A Handbook for theSheep Clinician7th EditionAgnes C. Winter and Michael J. Clarkson

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A Handbook for the Sheep Clinician

7th Edition

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A Handbook for the Sheep Clinician

7th Edition

Agnes C. Winter and Michael J. Clarkson

School of Veterinary Science, University of Liverpool, UK

www.cabi.org

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© CAB International 2012. All rights reserved. No part of this publicationmay be reproduced in any form or by any means, electronically,mechanically, by photocopying, recording or otherwise, without theprior permission of the copyright owners.

Library of Congress Cataloging-in-Publication Data

Winter, Agnes C.A handbook for the sheep clinician / A.C. Winter and M.J. Clarkson. --

7th ed.p. ; cm.

Clarkson's name appears first on the earlier edition.Includes bibliographical references and index.ISBN 978-1-84593-973-1 (hardback : alk. paper) -- ISBN 978-1-84593-974-8

(pbk. : alk. paper)I. Clarkson, M. J. II. Title.

[DNLM: 1. Sheep Diseases. 2. Sheep -- physiology. 3. VeterinaryMedicine. SF 968]

636.3'089758--dc232011034290

ISBN-13: 978 1 84593 973 1 (HB)ISBN-13: 978 1 84593 974 8 (PB)

Commissioning editor: Sarah HulbertEditorial assistant: Alexandra LainsburyProduction editor: Holly Beaumont

Typeset by SPi, Pondicherry, India.Printed and bound by CPI Group (UK) Ltd, Croydon, CR0 4YY.

Contents

About the Authors

Abbreviations

Preface

vii

ix

xi

1 Production 1

2 Reproduction 9

3 Vaccination 17

4 Thin Sheep 23

5 The Pregnant Ewe 35

6 The Periparturient Ewe 49

7 Newborn Lambs 61

8 The Lactating Ewe 75

9 Growing Lambs 79

10 Sudden Death 89

11 Lameness 95

12 Skin and Wool 107

13 Respiratory Diseases 119

14 Neurological Diseases 127

15 Eyes, Ears and Nose 139

16 Ticks and Tick-borne Diseases 143

17 Notifiable Diseases and Diseases Exotic to the UK and Northern Europe 149

18 Health Schemes 155

v

vi Contents

Appendix 1 Clinical Examination 161

Appendix 2 Neurological Examination of Sheep 164

Appendix 3 Checklist for Examination of a Sick Lamb 166

Appendix 4 Professional Development 167

Appendix 5 Revision Problems and Questions 169

Appendix 6 Suggested Answers 175

Index 185

About the Authors

Agnes Winter grew up on a small family farm in the Yorkshire Dales. After graduating fromLiverpool Veterinary School she worked in mixed practice in north Wales where her inter-est in farm animal work, in particular with sheep, developed further. With her Welsh farmerhusband she kept a flock of sheep, including a small flock of pedigree Wensleydales withwhich she had considerable success in the show ring. After some years she returned toLiverpool Veterinary School to undertake a PhD supervized by her co-author MichaelClarkson. After completion of this she became a lecturer, and later senior lecturer, in sheephealth. For the last four years of her academic career she was head of the Clinical Departmentand, on retiring, was made an Honorary Professor in the University. She remains an activemember of the UK Sheep Veterinary Society, of which she was President from 1987-88. Shehas written five other books on various aspects of sheep health and disease and has receivedseveral prestigious awards for her contributions to the sheep industry.

Agnes C. Winter BVSc, PhD, DSHP, DipECSRHM, FRAgS, MRCVSHonorary Professor, School of Veterinary Science, University of Liverpool2 Fossbridge House, Walmgate, York, YO1 9SYE-mail: a.winter@liverpool.ac.uk

Michael Clarkson was born in Yorkshire and graduated from Liverpool Veterinary School.He undertook specialist studies in the Liverpool School of Tropical Medicine where hetaught veterinary parasitology and did research on turkey coccidiosis, cattle trypanosomia-sis, liver fluke infection in cattle and sheep and a number of zoonotic infections, especiallyhydatid disease. Michael has worked in several countries including Kenya, Zambia, Peru,Chile and Libya. He was appointed Professor of Farm Animal Medicine by LiverpoolVeterinary School and studied the epidemiology of a number of important sheep diseasesincluding parasitic gastroenteritis, chlamydial and toxoplasma abortion and fasciolosisand continued his interest in hydatid disease. He taught sheep and cattle medicine andworked on a number of sheep farms developing sheep health programmes. He was appointedEmeritus Professor on his retirement and still undertakes research work at the VeterinarySchool. He has been a member of the UK Sheep Veterinary Society for many years, editedits Proceedings for 25 years, and was President of the Society from 1986-87.

vii

viii About the Authors

Michael J. Clarkson BSc, PhD, DVSc, DSHP, MRCVSEmeritus Professor, School of Veterinary Science, University of LiverpoolLeahurst Campus, Neston, CH64 7TEE-mail: vm01@liverpool.ac.uk

Agnes Winter and Michael Clarkson were the first two Royal College of Veterinary SurgeonsDiplomates in Sheep Health and Production and the first two RCVS-recognized sheepspecialists.

Abbreviations

AADs Amino-acetonitrile derivativesAGID Agar gel immunodiffusion testAHVLA Animal Health and Veterinary Laboratories AgencyAI Artificial insemination

BDV Border disease virusBLUP Best linear unbiased predictionBOHB BetahydroxybutyrateBSE Bovine spongiform encephalopathyBTV Bluetongue virusBVA British Veterinary AssociationBVDV Bovine virus diarrhea virusBZ Benzimidazole

CAE Caprine arthritis encephalitisCaMD Calcium borogluconate, magnesium and dextroseCAP Common Agricultural PolicyCCN Cerebrocortical necrosisCF Complement-fixingCK Creatine kinaseCLA Caseous lymphadenitisCNS Central nervous systemCODD Contagious ovine digital dermatitisCP Crude proteinCS Condition scoreCSF Cerebrospinal fluid

D value Digestibility valueDET Dry ewe therapyDM Dry matter

EAE Enzootic abortion of ewesEBLEX English Beef and Lamb ExecutiveEBV Estimated breeding valueELISA Enzyme-linked immunosorbent assay

ix

x Abbreviations

EM Electron microscope/microscopyEU European Union

FMD Foot and mouth diseaseFR Footrot

GGT Gammaglutamyl transferaseGSHPx Glutathione peroxidase

ID Interdigital dermatitisIM IntramuscularIV Intravenous

LA Long actingLM Levamisole and morantel (drugs)

MAP Mycobacterium avium subspecies paratuberculosisME Metabolizable energyMJ MegajouleML Macrocyclic lactonesMLC Meat and Livestock CommissionMOET Multiple ovulation embryo transferMRI Magnetic resonance imagingMV Maedi visna

NADIS National Animal Disease Information ServiceNSA National Sheep AssociationNSAID Non-steroidal anti-inflammatory drugNSP National Scrapie Plan

OP organophosphateOPA Ovine pulmonary adenocarcinoma

PCV Packed cell volumePGE Parasitic gastroenteritisPI3 Parainfluenza virus type 3PME Post-mortem examinationPMSG Pregnant mare's serum gonadotrophinPrP Prion proteinPT Pregnancy toxaemia

RCVS The Royal College of Veterinary Surgeons

SAC Scottish Agricultural CollegeSAHPS Animal Health Planning SystemSC SubcutaneousSCOPS Sustainable Control of Parasites of SheepSFP Single Farm PaymentSP Synthetic pyrethroidSPA Sheep pulmonary adenomatosisSVS Sheep Veterinary Society

TB TuberculosisTBF Tick-borne feverTSE Transmissible spongiform encephalopathy

VLA Veterinary Laboratories Agency (now AHVLA having merged with Animal Health)VMD Veterinary Medicines Directorate

Preface

The original idea for this book was to produce a concise practical clinical guide to thediagnosis, epidemiology, treatment and control of the common conditions affecting sheep inthe UK and an early version appeared in 1983. It was first used for teaching veterinary stu-dents at the Liverpool Veterinary School but we were encouraged when a number of veteri-nary surgeons and sheep farmers indicated that they found it helpful and it became wellknown as the 'Green Book'. The last edition was published in 1997 by the Liverpool UniversityPress, although the document has been updated internally every couple of years since then.

The present book has been considerably extended both in the information given on themain conditions and in the geographical range covered. Although the emphasis remains onthe common conditions affecting sheep in the UK, we have considered their importance inthe countries of northern and southern Europe and elsewhere including Australasia andother southern hemisphere countries and in North America. We have not discussed theconditions of sheep maintained for milk production, however, since that is a specializedarea mostly outside our experience.

The emphasis has continued to be on the practical clinical aspects of sheep medicine,concentrating on common and important aspects. No attempt has been made to cover moreunusual or obscure conditions. Knowledge of the details of pathology and the organismsinvolved has been assumed or can be sought elsewhere. Where specific drugs are referredto we have used the generic name; availability and legislative aspects of use refer to UKconditions and may vary in other countries.

We hope that this book will prove a useful practical handbook for dealing with the com-mon conditions of sheep, both as individuals and in flocks and will be helpful to veterinarystudents and practitioners and also to farmers and agricultural students and advisors.

We are grateful to many veterinary surgeons and farmers who have taught us so muchand have benefitted enormously from membership of the Sheep Veterinary Society. Weespecially acknowledge the contributions to the early editions from our colleagues BillFault and Alun Davies.

We appreciate the encouragement we have received and the care and attention givento the publication by the staff of CABI and especially by Sarah Hulbert, CommissioningEditor and Alex Lainsbury, Editorial Assistant.

Agnes Winter and Michael ClarksonJuly 2011

xi

1

Production

Structure of Sheep Industryand Economics

Sheep are found in almost every country inthe world and due to breeding and selectionare able to live in environmental extremesas wide as dusty deserts and snowy peaks.It has been estimated that there are overone billion sheep and lambs in the worldwith the greatest number in China with128 million followed by Australia with73 million, India 65 million, Iran 54 million,Sudan 52 million and Nigeria 35 million.New Zealand and the UK have a similarnumber of around 32 million. The USA hassix million and Canada less than one mil-lion sheep and lambs. Considerable num-bers of sheep are found in South America,especially in Argentina, Uruguay, Peru andChile.

In the countries of the European Union(EU), the UK and Spain have similar numbersof breeding ewes of around 14 million, withGreece, Italy and France having around sevenmillion with a total of around 60 million

It is important that veterinary surgeonsinvolved in sheep work should have a work-ing knowledge of the structure of the sheepindustry in their own country and shouldhave some appreciation of the value of indi-vidual sheep and the way that flock profita-bility can be improved by veterinary advice

and involvement. It is often said by veteri-nary surgeons that farmers are not willing topay for advice and on the other hand, manyfarmers complain that their veterinary sur-geon is not willing (or possibly not able!) toprovide an overall service for sheep. Thisservice should involve more than the occa-sional visit to investigate an abortion out-break, for example, or to carry out a caesareanoperation on a ewe which has been broughtto the surgery.

Probably the best way to becomeinvolved and experienced is to offer to helpwith the production of a health programmefor one of your farmer clients who has sheepas a secondary venture on a dairy herd towhich you are already carrying out regularvisits to advise on herd health. An alterna-tive would be one or more hobby flockswhere veterinary costs are often not suchan issue as on commercial farms and theowners are usually extremely enthusiastic.The knowledge which can be transmittedbetween farmer and veterinary surgeon ismutually beneficial and knowledge learnton one flock can then be offered to otherfarmer clients. Membership of organizationslike the Sheep Veterinary Society (SVS) andthe National Sheep Association (NSA) isessential for the successful sheep clinician.

Sheep are kept under a wide variety ofsystems which need to be understood for

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 1

2 Chapter 1

the clinician's own country. For example,in the UK the stratification system of hillor mountain, upland and lowland farmsshould be understood (see Fig. 1.1) and thephysical and financial performance ofthe three farm systems should form part ofthe veterinary input into the farm.

Many sheep clinicians have learnt andgained 'street credibility' by keeping somesheep of their own as there is nothing thatsheep farmers like talking about more thansheep! This personal involvement, even ona small scale gives experience on the pro-duction, marketing and disease problemsand the financial constraints which are sim-ilar on large commercial flocks.

It is also invaluable to know the mainbreeds of sheep and particularly those thatare likely to be encountered in the area inwhich you work. It would be an expert whowas able to identify the more than 60 breedsin the UK but finding information aboutexamples of the main breeds in the differ-ent layers of the stratification system is

Hill

Upland

Lowland

Fig. 1.1. Stratification of sheep in the UK.

relatively easy with the aid of the internetand the excellent charts which are availablefrom many sources such as the British WoolMarketing Board, for example. The mainhill breeds are Scottish Blackface, WelshMountain and Swaledale (Fig. 1.2), all ofwhich are now bred in large numbers andcan be found a long distance from their areaof origin. These breeds, bred pure on themountains for three or four lamb crops,then move to upland farms as draft eweswhere they are crossed with a ram of a long-wool breed, especially the Bluefaced orBorder Leicester (Fig. 1.3), to give the Muleor the Halfbred which forms the breedingewes of the lowland farms. These are thencrossed with a Down type ram, classicallythe Suffolk but including continental breedssuch as Texel and Charollais to produce theprime lamb for slaughter.

Figures for physical and financial per-formance are obtainable for many sheepsystems in many parts of the world byinternet searches from flocks involved in

Female lambreplacements

Hardy hill ewes x)purebred rams

Males

Older (draft)ewes

1Draft ewes x _Maleslong-wool ram

Half bredfemales

Halfbred ewes x Males

terminal sire andfemales

Finished lambs

Production 3

Fig. 1.2. Swaledale sheep in a hill farm environment.

Fig. 1.3. These are Bluefaced Leicesters that are crossed with Swaledales to create the Mule.

4 Chapter 1

recording schemes. These flocks are likelyto be above average in their production somay act as targets to improve productionby veterinary advice. In England, for exam-ple, EBLEX, the English Beef and LambExecutive produces information from theirrecorded flocks and divides this into theaverage of a particular sector and the per-formance of the top-third farms in that sec-tor. This may usefully form the basis forimproving a farm in the average section toone in the top third. This data is availableon the web site www.eblex.org.uk/businesspointers. The main factors which distin-guish the flocks in the top third of the sec-tor are number of lambs reared and stockingdensity suggesting several areas where vet-erinary input and the production of farmhealth programmes can contribute signifi-cantly to farm economics. Similar data isavailable for Scotland and Wales and formany other countries. Production figuresare usually expressed as a quantity per100 ewes which are put to the ram (tupped).Representative figures of lamb perform-ance in the UK are 110 lambs per 100 ewestupped for mountain farms, 140 for uplandfarms and 170 for lowland farms, with anaverage of 10% lamb mortality across allthree systems.

While the physical performance figuresdiffer little over recent years, the financialinformation shows marked differences dueto market conditions but up-to-date figuresfor the cost of cull ewes and prime lambscan be obtained online The sheep clinicianwill find this information invaluable in dis-cussions with farmers.

In the EU, there is a complex and mas-sive support mechanism for many agricul-tural systems including sheep whereasmany countries including New Zealand,Australia and the USA removed suchsupport many years ago. The CommonAgricultural Policy (CAP) of the EU madepayments based on ewe numbers or lambproduction but since 2005, this payment,known as the Single Farm Payment (SFP)has been independent of production. In theUK, this has resulted in a marked fall in thenumbers of breeding ewes from around19 million to below 14 million which is

doubtless partly responsible for the increasein prices for prime lamb in 2011. Differentmethods have been used to calculate theSFP for England, Scotland and Wales butproducers indicate that without such sup-port, which is likely to reduce, sheep farmswill be unable to continue to exist finan-cially. It is important to understand themain features of the schemes in the localarea as these may allow or demand a greaterinput from clinicians into health schemes,which are an essential ingredient for somepayments.

There are, however, so many variationsthat it is not possible to summarize thembut the clinician should be aware of theopportunities afforded by the SFP in theirown area. In any case, these may change fol-lowing the review of the CAP due in 2013.

Feeding Management

(This section provides general advice onfeeding sheep. See Chapter 4 for a practicalexercise on the specific common problemof how to assess a diet which is being fed tosheep for adequacy.)

Grass, either fresh or conserved as hayor silage is the main and cheapest food forsheep in the UK. However, because of sea-sonality of grass growth coupled with itseffect on quality and quantity of the cropand the varying requirements of ewesthroughout the production cycle, alterna-tive foods may be used to replace and/orsupplement grass, either grazed or con-served. Supplements include simple orcomplex rations of cereals and proteinsources and mineral supplements usedwhen copper, cobalt and selenium concen-trations are deficient in grass grown oncertain soil types.

Feeding the ram

Many rams are purchased by sheep farmerseach year. These, almost invariably, will bein condition score (CS) 3.5-4.5 having beenwell fed with concentrates in preparation

Production 5

for sale. It is important that this concentratefeeding is continued up to mating, at nomore than 400g/day. This should minimizethe effects of diet change from mainly con-centrates to grass only and at the same timeprepare the rams for the mating period dur-ing which concentrate feeding of the ramsonly can be difficult.

Rams already on the farm should havea CS of 3.5 (i.e. be fit not fat) 6-8 weeks priorto the beginning of mating. Overfat ramsusually have reduced reproductive perform-ance. Most rams will be in correct conditionprovided reasonable grazing has been avail-able during the summer months.

If there is insufficient grass and/or ramsare in poor condition, concentrates and haywill need to be provided during the pre-mating period and possibly during the mat-ing period itself. The amount of concentratesrequired will vary depending on CS butup to 600g/day of a concentrate containing160 g/kg (16%) crude protein (CP) can be pro-vided. Proprietary ewe concentrates shouldbe avoided, especially if large amounts arebeing fed, because of the high concentra-tions of magnesium and phosphorus whichthey contain, predisposing to urinary calculi.Coarse mixes of cereals, sugarbeet pulp andvegetable protein sources with a minimumaddition of minerals are recommended.

Feeding the ewe

Condition scoring is an essential guide tofeeding management (see Chapter 4).

Pre-mating

The production cycle can be considered toend and start at the time of weaning. At thistime, the CS of ewes will depend not onlyon the amount of food which has been avail-able but also on within-flock factors such asprevious suckling load. The period fromweaning to mating provides an opportunityto adjust the feeding so that ewes are inoptimum condition at mating.

