are not used to test for other abortion agents. Control of the disease is the preserve of the State Veterinary Service in Britain and test and cull policies

are pursued. Vaccination has been used in many national or regional eradication programmes, often in the early stages of control (see p. 1013).

Leptospirosis (see also p. 735) The disease in cattle is caused by the organisms collectively referred to as Leptospira hardjo (L. borgpetersenii serovar hardjo and L. interrogans serovar hardjo, previously named Leptospira interrogans serovars hardjobovis and hardjoprajitno, respectively). These are host-adapted serovars responsible for disease in cattle. In New Zealand there is little evidence that these are significant pathogens of cattle and their importance lies in their zoonotic impact (Bolin & Alt, 1998). Conversely, disease surveillance figures from New Zealand have found Leptospira pomona, a serovar that is not adapted to cattle, in 1.3 per cent of abortion cases examined (Thornton, 1991). In Victoria, Australia, experimental infection of pregnant heifers with a locally isolated strain of L. interrogans serovar hardjo failed to cause abortion or to establish fetal infection (Chappel et al., 1989). In Britain and Ireland leptospirosis is associated with infertility, abortion and milk drop. As it is difficult to detect evidence of infection in the fetus it is also difficult to determine the true significance of leptospirosis as cause of fetal death, however diagnostic rates of 1.7 per cent have been observed in Scotland (Caldow et al., 1996) while in Northern Ireland 42 per cent of aborted fetuses showed evidence of infection (Ellis et al., 1982). The disease is widespread in the national herd and bulk milk antibody testing showed 75 per cent of samples from dairy herds in England and Wales to have antibody present (Pritchard, 1999). Infection is through exposure to contaminated urine and leptospires penetrate intact mucosal surfaces to establish a bacteraemia. The agent localizes in the urinary and reproductive tracts and is passed in large numbers in the urine in the early stages of the disease and may be passed intermittently for prolonged periods thereafter. Spread of infection within a herd is most rapid during the grazing season, an observation that has been explained by the longer survival times for the organism that occur in the moist neutral pH conditions found at pasture in contrast to the more acid environment that prevails when animals are housed, particularly where ensiled forage is fed. Infection is generally considered to be introduced to a herd through the addition of infected cattle, but both sheep and horses can maintain the infection and one study has suggested that sheep, the use of natural service and the presence of water courses that have run through other farms may all be risk factors for leptospirosis infection (Pritchard et al., 1989).

Fetal Loss

As with several other infections, abortion occurs as a chronic sequel, following up to 12 weeks after what is often a subclinical acute infection of the dam. Aborted fetuses and placentas do not show any characteristic pathology that is of diagnostic value, but the time course of infection is such that the fetus may have been able to mount an immune response and produce antibody. This antibody can be detected in fetal fluid by the microscopic agglutination test (MAT). Isolation of leptospires from fetal tissues is a preserve of the specialist laboratory and is not routinely used as a diagnostic test. The fluorescent antibody test performed on cryostat sections or impression smears of fetal tissues found favour for some time but inherent difficulties of such techniques in autolytic tissues mean that these tests too are now less frequently used. Once again the detection of specific DNA may well become the technique of choice and several PCR methods have been described (Smith et al., 1994). The literature on maternal serological response is extensive and serves to underline the diagnostic limitations of serological techniques. The MAT has long been the standard test and principally detects antibody of the IgM class. These antibodies are produced as an early response to infection and may have fallen to undetectable levels by the time the animal aborts. The enzyme linked immunosorbant assay (ELISA) can be designed to detect a specific subclass of antibody or a mixture, but the commercially available ELISAs usually detect predominantly IgG. After infection an animal produces detectable levels of IgG by 21 to 28 days and these persist for prolonged periods. Serology does not allow the differentiation between vaccinal titres and those that follow natural infection. For these reasons maternal serology is of little value in the individual animal that aborts and is best used as a herd diagnostic technique on the understanding that it may have limited applications in vaccinated herds. In dairy herds a principal reason for controlling the infection by vaccination is to reduce the risk of zoonotic disease in those milking the cows, but one study has claimed an improvement in fertility indices after vaccination (Dhaliwal et al., 1996). In beef herds the risk of zoonotic infection is low and there is no published study to demonstrate the value of vaccination, although this is a commonly used control strategy. Similarly the use of quarantine, serological screening and antibiotic treatment of animals that are seropositive are measures that have been recommended (BCVA, 1992). A successful national herd control programme based on the application of biosecurity and test and cull exists in the Netherlands. In Britain a programme of accreditation of freedom of disease has operated since 1989 (MAFF, 1989). Both approaches offer the benefit of allowing

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the sale of breeding replacements accredited free of infection.

Bacillus licheniformis Bacillus species are saprophytes that are widely distributed in the environment and with the exception of Bacillus anthracis are generally considered to have little pathogenic potential. Species differentiation is not easy, but the principal isolate from bovine abortions is Bacillus licheniformis. Bacillus organisms have been isolated from 9.8% of fetal specimens (Caldow et al., 1996) and outbreaks of abortion associated with this agent are commonly observed (David, 1993). Just how an organism that is considered to have little pathogenic potential can appear to be such an important fetal pathogen is not clear. It has been suggested that the risk of abortion may be related to the weight of infection in the environment, either in silage or in other forage or in contaminated water. However, other factors may be important and in 45 per cent of fetuses where a diagnosis of Bacillus licheniformis abortion was made evidence of fetal infection with Neospora caninum was also found (Caldow et al., 1996). Despite this the experimental infection by the intravenous route alone has resulted in placentitis and abortion with lesions similar to those observed in naturally occurring incidents (Agerholm et al., 1999). Usually abortion occurs relatively late in pregnancy and lesions of a necrotizing placentitis are observed with thickening of the intercotyledonary areas and adventitious placentation. Suppurative bronchopneumonia and occasionally pericarditis can be found in the fetus. The organism is readily isolated from the placenta, fetal lung and fetal stomach contents, but on occasion the organisms can no longer be cultured from the fetus despite isolation from the placenta and the presence of typical pathology. There is no indication that the bacteraemia that precedes the abortion is associated with any clinical disease in the dam and no serological test has been developed. In herds experiencing outbreaks group treatment with antibiotic is sometimes advocated, but there is no evidence of efficacy. It is prudent to screen cows for the presence of other agents that may be acting as cofactors as well as to carry out bacterial counts on silage. A threshold of 104 colony forming units/g has been suggested above which forage should not be fed to pregnant cows (David, 1993). Other potential sources of the organism should also be investigated, including drinking water.

Listeria monocytogenes (see also p. 904) There are similarities between listeria and bacillus as causes of abortion, although Listeria monocytogenes is

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generally considered to be a more significant pathogen. It may be associated with clinical disease in the dam, but is usually only a sporadic cause of cattle abortion. Listeria monocytogenes is a small Gram-positive rod that grows rapidly in aerobic or microaerophilic conditions at temperatures of between 3 and 45°C. It can tolerate pH values as high as 9.6, but is inhibited by pH values lower than 5.6 and exists as a plant saprophyte or as an animal pathogen (Low & Donachie, 1997). It is these characteristics that are crucial to the epidemiology of the disease in ruminants, allowing growth of the organism in poorly fermented silage and infection by ingestion. The clinical syndromes most commonly observed in cattle are iritis and meningoencephalitis, with abortion an uncommon sequel of either of these. Silage feeding is associated with a risk of listeriosis, however disease can occur when animals are grazing pasture. In addition to L. monocytogenes, the closely related Listeria ivanovii is also isolated occasionally from cattle fetuses (Alexander et al., 1992). In listeric abortion the aborted fetus is often autolytic, but non-specific lesions of placentitis and fetal septicaemia may be seen (Barr & Anderson, 1993) and the organism can be readily isolated from fetal viscera, stomach contents and the placenta. Serological tests for exposure to listeria exist, but are not used in the diagnosis of bovine abortion. The same restraints on treatment and control of bacillus apply to listeria. High-risk forages, which in this case are poorly preserved silages with a pH greater than 5, should not be fed to pregnant cattle. In addition to ensuring conditions that promote good anaerobic fermentation during the ensilage process, measures should be taken to reduce soil and faecal contamination of the grass prior to and during harvesting.

Salmonellosis (see also Chapter 15; p. 850) According to British diagnostic data, salmonella organisms were isolated from 159 to 300 cases of bovine abortion in each of the years of 1994 to 1998 (MAFF, 1998a). During this period Salmonella dublin made up 82 per cent of these diagnoses. In contrast, S. dublin accounted for 31 per cent of the non-abortion salmonella cases in adult cattle whereas the figure for Salmonella typhimurium was 54 per cent (MAFF, 1998b). These data suggest that S. dublin is more likely to manifest as a primary abortion problem than is S. typhimurium. There is a variation in the number of S. dublin cases diagnosed on a regional basis, indicating an endemic problem in some areas. Salmonella organisms are members of the Enterobacteriaceae and as such can be found as part of the intestinal flora in many species of domestic animals and

wildlife. The carrier state is particularly important in the spread of the disease and S. dublin shows a greater tendency towards the carrier state than S. typhimurium in cattle. Studies on the epidemiology of S. typhimurium determinant type 104 have also demonstrated the important role of newly introduced animals in the spread of this disease (Evans & Davies, 1996). While it remains unclear how important wildlife are in initiating new outbreaks, infection was found to be maintained in rodent and wild bird populations after an outbreak. Infection of the placenta follows bacteraemia and extension to the fetus can follow from this. However, neither infection of the fetus nor indeed placentitis is required to cause fetal death or abortion. Where fetal infection has occurred gross lesions are non-specific; histological lesions of fetal septicaemia may be found and the organism may be isolated from fetal tissues and the placenta. If the cow is showing signs of septicaemia at the time of abortion it is advisable to attempt to isolate the organism from faeces. Serological tests for salmonellosis are available, but are not used routinely for diagnostic purposes in the investigation of bovine abortion. Once a diagnosis of salmonellosis has been made control rests on efforts to minimize further spread of infection within the herd through improved hygiene and thorough cleaning and disinfection. There are conflicting reports of the effectiveness of vaccination against S. typhimurium in the face of an outbreak (Davies & Renton, 1992; Mee & Malone, 1995), but a S. dublin vaccine is available and has been used successfully in endemically infected herds (Wray et al., 1989). The removal of S. dublin carriers after an outbreak appears to be an attractive course of action, but this approach is impractical as excretion is periodic. Faeces must be cultured with negative results on three occasions at 14-day intervals before an animal is considered to be free of infection. In addition, animals must be individually housed or stall-tied with this method as there is the possibility of passive excretion if animals are loose housed or at pasture (Radostits et al., 1994). Farmers should be aware of the risks that purchased breeding replacements pose and added animals should be placed in quarantine and screened by culture as above.

Campylobacter (see also p. 568) Venereal campylobacteriosis is considered to be an important cause of bovine infertility wherever natural service is used and abortions are a feature of this disease. Recent observations have suggested that the condition may be more prevalent in beef herds in Britain than has been widely presumed (Caldow & Taylor, 1997).

Fetal Loss

Campylobacter fetus is a microaerophilic, motile bacterium that has two recognized subspecies: C. fetus subsp. venerealis and C. fetus subsp. fetus. Differentiation has been based on the variation of antigenic and biochemical characteristics of the subspecies, notably that C. fetus subsp. venerealis will not grow in 1 per cent glycine whereas C. fetus subsp. fetus will. This differentiation is important, as C. fetus subsp. venerealis is considered to be adapted to the bovine reproductive tract and to be the cause of venereal campylobacteriosis, whereas C. fetus subsp. fetus is a gut commensal causing sporadic abortion in cattle. However, strains of the latter vary in their biochemical characteristics and strains identified as C. fetus subsp. venerealis have developed tolerance to glycine (Chang & Ogg, 1971). In addition, strains identified as C. fetus subsp. fetus, when used in experimental studies, have resulted in disease indistinguishable from that caused by C. fetus subsp. venerealis (Schurig et al., 1973) and field outbreaks of venereal campylobacter infertility associated with C. fetus subsp. fetus have been identified (MacLaren & Agumbah, 1988). It would therefore appear that strains of both subspecies are capable of causing venereal infertility and whenever C. fetus is isolated from abortion material the possibility of herd venereal infertility should be investigated. In the case of sporadic abortion not associated with venereal infertility, invasion from the intestinal tract is the probable route of infection. The venereal form of the disease is usually introduced to the herd via an infected mature bull and while younger bulls or breeding females are less likely sources, any animal that has previously been mated constitutes a potential source of infection. The use of hired bulls is considered to be a particularly high-risk practice. Infection in the bull follows natural mating with an infected cow, but is not associated with clinical signs or pathological changes. In mature bulls infection becomes established in the lumen of the epithelial crypts of the prepuce, while bulls younger than 6 years of age are more resistant to infection (Clark, 1971). In natural service the spread of infection is from the penis to the anterior vagina, where the organism becomes established before entering the uterus to cause a mild endometritis and salpingitis. Pathological changes are most pronounced at 8 to 13 weeks after infection and have resolved by four to five months (Dekeyser, 1986). Where conception has occurred embryonic death and a delayed return to oestrus, abortion or the birth of a live full term calf can follow. Of the abortions that are detected the gestational length is usually around four to five months. A marked placentitis and pericarditis may be seen on gross examination of the tissues and histological findings are of fetal septicaemia and pneumonia.