In lowland conditions, where highlambing percentages are expected, the CS atmating should be 3 or 3.5 but in hill flocks,

where much lower lambing percentages arerequired, the optimum score will normallybe 2.5.

Increasing the nutrition in the 2-3weeks pre-mating so that ewes gain 0.5 of aCS (flushing effect) will increase ovulationrate and reproductive performance if ewesare below CS 3. However, if ewes are ingood condition, flushing has little advan-tage over simply maintaining ewes in con-dition and there is a risk that flushing ewesalready in good condition will lead to ewesbecoming overfat which may result inreduced reproductive performance.

Grass, provided it is in good supply,should meet the requirements of the ewe formaintenance and some increase in bodycondition. However, in late lambing flocksin which mating takes place in late Novemberand December, grass will need to be supple-mented with concentrates and probablyconserved forage also. Feed blocks and liq-uid molasses diets can be an alternative toconcentrates and do not require to be replen-ished daily. The aim in these circumstancesshould be to have ewes in good condition3 weeks pre-mating and then to provide amaintenance ration for them over the matingperiod. If conditions are very wet, windyand cold, maintenance needs will increase.

Post-mating

MATING TO 42 DAYS During pregnancy20-25% of embryos/fetuses die and some ofthese deaths are caused by a combination ofincorrect nutrition and handling and climaticstress, the latter especially in late matingflocks. The aim should be to feed ewes atmaintenance level or just below. Both over-feeding, with ewes gaining in weight, or sig-nificant underfeeding will increase embryoand fetal losses. Above average losses mayalso be attributable to grazing low seleniumcontent herbage and to grazing pasture con-taining large amounts of red clover. Alternativeforage crops, such as kale and rape, shouldalso be avoided.

Low cobalt-content herbage has alsobeen found to have an important longerterm effect by reducing the vigour of thelamb at birth and its resistance to disease.

6 Chapter 1

Grass will meet the needs of the ewesfor nutrients in the post-mating period dur-ing the early part of the mating season, butin areas where cobalt and selenium areknown to be deficient in herbage, providinga small amount of concentrates containingenhanced amounts of these minerals may bebeneficial. It should be noted that cobaltand selenium concentrations of herbage areusually at their lowest in late summer andautumn and are most likely to be belowrequirements in wet seasons.

PERIOD 42-90 DAYS The fetus grows slowlythroughout this period but growth of fetalmembranes and the placenta is considera-ble, especially during the later weeks. Thisresults in an extra energy requirement abovemaintenance of approximately 2 MJ/dayat 90 days. However, 1 kg of body weightloss will provide 20 MJ of metabolizableenergy (ME), so the extra needs can easilybe met by a small loss in ewe condition.Only severe underfeeding will reduce pla-cental growth and hence lamb birthweight.Virtually no placental growth occurs after90 days.

The aim should be to maintain CS in the3-3.5 range for lowland ewes. Ewes whichhave been scanned to have three or morelambs should be carefully managed so thattheir CS does not decrease below 3-3.5, butin lowland ewes with twins and singles andin hill ewes carrying singles, some loss ofcondition (up to 0.5 CS) can be tolerated andwill be desirable in ewes in CS 4 or above. Incontrast, thin ewes and ewe lambs andshearling ewes which are still growing willneed an above maintenance ration; the MErequired for 1 kg live weight gain = 24 MJ.Grass will often not be abundant throughoutthe period and will have to be supplementedwith conserved forage and, in some cases,concentrates or feed blocks. Medium to goodquality hay or silage should easily meet thenutrient requirements of the ewe so, pro-vided these forages are available, concen-trate supplementation is unnecessary.

PERIOD 90 DAYS TO LAMBING During thisperiod, fetal growth accelerates rapidly withthe fetus doubling its size in the last 4 weeks

of pregnancy. Mammary growth also occurs,especially in the final 2 weeks before lamb-ing, when udder weight increases by morethan 100%.

The net result of the above is an increas-ing requirement for nutrients for fetal andmammary tissue growth and development.

The appetite limitations of the ewe dur-ing this period impose considerable restric-tions on ration formulation. The voluntaryfood intake is approximately 15 g/kg bodyweight (dry matter, DM) and is determinedby a number of factors.

In housed ewes, the intake of eweswhich have been sheared is approxi-mately 25% greater than those in fullfleece.During this 8-week period, appetiteincreases slowly to a maximum at2 weeks pre-partum. There is an equallyslow decline until a few days beforeparturition when appetite decreasesmarkedly.The digestibility of the forage, theamount of concentrates provided andthe type of forage all influence intake.

Quality of forage not only indicatesfeeding value, but also the daily intake. Hayis very variable in quality and a chemicalanalysis of a representative sample isrecommended.

Silage usually has higher ME and CPvalues than hay but DM intakes are lower(approximately 90%) than those of equiva-lent ME value of hay. Intakes increase withhigher DM concentrations up to 250 g/kgDM. The intake of long material in a big balewill be 85% of precision-chopped material.

Straws may also be used as forage.Spring barley varieties are most suitable butall cereal straws can be used.

Chemical analysis of the whole straw isnot a suitable means of assessing feedingquality because in most cases the ewes onlyeat the 25% of the straw which is most read-ily consumable and has the highest feedingvalue. The remainder should be discardedand used as bedding. Fresh straw should beprovided daily either in a rack or on thefloor. In the former system, uneaten strawshould be removed from the rack daily.

Production 7

Straw feeding value may be enhanced bytreatment with a strong alkali or urea.

The body tissue of the ewe may be con-sidered as a reservoir of nutrients which canbe built up and depleted to a certain extentwithout adverse effects provided the deple-tion occurs slowly. An alternate 'flat-rate'feeding system has been devised which uti-lizes this fact. It is first necessary to calcu-late the total concentrate needs of the eweover the period and then to provide the samedaily amount throughout the period. Ewesgain weight at first and then, as lambingapproaches, they lose condition. Practically,this is an easy-to-operate system and it alsoavoids the risk of metabolic acidosis occur-ring when ewes are fed large amounts ofconcentrates in late pregnancy. Lamb birth-weights are similar to those obtained whenewes are fed on the traditional increasingplane of nutrition, but especially in youngewes, colostrum production may be some-what reduced and there is increased possi-bility of hypocalcaemia. A single-step systemtherefore may be more appropriate withewes fed at a first flat rate up to approxi-mately 3 weeks pre-partum when the qual-ity of the concentrate can be increased andthen fed at a second increased flat rate untilthe end of pregnancy.

WATER REQUIREMENTS Housed pregnant ewesrequire a daily intake of 2.5 kg water inmid-pregnancy and up to 5 kg in latepregnancy.

Lactation

Colostrum production and consumption bythe lamb is crucial. Sufficient colostrumshould be available to meet the passiveimmunity requirements and also the energydemand in the first day of life. Output to 24hpost-partum will vary from 1.5 to 3.5kg.

In early lactation, ewes suckling singlesare likely to be producing a daily averageyield of 2kg or more, those suckling twins3kg or more and those suckling triplets 4 kgor more, provided they are well fed. Maximumdaily yields occur at approximately 4 weekspost-partum and will vary from 2 to 5 kg.After 4 weeks, there is a slow, steady decline

in yield but ewes will still be producing1.5-2 kg at 10 weeks after lambing.

Nutrient requirements largely reflectthe milk production of the ewe. The produc-tion of 1 kg of milk requires 7.1 MJ ME and72 g of metabolizable protein. Formulationof rations to meet these requirements ismodified by a number of factors including:(i) stage of lactation; (ii) body CS of the ewe;and (iii) foods which are available.

In the immediate post-partum period,ewes are hungry and careful rationing ofconcentrates to avoid gorging and conse-quent digestive upsets is necessary. Post-lambing DM intake increases steadily up to5-7 weeks of lactation. Despite this increasein appetite, lactation demands usually out-strip the intake and ewes usually lose con-dition in the first month of lactation. A lossof one CS is not uncommon and is fre-quently a reflection of high milk yields.Growth rate(s) of the lamb(s) are a goodindicator of milk yield in the early stages oflactation. Yields may be calculated fromlive-weight gain by assuming the DM con-tent of ewes' milk is 200 g/kg and the con-version ratio of milk solids to live-weightgain is 1:1.

In practice, many ewes will be at grassthroughout the lactation period. It is quitelikely that grass will be limited at the begin-ning, which results in a considerable lossin body condition. Limitation is indicatedby a sward length below 4 cm and ewesspending more than 9h/day grazing. Whensward length is below 2 cm, supplementa-tion should be given to provide almost allnutrient needs (i.e. forage and concentrates).When the sward length is 2-3 cm, concen-trates can provide approximately half ofnutrient needs.

Concentrate feeding is also a vehicle bywhich magnesium can be made available tothe ewe. An intake of 6g/day of calcinedmagnesite, equivalent to 4g of magnesium,should prevent hypomagnesaemia, whichcan be a problem in early spring when younggrass high in protein is being grazed. Highintakes of non-protein nitrogen and a rapidrate of passage through the gut both reducemagnesium absorption. Feeding of a high-energy concentrate food such as sugarbeet

8 Chapter 1

pulp should be a considered option to mini-mize the problem. Providing ewes with shel-ter to reduce environmental stress is alsobeneficial.

Feeding the Iamb

Providing the lamb with a supply of colos-trum is essential. Ideally, the lamb willreceive this from its dam within a few hoursof birth and will continue to suck its damand receive further amounts in the follow-ing 48 h.

Ewes also vary widely in production. Inthe first 24h, the mean yield should be 3.01but some ewes will produce 500 ml and oth-ers more than 41.

For details of substitute colostrumpreparations, see section on lamb survival(Chapter 7).

Most post-lambing mortality occurs inthe first few days of life and the major causeis starvation. Insufficient colostrum or milkmay be causative but the ewe not allowingthe lamb to suck and lack of sucking driveand udder problems, such as blocked teats,may also be responsible. Starvation after thefirst few days is usually the result of poorfeeding of the ewe in lactation, sore teats,mastitis or mismothering.

The lamb is dependent almost entirelyon the ewe's milk until 4 or 5 weeks of age.Solid food consumption will begin at 3-4weeks of age when the lamb starts to con-sume measurable amounts of grass and/or,if available, concentrate creep feed. Thistime is important as it is obviously whenlambs commence to ingest significant num-bers of parasite infective larvae.

Feeding the naturally reared lambpost-weaning

Most lambs will be weaned between 14 and22 weeks of age. Some of these, especiallysingle lambs, will be ready for slaughter atthe time of weaning and will be finished offon grass alone or grass with a minimumconcentrate supplementation in the autumnThe system depends on having available goodquality grass such as aftermaths (the fresh

grass growth after a crop of hay or silage hasbeen taken off) and cow grazing. If such pas-tures are not available, performance figureswill be disappointing partly because of lowintakes. Intakes and performance will alsobe depressed if the grass is deficient in traceminerals such as cobalt. The post-weaningperiod is particularly problematical, espe-cially if the grass is lush. In areas of cobaltdeficiency, providing concentrates whichcontain minerals could paradoxically bemore beneficial when there is lots of grassfollowing a good rainfall in the late summerand early autumn than in drier conditionswhen less grass is available.

Many of the lambs, especially wetherlambs from hill and uplands, will be man-aged so that they reach the required slaugh-ter weight between Christmas and Easter.During the winter period, these lambs maygraze green forage crops, turnips or sugar-beet tops. However, increasingly, they arebeing fed on silage with some concentratesupplementation. Growth rates of between<50 g/day and >200 g/day may be obtained,depending on the quantity and quality ofthe supplement provided. Farmers who rearstore lambs have the option of finishingthese store lambs early or late.

Grass silage if fed alone, even if of highDM and digestibility (D) values, will beunlikely to give growth rates in excess of80g/day. Part of the problem is that of lowintakes which become more apparent: (i) ifthe DM is below 220 g/kg; (ii) if the pH is<4.0; and (iii) if the material is big balerather than precision chopped. Maize silagehas also been fed successfully.

Supplementing silages with 200g con-centrates/day will increase total intake andgive growth rates between 120 and 150 g/dayand 400 g concentrates will give growth ratesof 175 -225g /day.

Shearing lambs in late summer andautumn usually results in higher foodintakes and improved growth and carcassweight performance. Shearing may be par-ticularly useful if the final finishing periodis indoors because of nutritional and non-nutritional factors such as reduced spaceallowance and cleaner sheep being sent formarket.

2

Reproduction

Control of Breeding

Most breeds in the UK are seasonally anoe-strus, although the Dorset Horn or polledDorset and its crosses and some continentalbreeds will breed throughout most of theyear. The Merino, which is a very importantbreed in countries such as Australia andSouth Africa, is not a strongly seasonalbreeder so can be stimulated to breed atmost times of the year. In seasonal breeders,the breeding cycle is controlled by decreas-ing daylight length and so ewes show peakoestrus activity in the autumn.

There are a number of methods whichadvance the breeding season or synchronizetupping and lambing.

Early breeding with progestogen sponges

Breeding may be advanced by up to 6 weeksby the use of progestogen sponges withinjections of pregnant mare's serum gonado-trophin (PMSG).

Medroxyprogesterone acetate and flug-estone acetate are different synthetic pro-gesterone-like compounds that have beenused by incorporation into sponges forintravaginal insertion. Currently, only flug-estone is available in the UK. Both may beused with the injection of PMSG at sponge

removal, which is essential in the season-ally anoestrus ewe. The farmer should bewarned that individual ewes react differ-ently to the same dose of PMSG and theresults are unpredictable.

Table 2.1 provides an example of aschedule for early lambing with progestogensponges (for normal conditions in the UK,although a similar schedule can be usedat any time during the breeding season bysubstituting appropriate dates).

Discuss with the farmer when thefinished lambs can be sold, and whether itis preferred that lambs are born beforeChristmas or after.

Roughly 70% of the ewes should lambto the induced oestrus and most havetwins. Results vary widely, according to:(i) breed; (ii) feeding; (iii) time of year; and(iv) weather. Test a batch of ewes andrecord the results in order to find outwhether the procedure is worthwhile on aparticular farm. The recommended dose ofPMSG ranges from 300 to 7501U at spongewithdrawal, with a higher dose in July thanin August. Ewes and rams should be ingood condition (CS 3) and fit. Put the ramsnear the ewes at sponge withdrawal, andput them with the ewes 48 h after with-drawal, for 48 h. If possible, remove ewesfrom the ram when they have been marked(raddled) convincingly, to avoid repeated

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 9

10 Chapter 2

Table 2.1. Example of devising a schedule for early lambing (15-23 December), working backwardsfrom desired lambing date.

Calculate Activity

Longest gestation 150 days'Shortest gestation 144 daysbLast mating dateFirst mating date'Sponges in for 14 days

Last lambing requiredFirst lambing anticipatedRemove ramsIntroduce ramsRemove spongesInsert sponges

Date

23 December15 December26 July24 July22 July8 July

'Counting 150 days back from 23 December the last mating date can be calculated (26 July).'Counting 144 days back from 15 December the first mating date can be calculated (24 July).'The sponges need to be removed 2 days before the rams are introduced (i.e. 22 July).

serving of favourites. Introducing rams atsponge withdrawal reduces the pregnancyrate drastically (68-40% in one trial). Twoweeks after first oestrus, put rams, with adifferent raddle crayon, with the ewes for1 week and then remove. The usual adviceis to allow one ram for ten ewes, though itis possible with some individual rams toachieve good fertility with more ewes.There are considerable differences betweenindividuals and between breeds in the abil-ity of rams to breed outside the usualseason.

Only well-managed farms can benefitfrom early, concentrated lambings. Housingand labour for lambings must be plannedwell or welfare is compromised and lambmortality may be high.

Out-of-season breeding with progestogensponges

It is generally agreed that in the UK disap-pointing results are obtained with mostcommercial breeds and hallbred ewes withtupping earlier than July though a success-ful attempt was made in 40 barren or abortedWelsh crossbred ewes in North Wales.Sponges were removed and 1000 IU PMSGinjected on 25 May. Twenty ewes lambed,producing 30 live and seven dead lambs,and the lambs fetched a high price whensold for slaughter.

Similar results have been obtained withMule (Bluefaced Leicester x Swaledale) ewesin June, with progestogen sponges and PMSGwith 50% of ewes becoming pregnant.

Frequent breeding with ewesof aseasonal breeds

With selected breeds, it is possible to producethree crops of lambs every 2 years. In practice,few people have achieved this although onesuccessful system produced lambs every8 months from ewes mated in December,April and August with Finnish Landrace xDorset Horn ewes and Down rams. Lamb salesapproached 300% and profitability was threetimes higher than in annual lambing flocks.

A sophisticated but very practical sys-tem of frequent breeding has been describedand developed over the past 30 years in theUSA by Cornell University, New Yorkknown as the Cornell STAR acceleratedlambing system. This system has beenapplied successfully by commercial primelamb producers in the USA. Dorset andFinn sheep and their crosses are used andbatches of ewes lamb every 2 months withindividual ewes achieving five lambings in3 years. No hormones or light regimes areused and the system results in a regular pro-duction of similar carcasses throughout theyear. The system is well described on theCornell University web site which includesan instructive and beautiful video and alldetails needed to implement a successfulprogramme (www. sheep. cornett. edu).

Synchronization of oestrus during the normalbreeding season with progestogen sponges

Sponges may be used in order to bring abatch of ewes into oestrus within a few hours

Reproduction 11

of each other, which may be useful to helpproduce a short lambing period, especiallyif used together with induction of lambing.

The sponges are removed after 12-14days and rams introduced 48 h later. Almostall the ewes will be tupped over a 12-hperiod and the majority will hold to service,provided adequate numbers of rams areused.

Early breeding with vasectomized rams

A vasectomized ram run with ewes 1-2months earlier than the usual start of thebreeding season will stimulate a large pro-portion of the flock to come into oestrusabout 3-4 weeks after his introduction. Theewes must be away from rams for 4-6 weeksbefore the teaser is introduced. This is alsoa cheap method of inducing synchronizedoestrus. A vasectomized ram may also beused to withdraw individual ewes, as theyare raddled, for service by a fertile ram, orfor artificial insemination.

Early breeding with melatonin

Melatonin is secreted by the pineal glandin response to darkness and can be admin-istered artificially by implant simulating shortday-length, which stimulates the reproduc-tive system of the ewe.

Melatonin is injected subcutaneouslynear the base of the ear with a specialimplanter. It can be used to advance the breed-ing season by 4-6 weeks so that for example,Suffolk-type ewes may be mated successfullyat the end of June by giving an implant about5 weeks earlier. It is vitally important that theewes should be in good condition and thatthey should be isolated from sight, sound andsmell of rams (and male goats) for 6 weeksbefore ram introduction.

Induction of lambing

Predictable lambing dates can be achievedby injecting 16 mg of betamethasone ordexamethasone at 140 days of gestation or

later. This system has been used to batchlamb at times when labour is present, thusreducing lamb mortality.

As an example, in a trial at LiverpoolUniversity, 33 ewes were selected for injec-tion with 16 mg betamethasone at 9.00 p.m.on day 142 of pregnancy (Saturday). Twoewes lambed before treatment, three within24 h, three between 24 and 36 h, and 24between 36 and 48 h (9.00 a.m.-9.00 p.m.Monday). Only one ewe lambed later, 55 hafter treatment. It is clearly possible togive better attention to ewes, and to giveattendants a rest, particularly avoidingthe few ewes at the end of a group withlong gestations. Side effects appear to benegligible, but if some ewes have beenmated after the recorded service date (e.g.one cycle later) there is a serious riskof abortion.

Ram Examination

This is best done 2 months before tuppingtime as part of a flock health visit (Figs 2.1and 2.2). About 10% of rams have poorfertility. Many of these can be detected bypalpation of testicles without the need forelectroejaculation but there are some condi-tions which are missed if examination offresh semen is not carried out.

Examination of a ram lamb before use,or of a freshly-bought ram, is a wise invest-ment. An infertile ram which is not detectedcan lead to ewes lambing 2 months late.If several rams of the same breed worktogether, an individual infertile ram maynever be detected and may result in a reduc-tion in overall fertility of the flock.

Any history based on good breedingrecords is valuable. Illness, however brief,can lead to temporary infertility up to andbeyond 2 months later. If the ram is exam-ined before entry to the flock, his conforma-tion and any inherited condition should bechecked. Teeth should make contact withthe dental pad. Orf should be looked foraround the lips. The CS should be 3 to 3.5.Feet should be checked; about 50% of ramswere found to have severe foot lesions inone survey, which can drastically reducefertility.

12 Chapter 2

Fig. 2.1. Rams should be checked over 6-8 weeks before putting in with the ewes.

Fig. 2.2. These Texel rams (foreground) with a group of ewes are showing the Flehmen response (curling theupper lip) which helps detect ewes in oestrus.

Before the breeding season (before Julyin the UK), the size of testicles and numbersof spermatozoa are lower, especially inbreeds with a short breeding season.

The testicles should be of similar size,very resilient (turgid) and move freely in thescrotum (compare with others of the sameage and similar breed). The scrotal circum-ference ranges from 30 to 44 cm in maturelowland rams and from 30 to 40 cm in hillbreeds. The scrotal circumference of ram

lambs at 9 months old should be at least28 cm in lowland and 26 cm in hill breeds.Testicular hypoplasia is incurable: no sper-matozoa are produced, though libido is nor-mal. The head and tail of the epididymisshould be palpated for evidence of pain,lumps or adhesions since epididymitis is acommon cause of reduced fertility in rams.A variety of organisms may be associatedwith epididymitis but Brucella ovis infec-tion is of great importance in southern

Reproduction 13

European countries, Australia, New Zealand,South Africa and North and South America.Control schemes have been described whererams are tested and culled and this has beensuccessful in eradicating the infection in theFalkland Islands and in some flocks in NewZealand and elsewhere. This infection is notpresent in the UK where it is a notifiable dis-ease but other bacteria have been found inepididymitis cases including Mannheimiaand Histophilus.

The penis can be extended with care,with the ram in the sitting position, to checkfor rare defects, by holding the prepuce andpushing forwards with the other hand at thesigmoid flexure, which is found at the baseof the testicles. (Have a bit of practice so youcan do it well!)

There are a number of battery-operatedelectroejaculators which are used to obtainsemen samples from rams. The tip of theprobe should be on the pubic brim, but thereare marks to act as a guide to the depth ofinsertion in the average ram's rectum. Themethod has been criticized on welfaregrounds and it seems preferable to avoidelectroejaculation unless there are stronggrounds for suspecting the ram is infertile inthe absence of obvious physical abnormali-ties. In addition, it seems reasonable to giveup if a sample is not obtained after three orfour attempts and to try again later. The ramcan stand or lie. The semen can be collectedin a warm beaker or into a small transparentplastic bag. Between 0.5 and 2m1 of densecreamy semen is normally collected from afertile ram. Semen obtained by electroejacu-lation is not necessarily typical of a naturalejaculate and some breed societies requireexamination by artificial vagina, which oftenneeds training (for the ram!) or semen can berecovered from the vagina of a ewe justserved by the suspect ram.

Semen examined immediately on awarm slide in a warm room should showgood wave motion (as if being vigorouslystirred) as seen in bull semen. If a poor sam-ple is obtained, a second sample should nor-mally be taken. After mixing one drop ofsemen on a warm slide with five drops ofnigrosin-eosin (1.67g eosin, 10.0g nigrosin,100 ml water) for 3min, a smear can be made.

Further evidence of the likely fertility is pro-vided by: (i) the total number of spermato-zoa; (ii) the number of live (unstained)spermatozoa; and (iii) the number of sper-matozoa free of morphological abnormali-ties. Smears can be stained by Romanowskymethods as used for blood smears to detectthe presence of polymorphs, suggesting aninflammatory response.

If the history and examination of theram and semen show reduced fertility, treat-ment is not normally possible. A potentiallyvaluable ram may be tested again 2 monthslater, as infertility is occasionally tempo-rary. A report should always remind the cli-ent that the only final evidence of fertility isthe production of lambs.

Rams should be permanently marked foridentification and reports should be made onthe special certificates designed by the BritishVeterinary Association (BVA) 'Certificate ofVeterinary Examination of a Ram Intendedfor Breeding' which can be downloaded byBVA members or found on the SVS web site(www.sheepvetsoc.org.uk). This certificatealso contains guidelines for semen collectionby electroejaculation.

Urolithiasis

This is mainly a hazard for the housed2-4-month-old castrated male lamb fed a lotof concentrate, although it does occasion-ally occur in adult males, particularlyheavily-fed pedigree rams. The fine sand-like calculi, usually consisting of magne-sium ammonium phosphate, obstruct thepenis either at the vermiform appendage orat the sigmoid flexure.

Clinical signs

The lambs show discomfort with strain-ing (`hiccups'), kicking at the abdomen,twitching of the tail and generalrestlessness.A precipitate of crystals may be foundon the preputial hairs which are oftendry and sometimes bloodstained.

14 Chapter 2

'Water belly' may occur, with urineleaking subcutaneously from a rupturedurethra, or into the abdominal cavityfrom a ruptured bladder.

Treatment (not easy, but urgent)

Assess the state of the animal as treatmentdiffers depending on whether salvage orretention of breeding potential is the aim.Check whether the bladder is intact byultrasound or paracentesis, and considerdecompressing the bladder with a long nee-dle through the abdominal wall. For valua-ble breeding animals, take blood forhaematocrit, urea, creatinine and potas-sium, sodium and chloride concentrations.

Possibilities then are:

Examine the vermiform appendage. Ifthis is obstructed, cut it off at the basewith a pair of clean scissors. If you arelucky and this is the only obstruction,urine will flow, but keep a close checkas blockage may recur.Give a spasmolytic and analgesicinjection.If the obstruction is higher and the ani-mal is not required for breeding pur-poses, do a perineal urethrotomy undersacrococcygeal anaesthesia. If urinestill does not flow, you can attempt ret-rograde flushing into the bladder, butcatheterization is difficult because ofurethral diverticulum.For non-breeding animals again, ampu-tation of the penis can be carried out,exteriorizing the stump through theskin incision below the anus. This isprobably the best method where ure-thral rupture has occurred.For breeding animals, either:. do a laparotomy, open the bladder

and attempt to flush down the ure-thra. This is also an option if thebladder has already ruptured andrepair is to be attempted; or

. insert a Foley catheter into thebladder via the laparotomy andexteriorize the tube through theincision. The bladder can be flusheddaily with Walpole's solution in an

attempt to dissolve the stones.Flushing with a solution of solubleoxytetracycline, which is acidic, isworth considering.

For all cases correct the fluid deficitand electrolyte balance with intrave-nous (IV) fluids.For all cases drench twice daily with5g ammonium chloride or other urineacidifier, but not until metabolic acido-sis has been corrected.

These cases are always a worry and theprognosis is always guarded.

Control

When cases are occurring

Check the type and amount of concen-trate being fed. Make sure it is formu-lated for feeding to breeding rams orfattening lambs and is not being fed inexcessive amounts.Ensure plenty of fresh water is available.Supply salt (NaC1) as licks, or in theration or in the drinking water.Add 2% ammonium chloride to theration.Contact the food supplier to alert themto a possible problem, particularly iffeeding instructions have been cor-rectly followed.

In future

Ensure no magnesium is added to con-centrates; do not exceed 200g MgO /t.Ensure calcium:phosphorus ratio is atleast 1.2:1 up to 2:1; include 1.5% groundlimestone in the diet if necessary.Ensure there is a minimum of 1% saltin the concentrate.Ensure there is plenty of fresh wateravailable.Avoid castration.

Artificial Insemination (Al) and MultipleOvulation Embryo Transfer (MOET)

There have been considerable advances inthe use of these techniques over the past

Reproduction 15

20 years and although ethical objectionshave been raised to the use of laparoscopictechniques, the stress to ewes when thistechnique is used by experienced veteri-nary surgeons is slight. Superior siresbased on objective criteria are now availa-ble so the arguments for breed improve-ment are considerable and offset the minorsurgical interference needed. The expan-sion of Sire Reference Groups (see later)has necessitated the use of AI with frozendiluted semen, which can only be donesuccessfully by laparoscopic techniques.Commercial companies are now activelypromoting AI, by cervical and laparoscopictechniques, and MOET is also availablecommercially and widely used in manycountries. Throughout the UK, a widerange of breeding services including AIand MOET are available from Innovis(www.innovis.org.uk) and have beenresponsible for great advances in flock per-formance. Similar organizations exist inmost sheep-producing countries.

Al with fresh semen

Synchronization of ewes with progestogensponges and injection of PMSG at with-drawal is used, with AI 56h after spongewithdrawal. Fresh semen can be placed inthe vagina but better results are obtained byplacing semen by pipette just into the cer-vix. One ejaculate will inseminate 20 eweswith a conception rate of around 70%. Thisprocedure has been used for many years inlarge flocks in Eastern Europe.

Al with frozen semen

Conception rates with frozen ram semengiven into the cervix are low (30%) and dueto the tortuous nature of the cervical canalin ewes it is extremely difficult and oftenimpossible to place the semen into theuterus, although attempts have been madeto develop transcervical AI.

This is the reason for intrauterineinsemination by laparoscopy, under localanalgesia, with diluted frozen ram semen so

that one ejaculate can inseminate 100 eweswith a conception rate of 60-70%.

Breed and Flock Improvement

Breed improvement has always been a fea-ture of sheep farming from its earliest daysin the development of different breedssuited to particular areas of the world. Thenaming of breeds of sheep according to thegeographical area of origin such as Suffolk,Clun Forest and Swaledale indicates theselection which has taken place over centu-ries. The selection of rams and ewes accord-ing to breed standards was also an attemptto improve flocks though physical featureswere not necessarily associated with pro-duction criteria. In the past 40 years, record-ing of data on production, the recognitionthat much of this data is genetically inher-ited and the introduction of breeding tech-niques such as AI and MOET have givensheep breeders objective measurements toguide improvements and have made markedadvances in flock performance.

In the UK, the Meat and LivestockCommission (MLC) introduced sheeprecording schemes in the 1970s as itsSheepbreeder Services and these schemesprovided an enormous stimulus to ramimprovement and thus to flock geneticimprovement. The traits identified havebeen chosen in order to effect the perform-ance of sheep under UK conditions for meatproduction but similar methods have beenused in Australia and other southern hemi-sphere countries where the main sheepproduct is wool. Twenty years ago a moreambitious ram evaluation scheme was intro-duced by Signet Breeding Services in theUK which offered best linear unbiased pre-diction (BLUP) technology to their recordedSheepbreeder flocks. This system identifiessuperior rams for a number of criteria andthe production of estimated breeding values(EBV) for each criterion and has now beenextended to include ewes and lambs in ped-igree flocks. The pedigree and performancedata are analysed to estimate how much of asheep's performance is due to its geneticmakeup and how much to the flock envi-ronment. The standard performance traits

16 Chapter 2

are: (i) litter size; (ii) maternal ability (milkproduction); (iii) lamb 8-week weight(a measure of milk production); (iv) anumber of traits obtained by lamb examina-tion at 21 weeks including weight and mus-cle and fat depth by ultrasound examination;and (v) mature size by weight at first lamb-ing. More recently, computed tomographyhas been applied to selected animals toextend the number of traits to include:(i) carcass live weight/fat weight; (ii) carcassshape; and (iii) faecal egg count as a meas-ure of genetic resistance to nematode worms.All these measurements are carried out onlambs at 21 weeks old.

An EBV is measured in the same unitsas the trait (e.g. 8-week weight in kg) andexpressed as a positive or negative valuecompared with the average for the trait.A ram having a value of +5 kg for 8-weeklamb weight, for example, means that onaverage, its progeny will be 2.5 kg betterthan those from a ram with a zero value,since only half its genes are transmitted.A recorded ram will have a value for eachtrait and in addition, different individualEBVs are combined to give breeding indexesto identify superior rams for the differentstratifications in the UK sheep industry (seewww. signetfbc. co. uk).

Similar schemes are used in other coun-tries including Australia in which one EBVis for wool fibre diameter and in NewZealand, where a total of 94 individualEBVs are measured with around half fortraits associated with wool and half formeat. Additional traits are likely to beincluded in future developments in sheepbreeding as the genetics of production anddisease factors are studied further.

Many breed societies now use SireReferencing Schemes and EBV values toincrease the rapidity with which geneticimprovement can be used across flocks byidentifying superior rams from the wholebreed. In these schemes, AI is used on allfarms in a Group Breeding Scheme withsemen from the same rams so that geneticcomparisons can be made even though theenvironment and husbandry of the farmsdiffer. 'Nature' is thus separated from`Nurture'!

It is also clear that commercial sheepfarmers should purchase rams with knownEBVs for traits that are needed to improvetheir own flocks and the financial indica-tions are that the investment of around £600per ram compared with £500 for an unknownram will be repaid in extra revenue fromlamb sales of around £3.00 per lamb sold.

3

Vaccination

A vaccination schedule should be in placeas part of each flock health plan, based uponthe particular disease risks within the flock.Always read the data sheet before using vac-cines as instructions and protocols some-times change (Fig. 3.1). At the time ofwriting, vaccines are available in the UKand many other sheep-producing countriesfor control of the following:

clostridial diseases;pasteurellosis;combined clostridial diseases andpasteurellosis;enzootic abortion of ewes (EAE);toxoplasmosis;footrot (FR);erysipelas;louping-ill; andorf.

Other diseases for which vaccinescan be used in special circumstances inthe UK are caseous lymphadenitis, botu-lism and Johne's disease. In some coun-tries, exotic diseases such as foot andmouth disease (FMD), sheep pox andBrucella melitensis may be controlled byvaccination.

Bluetongue vaccine was used in the UKwhile the threat of disease existed (seebelow for more information). See also underspecific diseases in relevant chapters.

Clostridia! Diseases

Clostridial diseases (see Table 3.1), otherthan tetanus and botulism, generally causerapid collapse and death, therefore diagno-sis and control are key issues. The diseasesare an ever-present risk in virtually all flocksand should be controlled by vaccination.It is common for mistakes to be made in tim-ing of vaccine administration or acciden-tally missing individuals or groups. It isalso quite common to find farmers who donot routinely use these vaccines either onthe grounds of cost (questionable as they arenot expensive) or the mistaken belief thattheir farm is not subject to this group of dis-eases. Clostridial organisms are commonlyfound in the intestinal tract, are widespreadin soil and form resistant, long-lastingspores, so it is never safe to assume freedomfrom these diseases.

Vaccination against clostridial diseases

There are several vaccines available rangingfrom comprehensive '8- or 10-in-1' to sin-gle component for blackleg. Mannheimia(Pasteurella) haemolytica and Pasteurellatrehalosi antigens are also combined withclostridial in one of the commonly used vac-cines. By using a multicomponent vaccine

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 17

18 Chapter 3

Fig. 3.1. Vaccination should be carried out carefully and cleanly.

Table 3.1. Clostridia! infections and associated diseases.

Disease Clostridium sp. Age affected Season Trigger factors

EnterotoxaemiasLamb dysentery'Struck'

Pulpy kidney'

BraxyaBlack disease'Bacilliary

haemoglobinuriaaAcute abomasitisb

Gas gangrenesBlackleg'Big head

NeurotropicTetanus'Botulismc

perfringens type Bperfringens type C

perfringens type D

septicumnovyi type Bnovyi type D

sordellii

chauvoeinovyi type A

tetanibotulinum

<2 weeksGrowing lambs

and adults>2 weeks

4-8 monthsAdultsAdults

SpringSpring

Any

AutumnWinterWinter

Growing lambs Springand adults

AnyAdults

AnyAny

2 weeks-4 months SpringAdults Any

Flush of milkFlush of milk or

grassFlush of milk, grass

or concentratesFrosted foodLiver flukeLiver fluke

Intensive feeding

Injury, woundsFighting, wounds

Docking, castratingToxin in food

'Included in 8-in-1 vaccines.'C. sordellii is increasingly being implicated by laboratories as a cause of death; included in 10-in-1 vaccine.'C. botulinum is rare in sheep and usually associated with chicken litter but is included for the sake of completeness.

and efficient primary and secondary doses,it is possible to maintain a protective level ofimmunity throughout the year in both ewesand lambs, against all the common clostrid-ial diseases. Vaccines containing fewer anti-gens may be cheaper and are sometimesused for growing lambs, but it is arguably

better to have a fully comprehensive insur-ance policy for these killing diseases.