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Diagnosis of C. fetus as a cause of abortion rests on the isolation of the organism from the fetus. As faecal contamination of the placenta may occur after the abortion, isolation from the placenta should not be considered diagnostic unless reinforced by histopathology. After venereal infection in the cow, antibody is secreted in the uterine and vaginal fluid. Of this IgG is the most important component and can be detected eight weeks post infection, but is largely undetectable by six months. IgA is produced by three to five weeks and is still detectable for up to a year after infection (Corbeil et al., 1974). Despite recovery, the development of immunity and the establishment of normal pregnancies, C. fetus has been isolated from the vaginal mucus more than a year after infection (MacLaren & Agumbah, 1988), creating the potential for cows as well as bulls to maintain the infection in the herd from one year to the next. The sampling technique most frequently used in bulls in Britain is the collection of sheath washings (BCVA, 1995) and phosphate buffered saline (PBS) is adequate for the lavage fluid provided samples are relatively free from gross contamination and transported to the laboratory within four to six hours. However, where immediate delivery to the laboratory cannot be achieved the use of transport enrichment medium (TEM) has proved to be effective in maintaining the viability of the organism (Hum et al., 1994). A fluorescent antibody test is available, but does not allow differentiation between the two subspecies and it is of limited value in the diagnosis of the disease. Vaginal mucus should also be collected without gross faecal contamination and this can best be achieved by using pipettes with the end closed off and perforations made in the last few centimetres. Twenty ml of PBS are injected through a 60 ml syringe and then aspirated back, bringing with it vaginal mucus (Lander, 1983). As with sheath washings, TEM can be used if there is to be a delay of more than six hours between sample collection and the inoculation of media. In the vaginal mucus agglutination test (VMAT) antigens prepared from C. fetus are used to detect agglutinins in the vaginal mucus. Immunoglobulin A is the antibody present in the mucus, but where serum or blood contaminates vaginal secretions false positives can arise as serum antibody to C. fetus is common in cattle (Wilkie & Winter, 1971). In addition, where cattle are in oestrus, large amounts of mucus is produced, IgA is diluted and false negatives can occur. Problems have been reported with the test and it has been suggested that only 50 per cent of infected animals will be positive by VMAT and of those 50 per cent will be negative six months after infection. An enzyme-linked immunoassay has been developed to overcome some of the problems experienced in using the VMAT (Hewson

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et al., 1985; Hum et al., 1991), but the test is not currently used in Britain. As a consequence of the delay between infection and investigation in most herds and the cows’ ability to clear the infection as well as the limitations of the vaginal mucus agglutination test it is necessary to sample a minimum of 12 cows. Where endemic infection is suspected animals in their first year in the breeding herd should be sampled to offer the best chance of achieving a diagnosis. Bulls should be sheath washed in the course of a herd investigation, but a negative result is of little value as the screening is a relatively insensitive test. Artificial insemination using semen from campylobacter-free studs offers a simple and successful method of control, but for some herds, particularly where mating occurs at grass, this may not be practical. Vaccination is used in many countries where the disease occurs in range cattle and a vaccination programme to eradicate infection from within a herd has been described (Hum & MacInnes, 1987). Antibiotic treatment of the bulls is suggested as an additional measure (Hum et al., 1993). However, there is no licensed vaccine in Britain and an emergency vaccine must be produced under the authority of the Veterinary Medicines Directorate (see Chapter 59). Prevention can be achieved by maintaining a strict closed herd policy, but in practical terms the purchase of virgin heifers and virgin bulls does not constitute a risk. Difficulties arise where bulls have to be replaced at short notice. In these situations a synchronization and insemination programme would offer the safest course of action with a young unproven bull used to sweep up. If mature bulls are used these should be screened and treated with antibiotics (BCVA, 1995).

Miscellaneous bacteria Species of bacteria associated only with sporadic abortions can be split into those that can be readily isolated from the posterior reproductive tract of the normal animal and those that cannot. The former category includes organisms such as Haemophilus somnus, Arcanobacterium pyogenes, Streptococcus dysgalactiae, Mycoplasma bovis and Ureaplasma diversum. These may gain entry to the uterus through the cervix as a sequel to some other disease process affecting the fetus. It is possible that strain differences in virulence exist, but at the present time these agents should be considered to be of minor importance. Ureaplasmas have been suggested as important, but isolation methods for these organisms are rarely employed in diagnostic laboratories (Sanderson & Chenoweth, 1999).

The second category includes Yersinia pseudotuberculosis, Mannheimia haemolytica, Erysipelothrix rhusiopathiae and Staphylocccus aureus where infection of the fetus follows bacteraemia in the dam. Arcanobacterium pyogenes may also gain entry to the conceptus in this way and experimental infection via the intravenous route with this organism has resulted in abortion (Semambo et al., 1991). These infections are unlikely to represent a herd problem and as such do not merit further discussion.

Protozoal causes of abortion Trichomoniasis Bovine trichomoniasis is caused by the protozoan parasite Tritrichomonas fetus and is a venereal disease responsible for early embryonic death, infertility, pyometra and abortion. It is a particular problem in range cattle, where as many as 50 per cent of the herds may be infected (Dennet et al., 1974). There is no recent report of the disease from within Britain, but there is no biological barrier that would prevent the disease from occurring here and diagnostic laboratories in Britain do not routinely use techniques that would identify the presence of this agent. Therefore trichomoniasis should be considered in the differential diagnosis in herds using natural service where infertility, abortions and pyometra are observed. Although most pregnancies are lost at around 17 days after conception, one review reported that death can occur at any time up to the fifth month of gestation (Yule et al., 1989), and fetal infection has also been demonstrated in late abortions and in full term calves (Rhyan et al., 1988). No specific gross changes are seen in the abortion material. Histological examination reveals lesions of placentitis and pyogranulomatous bronchopneumonia with evidence of tissue invasion with the parasite (Rhyan et al., 1995). The organism can be cultured from vaginal discharges, preputial smegma and fetal tissues by using a specific medium in a pouch system (Kvasnicka et al., 1996). Trichomoniasis can be controlled through the use of artificial insemination and commercial vaccines are available in the countries where the disease is endemic.