Two doses of vaccine at a 4-6 weekinterval produce sufficient antibodies toprotect a ewe for the first year with suffi-cient spare, via colostrum, to protect itslamb(s) for up to about 16 weeks, providing

Vaccination 19

the secondary or booster dose is givenapproximately 1 month before lambing(Fig. 3.2). In subsequent years, only one pre-lambing booster injection is required to pro-tect both ewe and lamb(s).

Assuming a flock to have no initial pro-tection, one effective vaccination scheduleis as follows.

Ewes

Primary as soon as possible.Secondary - 4-6 weeks later.Booster - 4-6 weeks before lambing.Repeat booster annually.

Lambs (ewe and ram)

Those to be kept over 16 weeks (for slaugh-ter or breeding):

Primary - at 10-12 weeks.Secondary - at 14-16 weeks.Booster (for breeding lambs only) withthe adult ewes and rams pre-lambingtime.

Bought-in ewes (for breeding)and store lambs (for slaughter)

Unless there is reliable vaccination infor-mation, it is best to assume that these have

not been vaccinated, or at least that theirimmunity has waned and give them the fullcourse of primary and secondary injections,starting as soon as possible after purchase.A short cut is often taken with the bought-inewes (with some justification if there are noobvious winter clostridial risks, e.g. blackdisease) and that is to vaccinate them onarrival but delay the secondary injectionuntil 4-6 weeks before lambing, but thisstrategy can be risky.

Bought-in rams

If their vaccination status is in doubt, givetwo doses at a 4-6 week interval, followedby an annual booster.

Lambs out of unvaccinated or inadequatelyvaccinated ewes

These lambs should either be vaccinated(primary in first week, secondary at 6 weeks)or rely on 200 ml of colostrum (fresh or fro-zen) taken from a vaccinated ewe and givenat birth.

In an outbreak

Control measures in the rest of the flockconsist of:

Fig. 3.2. These newborn lambs are born with no antibodies and are dependent on colostrum to acquire them.

20 Chapter 3

Remove sheep from the predisposingsource (where possible), for exampletake off the lush grass or reduce theconcentrates.Give an antibiotic injection (e.g. peni-cillin) for those with local infection, forexample 'gas gangrene' and tetanus.Give antitoxin, if available, to all at risk,but in the UK this is now only availablefor tetanus. As the protection providedby antitoxin persists for only approxi-mately 2 weeks, it is appropriate to injecta primary dose of vaccine at the sametime (but at a different site), followed bythe secondary dose of vaccine 4 weekslater, thus providing both immediateand long-term cover; the potency of theantigen overcomes any significant inter-ference by circulating antibody.

Pasteurellosis

In flocks experiencing pasteurellosis, acombined vaccine containing clostridialand Pasteurella antigens is often used onthe same schedule as for clostridial vaccina-tion. A specific vaccine for pasteurellosis isavailable if, for any reason, the combinedvaccine is not suitable. Note that passiveantibodies to Pasteurella/Mannheimia spp.obtained by lambs from colostrum only pro-tect for 2-4 weeks compared with up to 16weeks for clostridial protection. If pneumo-nia is a problem in young lambs they can bevaccinated with a single vaccine from 3weeks of age with a booster after 4 weeks.

Abortion

Effective vaccines are available to protectagainst EAE (caused by Chlamydophilaabortus) and toxoplasmosis (Toxoplasmagondii).

Although there has been an effectivedead vaccine to protect against EAE, this isnot available at the time of writing. It hadthe advantage of being able to be adminis-tered to already pregnant ewes. The availa-ble vaccines are live and must be given at

least 4 weeks before mating. Boosters arerecommended a few years after the initialdose, but in practice most sheep are onlyvaccinated once.

The vaccine against toxoplasmosis is alive vaccine and should only be given tonon-pregnant sheep at least 3 weeks beforetupping. The EAE vaccine and that for toxo-plasmosis can be given at the same time butfrom different syringes at different sites (e.g.on each side of the neck).

Footrot (FR)

One vaccine is available and should be usedas part of a package of control measureswhen dealing with an infected flock. It is adead vaccine containing ten strains ofDichelobacter nodosus. It is prepared in anoily adjuvant which can lead to lumpsdeveloping at the injection site. The vaccinecan be curative as well as preventive, with aresponse usually noticed after a single dose.Boosters are needed, the frequency and tim-ing depending on individual flock circum-stances and identification of particularhigh-risk times for disease spread.

Monovalent vaccines have been usedin some places where only a single strain ofD. nodosus has been implicated, for exam-ple in Nepal. Research is ongoing looking atcandidate antigens in order to develop abetter vaccine for the future.

Erysipelas

In flocks experiencing problems of chronicarthritis of lambs shown to be caused byErysipelothrix rhusiopathiae, or where post-dipping lameness is a recurrent problem,vaccination with an erysipelas vaccine isusually highly effective in preventing futureproblems. The vaccine is a dead one andrequires two injections 3 weeks apart to pro-duce immunity. Young lambs are protectedthrough colostral antibodies so vaccinationshould be carried out on a similar scheduleto clostridial vaccines, with pre-lambingboosters in succeeding years.

Vaccination 21

Louping-ill

This vaccine is obviously only necessary intick areas where louping-ill is a known orpotential problem. The vaccine is a deadone and requires a single injection repeatedevery 2 years. Lambs from vaccinated ewesare protected by colostral antibodies for 2-3months.

Bluetongue

Bluetongue suddenly appeared in northernEurope in 2006 and continued in 2007 caus-ing devastating losses in some sheep flocks.Cases appeared in the east of England in2007. A vaccine against the specific sero-type (8) was developed and was widelyused in 2008 and 2009. This has resulted inno further disease in the UK and a hugereduction involving this serotype else-where. The disease remains active in coun-tries around the Mediterranean and involvesother serotypes which always pose a poten-tial threat. The use of vaccine will now

depend on the disease risk. The UK has nowbeen declared free of the disease and vacci-nation is no longer allowed, however,should the disease recur, it is likely thatvaccination will again be used.

Orf

Orf vaccine is different from all of the above,being applied to a scratch on the skin ratherthan being injected. It consists of live virusand should not be used in flocks whichhave no previous history of the disease.Care needs to be taken in its use. A scabforms at the vaccination site and this con-tains live virus and may be shed into theenvironment for up to 7 weeks. It is there-fore important that contamination of lamb-ing pens and fields is avoided by not puttingrecently vaccinated sheep into them. Ewesshould not be vaccinated within 7 weeks oflambing. It can be used in lambs but riskstransmitting infection to ewes' teats. Aswith all vaccines, read the data sheet thor-oughly before recommending!

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4

Thin Sheep

Thin ewes are interesting and important forthe following reasons:

They are common which shouldencourage us to do something aboutthem.The causes are not infinite; in fact, formost cases, the list is short:

lack of food;inadequate teeth - particularly thecheek teeth; andchronic disease, for examplechronic lameness (joints rather thanfeet), chronic fasciolosis, chronicpneumonias, Johne's disease.

This should encourage us to diagnose themaccurately.

If there are many thin ewes, look first atthe food and the number of fetuses orlambs; if there are a few thin ewes, alsolook at the 'fangs' (teeth) and the faeces;if there are only one or two thin ewes,also look at the limbs and the lungs.Thin ewes have suffered an insult forsome time, which may imply irreversi-bility (i.e. they may not get better).Thin ewes are not 'worth' much, butdeserve a lot because they represent aserious welfare problem.Thin ewes are generally unprofitable,for the following reasons:

If at tupping, their ovulation ratesare reduced and therefore they pro-duce fewer lambs.If in late pregnancy, they producesmaller lambs and risk pregnancytoxaemia.If at lambing, they produce lesscolostrum and show less interest intheir lambs, which in turn are moresusceptible to disease.If in early lactation, they produceless milk leading to poor growthrate in their lambs.

Condition Scoring

One of the reasons for thin ewes being com-mon is that the fleece masks their conditionand it is only when the ewe is shorn or han-dled that the thinness is disclosed, so thatthe condition has continued for much longerthan would have occurred in other species.Condition scoring (Fig. 4.1) was introducedto overcome this problem and is now anessential tool in good flock management aswell as in the clinical examination of indi-vidual sick sheep. In some countries (e.g.New Zealand, Australia) body weight is anessential monitoring tool, but cannot begenerally applied in the UK because of the

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 23

24 Chapter 4

Fig. 4.1. Condition scoring by feeling muscle andfat cover over the loin is a vital technique.

large number of breeds and wide variationin mature body weight whereas a morestandard breed type is found in these othercountries. Condition scoring does not sufferfrom breed differences though it will benecessary to use different ideal target scoresfor different breeds, particularly betweenmountain and lowland sheep.

The crucial element in the technique isto decide by feeling the mid-lumbar region,whether the ewe is 'too thin' or 'too fat' orjust about right, so that action follows, forexample, by separating and supplying extra,or occasionally less, food (see Fig. 4.2).

A number score (1 to 5, where 1 isemaciated and 5 is so fat you can't feel any-thing else) is given and it needs practiceacross the full range of scores and stand-ardizing with other scorers from time totime. Each time of condition scoring usu-ally requires doing a few 'to get your handin', but it is a technique that is learntquickly and needs no kit, only one sensi-tive hand! Half scores are useful as mostpeople find the distinction between full

Score 1 - transverse processes and spinesharp, bones easily felt, little muscle, no fat

Score 2 - transverse processes and spineeasily felt, some muscle but still feels hollow

Score 3 - requires pressure to feeltransverse processes, spine rounded, goodmuscle cover feeling rounded

Score 4 - spine just detectable with pressure,transverse processes barely detectable evenwith pressure, muscle covered with fat

Score 5 - thick fat cover, no bones palpable

Fig. 4.2. Condition scoring: descriptions of the mid-lumbar region denoting condition score (CS) 1 to 5.

Thin Sheep 25

scores too large for decisiveness. It is usu-ally possible to teach the technique rapidlywith agreement within half a score.

Two vital times when farmers shoulduse the technique of condition scoring theirflock are 6-8 weeks pre-tupping and 6-8weeks pre-lambing, because then thereis time to alter events by, for instance,reallocating resources such as food, housingand shepherding. Repeat scoring in about4 weeks is advisable because at least it willsuggest what the future holds, although itmay be too late by then to alter some of theevents, particularly late in pregnancy whenthe demands by the lambs are high. Lowlandewes with a CS of less than 3 (hill 2.5) shouldbe separated and clinically checked. Mostwill require more, perhaps better food, whilesome will require treatment or even culling.

Assessing a Feed Ration forAdequacy -a Practical Problem

One of the simple nutritional problemswhich the practising veterinary surgeon cancarry out is to decide if a group of sheep arethin because of inadequate feed or if somespecific disease is involved. The followingsteps illustrate how to investigate the prob-lem by an examination of what is being fedto the thin ewes. It should be emphasizedthat it is a simplification but will indicate ifthere is a gross inbalance in the require-ments and the intake of the ewes. It has beenused by student groups and by us over manyyears and usually works!

Is thinness in a group of ewes due to feedor is something else responsible?

The most common problem is when a groupof pregnant ewes are housed and a signifi-cant number of them are in poor condition.

Work on metabolizable energy (ME) only

STEP 1. Assume the following approximateME requirements of a 70kg ewe, which isaround the average weight of a lowland ewe:

Maintenance 10 MJAt lambing with two/three lambs 20 MJFull lactation 30 MJ

These figures are easy to remember and anystage of gestation can be obtained by linearextrapolation between maintenance at 80days and lambing at 145 days (e.g. day 115is approximately 15 MJ).

If the ewes are significantly different inweight from this, maintenance ME can beobtained by the formula:

ME = 0.4(body weight)° 75

For example for a 70 kg ewe ME = 0.4 x 24.2= 9.7 MJ (rounded off above to 10 MJ).

Does the ration supply these requirements?

STEP 2. Examine the concentrateconsumption:The farmer may know how many kilogramsare fed daily or may state, for example, that`six bucketsful are given to the group'. Weigh abucketful and calculate how many kilogramsare fed to the group. Count the number of ewesand let the quantity fed per ewe be 'c'.

1. Check the ME of the concentrate.This may be: (i) obtained by asking the man-ufacturer; (ii) calculated from formulae; or(iii) assumed to be about 12.4 MJ/kg DM.This assumption is risky since some feeds(usually cheap) may be as low as 11.0 MJ/kgDM. Take great care to distinguish betweenvalues given by manufacturers for air-dry oroven-dry material. It is assumed that thevalue obtained is for oven-dry material(i.e. true DM).2. Remember that the megajoule in (1) willbe per kilogram DM. Since concentrateshave a DM of about 85%, the DM intake willbe 0.85c.3. Calculate the mean intake of each ewefrom the concentrate:

ME intake concentrate = 0.85c x MJ(e.g. 0.85c x 12.4 = 10.5c)

STEP 3. Examine the forage consumption:The farmer may state that this is given ad libi-tum which should mean that there is alwayssome available for the ewes (i.e. hay in therack all day or self-feed silage). If this is not

26 Chapter 4

true when you visit the farm, the quantity fedmust be measured by weighing a bale andasking how many bales are fed per day. If theforage is truly available ad libitum, work onforage being consumed to appetite. (This is aproblem in the calculation since so manyfactors influence food intake but a check isincluded later - see STEP 5).

(In the example given below it isassumed that the ewes are being given hay,but the calculation for other forages such assilage is identical. It is probably even moreimportant to have the forage analysed asthere are greater variations than for hay. TheDM content of hay is around 85-90%whereas that for silage is 25-30% so a muchgreater weight of silage must be eaten to pro-vide the same energy. It should be remem-bered that care must be taken with silageproduction to reduce the risk of listeriosis.)

1. Calculate forage consumed.Assume a 70 kg ewe has an intake of approx-imately 1.5 kg DM, which is reasonable ifthey are fed medium or good quality hay.If the hay is poor, with a ME of 8, the intakewill be less, around 1.25 kg DM.

DM forage consumed= 1.5 - concentrate consumed= 1.5 - 0.85c

2. Calculate the ME of the forage.This can be obtained by: (i) analysis; (ii) cal-culation; or (iii) by estimating the qualityand assuming that poor, medium and goodquality hay will have values of approxi-mately 8, 9 and 10 MJ/kg DM, respectively.The values for silage are higher than for hayand the corresponding values are 9.5, 10.6and 11.7, respectively.

ME intake forage = (1.5 - 0.85c)x ME forage

For example with medium quality hay= (1.5 - 0.85c) x 9

STEP 4. Calculate the total ME intake:

Total ME intake = ME from concentrateplus ME from forage

= 0.85c x ME concentrate+(1.5 - 0.85c)x ME forage

For example:Total ME intake = 0.85c x 12.4

+ (1.5 - 0.85c) x 9

STEP 5. Look at modifying factors on thefarm:These calculations have made a number ofassumptions, some of which can be checkedon the farm.

1. Check that your calculation of forageagrees roughly with what is fed (i.e. weighand count bales).2. Allow for wastage of forage if this is not fedad libitum, which will depend on its quality.Look at the bedding and see how much haycan be seen and observe the ewes eating andsee how much they reject. As an estimate,wastage of good hay will be about 5% and canbe ignored but poor hay may have wastage of20%. Make an allowance for this in your cal-culations unless the hay is truly ad libitum.3. Look at the trough space which should beat least 45 cm for each ewe in the group.Watch the ewes when they are given con-centrates and see if many are forced to snatchsmall quantities and keep moving. Each eweshould be able to stand fairly quietly and eatits share. Watch for bullying which may giverise to a small number of thin (bullied) eweswith the rest normal or overfat.4. Ask if there are any ewes with particularrequirements. We have assumed that theewes are uniform but different lamb num-bers, initial condition, etc. may need to betaken into consideration.

A calculated example

A 70 kg Mule ewe at 115 days of gestationgiven hay ad libitum with an analysis of9.0 MJ/kg DM and 0.25 kg of a concentratewith ME of 12.4 MJ/kg DM. Is this diet ade-quate to maintain body condition?

Requirement = approximately 15 MJ

Intake = 0.85 x 0.25 x 12.4 + (1.5 - 0.85x 0.25) x 9 (from STEP 4 above)

Intake = 14.2, which is just less than require-ment, so some loss in condition will resultand it would be preferable to increase theconcentrate fed slightly.

Thin Sheep 27

Teeth

It is very important to be able to examinesheep teeth properly, not only for ageing(see Fig. 4.3 and Table 4.1) but also becausefaulty teeth are one of the most commoncauses for adult sheep to be thin (Fig. 4.4).

With regards to teeth the followingpoints are worth noting as there is a lot ofvariation within and between flocks, andsome confusing features:

Eight worn permanent incisors canlook like eight temporaries and viceversa, especially in mountain breedssuch as Welsh Mountain. Generally,the temporaries are smaller, more

I '10'41,

..11

11111,1

triangular and without a table (i.e. aflat surface). However, since this meansthat a yearling is being comparedwith an old ewe, it is generally possi-ble to tell the difference by generalobservation so common sense is neededrather than unthinking applicationof the data shown in Table 4.1 andFig. 4.3.The permanent corner incisor is usu-ally less obvious than the other perma-nent incisors (it sometimes nevererupts). It can look like a temporarytooth, making the sheep appear like a3-year-old (six teeth).In rapidly growing lowland breedseruption of incisors can take place

Eight temporary teeth - the animalis less than about 1 year 3 months old

One pair of permanent teeth - about 1.5 years old

Two pairs of permanent teeth - about 2 years old

Three pairs of permanent teeth - 2.5-3 years old

Full mouth - more than 3 years old

Remember that a full set of small permanent teeth can looklike temporaries - look at the animal to gauge if it is old or young.

Fig. 4.3. Teeth and ageing.

Table 4.1. Ageing - a rough-and-ready guide (see points worth noting in text).

Age (years) Incisors Cheek teeth (one side)

Up to 1 (lamb, hogg) Four pairs (eight teeth) temporary

1-2 (yearling, shearling) One pair permanent (two teeth),three pairs temporary

2-3 Two pairs permanent (four teeth),two pairs temporary

3-4 Three pairs permanent (six teeth),one pair temporary

Four pairs permanent (full mouth)Rising 4 and over (sometimesto a grand old age)

Old sheep Less than four pairs permanent(broken mouth)

Three premolars - temporary,two molars - permanent

Three premolars - permanent,three molars - permanent

As above

As above

As above

May lose some premolarsand/or molars

28 Chapter 4

Fig. 4.4. Examining the incisor teeth gives a good indication of age.

earlier than indicated in Table 4.1. Thefirst set of permanent incisors can bepresent by 15 months, the second set by21 months, the third set by 2 years 3months and a full mouth by less than 3years.Age the sheep in relation to the time ofyear and the normal time of lambing(e.g. in the autumn in the UK, mostsheep will be X years plus or minus6 months, while in the spring they willbe just X years, since most ewes areborn in March).Periodontal disease causes prematureincisor and molar tooth loss and sheepthen look older than they really are.The first and second molars (fourthand fifth cheek teeth) are present earlyin the lamb's life and a year or morebefore the temporary premolars areshed and the permanent premolarserupt. The region between the thirdpremolar and the first molar is, there-fore, a very susceptible site for foodimpaction and progressive disease,starting in the first year or so of life. Itis almost certainly the reason why themid-ramus is the area most promi-nently affected (lump and sinus) inperiodontal disease of the cheek teethwhich is the area where careful exami-nation should be carried out.

Teeth problems

Incisors

Very occasionally, faulty eruption occursand a dentigerous cyst may result whichultimately causes considerable bonydeformity and may cause premature cullingthough it is surprising how efficiently suchsheep maintain condition. Malposition inrelation to the dental pad (over or under-shot) is quite common but it is probably notsignificant unless extreme. It has low herit-ability, and the selection for good apposi-tion (bite or occlusion) is unreliable before3 years old. Premature loss of incisors (bro-ken mouth) is extremely common and isconnected with periodontal disease.

To some extent, tooth eruption alwayscauses a local Ids', but in many sheep thereis a serious progressive gingivitis leading togum recession early in life, and subsequentloosening of teeth following subgingivalplaque formation and periodontitis.Osteomyelitis, abscessation and sinus for-mation are natural consequences of the ini-tial gum pathology. The reason for suchserious progression is uncertain; the role ofsome oral bacteria has been investigatedand there is a strong suspicion that grittyfood may be involved, which may help toexplain why the prevalence of the disease is

Thin Sheep 29

much higher on some farms than others,where the soil types and grazing environ-ments differ. Sometimes, there is a family orbreed prevalence within a flock, suggestinga genetic component.

Premature loss of incisors in hill andupland sheep reduces the ability of ewes tomaintain body condition and to feed theirlambs well, and so often results in prema-ture culling. Its effect on lowland sheep isnot so serious providing the cheek teeth arenot involved, and therein lies the problem.Broken-mouthed sheep should always havetheir cheek teeth checked, because incisorloss often means molar loss, although occa-sionally the incisors may appear healthywhile the cheek teeth are not (and viceversa). So the customary reliance on incisorexamination alone (ageing) can be very mis-leading and all thin sheep need their cheekteeth examining by external examination ofthe jaws. Studies have shown a poor corre-lation between incisor loss and body condi-tion but a good correlation between molartooth disease and condition.

Cheek teeth

First examine from outside (most problemscan be detected by this method, but a moredetailed examination can be done if consid-ered really necessary - see below).

Note CS, dribbling, staining of lips andmouth, mouthing (when trying to eat) andquidding (swelling of cheeks with wadsof food and spilt quids and cuds on theground). Observe sheep chewing the cudand regularity of movement of lower jaw.Feel along the outside of the cheek forevidence of pain (flinching on pressure)and for irregularity of teeth (shearmouth and wave mouth).Feel with finger and thumb along thetwo rami for bony swellings and miss-ing teeth.Compare the thickness of the rami witheach other, but also with a normalyoung animal - bilateral thickeningmay be missed if you are unfamiliarwith the normal, though it is usual foronly one side of the mandible to be

involved which allows comparisonbetween them.Note whether there are dischargingmaxillary or mandibular sinuses.Note abdominal distension for ruminal`impaction' and/or pregnancy (likely todevelop pregnancy toxaemia).

Now look inside if you really need to,but remember sheep cannot open their jawswidely and it may cause, at the least, dis-comfort to force them apart. Make sure theanimal is facing the light (and have a goodtorch) and also have a good gag (e.g. block ofbevelled hard wood 12 x 2 x 2 cm or a sheepgag). With the gag in place, note any gaps(particularly common in the lower jaw),irregularities, loose teeth, food impactionand spikes. Look particularly in the mid-third region (check teeth three and four): ifthere are gaps, the corresponding upper (orlower) tooth lengthens through lack of wear,making it even more difficult and painfulfor the sheep to chew properly.

Be very careful in inserting a fingersince the edges of the teeth are usuallyvery sharp and it is easy to sustain apainful cut.We have found increasingly that we candetermine the presence of molar toothproblems by external palpation andrarely resort to the use of a gag to exam-ine inside the jaw.

Treatment

Assess whether it is worth doing any-thing other than cull. Some action usu-ally must be taken on grounds of welfareas well as economics, but dentistry pro-vides only temporary relief and mayonly be indicated in late pregnancy inorder to allow the ewe to produce valu-able lambs which will probably have tobe reared apart from the ewe.Loose incisors are often best removedrather than left and can usually beremoved without anaesthetic. Removeobvious loose molar teeth under seda-tion or light anaesthesia and injectlong-acting (LA) antibiotic twice at

30 Chapter 4

4-day intervals. Ewes can thrive, givena chance, without any incisors (`gum-mers') providing their cheek teeth arehealthy. Molar rasping may have short-term advantage, but is very difficult todo effectively.Feed high quality concentrates and rough-age that are comfortable to eat and sepa-rate from greedy competitors. Proprietarynuts are usually too hard. A useful mix is40% whole barley, 40% sugarbeet pulp,17% soya and 3% minerals.

Control

Check feeding and breeding. A fault in Ca/P,vitamin D, copper and fluorine levels in thefeed should be considered, as well as gener-ally inadequate feeding which may lead toexcessive soil eating (which compounds theproblems of mineral deficiencies and gumirritation). The prevalence in a flock may sug-gest genetic factors, in which case the ram(s)or even the breed needs changing. Feedingblocks and roots may not promote incisorloss, but certainly require healthy teeth.

Fasciolosis

Fasciolosis, most importantly Fasciolahepatica (liver fluke) infection, is of immenseeconomic importance in sheep throughoutthe UK and most sheep-producing countriesof the world. Some years ago, it was only amajor problem in the wetter west of the UKbut it is now much more widespread perhapsdue to climate change. No effective immu-nity develops in sheep, unlike cattle, andthus disease can occur in any age of sheep.A high proportion of the flock is usuallyaffected in epidemic years. E hepatica has awide host range including humans and wildmammals which makes control difficultwhere mixed host species occur on farms.

Clinical disease is associated with theecology of a mud snail of the genus Lymnaea(Galba) often with different species in differ-ent countries though all have similar habi-tats, so that work on one species can beextrapolated to others and rational controlprinciples suggested. In the UK, the snail is

Lymnaea (Galba) truncatula. All these snailsare small (a maximum of 10mm thoughmuch smaller snails can support the devel-opment of the fluke) and are found in muddyareas at the edge of streams and ditches.When searching for the snails, it is often use-ful to look for dried mud on the snail shellwhich means that it stands out on the muddyhabitat. The development of the stages in thesnail is dependent on a minimum tempera-ture of 10°C and moist habitats which allowsthe important times for the appearance ofdisease to be forecast from meteorologicaldata, even if the country has never been vis-ited or studied! The epidemiology of the dis-ease is dependent on wet conditions for acumulative period of 12 weeks during themonths when the temperature is above 10°C.This association allowed a forecast to bemade dependent on meteorological condi-tions and resulted in very effective controlschemes being devised. In the UK, this inval-uable forecast is still produced in the NationalAnimal Disease Information Service (NADIS),available online at www.nadis.org.uk.

In summary, acute disease, associatedwith migrating immature flukes, is most com-monly seen from October to February after awet summer, and chronic fasciolosis, in whichadults are found in the bile ducts, is seen fromDecember to April. A subacute form of thedisease has been described as occurring inDecember and January when a mixture ofadult and immature flukes will be present.The best way to decide if a farm has liver flukeis to take faeces from between ten and 20untreated thin ewes in December to May andlook for eggs, though eggs are likely to bepresent all the year round in untreated ewes.

Acute fasciolosis

Sudden death may occur in sheep of all agesin epidemic years and the mortality can bevery high. Affected animals may be seenwith extreme weakness, severe anaemia(packed cell volume (PCV) of 10%), abdom-inal pain and ascites. The liver is enlargedwith haemorrhagic tracts. Eggs are not foundin the faeces and there are usually over1000 immature (0.5 cm long) flukes in the

Thin Sheep 31

substance of the liver. Acute disease is seenabout 6-8 weeks after the ingestion of alarge number of metacercariae.

The flock should be treated (triclabenda-zole is effective against all stages of the parasitefrom 2 days old onwards unless resistance hasdeveloped, which is not common as yet) andmoved to a clean pasture, wherever possible.The metacercariae will remain viable for sev-eral months, especially over the winter, so donot return sheep to the pasture containing anextensive snail habitat before the end of May.

Chronic fasciolosis

Affected animals show a progressive loss incondition proceeding to emaciation, andsigns of anaemia will be present, since thePCV is usually about 15%. Mucous mem-branes are pale and the nictitating membraneis pale and oedematous Pflukey-eyel. Ascitesoften occurs but sub-mandibular oedemaPbottle-jawl, often described as being typi-cal of chronic fasciolosis, is uncommon anddoes occur in other clinical conditions. Woolyield is reduced even in light infections, as isthe milk production of ewes, thus resultingin reduced weight gain in the lambs. Theliver is small and cirrhotic, the bile ductsenlarged and thickened. There are usuallyabout 250 adult flukes present and eggs canbe found in the faeces. The prepatent periodis about 10 weeks but chronic fasciolosisusually occurs some weeks after patency.

Control

This is based upon strategic anthelminticuse and knowledge of the environmentalconditions which are needed to allow thedevelopment of the fluke from egg to infec-tive metacercaria, on the ground and in thesnail, L. (G.) truncatula. This mud snailmeasures up to 10 mm in length and theoperculum is on the right side when heldupright. There are, however, a number ofrather similar snails which can easily beconfused with L. truncatula.

In the UK, the most important cycle ofinfection involves the 'summer' infection of

snails which results in the main pastureinfection with metacercariae occurring inSeptember and October. The 'winter' infec-tion of snails occurs when snails becomeinfected in October of one year and the lifecycle is complete in May and June of the nextyear. This can give rise to acute fasciolosis inJuly and August rather than in the autumn Itis a rare occurrence in the UK because May isusually a dry month and the over-winteredsnails commence to die off at this time.

Use of anthelmintics

Modern anthelmintics act against immaturestages as well as against adults. Some drugs,such as triclabendazole are effective againstthe very early stages (from 2 days old), oth-ers against somewhat older, immature flukes(rafoxanide, nitroxynil, closantel from 4 to 6weeks old) while some drugs are only effec-tive against adults (oxyclozanide, albenda-zole). Closantel also prevents egg layingby adult flukes for over 10 weeks.Triclabendazole is the drug of choice in thetreatment of acute fasciolosis. Drugs are avery important part of any control pro-gramme, the aim of which is to prevent flukeeggs being passed by the sheep (or cattle) sothat the infection rate of snails is greatlyreduced. Field trials with rafoxanide haveshown that if all adult sheep are treated inmid-April, followed by a second treatment6 weeks later, the summer infection isreduced to a very low level. Further treat-ment in October and January reduced flukeburdens over a 3-year period to about 10%of pre-trial numbers, and resulted in consid-erable increase in wool yield and lambproductivity (the extra revenue from fleecesales was sufficient to pay for theanthelmintic treatments). This work wasdone in an area where fluke was widespreadand habitats extensive, and in areas of lighterinfection it would probably be sufficient totreat in April, October and January. Goodresults have been obtained on a high-riskfarm by the treatment of all sheep with tri-clabendazole in January or February andthen every 3 months. Although snail num-bers increased, the number of infected snailswas very low and the prevalence of infec-tion in the sheep reduced by about 75%.

32 Chapter 4

These months are based on UKconditions but it is easy to extrapolate toconditions in other countries includingthose in the southern hemisphere by con-sulting local meteorological information.

Although anthelmintic resistance toF. hepatica is not as common or widespreadas to intestinal nematodes, flukes resistantto triclabendazole have been described insheep in many parts of the world includingthe UK and Australia. Field studies onsheep harbouring the resistant adult flukesshowed that they were susceptible to clos-antel, nitroxynil, albendazole and oxycloza-nide; younger resistant flukes are probablysusceptible to rafoxanide and nitroxynilfrom 4 to 6 weeks old as above.

Short-term control

The publication, UK VET Livestock has a regu-lar section called 'Parasite update and forecast'which includes a liver fluke forecast. This isextremely valuable and can be used to avoidacute fasciolosis in epidemic years by prevent-ing sheep from ingesting large numbers of cer-cariae from September onwards by:

removal of sheep to a pasture with nosnail habitats; orfencing off small habitats.

Sheep should be kept away from habitatsuntil May of the following year since meta-cercariae are long lived during wintermonths. If sheep must be grazed on habitatsduring the winter in epidemic years sinceno other grazing is available, anthelminticswhich are effective against very youngflukes given at 4-6 week intervals may helpin preventing serious disease. This is notvery satisfactory however, and it is prefera-ble to use control measures which preventsuch heavy pasture contamination.

Long-term control

This used to be based on improved drain-age and even use of molluscicides (it is nowmany years since use of these was contem-plated) but current support for wildlifehabitat improvement means that farmersare more likely to be encouraged to keep

boggy ground rather than drain it!Improvement of hill grazings with basicslag and lime also no longer takes place.This increased the pH and allowed previ-ously unsuitable land to become very suit-able for snail multiplication. Severeoutbreaks of fasciolosis were seen on theseimproved pastures where previously theacid pH of the peat prevented extensivehabitats.

Control therefore has to rely on:

fencing off habitats if feasible; andprophylactic use of anthelmintics toreduce pasture contamination witheggs so that the proportion of infectedsnails is reduced.

On many farms where habitats are few andsmall, eradication is possible by a logicalcombination of these principles.

A survey of snail habitats is essentialbefore any of these control schemes can bedeveloped. This may be done by the veteri-nary surgeon with a large-scale map of thefields and an experienced eye for suitablesnail habitats.

Johne's Disease (Paratuberculosis)

Johne's disease is found in older sheep inmost sheep-producing countries of theworld. However, it is not diagnosed veryoften but it may be much more commonthan we realize since diagnosis is difficultand there are many sheep which harbourthe causative organism Mycobacteriumavium subspecies paratuberculosis (MAP;synonym Mycobacterium johnei). It needsto be on one's list of causes of thinness inmiddle-aged ewes. However, it can becomeestablished in a closed flock, and a 10%incidence has been recorded in some flockswith an even higher prevalence in someabattoir surveys.

Diagnosis

The typical story is of a few dirty-tailed andbroken-woolled ewes of about 3 years of age

Thin Sheep 33

which are unaccountably thin (feed andteeth okay), often deteriorating soon afterlambing. The disease is similar to that incattle but there are a number of specificfeatures:

Scouring is not so obvious, often beingintermittent with only soft faeces.As with most debilitating diseases ofsheep, the fleece pulls out easily (woolbreak).As well as the common ovine strain,there is also a yellow pigmented strainwhich occurs in some restricted geo-graphical areas and can be seen atnecropsy, staining the intestine.The organisms are not easily found inthe faeces though it may be worth-while staining a faecal film for theacid-fast bacteria by the Ziehl-Neelsentechnique but no conclusion shouldbe drawn from a negative result.A necropsy with gut histology is usu-ally required to establish the diagno-sis in a flock and thereafter it is oftenassumed that thin ewes are caused byMAP.Individual complement-fixation testsare unreliable and are really only foruse as a flock test. Similarly, anenzyme-linked immunosorbent assay(ELISA) is available though cannot berelied on.Since the disease is a protein-losingenteropathy, it has been suggested thatthe very low serum albumin concentra-tion seen in Johne's disease in sheep(mean of 14.1g/1 cf. normal 32.7 g /1),together with a normal globulin con-centration, may be useful as a screeningdiagnostic test.Many different strains of MAP areknown in a wide range of hostsincluding cattle, deer and rabbits andthe organism is found in Crohn'sdisease in humans, giving rise tofears that this disease is associatedwith poor pasteurization of milk.There is still considerable debate asto the relationship between thesestrains.

Control

Cull clinical cases and fatten their lambsfor slaughter rather than keeping themfor breeding. Infection occurs by inges-tion of MAP by young lambs with clini-cal signs developing 2-3 years later.Vaccination - live, attenuated vaccinesare used in many countries and can beimported specially into the UK with per-mission from the Veterinary MedicinesDirectorate (VMD). Experience hasshown that injection of lambs at about3 months of age increases their resist-ance to the disease, slows shedding ofbacteria and reduces clinical disease. Itdoes not prevent infection.Ensure good control of other debilitat-ing conditions (e.g. lack of food, worms,fluke and cobalt) which appear to pre-dispose to the development of the clini-cal disease and the shedding of largenumbers of bacteria.Think carefully about the use of surpluscolostrum in flocks which keep lambsfor future breeding. Infection can bespread through this route, therefore inproblem flocks use of commercial sub-stitutes may be a wiser choice.

Chronic Respiratory Diseases

The two slow virus diseases affecting thelungs, maedi visna (MV) and ovine pulmo-nary adenocarcinoma (OPA otherwiseknown as sheep pulmonary adenomatosis,SPA, or Jaagsiekte), can both lead to anincrease in the number of thin older (youngadult) sheep, and be the cause of prematureculling (see Chapter 13).

Caseous Lymphadenitis (CLA)

This chronic bacterial disease can alsosometimes cause wasting in older animalsbut is more often seen as abscesses in exter-nal lymph nodes (see Chapter 12).