Neosporosis (see also p. 283) Protozoal abortion has been recognized as a problem in the dairy herds of California since the mid 1980s (Anderson et al., 1991) and around the same time a protozoan parasite of dogs was identified in Norway

Fetal Loss

(Bjerkås et al., 1984). This was subsequently named Neospora caninum (Dubey et al., 1988) and the link was made to the infection of cattle (Thilsted & Dubey, 1989). Since then N. caninum has been identified as a cause of abortion in many parts of the world and a major volume of research publications has been generated (Dubey, 1999). Serological studies have found evidence of exposure to the organism in 16 per cent of aborted fetuses in Scotland (Buxton et al., 1997) and in 13 per cent of cows that aborted in Northern Ireland (McNamee et al., 1996). Outbreaks described range from 11 per cent of cows that aborted in one herd in England (Dannatt et al., 1995), to as many as 57 per cent of a herd in The Netherlands (Wouda et al., 1999). While neosporosis is a recently recognized disease there is nothing to suggest that the parasite or the disease is new. Neospora caninum is an apicomplexan protozoan closely related to Toxoplasma gondii and although the complete life cycle of the parasite is still to be determined dogs have been shown to be a definitive host and to pass small numbers of oocysts in faeces from 8 to 23 days after experimental infection (McAllister et al., 1998). Tissue cysts and tachyzoites have been found in cattle, sheep, goats and horses and it is possible that the intestinal stage of the life cycle is not limited to the dog. Vertical transmission occurs in addition to the point source outbreaks, where cows are presumed to be infected for the first time and abort. As post natal infection rates are probably as low as 1 per cent (Hietala & Thurmond, 1999) most cases are due to vertical transmission where an infection rate of 95 per cent has been found (Davison et al., 1999). Infection of the fetus may often be a relatively benign event and care should be taken in attributing significance to evidence of infection in an aborted fetus (Thurmond et al., 1997). Coinfection with other agents is often found and potentiation or the presence of factors that cause immune suppression in endemically infected herds may explain some of the cases that appear as epidemics (Bartels et al., 1999). Experimental infection of pregnant cattle has resulted in fetal death and lesions indistinguishable from those seen in naturally occurring outbreaks (Barr et al., 1994). Abortion most frequently occurs in the second half of pregnancy and the commonly observed lesions are limited to placentitis, focal non-suppurative encephalitis, non-suppurative myocarditis and myositis and widespread non-suppurative infiltrates in other organs (Anderson et al., 1991). The tissue cysts are well tolerated and the host response is limited to the tachyzoites. Histological examination of the fetus is important in order to determine the severity and therefore the significance of the lesions in terms of fetal death (Thurmond et al., 1999). The histological appearance of

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the lesions is considered significantly characteristic to warrant a diagnosis and immunohistochemistry gives further specificity to this. Autolysis often hampers examination although tissue cysts do survive and may be recognized. The fetus is capable of mounting an immunological response to neospora infection and detection of specific antibody in fetal or precolostral sera is a reliable indicator of fetal infection, but not of infection causing fetal death (Otter et al., 1997). At present, despite the availability of molecular biological techniques for the detection of neospora DNA they are not routinely used for diagnostic purposes. Maternal infection is followed by the production of antibodies within 14 days that peak by 46 days and in most cases the time lag between maternal infection and abortion is such that antibody production will have peaked before the abortion and may occasionally have fallen to undetectable levels by two months after the abortion (Wouda et al., 1999). In the congenitally infected individual there is fluctuation in antibody level and at times antibody is undetected. The observations that congenitally infected animals have been found to have a higher risk of abortion at their first gestation compared to the second gestation and that abortions occurred at an earlier stage in the first gestation than subsequently suggest the possibility of a protective immunity developing in infected animals (Thurmond & Hietala, 1997). Given the close relationships between neospora, toxoplasma and sarcocystis species there were concerns that serological cross-reaction could occur, however it has been shown that such crossreactivity is negligible and of no importance diagnostically (Dubey et al., 1996). The lack of a complete understanding of the life cycle and knowledge of the range of definitive hosts has led to a cautious approach to control, but there seems a clear argument emerging in favour of culling seropositive animals from the herd. These have been shown to have lower levels of production and suffer a higher risk of abortion than seronegative cows within the herd. By using information from the literature in a mathematical model it has been shown that annual culling of seropositive animals was the most effective and rapid method of control. Effective control at a slower rate could be achieved if the action was limited to excluding the offspring from seropositive cows from the breeding herd (French et al., 1999). At the present time the question of the cost-benefits of these strategies has not been addressed, but given the large outbreaks that can occur, action to prevent a sudden catastrophic, albeit low-risk, occurrence might be justifiable. Irrespective of culling practices, all fetuses, placentas and cattle carcases should be disposed of in a way that prevents recycling of N. caninum infection through definitive hosts.

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Other infectious agents causing abortion Chlamydia and rickettsia Q fever, Chlamydophila abortus and Cytocoetes phagocytophilia have all been identified as occasional causes of bovine abortion. There is serological evidence of exposure to the agent of Q fever in Britain (Paiba et al., 1999), but no recent report of abortion in cattle due to this agent. Occasionally a purulent placentitis and the presence of elementary bodies in modified Ziehl Neelsen stained smears of placenta and stomach contents are observed. Establishing the precise aetiology in these cases can be difficult, but Chlamydophila abortus has been isolated from such material and in one report the strain was found to be identical to that responsible for chlamydial abortion in sheep (Griffiths et al., 1995). The outbreak may have been the result of close contact between cattle and an infected sheep flock on the same premises. Cytocoetes phagocytophilia, the cause of tick borne fever (TBF), will cause abortion in cattle when first exposure to ticks occurs during pregnancy. Diagnosis can be difficult to confirm, as there is no longer parasitaemia by the time the abortion occurs. A presumptive diagnosis may be based on the herd history and the presence of ticks and antibody to the TBF agent.

Mycotic abortion Mycotic abortion with placentitis and fetal infection is reported throughout the world. In one detailed study 7 per cent were mycotic abortions and Aspergillus fumigatus infection accounted for 62 per cent of these (Knudtson & Kirkbride, 1992). Other species of fungi have been reported and it would appear that most are opportunist pathogens. The source of these infections is often poorly preserved hay or ensiled feed that has undergone aerobic fermentation. Placentitis follows a septicaemia that has resulted from either ingestion or inhalation of spores from the environment. The placenta is frequently thickened and may be of a leathery appearance. White plaques on the skin of the fetus are an occasional feature of this disease, but apart from this gross lesions are seldom observed. At the microscopic level hepatitis, pneumonia and placentitis are evident and Grocott’s stain can be used to reveal fungal hyphae in fixed sections. Fungal elements can be seen on direct microscopy of the placenta and the stomach contents, the latter being diagnostic. These organisms are readily cultured from the fetus and the placenta, but environmental contamination after the abortion has occurred may explain isolation from the placenta alone. There is little information on the development of

immunity after infection or whether the cow is likely to return to normal fertility. Prevention of mycotic placentitis is by reducing the degree of fungal contamination pregnant cows are exposed to, particularly in preserved forage. Fungal growth occurs in other feedstuffs and bedding materials and after a diagnosis of mycotic abortion the management system should be reviewed in order to identify possible sources of these organisms. A visual examination of suspect materials may be sufficient, but where doubt over the source remains it is also possible to use quantitative culture methods to assess the degree of fungal contamination and to identify the organisms present.