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5

The Pregnant Ewe

Ultrasound Scanning - Diagnosisof Pregnancy and Number of Lambs

Ultrasound scanning of pregnant ewes hasbecome a widespread valuable technique insheep husbandry throughout the world. Inmany situations, it is sufficient to know ifthe ewe is pregnant or not but the techniquehas the additional value in flocks with highlambing percentages, to distinguish thenumber of fetuses. Ewes can then be markedand separated and fed appropriately fortheir fetal burden.

Commercial operators and veterinarysurgeons have provided ultrasound servicesin Australia, New Zealand and the UK andin many other countries. Most operatorsoffer a service which includes the determi-nation of fetal numbers.

It is important that the operator scans alarge number of ewes regularly to maintainexpertise in detecting fetal numbers andaccuracy will then be over 98%. An experi-enced operator can scan 80-120 ewes/h.Several veterinary practices with a largenumber of sheep clients operate scanningservices which help in the introduction ofsheep health programmes on to the farms.

The value of the technique is that:(i) barren ewes can be sold when prices arehigh or fed less; (ii) ewes with single lambscan be fed less, saving feed and avoiding

over-large lambs; and (iii) ewes with twoor more lambs can be fed more concen-trates which should reduce the possibilityof loss of condition and pregnancytoxaemia (PT).

The ewes are scanned in the standingposition without shearing and purpose-builthandling systems allow large numbers ofewes to be scanned in a day. For accuratediagnosis of fetal numbers, the fetusesshould not be less than 50 days and notmore than 100 days gestation. Allowing fora 28-day period with tups in the flock, thismeans that the flock should be scannedbetween 80 and 100 days from the time thatthe tups were turned out with the flock.

The main alternative is regular condi-tion scoring and transfer of thin ewes togroups fed more concentrates. This avoidsthe need for pregnancy diagnosis, butrequires regular examination by goodshepherds during late pregnancy.

Housing

The practice of housing pregnant ewes dur-ing the last 2 months of pregnancy or in wet,cold climates for longer periods has becomeadopted in the UK and many northernEuropean countries and in other countriessuch as the USA (Figs 5.1 and 5.2).

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 35

36 Chapter 5

Fig. 5.1. Heavily pregnant sheep are often housed for lambing.

111 1,11,11111111111111111111 1111111r1111111111M1111

Fig. 5.2. This shed holds a large flock of pregnant ewes divided into suitable groups.

Advantages

Housing prevents damage to the pastureby the sheep, which otherwise poachland during the wet winter and nibbleyoung grass shoots in February and

March. This is particularly importanton wet, heavy land where removing thesheep in winter results in good grassgrowth in April when ewes are lactatingheavily. This strategy allows an increasein stocking rate which is necessary if

The Pregnant Ewe 37

the costs are to be covered. Housingusually commences in December/January and sheep are turned out nearthe end of March, depending onweather.Housing improves the working condi-tions of the shepherd and protectssheep (and newborn lambs) fromextreme weather conditions. Ewes aremore carefully observed and shep-herded during lambing which reduceslambing losses.Housing allows ewes to be sorted intodifferent batches according to CS,number of lambs being carried (if ultra-sound pregnancy detection is used),state of teeth, lambing dates, etc. Thefeeding of the ewes is more controllableand regular condition scoring allowsappropriate adjustment to feeding to bemade.Housing reduces the wastage of food,both forage and concentrates, if well-designed racks and troughs are used,whereas considerable wastage occursin adverse weather if fed outside.Housing allows the winter shearing ofewes.

Disadvantages

Capital costs: these depend on the typeof building and whether existing build-ings can be modified. The buildingdoes not need to be of complex design,the cheapest being the 'polythene tun-nel'. The latter is composed of steelhoops covered with polythene and usu-ally with walls of plastic mesh. Thepolythene covering has to be replacedperiodically, some types every 3 or 4years, but some last 10 years. Mostbuildings may be used for some otherventure (e.g. calves) during the summerand autumnDisease risks: intensive housing mayincrease the risk of certain diseasessuch as neonatal scours, coccidiosis,FR and pneumonia but these can becontrolled by good construction andmanagement.

Food and bedding costs: food costs inMarch will be increased because theyoung grass is deliberately not madeavailable to the ewes but this will bebeneficial in the long run. Straw is anadditional cost.

Principles of Design

Site

The house should: (i) be convenient for theshepherd; (ii) be sheltered from the prevail-ing wind and snow; and (iii) have readyaccess to water and electricity.

Design

It is usual to have a wide centre passage,which allows access for feeding silage, ormay hold hay and concentrate feed, and canbe used for individual lambing pens later.Pens to hold 30-60 ewes are sited on eitherside of the passage. The centre passageshould be concreted but hardcore is best forthe pens to permit good drainage. The sizeof the pens varies with breeds and shearingbut should allow 1.0 -1.3m2 (10-14 ft2) perewe at least. It is most important that theewe should have ample trough space(0.45 m/18 inches each). A useful design isto have removable, double-sided pen divid-ers, each side consisting of a lower foodtrough and an upper hay rack with a centralwalkway between the two sides. Groundlevel 'walk-through' troughs are also oftenused for hay feeding. Alternatively, silagecan be floor-fed in the passage with ewesreaching through a simple barrier, with con-centrates also fed similarly, or scattered onthe (clean) bedding. Straw bedding shouldbe provided; about two bales of straw areneeded for each ewe for a 3-month period.Slats can be used, but ewes should not lambdown on them. The house must be well ven-tilated by Yorkshire (slatted) boarding, plas-tic mesh or open sides but be draught proofat sheep level by having solid walls to aheight of 1.0-1.2m. Water may be providedin troughs, self-fill bowls or continuousflow along a rainwater gutter. The water

38 Chapter 5

should be at a height that the sheep canreach but not too low or it will become con-taminated with faeces and thought shouldbe given to the increase in bedding heightwhich occurs during housing. Good lightingis essential as are power points for shearingand particularly for infra-red lamps over theindividual lambing pens and for the shep-herd's kettle!

Shearing Housed Ewes

For many years in the UK, the winter shear-ing of ewes was done when the ewes werehoused since this: (i) reduced heat stressand humidity which predisposes to pneu-monia; (ii) enabled more ewes to be kept inthe same space; (iii) increased food con-sumption and lamb birthweight; and (iv)enabled easy observation of lambing eweswithout handling. It also provides somecontrol of lice and keds since they breedmore rapidly in thick wool.

There were, however, disadvantagesassociated with the practice. If conditionswere extreme, ewes became too cold andhuddled together and it was necessary toallow at least 2 months' wool growth beforeturnout which may coincide with badweather and thus delay turnout. There wereincreased feed costs and single lambs maybe too large, causing dystocia and 'woolslip', associated with stress, was commonIn addition, the thick fleece which followedin the summer caused ewes to be too hotand distressed.

As a result of these disadvantages thepractice seems to have died out and it isunusual to find sheared ewes in houses dur-ing the winter.

Abortion

The incidence of abortions in 'normal'flocks is usually quite low (1-2%) and istolerated by the farmer without investiga-tion. However, it must be remembered thatmany of these abortions are caused by path-ogens or nutritional disturbances, which

also cause: (i) apparently 'barren' ewes;(ii) fetal mummies; and (iii) very weak non-viable premature lambs. Abortions, there-fore, even in small numbers should alwaysbe considered as only part of the losses inthe production process and farmers shouldbe questioned about these other aspects ofreproductive loss before dismissing them asunimportant.

When, however, an infectious abortionagent is introduced into a fully susceptibleflock, the incidence of abortions is oftenalarming and is recognized as a 'storm'.

Causes

All abortions should be regarded as infec-tious until proved otherwise. Although theprevalence of the different types of infec-tious abortion varies from year to year andfrom area to area, overall the four most com-mon causes of infectious abortion through-out the UK are:

EAE caused by Chlamydophila abortus;Toxoplasma;Campylobacter; andSalmonella - various serotypes.

Although these four infections are the mostimportant in the UK, some do not occur inother countries and the relative importanceof each will be indicated when dealing witheach specific infection. In summary, theseare the most common causes in countries innorthern Europe. Bruce lla melitensis, whichdoes not occur in the UK, where it is notifi-able, is common in southern Europe and isan important zoonosis. Campylobacter ismore important in North America than inthe UK. Australia and New Zealand are for-tunately free of EAE.

A number of other agents can causeabortions, but these are generally sporadicoccurrences which are relatively insignifi-cant. These include:

Border disease virus (BDV);Listeria;tick-borne fever (TBF) - Ehrlichia;Q fever - Coxiella;Arcanobacterium pyogenes;

The Pregnant Ewe 39

Yersinia pseudotuberculosis; andfungi.

Reports from diagnostic laboratories giveuseful figures to indicate the relative impor-tance of the infections in different countriesof the world.

For the UK, annual reports fromVeterinary Laboratories Agency (VLA) labo-ratories (now AHVLA having merged withAnimal Health) give a good indication ofabortion trends over at least the previous8 years (good for other disease informationtoo! - see www.defra.gov.uk/ahvla and inthe site A-Z find 'VIDA' in the index page;VIDA is the Veterinary InvestigationSurveillance Report). Table 5.1 shows fig-ures for the years 2005-2009 inclusive, 2009being the latest completed figures. Each fig-ure is a separate incident, not the totalnumber of samples received and may there-fore include several individual ewes. Thefigures show a trend for a reduction in EAE(Chlamydophila) and Toxoplasma whereasCampylobacter and Salmonella incidentsremain similar for each year, perhaps reflect-ing the use of the vaccines for EAE andToxoplasma.

It might be thought that since almosthalf the incidents do not result in a definitediagnosis, laboratory investigation of abor-tion outbreaks is unrewarding and notworth the costs involved. However, as ageneral rule, if there is a significant abor-tion problem and the laboratory receivessufficient useful material, the cause will beidentified allowing the appropriate specificcontrol to be instituted and perhaps allow-ing treatment of the ewes which have notyet aborted. The most likely reasons for

Table 5.1. Abortion incidents reported by the VLA2005-2009 inclusive.

Number of incidents

Total abortion incidents 10,493Diagnosis not reached 5,045 (48.1%)Chlamydophila 2,152 (20.5%)Toxoplasma 1,484 (14.1%)Campylobacter 675 (6.4%)Salmonella spp. 291 (2.8%)Other diagnoses 846 (8.1%)

laboratories failing to arrive at a diagnosisare that the material submitted is unsuita-ble and incomplete and may be just the`odd' abortion from the 'normal' flock. Inaddition, laboratories may only test for alimited number of infectious agents, thoughall will look for the four main agents.

In order to allow the laboratory the bestpossible chance of finding a causal agent,the following materials should be submittedas soon as possible after the abortionincident:

Fresh fetal membranes with cotyledons(if these are not available then supplyswabs from the wet skin of the fetus orof vaginal discharge).Fresh fetus(es).Information, which will include:O size and nature of flock (e.g. is it

self-contained? Are the abortionsin a particular group such as pur-chased, yearlings?);feeding of flock;previous abortion history, includ-ing any laboratory reports;dates of lambing;facilities for isolation; andpossible reasons for the abortion(s)for example handling and dosing,predisposing diseases such as flukeand PT and dogs (though the evi-dence for the latter is slight!).

It may also be useful to submit a clottedblood sample (red tube) to test for serumantibodies for Toxoplasma or EAE (it isworth tagging aborting ewes so thatthey can be identified later). However,it is best to leave this for 1-2 weeks andonly submit the sample if no diagnosiswas reached from the fetal membranesor these were not available.

Remember that some ewes can pro-duce twins, one of which is apparentlynormal, and the other abnormal andinfected. A flock may be infected withmore than one pathogen (e.g. Toxoplasmaand EAE) so that it is worth continuing tosubmit aborted material to the laboratoryeven after the first positive diagnosis hasbeen established (perhaps 10% of subse-quent abortions).

40 Chapter 5

General advice

Isolate the aborting ewe and retain thefetus(es) and membranes for laboratoryinvestigation; treat these as infectious(use polythene gloves and bags), notforgetting the public health risksfrom Chlamydophila, Salmonella spp.,Listeria, Q fever and (less directly dan-gerous) Toxoplasma (since oocysts arethe most dangerous stage).Chlamydophila is particularly danger-ous for pregnant women and theirunborn children and they should notbe involved with the lambing flock,since abortion may arise in a clean flockwithout notice! Keep aborting ewes inisolation until a positive diagnosis hasbeen made and until obvious vaginaldischarge has ceased (up to 3 weeks)and tag so they may be identified later,if necessary, for blood sampling or cull-ing. If the ewe is ill, antibiotic therapyshould be given but only after vaginalswabs have been obtained to submit tothe laboratory.Do not use aborting ewes or ewes pro-ducing premature lambs as foster moth-ers until it is known to be safe to do so.It is usually better to retain abortingewes and not sell them, because in gen-eral, they will now be immune to atleast one pathogen and not abort again.For Campylobacter, it may be worthallowing the aborted ewes to mix withthe ewes which have already lambed,and so induce general flock immunity(i.e. 'move on' rather than 'move back').It is essential, however, to be absolutelycertain that Chlamydophila is not alsopresent before recommending this prac-tice. (Mixing ewes that have abortedwith Chlamydophila will increase thenumber of latently infected animalswhich may then abort the next year!).It is no longer sound advice for bought-insheep to mix with the resident sheep,the general farm environment andon-the-farm food before tupping, for avariety of biosecurity reasons. Theyshould, where possible, lamb separatelyin their first season on the farm, in case

they are infected with Chlamydophilaand introduce EAE into the whole flock.An abortion 'storm' is usually notrepeated in subsequent seasons andsubsequent fertility is good, unless adifferent pathogen is introduced.At the time of abortions, those ewes yetto lamb should be kept apart from theinfected group and spread out, and thepossibility of therapy (see specificinfections) should be considered.Where possible, they should not lambin the same area as the infected group,or at least the lambing yard should bere-strawed.

Enzootic Abortion of Ewes (EAE)

This form of abortion is the most commonlydiagnosed in the UK and most northernEuropean countries but is notably absentfrom Australia and New Zealand. EAE iscaused by C. abortus, a highly specializedbacterium which parasitizes host cells, inwhich it undergoes a complex life cycleinvolving the formation of reticulate andelementary bodies.

Although chlamydiae are bacteria andare susceptible to certain antibiotics, theyrequire 'virological' (tissue-culture) tech-niques for their isolation and propagationand cultural confirmation of diagnosis isnot routinely available.

Infection of pregnant women causesdeath of the fetus and abortion and a veryserious life-threatening disease in themother, though only a small number ofcases have been reported. Considering thewidespread prevalence of EAE, it is perhapsnot very infectious to humans though thebest advice is that pregnant women shouldnot be involved with lambing flocks.

Clinical signs

Abortion occurs in the last 2 or 3 weeks ofpregnancy with no evidence of illness in theewes. The pathology of infection is essen-tially a necrotic placentitis so lambs usually

The Pregnant Ewe 41

appear fresh and show little or no grosspathology, although the abdomen is some-times distended with blood-stained fluid. Inaddition to aborted fetuses, premature andweak live lambs, and even apparentlyhealthy lambs but with infected membranes,are seen. Fetal membranes are sometimesretained, which may lead to metritis, butusually no clinical signs are seen inthe ewes.

Epidemiology

The most important source of infectionis from aborting ewes since the organ-ism is mainly excreted at the time ofabortion and in subsequent vaginal dis-charges, which resolve in a maximumof 3 weeks. Infection is, therefore,mainly spread at lambing time and therate of infection and the developmentof flock immunity is usually slow. Few`storms' occur but the incidence ofabortions tends to persist for yearsunless otherwise controlled. The dis-ease is almost unknown in hill flockswhere the management at lambing isless intensive than lowland, whereas itrepresents a serious and increasing haz-ard for sheep lambing under intensive,housed conditions.Infection is introduced to a 'clean' farmby the purchase of ewes which arelatently infected. The chlamydiae aremobilized during pregnancy, givingrise to abortions etc. 1 year after theewe became infected. No serologicalresponse can be detected during the`latent' infection and there is no methodof deciding whether purchased ewesare infected. Since only a few pur-chased ewes may be infected and abort,material may not be submitted for diag-nosis and the disease is not recognizeduntil a much greater number of ewesabort at the next lambing season.The characteristic picture, therefore, isthat the first season of infection showsitself as a few purchased ewes abortingor producing premature lambs; thenext one or two seasons, abortions and

stillbirths occur in all age groups andthe following seasons abortions etc. aremainly confined to yearlings andbought-in sheep, since the older eweswill have acquired immunity, which isdependent on infection of membranes.Lambs can be infected at birth fromtheir mother or other ewes and produceinfected lambs and membranes at theirfirst lambing (which may not be untilthey are shearlings) and then becomesolidly immune.Ewes infected for the first time in latepregnancy do not usually abort thenbut may do at their next pregnancy. Ittakes about 40-50 days from infectionto abortion which means that infectionand abortion can occur within the samelambing season if batch lambing ispractised. Ewes with lambing dates ofmore than 6 weeks apart should not bemixed close to lambing.Intestinal chlamydiae are common insheep but the majority of these arenow described as a separate species,Chlamydophila pecorum. The intestinemay also act as a reservoir of the abor-tion chlamydia, C. abortus, but there islittle evidence that clean ewes becomeinfected from these chlamydiae.Rams can become infected and mayshow epididymitis, but it is generallyaccepted that there is little likelihoodthat infection will be introduced into aflock or transmitted within a flock byrams. However, it seems unwise to pur-chase rams from flocks which areknown to be infected.Chlamydiae are not transmitted in themilk of infected ewes.Some workers have reported that eweswhich have previously aborted mayshed chlamydiae at subsequent oestrusperiods, but there is no strong evidencethat this is an important route of trans-mission. Most aborted ewes are consid-ered to be solidly immune.Recently, Chlamydophila of the vac-cine strain have been isolated from afew cases of abortion but it is acceptedthat this is no reason to cease vaccina-tion as a control method.

42 Chapter 5

Diagnosis

There is usually an obvious placentitis withthickening and necrosis, so look for thembefore sending to the lab. The lesions ofabortion caused by Y. pseudotuberculosisare very similar and the membranes shouldbe stained for chlamydiae and subjected tobacteriology for this agent. Modified Ziehl-Neelsen staining of smears from chlamydia-infected cotyledons will usually show largenumbers of intracellular inclusion bodies.However, infection may not be very obviousin the placenta when organisms are few andtissue culture has revealed organisms wheresmears have been negative. If no membranesare available, smears can be made from thewet skin/fleece of a recently aborted fetus orfrom the vagina of the ewe for 24 h or soafter abortion. Examination of the sera of anaborting ewe for complement-fixing (CF)antibodies will usually show a titre of atleast 64 if EAE was responsible, but it is notusually necessary unless membrane mate-rial is not available. Interpretation of CFtitres must take account of vaccination his-tory and previous abortions because thesemay produce persistent titres. Kits are nowavailable which will identify chlamydiaantigen in membranes.

Treatment

Aborting ewes rarely require any treatmentother than isolation until their dischargescease. It is wrong to mix these sheep withlambed ewes until discharges cease sincethe lambed ewes may become latentlyinfected and abort next year.

A decision has to be taken immediatelyafter a positive diagnosis has been made asto whether it is worth treating the ewes yetto lamb. This decision will be influenced bythe size and value of the flock as well as aguess as to what the subsequent abortionincidence is likely to be! Oxytetracycline iseffective against chlamydiae and injectionof an LA preparation will maintain preg-nancy until nearer the expected lambingdate. Injection could be repeated 2 weeks

later for ewes which appear not to be closeto lambing. Oxytetracycline does not steri-lize the infection so membranes are stillinfective. It is as well to warn the farmerthat, despite treatment, some ewes may stillabort or produce weak lambs.

In the first year after an outbreak in avaluable flock, it may be worth injecting LAoxytetracycline 6 and 3 weeks prior to theexpected lambing date to reduce abortionsin ewes which are latently infected.

Control

If EAE has been diagnosed

The following measures should be employed:

Reduce transmission to other ewes.. Remove and destroy all mem-

branes, whether believed infectedor not (on-farm burial is not nowlegal therefore they should be burntor disposed of with dead lambs).Attempt to clean up the area in thelambing shed and cover with cleanstraw.The use of aborted ewes to fosterlambs should be discouraged but,if practised, the lambs must be sentfor slaughter and females notretained for breeding since it ishighly probable that they will havebecome latently infected.Ewes which abort should be keptsince they will be immune andmost evidence suggests that theywill not continue to shedchlamydiae.

Protection of ewes by vaccination.There are two Chlamydophila vaccinesbut both consist of the same live heat-sensitive strain. Vaccination not onlyprotects against abortion but alsoreduces the number of chlamydiae shedat lambing.

Vaccines should be given in the4 months prior to mating, but not within4 weeks of the ram being introduced.Boosters are not usually given. Althoughthe vaccine is live, the chlamydiae do not

The Pregnant Ewe 43

usually persist in the vaccinated ewe.Vaccinating ewes which have been infectedthe previous lambing season (i.e. the latentcarriers) reduces the abortion rate by about50% so the farmer should be warned thatvaccinated ewes might abort or produceweak lambs. Great care should be taken toprevent self-injection of the vaccine since itcontains live chlamydiae and it is wise thatpregnant women should not handle the vac-cine at all. The wearing of gloves and the useof a guarded needle system is essential.

If EAE is not present on the farm

The following strenuous efforts should bemade to prevent its introduction:

Maintain a self-contained flock. Nofemale breeding stock or lambs for fos-tering should be purchased except fromknown clean flocks and although it isgenerally believed that rams are of littlerisk, it is preferable to use the same pre-caution in their purchase. The penaltyfor introducing EAE is so severe that nosheep is a bargain!Purchase replacements from flockswhich are monitored free from EAE aspart of the Premium Health Scheme ofthe Scottish Agricultural College (SAC)or on other well-attested evidence.Lamb purchased ewes separately fromor later than the 'home' flock for thefirst year and investigate all abortionsand apparently barren ewes, carefully.

Toxoplasmosis

Caused by Toxoplasma gondii, a coccidianprotozoan, in which tissue cysts are foundin virtually all mammals including man,and in birds, and in which a sexual cycle iscompleted only in cats and other Felidae, toproduce resistant oocysts. When susceptiblesheep ingest sporulated oocysts (Toxoplasmaresemble Isospora oocysts, with two sporo-cysts each containing four sporozoites), thesporozoites penetrate the epithelial cells ofthe small intestine and are distributed tomany organs, including muscles, brain and,

in pregnant ewes, the placenta. Multiplicationoccurs and cysts develop in these sites,which remain viable for the life of the sheepbut are not mobilized. This means thatadverse effects are only seen in pregnantewes soon after the ingestion of oocysts.A solid immunity develops about 4 weeksafter infection which lasts for life.

Infection of susceptible pregnant womenby oocysts or from tissue cysts in under-cooked meat may result in abortion or fetalabnormalities including hydrocephalus.

Clinical signs

These depend on the stage of gestation atwhich infection takes place.

If oocysts are ingested in the first 60days, fetal death and resorption occurs.If the rams have been removed the eweswill then appear to have been barren or,if the rams are still present, the eweswill be served again.Infection between day 60 and day 120results in the typical signs - abortion inlate pregnancy, often with mummifica-tion of one or more fetuses, or with oneor more stillborn lambs, or the produc-tion of weak lambs.Infection after day 120 results in aninfected normal lamb which becomesimmune.

The ewes are not obviously ill, thoughthey do have an increased temperature andlose appetite a few days after infection.Abortion usually occurs about 30-50 daysafter ingestion of the cat oocysts.

Epidemiology

Sheep become infected by oocystspassed in cat faeces. Infection and abor-tion can result from infection with asfew as 200 oocysts. The most likelysources of infection to sheep are bycontamination of stored grain or hay orfrom pasture, by the spreading ofmanure containing cat faeces or by cats

44 Chapter 5

defaecating on the pasture. The oocystsare very resistant and remain viable formany months.Immunity following infection is strongand ewes never abort more than once. Ifinfection occurs outside pregnancy, theewe will become immune, withoutshowing any signs.Although it is known that rams canexcrete the organism in their semen fora short time after infection, this doesnot seem to be of importance and infec-tion at this time, of course, would notresult in abortion.Ewes do not become infected by eatinginfected membranes, that is directewe-to-ewe transmission at lambingdoes not occur.As mentioned above, vertical transmis-sion occurs if susceptible ewes ingestoocysts after 120 days of gestation.However, although infected ewes haveviable Toxoplasma cysts in their tissuesfor life, their mobilization and verticaltransmission probably occurs veryrarely.Young cats first become infected whenthey commence to hunt, particularlyfrom mice, and shed many millions ofoocysts over a few days about a weeklater.

Diagnosis

Fresh fetal cotyledons often showsmall (2 mm) white necrotic or calci-fied foci - 'white spot placenta' or`frosted strawberries', often attachedto brown, dry mummifying fetuses.The white foci are often easier to see if amicroscope slide is placed on the coty-ledon, or the cotyledon pressed againstthe side of a clear polythene bag.Direct immunofluorescent antibodytechniques on sections or smears ofcotyledons show brightly fluorescingtachyzoites or cysts.Serology on pleural or peritoneal fluidsof stillborn lambs, live lambs beforethey have taken colostrum or IgM anti-body in post-colostral live lambs, as the

presence of antibody in the fetus indi-cates an active infection in the uterus atthe dangerous time.Histology or smears of placenta andhistology or squash preparation of fetalbrain may show Toxoplasma cysts or aspecific cell reaction.The detection of specific antibody byvarious techniques (e.g. indirect hae-magglutination, latex agglutination,ELISA) is useful in epidemiologicalstudies but antibody persists for yearsand serology is of little value in indi-vidual aborting sheep. Paired sera takenat abortion and 2 weeks later with amarked increase in titre may behelpful.

Treatment and control

During an outbreak of toxoplasmosis,aborting ewes are not dangerous toother ewes, nor useful in transferringinfection and therefore immunity, sothere is no obvious justification in con-tinuing to isolate them once the diagno-sis has been established. However, thefarmer can easily become confusedwith this exception to the rule, and onemust also always be aware of mixedinfections, especially with C. abortus.Abortions and fetal membranes shouldbe handled with disposable gloves dueto the zoonotic risk.During the outbreak there is usually lit-tle to be done other than to grin andbear it, although it is prudent to look forthe possible ways that sheep could haveingested cat faeces containing oocystsand postpone feeding any contami-nated material until after lambing. Keepcats away from cereals, hay and bed-ding likely to be available to pregnantsheep (pelleted concentrates are likelyto be safe since they are subject to hightemperatures).The organism is, however, susceptibleto sulfonamides and injection of a highdose (four times the normal dose) isworth considering (there is no licensedsheep product but cattle products are

The Pregnant Ewe 45

available), although some fetuses willbe dead and undergoing mummifica-tion at the time of treatment. Treatmentof experimentally induced toxoplasmo-sis in ewes with a combination ofsulfamezathine and pyrimethamineresulted in more live lambs and lesspathology than untreated controls.After lambing, retain the aborters andmaintain within a closed flock, or intro-duce bought-in replacements to thefarm environment for as long as possi-ble before tupping so that they areexposed to material likely to containcat oocysts.A commercial vaccine was first mar-keted in New Zealand and has been usedwidely in the UK and elsewhere. It con-sists of live attenuated tachyzoites andis injected into non-pregnant ewes atleast 3 weeks prior to tupping and canbe given at the same time as an EAE vac-cine but at a different site. The vaccineis given via the intramuscular (IM) route,multiplies in the sheep for a few daysbut does not give rise to tissue cysts inthe muscles. It is infectious to humansand the same precautions as are neces-sary for the live vaccines for EAE mustbe used. It is assumed that immunity isboosted by natural infection so it is usualto only vaccinate once.Chemoprophylaxis with decoquinategiven in pregnancy (perhaps to pur-chased ewe-lambs only, during mid-pregnancy) at a concentration designedto produce 2.0 mg/kg body weight iseffective in reducing abortion and is pal-atable. The problem is that it is unusualto feed concentrates during the suscepti-ble period (60-120 days gestation) andthus costs are increased and practicalproblems of feeding ewes at this time areencountered. Under most circumstances,vaccination is the better option but thismust be planned before tupping.

Campylobacteriosis (Vibriosis)

The organism causing this form of sheepabortion was originally classified as Vibrio

fetus, leading to the disease being calledvibriosis but it is now agreed that it belongsto the genus Campylobacter. Sheep abortionis caused by Campylobacter fetus fetus andCampylobacter jejuni. It is particularlyimportant in New Zealand and NorthAmerica.

Clinical signs and epidemiology

Infection is ingested and is primarilyintestinal. It is therefore excreted inthe faeces from symptomless carriers,which often introduce infection into asusceptible flock.Ewes are rarely ill at the time ofabortion.Birds (e.g. crows and magpies) andvoles may introduce the infection to aflock as well as introduced carriersheep; the infection is then spread fromsheep to sheep via faeces, abortions andpersonnel.Early fetal loss is rare as ewes appear tobe resistant in the first 3 months ofpregnancy; campylobacter infection istherefore not associated with 'barrenewes'. Bacteraemia follows infection inlater pregnancy followed by placentalinfection which results in abortion7-25 days after infection.Immunity following infection is strongto a particular serotype of which thereare three in the UK and many more inother countries like New Zealand, andsubsequent fertility is good. Outbreaksmay re-occur every few years becauseof lack of immunity in replacementstock, but usually abortions are few innumber after the initial year ofintroduction.

Diagnosis

There are no visible lesions in the placentathough visible focal necrosis of fetal liver issometimes present but the organism can beidentified in smears or cultured from coty-ledons, fetal stomach or liver. Campylobacter

46 Chapter 5

is not difficult to culture, but exact typing is Clinical signs and epidemiologycomplicated. Serology is not helpful.

Treatment and control

Usually the individual aborting ewedoes not require any therapy. Once thediagnosis is confirmed, such ewesshould mix with the ewes which havealready lambed, but not with the preg-nant sheep.The remaining pregnant sheep must bekept away from the infection as far aspossible and spread out, although thenumber and spread of abortions maynot make this possible. Considerationshould be given to antibiotic treatmentof groups of pregnant ewes, with, forexample, penicillin and streptomycinfor 2 days or LA oxytetracycline.The farmer should consider keeping aclosed flock, although infection can beintroduced by birds. Aborting ewesshould not be sold. If replacements arebought then they should be mixed withthe resident flock for as long as possiblebefore mid-pregnancy, but separated inlate pregnancy.Effective vaccines are not available inthe UK but are used in other countriessuch as Australia and New Zealandwhere the disease is more common.

Salmonellosis

One sheep-specific salmonella, Salmonellaser. Abortusovis, causes abortion as do anumber of other less-specific serotypesincluding Salmonella ser. Typhimurium,Salmonella ser. Dublin and Salmonella ser.Montevideo. S. ser. Abortusovis is nowrarely reported in the UK but is found else-where. Abortion is the only clinical signwith some serotypes like S. ser. Abortusovisand S. ser. Montevideo but some serotypesare much more pathogenic for ewes, result-ing in severe illness and death in ewes. Thisis particularly true for infection with S. ser.Typhimurium and S. ser. Dublin.

Abortions occur mainly in the latterhalf of pregnancy, although apparentlybarren ewes may reflect earlier fetalloss.Ewes may also be ill at or beforethe time of abortion: some scour,some die, some have an offensivesmelling vaginal discharge for aweek or more.Except for S. ser. Montevideo, lambsare often ill at or soon after birth,and develop a fatal septicaemia orpneumonia.Symptomless carriers are found in bothewes and lambs though the serotypeswhich cause the more severe disease inewes often result in a solid immunitywithout carrier status in those eweswhich do recover.A measure of immunity to a particularserotype is apparently induced becauseit is uncommon for ewes to abort thenext season.

There areplacenta.Salmonella is

Diagnosis

no obvious lesions in the

usually easily culturedfrom membranes and fetus, providingfaecal over-growth is avoided (a possi-bility if only vaginal swabs areprovided).Blood testing and rectal swabs providelittle worthwhile information.

Treatment and control

Salmonella is frequently found to be sensi-tive to a range of antibiotics in vitro andtheoretically treatment of individual sickanimals is indicated. In practice such treat-ment frequently fails to cure the sick or ster-ilize the carrier. Consideration must begiven in any salmonella outbreak to therisks of infecting humans and to producingdrug-resistant organisms.

The Pregnant Ewe 47

The principal aim in the control shouldbe to:

Reduce the weight of infection by theisolation of aborting, scouring and sicksheep.Prevent further infection of pregnantsheep, as far as possible, by keeping theaborting group (usually the nearest toterm) separate from other groups yet tolamb.Upset the flock as little as possible andmake sure food (hay or concentrate) isalways available, particularly immedi-ately following flock movement.Try and ensure that most of the flockbecomes immune after lambing byspread from carrier ewes to non-pregnant ewes (i.e. mix recovered abort-ers with ewes that have lambed).

Avoid re-introduction of the disease fromsources such as: (i) 'foreign' slurry; (ii)bought-in sheep and other grazing stock;and (iii) infected feed (including bird fae-ces). Attempts should be made to preventbirds, especially magpies, entering sheephouses and feeding from the sheep troughs.

Q Fever (Coxiella burnetii)

This has recently been a problem in Germanyand the Netherlands where there have beenmany outbreaks of disease in sheep andgoats and associated human disease. Controlmeasures have included slaughter of preg-nant animals to reduce the risk of zoonoticspread; however a vaccine is now availableto aid control.

Box 5.1. Schmallenberg Virus

As this book went to press, an apparently completely new virus disease of cattle, goats and sheep wasemerging in countries in northern Europe. Named after the German town near which it was first identi-fied, the disease has now also been diagnosed in the Netherlands, Belgium and on 23 January 2012 inflocks in some eastern counties of England. The disease causes fetal malformations (hydranencephaly,arthrogryposis and scoliosis) and stillbirths, affecting up to 50°A) of lambs in infected flocks. The causalorganism has been identified as an orthobunyavirus transmitted most probably by midges (Culicoidesspp). Initial infection probably occurred during late summer/early autumn 2010 in ewes in earlypregnancy, with the results not evident until lambing time. At the time of writing no decision has beenmade regarding making the disease notifiable or not, or possible control measures. Latest information isavailable at www.defra.gov.uk/ahvla

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6

The Periparturient Ewe

Farmer's First-aid Cupboard

This is the time of the production cycle atwhich most can go wrong and is whenmost vets have their main contact withsheep. Remember 'animals under yourcare' guidance for prescribing drugs - theflock should be seen within reasonabletime prior to dispensing items such asantibiotics. Here is a list of items thatshould be available on farm well inadvance of lambing time:

lubricant (petroleum jelly or soapflakescan be used as alternative);arm-length disposable gloves;disposable paper towels;prolapse harnesses;lambing cords and snare (Hughes snareor make one from plastic-coated cable);lamb stomach tube and syringe or funnel;frozen colostrum (200ml lots) - preferablyewe, but goat or cow as an alternative;commercial dried colostrum is usefulfor an emergency;antibiotic injection;antibiotic aerosol;antibiotic oral doser for lambs;antibiotic ophthalmic preparation;dextrose 40% injection;calcium borogluconate injection (400 mlbottles of 20% Ca);

oral twin-lamb disease remedy;tincture of iodine (e.g. in a spray);cotton wool;surgical spirit;needles 16G x 1" (i.e. 16 gauge 1 inch),18G x 1", 19G x 1", 21G x 5/8";sharps container;syringes 50, 10, 5 and 2 ml; andthermometer.

Important Periparturient Problems

The major problems to be faced (Fig. 6.1)will be dealing with:

abortions (see Chapter 5);metabolic diseases;prolapses; andobstetrical problems.

Metabolic Diseases (PT, Hypocalcaemiaand Hypomagnesaemia) -a Clinical

Approach

This is a particularly difficult set of condi-tions to cope with, mainly because:

They are difficult to differentiate clinically.They may coexist.

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 49

50 Chapter 6

" I 11111filli fl rll r Ili Mill

Fig. 6.1. Individual pens allow ewes with health problems to be cared for as well as for separating eweswith newborn lambs.

The farmer has often already treated theanimal and confused the picture withvarious treatments as well as causingdelay in diagnosis.A number of cases may occur at thesame time.The results of treatment are oftendisappointing.Prevention is not simple.