Non-infectious causes of abortion The failure to identify an infectious cause in many cases has led to the suggestion that non-infectious causes are of importance (Norton & Campbell, 1990). Nutritional factors that may be involved include excess dietary protein or non-protein nitrogen and selenium or iodine deficiency. Twin pregnancies are associated with shorter gestation lengths and an increased rate of abortion (Echternkamp & Gregory, 1999). Various poisonous plants have been implicated, but none is indigenous to Britain. Ponderosa pine (Pinus ponderosa) and locoweeds (Astralagus sp.) cause significant problems in some areas of North America. Deaths due to aflatoxicosis and to nitrate toxicity may be preceded by abortion, suggesting that either the fetus is marginally more sensitive to any toxic effect than the dam or that fetal death is the consequence of the clinical disease in the dam. However, the literature fails to support non-infectious causes as a numerically significant cause of abortion in cattle (Norton & Campbell, 1990) and in the UK only iodine deficiency, manifest as hyperplastic goitre in full-term stillborn calves, is of importance. The condition is mainly reported in beef herds or in dairy heifers and is thought unlikely to affect dairy cows due to adequate dietary iodine intake. A threshold of 15 g for the weight of the intact gland, above which goitre is suspected, has been in common use. A better indicator is the ratio of thyroid weight to fetal body weight where the threshold value is 1 : 3000. However, oedema of the head and neck in stillborn calves can render this unreliable (Gee et al., 1989) and histological examination of the gland to confirm the presence of a colloid goitre is recommended (Capen, 1993). There does not appear to be any suggestion that goitrogenic factors should be considered and the inclusion of iodine in an oral mineral supplement should prevent the condition (see pp. 257, 301).

Fetal Loss

Investigation In abortion outbreaks in cattle herds abortions are frequently irregular and the single abortion may mark the start of an outbreak that does not become apparent for several weeks. An observed abortion may also represent a more extensive underlying herd problem and therefore there is justification for investigating every abortion. However, there are concerns over unnecessary costs and the diagnostic rate has been found to be higher in cases where there has been more than one abortion in the herd previously (Caldow et al., 1996). Since there is a statutory requirement to report all abortions in Britain there is the opportunity to discuss the problem with the client and to carry out the investigations considered necessary in each individual case. Investigations should follow a standard pattern: (1) (2) (3) (4) (5)

History Clinical examination of the cow Necropsy of fetus Collection of samples for the laboratory Interpretation of results

History The use of a standard form allows the systematic collection of the important details of the individual cow as well as production system, cow numbers, age structure, biosecurity measures, replacement policy and source of replacements (Fig. 37.1). Details on the feeding system and how feeds are stored are also of relevance. This can usefully be expanded to include details on herd fertility, retained membranes and any background clinical problem that may be of relevance. Careful evaluation of the information is essential to guide the investigation and to indicate the diagnostic tests to be employed.

Clinical examination In most cases examination does not yield useful information, but it is important to exclude conditions such as acute salmonellosis, summer mastitis or tick borne fever and to allow treatment if the cow is ill. At this time a blood sample for serology should be collected and if salmonellosis is suspected a faeces sample as well. Where stillbirth is the problem the body condition of the cow should be assessed and other cows in late gestation can also be examined in this way. Where the majority of animals in the group have scores of 3.5 and above there is cause for concern over excessive body condition. Even when it has been decided to limit diagnostic tests to those required for brucellosis, a serum sample can be stored frozen for possible retrospective examination.

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Examination of the fetus and placenta In the ideal situation, the entire aborted calf and fetal membranes with the appropriate samples from the dam should be delivered directly to a veterinary diagnostic laboratory. Where transport difficulties or other delays preclude this, the field veterinarian should collect appropriate samples while carrying out a necropsy of the fetus. A standard approach to the examination should be adopted and the appropriate information recorded. The measurement of the crown–rump length can give an approximation of gestational age. A formula to estimate the fetal developmental age from the crown–rump measurement is x = 2.5(y + 21), where y is the crown–rump length in centimetres and x is the gestational age in days. Measurement of the weight of the carcase is particularly important in stillbirths to explore the possibility of dystokia due to fetal maternal disproportion and for comparison with thyroid weight, for the diagnosis of hyperthyroidism. Other important features to be aware of include the presence of white plaques of fungal hyphae on the skin of fetuses where there is fungal involvement. Meconium staining of the perineum or the presence of meconium in the airways or fetal stomach indicate fetal anoxia consistent with placentitis or the prolonged parturition of dystokia. Haemarthrosis of the shoulder or hip joints may be seen in dystokia cases. Traumatic lesions in fetuses where dystokia has not been the problem are occasionally observed and while trauma may be the cause of the abortion other causes should not be excluded too early in the investigation. Lesions of pericarditis, pleurisy, pneumonia or hepatitis can all be found on the gross examination, but none of these changes is specific. In calves that have lived for a short time after birth it is important to record whether the calf has fed as this prevents useful bacteriological examination of the stomach contents,but also means that maternal antibody may have been absorbed, interfering with fetal serological tests. When the placenta is available as much of the surface area of the allantochorion as possible should be examined. Lesions can be focal and may be overlooked if insufficient care is taken. Commonly observed lesions are intercotyledonary thickening, necrosis of cotyledons and adventitious placentation. The last lesion is considered to be a chronic response to insufficient placental area and is seen following placentitis.

Collection of samples for laboratory investigation If samples are collected in the course of a necropsy on the farm, the collection and transport of samples to the laboratory should have been discussed with the laboratory personnel. The samples required and the means of

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Reference Number: C2………………………………… CASE HISTORY

Date of Abortion/Stillbirth………………………………

Ear no. of dam……………………………………………………………… Age of dam……………………………… Due on…………………… Source of dam……………Home bred

Purchased

Breed……………………………………… Vaccination: BVD L. hardjo No. of abortions……………………

Dam…………………………………………

Sire…………………………………………

Other………………………………… No. of stillbirths……………………

No. of weak calves……………………

Group size…………………………

Total cows………………………………

IBR

Calving starts……………………… Replacements:

Home bred

Bought in

Mixture

Method of service

AI only

Natural only

Both

Have hired bulls been used? Yes Production: Beef

No

Dairy

Body condition score of cows/heifers: …………………………………

HOUSING/MANAGEMENT Roughage Concentrate Mineral/trace element supplements

HERD FERTILITY (Dairy) Average days to conception All serves pregnancy rate % barren after p.d. positive

HERD FERTILITY (Beef) No. of barren cows Length of breeding/calving season

DETAILS OF PARTURITION Degree of assistance required/use of calving aid: ……………………………………………………………………………………………… Calf alive at onset of assistance: YES Placenta expelled with calf: YES

NO NO

Vet involved with calving:

YES NO Other information: …………………………………………………………………………………………………………………………………… ………………………………………………………………………………………………………………………………………………………… Fig. 37.1

A standard form to collect systematically important information when investigating fetal losses.

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preservation are determined by the causes of abortion that occur in an area and on the diagnostic facilities available to the laboratory. Nevertheless, basic rules do apply. The minimum sample required for bacteriology is fetal stomach contents. These can be collected using a sterile vacutainer and needle through the unopened abomasal wall. Where the placenta is available a cotyledon representative of the lesions observed should also be submitted fresh. Samples may also include fetal liver and lung, allowing slightly higher diagnostic success for some bacterial causes of abortion. It has been suggested that in cases where the fetal membranes have been retained a placentome is removed manually per vaginum (Johnson et al., 1994) for bacteriological and histological examination. However, this is not required when the fetus is available for examination. Fetal blood or fluid can be collected from any body cavity, again by using a vacutainer. This sample is used for serological tests for BVD, neospora and leptospira. Fetal thyroid, spleen, kidney and brain are all tissues that can be used for virus isolation for BVD, while the placenta is the sample of choice for BHV1. Histopathological examination is particularly useful to determine the significance of fetal infection with N. caninum or BVD, to confirm the significance of apparent thyroid enlargement and for further investigations where the standard screen for infectious disease is negative. The tissues of most value to collect are brain, lung, liver, thyroid (in stillbirths) and a cotyledon. It is important to be guided by the pathologist as to how these samples should be fixed. Tissues for histology must never be frozen. The minimum samples are fetal stomach contents for bacteriology and fetal blood or serum for serological tests. These may be the samples of choice when investigating what appears to be a single abortion. If subsequent abortions occur then the range of tests can be extended.

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precedes abortion so that paired serology is valueless. As many of the infections of importance tend to be endemic and circulating antibody may persist for long periods the presence of maternal antibody at the time of the abortion can only be taken to show that the cow has been exposed to the agent. The converse applies when the MAT is used for leptospirosis as the IgM antibody response can be so transient that the dam may be seronegative at the time of abortion. In essence, serology tests in the dam are of more value when used to exclude infection with negative results than to attempt to confirm a diagnosis with positive results. This should not discourage the use of these techniques to establish whether or not there is evidence of these diseases in the herd, as control strategies may still be required. Evidence of the involvement of several infectious agents is often found in the course of an outbreak, underlining the importance of proper evaluation of the results, but also raising the question of a potentiation effect amongst agents.

Prognosis For the individual cow the prognosis is usually favourable as long as any systemic disease or uterine infection is detected and treated. After abortion, oestrous cycles start quickly and, in general, subsequent pregnancy rates are satisfactory. Prognosis for the rest of the pregnant animals in the herd is a more serious consideration and varies with the diagnosed cause of abortion.

Conclusion Abortions are often the most obvious manifestation of an underlying herd problem that may be of significant financial importance to the owner of the cattle herd. Failure on the part of the veterinary surgeon to pursue or advise correctly could have a severe penalty for the producer.

Interpretation of results When evaluating results it is important to consider them in relation to the diagnostic criteria for each disease. Hence, while the presence of antibody to BVD or to N. caninum is considered to indicate fetal infection, it must be remembered that infection of the fetus need not necessarily be lethal, especially as gestational age increases. Similarly, the isolation of foetopathic bacteria or fungal organisms from the placenta in the absence of histopathology is of no value as they may arise from environmental contamination after the placenta has been passed. In the majority of infections maternal infection

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and infection and the immunofluorescent localization of the organism in infected heifers. Canadian Journal of Comparative Medicine, 35, 301–12. Wouda, W., Bartels, C.J.M. & Moen, A.R. (1999) Characteristics of Neospora caninum-associated abortion storms in dairy herds in the Netherlands (1995 to 1997). Theriogenology, 52, 233–45. Wray, C., Wadsworth, Q.C., Richards, D.W. & Morgan, J.H. (1989) A three-year study of Salmonella dublin infection in a closed dairy herd. Veterinary Record, 124, 532–5. Yule, A., Skirrow, S.Z. & BonDurant, R.H. (1989) Bovine trichomoniasis. Parasitology Today, 5, 373–7.

Chapter 38

Bull Infertility D.N. Logue and W.M. Crawshaw

Introduction Bull use in the UK The role of the veterinarian in bull use Preventing infectious infertility and other diseases Preputial washing Infectious disease control Investigation of bull infertility History Examination of the bull for breeding soundness Manifestations, aetiology, treatment and prognosis of bull infertility Failure to mount Failure to achieve intromission Failure to thrust and ejaculate after intromission Normal service with a poor pregnancy rate Conclusion

594 595 596 596 597 598 598 598 599 610 610 612 616 617 624

Introduction Since the domestication of cattle the bull has been a talisman and the desire to own a special bull a particular urge in all stock rearing countries. The bull is a symbol of power in the East, where Indra the sky deity is represented in myth as a mighty bull, while in the West as an example there is the Celtic legend of the Brown Bull of Quelgny stolen by Queen Mae of Connacht from Dara in Ulster only to be retrieved by the hero Cuchulain. Time has not diverted man a great deal from this interest in bull lineage and the performance of his offspring! The development of methodologies to assess the transmission of superior economic traits from bulls to their progeny over the last 50 years has been one of the success stories of the cattle industry. However, like the Brown Bull the truly outstanding sire is still very rare and the purchase of a young unproven bull is a gamble. Despite this the repeated need for young bulls (no bull is immortal) means that many are bought with this vision in mind, despite the difficulties in achieving it. When all breeding was by natural service the potential for genetic improvement by a good bull was very limited. Furthermore, selling, sharing and hiring animals resulted in the spread of venereal disease with some disastrous results for those affected farms. Artifi594

cial insemination (AI) has proved to be one of the most successful reproductive technologies and it became a commercial reality in the UK just before the end of the Second World War. AI has fulfilled two objectives: firstly, it set in motion more focused genetic improvement coupled with the widespread use of good bulls and secondly, it has limited the spread of venereal diseases. Unfortunately, the expression of oestrus in the cow varies in time of occurrence, duration and intensity and many farmers find accurate and, more particularly, efficient oestrous detection difficult and time consuming. Furthermore, particularly in large beef suckler herds under essentially range conditions, oestrous detection and the handling of cattle for AI are less practical. These factors ensure that many farmers continue to use natural service entirely or partially even though, due to the genetic improvement from AI, dairy farmers in particular could afford to have a longer calving interval and yet still expect to have the same financial returns (Hillers et al., 1982; Stott et al., 1999). The problem is illustrated by a study of UK national cattle population statistics where only approximately half the cows are bred by AI (Logue & Isbister, 1992), this figure being considerably higher for the dairy herd. Although confidentiality has stopped many of these statistics being easily available in the UK we have no reason to believe the proportion has changed. However, this figure may increase following the 2001 foot and mouth disease outbreak. In the USA the proportion bred by AI is probably a little higher (70 per cent). In addition, there have been a number of factors that have counteracted the undoubted improvements in the efficiency of AI. (1) The economics of dairy and beef production have resulted in a general trend to larger herds with fewer staff and so less time available for oestrous detection. Furthermore, the continuing financial pressure to cut costs has also made many dairy farmers economize by changing from paying for a technician AI service to inseminating their own cows (DIY AI). Many of these people keep a bull as a precaution against poor fertility arising from a doubtful insemination technique. Unfortunately, no figures are produced for the number

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Table 38.1 Number of cows in DIY AI herds (Anon. 1988).

DIY licences Average herd size Number of cows Cows inseminated (assuming 75%) by DIY AI

England and Wales

Northern Ireland

Scotland

Total

3 300 69 227 700 170 775

1 000 37 37 000 27 750

700 89 54 300 40 725

5 000 – 319 000 239 250

Table 38.2 UK dairy cattle statistics (Anon. 1979, 1988, 1998). Year

Cow numbers ¥ 106

Herd size

1960 1970 1980 1990 1997

4.01 4.55 4.69 4.43 4.41

20 31 55 67 72

of cows inseminated in the DIY AI sector in the UK. However, census data, the number of DIY AI licences issued by area and the assumption that 75 per cent of the cows in each herd are inseminated does allow an estimate (Table 38.1). It can be seen that DIY AI probably accounts for less than one in five of all dairy cow inseminations in the UK. (2) The gradual increase in herd size has meant that the added costs of keeping one or even several bulls are relatively lower per unit of production. For example, in the UK, dairy herd size has increased dramatically over the last 30 years (see Table 38.2), and this has been mirrored in Europe and in virtually all countries with an advanced dairy industry. (3) A further effect of the larger number of cows per herd has led to a more predictable production of heifer replacements because the male : female ratio remains nearer to the expected 50 : 50 as the numbers increase. This has meant that a definite block of heifers of similar age can be released for natural service. (4) In many beef and dairy herds, calving, and thus breeding periods, are concentrated into relatively short periods of time for production and management reasons. This leads to a requirement for high oestrous detection rates and high fertility, both of which are best achieved by using a combination of AI and natural service. (5) Finally, in the past an important reason for using AI was to reduce the introduction of disease. With the

increasing improvement in the health status of the national herd in many countries there is less pressure for AI use for this reason alone. However, this confidence is likely to be misplaced unless the farm takes adequate precautions when acquiring bulls.

Bull use in the UK It is worthwhile defining the various types of herd breeding policy since this will influence the management of the bull and may give a guide to the needs of the unit with regard to disease control. Four basic types of policy can be recognized: (1) Beef suckler herd. The principal demand is to produce calves for finishing. The cows are mated while suckling. For many years and in most geographical locations it has been axiomatic that this system operates at highest efficiency when there is a short (but efficient) breeding period (Kilkenny, 1978). Ideally this should be less than 10 weeks and demands very high levels of fertility in both bull and cow. (2) Dairy heifers. A considerable proportion of dairy herds use natural service when breeding heifers. This is mainly to avoid oestrous detection and the need to gather the individual heifer for AI when often these are run on a more remote area of the farm. (3) Sweeper bull. This term usually refers to the running of a bull after a fixed period of ‘AI-only’ breeding. Generally, in dairy cattle, the bull used is a beef breed and thus any calves born are easily distinguished from purebred dairy calves. The use of synchronization and fixed-time AI with batches of maiden heifers using an easy-calving sire has to some degree replaced natural service in both dairy and beef heifers, but in many herds those heifers that return are served by a sweeper bull. The timing of the introduction of the sweeper is paramount since mating pressure will obviously depend on the number of non-pregnant cows or heifers left after the AI breeding period. Clearly a

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drop in the pregnancy rates achieved with AI can result in an increase of mating pressure. (4) Modified sweeper. The sweeper bull is utilized for mating selected cows throughout the breeding season, for example cows of low genetic potential, repeat breeders, cows not exhibiting firm signs of oestrus and cows with a history of being difficult to get in calf. Subsequently, the bull is used as a ‘true’ sweeper. Finally, a minority of dairy herds still primarily use natural service.

The role of the veterinarian in bull use The role of the veterinarian in the control and monitoring of bull fertility is three-fold (see Box 38.1). Veterinarians should be authoritative in these roles for their clients or be able and willing to refer matters to another veterinarian with the appropriate resources if the occasion demands.

Preventing infectious infertility and other diseases Before considering the reproductive performance of the bull on the farm the first priority must be to keep disease out! No veterinarian or farmer should be without some appreciation of the risks that are being taken by the purchase of a bull (or even semen or embryos). In addition to the notifiable diseases (such as foot-and-mouth disease) there are a whole plethora of others that can cause economic loss. Unfortunately in the past, farmers in the UK, and for that matter elsewhere, have been pretty cavalier in their attitude to introducing disease. Veterinarians, by discussing these issues with their clients, can do much to reduce the risks of introducing disease and so protect the viability of their clients’ farms. The loss of output arising from the Box 38.1 Role of the veterinarian in bull fertility. (1) (2)

(3)

Preventing the introduction of infectious infertility and other diseases to the farm Assessing fertility and the level of investigation that is needed: (a) before purchase (b) after purchase (c) before use each breeding season (d) after poor fertility results Monitoring herd fertility (including the bull) by the assessment of breeding records

damaging effects of infectious disease impacts significantly on efficiency. The most important source of infectious disease for cattle is other livestock, particularly cattle. Uncontrolled movement of a bull into a herd carries a significant risk of introducing disease. This can be minimized by the following measures but presupposes that other biosecurity precautions are in place: (1) Bulls (and any other cattle) should be purchased only from herds certified free from specific diseases of concern by reputable cattle health schemes such as those registered with the Cattle Health Certification Standards (CheCS) body in the UK. While individual farm programmes can be undertaken or declarations made by the farmer and his veterinarian to the effect that a particular disease has not been seen, clearly these will have less certainty. The latter point is illustrated by Kallis et al. (1999) who revealed by faecal culture that 40 per cent of 100 Dutch dairy herds considered to be free of Johne’s disease on the basis of owner and veterinary declaration were actually infected. (2) Quarantine incoming cattle before entry into the main herd to allow testing for diseases that may be carried and development of any incubating diseases. In most cases four weeks should suffice, but this depends on circumstances and the diseases under consideration. Quarantine could also be applied to other species of livestock entering the farm that potentially carry diseases infectious to cattle. (3) During the quarantine period an adequate testing programme and/or prophylactic treatment against diseases of concern should be employed. The latter may be necessary where testing is unreliable or gives an equivocal answer (e.g. for venereal campylobacteriosis and Leptospira hardjo). The diseases of importance vary with country and area and are determined by the economic or practical importance of the disease, an assessment of the risk of introducing the disease, the availability of low cost and reliable tests and whether or not the disease is already present in the herd. In the UK the following nonstatutory diseases are suggested as being worthy of consideration based on their prevalence and the economic impact that they may have on the herd. Bovine virus diarrhoea virus (BVDV) Infectious bovine rhinotracheitis virus (IBRV) (bovine herpes virus 1 [BHV-1]) Leptospira hardjo Johne’s disease (paratuberculosis) Venereal campylobacteriosis Salmonellosis (especially S. dublin)

Bull Infertility

Whilst neosporosis is a significant cause of bovine reproductive failure any epidemiological role of the bull is undetermined and the reliability of current laboratory tests for detecting carriers remains questionable. However, the precautionary principle suggests it is unwise to acquire bulls bred in herds infected with Neospora caninum at least until more is known about this infection. Outside and unfortunately even within the UK, diseases considered notifiable in the UK such as brucellosis and tuberculosis also need to be considered. The two most important true venereal diseases are trichomoniasis and campylobacteriosis, although there is evidence for the venereal transmission of some Ureaplasma sp., Mycoplasma bovigenetalium, BHV-1, brucellosis and even Haemophilus somnus. Bovine trichomoniasis is a venereal disease characterized by early to mid-gestation pregnancy losses, reduced calving rates and pyometra; it is caused by the flagellated protozoan Tritrichomonas fetus. As far as is known, it is transmitted by venereal contact only. Campylobacteriosis, which also presents as a large increase in returns to service with early to mid-gestation pregnancy losses, is classically caused by C. fetus venerealis. However, there is evidence that this organism does not always follow the classic laboratory identification procedures and this has led to the proposition of C. fetus intermediatus, which also appears to cause the same clinical problems in cattle. This organism has many of the properties of C. fetus fetus. In these two venereal infections the bull is the long-term carrier of the organism, apparently without ill effects (i.e. no visible lesions are evident in recently or chronically infected bulls) and a distinct correlation exists between age and infection, with older bulls being far more likely to sustain an infection than younger bulls. Infection of the female occurs at the time of coitus. Diagnosis of campylobacteriosis in the female is by examination of vaginal mucus, collected by the method of Lander (1983), for antibody by the vaginal mucus agglutination test (VMAT) and for the bacterium by culture. Since antibody takes some time to appear after an infected service and false negative VMAT results are common, at least 12 cows should be sampled at least 50 days after a potentially infected service. Cows with blood in the mucus can give false positive results and cows in oestrus are more likely to give false negative results and such animals should not be sampled. In the bull, demonstration of the Campylobacter fetus bacterium in preputial washings by fluorescent antibody test and culture is used in the UK for diagnosis. Where samples of vaginal mucus or preputial washings are collected with a view to culture they should reach the laboratory within six hours of collection due to the fragility of the bacterium. Alternatively, samples can be submitted in transport

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enrichment medium. Negative laboratory results in the face of a strong history of infertility and natural service and no other obvious causes should be viewed with suspicion.

Preputial washing The method of preputial washing used routinely by the Scottish Agricultural College is summarized below.

Protocol for sampling bulls for Campylobacter fetus sp. screen Materials required:

• • • • •

Recovery fluid: 60 ml phosphate buffered saline (PBS) (sterile). Sampling catheter: 10 cm length of 3.5 ¥ 6.5 mm portex tubing (sterile). 60 ml syringe: attached to catheter (sterile). 3 ¥ 20 ml sterile sample bottles. Individual set of sampling materials for each animal sampled.

Procedure:

• • • •

• •

• • • •

Clip preputial hairs. Wash preputial orifice with warm water. Do not disinfect. Load syringe with 60 ml warmed PBS. Insert catheter as far into prepuce as possible. Clamp one hand over preputial orifice to seal around catheter and hold it in place (use hand nearest bull’s head to facilitate massage with the other hand). Pass 60 ml warmed PBS through catheter. Leave syringe in place. Retain fluid and catheter in prepuce by continuing to clamp one hand over preputial orifice and massage thoroughly along full length of prepuce to scrotum for one minute. Collect fluid into the original syringe by withdrawal using the plunger as the catheter is slowly withdrawn. Dispense sample into sterile containers and label. If the bull urinates during collection the sample should be discarded and the process repeated. All samples should be submitted to the laboratory within 6 hours of collection.

With preputial washings false negative results are again to be expected on a single screening, indeed four screenings have been recommended (Dufty, 1967) before a bull can be confidently declared free of infection. A more practical approach to reducing the risk of introducing this infection may therefore be prophylactic treatment of purchased, previously bred bulls by

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preputial lavage with penicillin and streptomycin antibiotic (Melrose et al., 1957) during the quarantine period. This could be refined by employing prophylactic treatment after a single negative preputial wash screening. Nevertheless, the most reliable way to prevent introduction of this infection is to acquire only unbred males and females. Control in infected herds is by disposal of infected bulls, suspension of natural service and use of AI with uninfected semen for 2 years (Clark, 1971) for all exposed cows, thus allowing the cows to develop immunity and eradicate the organism. Where this is not practicable, use of autogenous vaccine (there is no licensed vaccine in the UK), only using young bulls (50