However, if one tries to keep one's feet on theground, some sort of logic can prevail whichshould lead to a satisfactory outcome.

Clinical diagnosis

It is always useful to take a pre-treatmentblood sample (red or green top for Ca, Mg,betahydroxybutyrate (BOHB); grey top isneeded for glucose and P). This is thenavailable if the animal(s) fails to respondto treatment. If it recovers, your diagno-sis was correct! Treatment needs to beprompt for all three conditions, otherwisethe prognosis is hopeless; hence therapyby the farmer is usual, with the vet beingcalled if usual treatments fail or many ani-mals are affected. It is important to empha-size the necessity to treat early - delayleads to permanent damage (especially

with PT) or death with loss and dissatisfac-tion all round.

If the diagnosis is uncertain

A 'rough-and-ready' approach is:

1. Take pre-treatment blood sample (red orgreen and grey tubes) for Ca/Mg/glucose/BOHB estimations.2. Give 20-40 ml of a calcium borogluco-nate, magnesium and dextrose (CaMD) solu-tion and 20-40 ml dextrose 20% slowlyintravenously.3. Give 50-100ml CaMD subcutaneously.4. Give electrolyte and/or propylene glycolorally.5. If there is no response send bloods foranalysis and review your diagnosis, check-ing particularly for signs of listeriosis.

Pregnancy toxaemia (PT twin-lamb disease)

This occurs in the last month of preg-nancy and before spring-grass growth.It affects thin ewes (CS 2 or less), lesscommonly it may occur in overfat ewes.Insufficient food has usually been given,particularly concentrates, although poorquality forage also contributes to thecondition. Underfeeding has usually

The Periparturient Ewe 51

gone on for some weeks but also may besudden (e.g. following bad weather ormovement).Affected ewes are usually old and mayhave broken mouth and molar prob-lems, but shy young ewes with inade-quate access to limited feed may also beaffected.Affected ewes usually have a largeabdomen (two or more lambs).The first sign is refusal of feed. Affectedewes become separated from the rest ofthe flock, are easy to catch, apparentlyblind and stand motionless, showingfine tremors and may develop convul-sions on handling.Test the urine (obtained by occludingnostrils for a few moments). A rapidand strong positive result for ketonessuggests PT; a negative result makes itunlikely.The blood sample shows level of BOHBis >3 mmo1/1.If not treated, the condition progres-sively worsens over days and the ani-mal dies.

Treatment

Treat as soon as refusal of feed isnoticed - don't 'wait until tomorrow tosee what happens', it may be too late!Treatment by the farmer on the firstday - administer proprietary PT oraltreatment and/or 50 ml propylene gly-col orally and repeat in a few hours.Offer good hay and a little high energypalatable concentrate (e.g. flakedmaize). You hope that the ewe willbegin to feed by then. If the owner isprepared to give the time, hand feedingcan start an improvement. If housed,turning out for a few hours on to goodgrass, if available, may help to improvethe appetite.Treatment by the vet - give 50-100 mldextrose 40% plus 50 ml Ca 20% intra-venously (use the cephalic or jugularvein and inject very slowly to avoidadverse effects on the heart) in additionto the above oral treatment. Dextrosecan be repeated after a few hours.

If there is no response, review yourdiagnosis and prognosis.The next day - if the ewe is improving,continue with a drench until the ewe isfeeding well, then monitor carefully.Avoid repeated propylene glycol formore than 2 or 3 days as it appears tolead to scouring.If the ewe is not improving, eitherslaughter, or if less than 1 week beforeterm, abort the lambs by 8 ml (16 mg) ofbeta or dexamethasone, or perform acaesarean section. The outlook is pooranyway - it takes 36-48h for inducedlambing to take place, and the lambswill be dead or have low viability.A caesarean is also unlikely to produceviable lambs, but may save the ewe ifit is not in irreversible stage of disease(it is definitely not worth doing if theewe is comatose).Remember, early treatment is essen-tial; delay will lead to loss of ewe and/or lambs.

Control

Condition score the sheep 6-8 weeksbefore lambing is due to start and splitaccording to condition; also separateshy feeders.If ewes have been scanned, split themaccording to fetal numbers but use the CSas well. Put thin ewes scanned for a singlelamb with the twins group and thin onesscanned for twins with the triplet group.Feed more good quality concentrates(including some whole grain) to allsheep below CS 3, preferably givingtwo feeds daily. Be careful not toincrease concentrates too quickly asthis may lead to acidosis. Check thequality of concentrates - contact manu-facturer for details of ME value.Check the quality of hay or silage - feedthe best available to ewes expectingtwins or triplets.If possible, give access to green grass. Ifthe problem was precipitated by hous-ing, consider turning out again. Givemore feed outside and re-house wheneating well.

52 Chapter 6

Consider giving high energy or pro-tected energy self-help blocks.If outdoors, try to move the ewes tomore sheltered fields.

In future, scan ewes at 50-80 days ges-tation and mark according to the fetal load.About 2 months before lambing, conditionscore all the ewes and split them accordingto fetal load and body condition and feedaccordingly. Check the CS again at the timeof vaccination. Select the best forage for latepregnancy. The season with the lush autumn(therefore high ovulation rate) and hardwinter is the one which can create the worstproblems. The loss in condition is maskedby fleece growth, hence the need to handlethe sheep.

Remember, it is dangerous to assumesheep with a heavy fleece are in goodcondition by just looking at them.

Hypocalcaemia (trembling,lambing sickness)

This is most common in late pregnancyrather than early lactation, in contrastto cattle, but can occur just afterlambing.It can affect ewes in any condition.Affected ewes show typical signs of`milk-fever' - ataxia, leading to recum-bency, depression and atony (bloat, nofaeces, etc.) and loss of consciousness.In the later stages, saliva or regurgitatedrumen contents may trickle down thenose. It is easy to assume this is a nasaldischarge and to misdiagnose it aspneumonia.Often there is a history of recent move-ment (e.g. the ewes have been gatheredfor vaccination or housing) and a delayor sudden change in feeding, thereforea number of ewes may be affectedsimultaneously.The blood sample shows level of Ca is<0.8 mmo1/1.If not treated, the condition progres-sively worsens over hours and theanimal dies.

Hypocalcaemic ewes may go on to developPT, especially if they have not eaten forseveral hours.

Treatment

Give 20-40 ml Ca 20% intravenously slowly(the cephalic vein can be used if the jugularis hard to find) and 50-100 ml Ca 20% sub-cutaneously. You expect the ewe to respondlike a cow with milk fever, eructating, defae-cating and even 'walking off the needle'.

If it does not respond, review your diag-nosis. In particular, consider the possi-bility of listeriosis.

Control

Watch the flock after movement andhave a calcium injection handy.If the flock is being moved any distance(walking or by wagon) provide hay andconcentrates before leaving and onarrival.In theory, keeping the calcium content ofthe diet a little below requirements untilthe last month of pregnancy then increas-ing the content in the ration should helpin control, but this method is much moredifficult to operate than with cattle,because of the spread of lambing.

Hypomagnesaemia (grass staggers)

This nearly always occurs after lamb-ing, when the ewe is rearing twins andis at peak lactation (i.e. there is a bigmetabolic drain on the ewe).Usually it occurs when the animal isgrazing lush grass (low in magnesium,low in fibre), but occasionally when onbare pastures (insufficient food).Signs, if seen, come on very rapidly:excitable, tremors leading to convul-sions and rapid death. Often the animalis simply 'found dead'.The blood sample shows the level ofMg is <0 6 mmo1/1, sometimes coexist-ing with hypocalcaemia (hence theconfusion).

The Periparturient Ewe 53

If not treated, the conditionsively worsens over minutesanimal dies.

Treatment

progres-and the

Give 20 ml CaMD intravenously (wherepossible, but if ewe is twitchy this may bevery difficult) and 50m1 MgSO4 25% subcu-taneously. You hope that the ewe willquickly become less excitable and behavenormally within an hour, but some equallyquickly die.

Remember, don't give MgS0, 25%intravenously!

Control

Watch the flock after movement on tolush or bare fields and have a magne-sium sulfate injection handy.If on lush pasture, move the animals topoorer grass, until a magnesium sup-plement is added.Feed extra magnesium (up to 14 g MgO/day) via:. magnesium-enriched cake; or. magnesium-enriched feed blocks

or molasses licks (less reliable thanabove); or

. magnesium-intraruminal bulletsgiven just before turnout or the riskperiod - they last 3-4 weeks.

Give extra food to those animals whichare under-fed.Provide shelter.

The cost of supplementation has to beweighed against probable losses, based onprevious flock history or estimated risk.

Prolapses

Epidural anaesthesia

Epidural anaesthesia is a valuable techniquewhich should be more commonly used fordealing with vaginal prolapses and difficultlambings, or any other condition causingexcessive straining.

Control of straining can be achieved for24-36 h by the correct choice of drugs:

Local anaesthetic - this will give anal-gesia for 2 -4h; the hind limbs will beaffected if more than 2 ml is used.Local anaesthetic plus 2% xylazine -the addition of xylazine will prolongthe action for up to 36 h and is particu-larly useful to control straining associ-ated with prolapses. Draw up 1.75 ml(35 mg) of 2% lignocaine and add0.25 ml (5 mg) xylazine.2% xylazine - given alone this takes upto 1 h to produce an effect, but thenlasts for up to 36h. A dose of 0.25 ml(5 mg) is made up to 2.5 ml with sterilewater.

Epidural technique

The best site is the sacrococcygeal space(locate the first intercoccygeal space whichis easily identified by manipulating the tail,and then feel forward for a depression indi-cating the sacrococcygeal joint which haslittle mobility). The site should be clippedand surgically prepared. For a ewe, a 20G x1-1.5" needle is inserted in the midlinewith the bevel facing cranially (a 21G x 5/8"needle for lambs). The needle usually needsto be angled with the hub caudal to the ver-tical at an angle of 10-45° (very variable).Advance the needle slowly until a loss ofresistance indicates entry of the epiduralspace (the ewe may wag her tail at thispoint). Inject the contents of the syringe(preferably warmed to body temperature)slowly. Success is indicated by loss of tonein the tail and loss of sensation in the peri-nea' area. The first intercoccygeal spacemay be used if difficulty is experiencedfinding the sacrococcygeal space, but resultsare not as reliable.

Vaginal prolapse (eversionof the vagina/cervix)

This is an important problem, the cause ofwhich is still uncertain. The incidence,although generally low (1%) and very low

54 Chapter 6

in hill sheep, is sufficient to be a worry, andin some flocks over 5% of the ewes areaffected over a short period. Minor pro-lapses may not cause much disturbance,popping in and out as the ewe gets up andlies down, but if left, severe complicationsoften arise which endanger both the eweand the lambs; the condition must thereforealways be taken seriously and treatedquickly.

The prolapse usually occurs in the last3 weeks of pregnancy (although it may occuras early as 6 weeks pre-lambing), particu-larly during the last week, in ewes carryingmore than one lamb. There may be an asso-ciation with a particular breeding line orbreed of ram but this is unproven. Ewes thatprolapse almost invariably do it again nextyear. Cases therefore need to be marked forculling, as well as to spot breed connec-tions. It is possible to keep such ewes (e.g. ifvaluable pedigree animals) providing that asuitable external support is put on at thefirst sign of the prolapse reappearing.

Many causes have been suggestedincluding: (i) multiple lambs; (ii) conditionof ewe (too fat or too thin!); (iii) gut fill androughage; (iv) calcium deficiency; (v) hor-mone imbalance; (vi) short docking; (vii)steep ground; and (viii) coughing. In otherwords, there is no one obvious predisposingfactor.

Treatment

If treated in the early stages, replacement ofthe prolapse is usually easy. If there is adelay, damage and subsequent swelling pro-vokes further straining and the urethra maybecome kinked, preventing urination andthe vicious cycle of even more straining isinitiated.

Clean the prolapse and examine thecervix to check that no fetal membranesare visible. If they are, lambing hasstarted and the ewe must be carefullyobserved after replacement of the pro-lapse and assistance given if progressdoes not occur.Epidural anaesthesia should be usedin cases showing severe straining.

This will assist in replacement, allowsuturing if considered necessary, andcan give prolonged relief from strainingif xylazine is administered in additionto local anaesthetic.It may be helpful to raise the hind endof the ewe before gently replacing theprolapse. Urine will usually be passedas soon as the urethra is straightened.Incomplete dilatation of the cervix(ringwomb) is a common sequel soassistance to lamb or a caesarean maybe necessary.

Retaining the prolapse

Non-invasive methods are preferred and arevery successful if the prolapse is caughtearly (Fig. 6.2). More serious cases mayrequire suturing of the vulva.

The most common methods are:

Wool-tying - this is sometimes used byfarmers for only the simplest cases, andis not applicable for shorn ewes! It is nogood if animal is straining. It is not amethod for the vet to use.Application of a harness (truss) using:

String (there is a danger of cuttinginto skin).Soft rope - this is a simple and suc-cessful method with a reduced riskof chafing.Commercial truss made of webbing -several varieties are availablewhich work well if fitted correctly.This is the method of choice.

Intravaginal devices (`spoon') - thesesupport the cervix but can cause irrita-tion and may be pushed out.Suturing (under epidural anaesthesia) -there are several patterns includingmattress sutures and Buhner suture (seeFig. 6.3). These may tear out if strainingrecommences and need removing atlambing.

As complications are common, such as per-sistent straining, ringwomb and dead lambs,the ewe requires special observation. Toreduce abdominal pressure, the quantity ofroughage should be reduced and antibioticcover provided where there is obvious

The Periparturient Ewe 55

Fig. 6.2. This Herdwick sheep has had a cervical prolapse which is being managed by use of a harness.

damage or infection. Non-steroidal anti-inflammatory drugs (NSAIDs) are alsobeneficial.

Treated ewes must be observed care-fully for the onset of lambing - if a har-ness or suturing has been used, thesewill need to be taken off once lambingis underway.

Control (difficult whenthe cause is not clear)

Assess the ration, in particular the qual-ity and quantity of the roughage in rela-tion to the ewes' CS and fetal load.Look at feeding arrangements - too lit-tle rack or trough space leads to push-ing which may increase intra-abdominalpressure.Encourage regular exercise. Housedewes may become lazy.Mark, record and cull cases before thenext breeding season.Consider these records and note sus-ceptible lines and breeding.

Post-lambing prolapse of the cervix

This can occur several days or even weeksafter lambing and usually follows damage at

lambing, particularly tearing of the cervix,which becomes swollen and inflamed, trig-gering straining. They can be difficult toreplace because the pelvic ligaments havetightened up, and difficult to retain inplace - suturing the vulva may be neces-sary, with the suture left permanently untilculling, which is definitely indicated.

Vaginal rupture/intestinal prolapse

This catastrophe follows a rupture of thevaginal wall near the dorsum of the cervix,with loops of intestine prolapsing throughthe vulva. Death from shock is rapid. If theewe is found alive an emergency caesarean,then immediate euthanasia may be per-formed, but the chance of survival of thelambs is poor. The cause is unknown.

Uterine prolapse

This usually occurs immediately after lamb-ing and, providing the uterus has not beendamaged or become chilled, the ewe is notoften obviously shocked. The uterus shouldbe cleaned and fetal membranes carefullyremoved if easily detached, or trimmed ifstill tightly attached. With the aid of epidural

56 Chapter 6

The suture can be placed, under epidural anaesthesia, using either a Buhner needleor an ordinary large curved suture needle. The Buhner needle has the eye at the pointso is inserted then threaded but the same end result can be achieved using either type.

/(C

Step 1 - Place the suture subcutaneously to one side of the vulva

Step 2 - Using the same exit points, the suture is similarly placedon the opposite side of the vulva

Step 3 -The suture is tightened leaving sufficient space for the eweto urinate comfortably

Step 4 - The free ends are tied in a secure bow. Do not cut off theends - this is so the suture can be undone and retied ifnecessary

Fig. 6.3. Inserting a Buhner suture.

The Periparturient Ewe 57

anaesthesia and with the ewe's hind endraised, the uterus is usually easy to replace.Care needs to be taken not to damage it andcheck that the horns are fully everted intotheir correct position. A truss or suturesshould be used to prevent a recurrence.Some prolapses occur a few days after lamb-ing, and then shock is often more seriousand death is common

Abdominal Muscle Rupture

The rupture may involve any part of theabdominal wall although most commonlyaffects the left side, presumably because ofthe weight of the rumen. It occurs in latepregnancy in lowland ewes carrying twinsor triplets and although the ewe is not usu-ally distressed or disturbed at first, compli-cations may arise from trapping of thecontents and it may interfere with lambing.Surgical correction is usually impossible.Affected ewes need assistance lambing (roll-ing on to their back may make reaching thelambs easier) but a caesarean may be needed.Old ewes are most prone, particularly if theyare too thin, and perhaps if they are squeezedor knocked during handling and housing.

Obstetrical Problems

It has been calculated that:

70% of ewe deaths occur at or nearlambing.At least 75% of lamb deaths occur at ornear lambing.90% of vets' visits occur at or nearlambing.

These figures demonstrate that parturitionis a high-risk occupation and also that vetsare very dependent upon this time for theircontact with sheep farmers; but it is reward-ing work!

Manipulation of lambs within theuterus is relatively easy in most breeds, par-ticularly for small hands, and limitedembryotomy and caesarean operations aresimple procedures.

There are particular problems associ-ated with certain breeds and different prob-lems presented in hill and lowland flocks.

The seasonal pattern of lambing presentsproblems, with: (i) sudden numbers andlack of practice; (ii) a large susceptible popu-lation; and (iii) very intensive conditions.

Shepherd interference is common andthe lamb(s) are often dead when the vet'sassistance is sought, although valuable pedi-gree ewes may be presented for a caesareansooner rather than later, particularly if carry-ing a large single or for a large lamb in poste-rior presentation. The shepherd's job isusually quite different from the vet's - theshepherd has a problem of numbers, timing(when to interfere), observation, cleanliness,and often simple manipulations or theremoval of 'tight' lambs in normal presenta-tion and position, and to ensure the lambsare not smothered and/or mismothered. Thevet's role is: (i) to deal with difficult lamb-ings; (ii) to educate the shepherd when it isbetter to leave well alone and seek help(but remember that many shepherds areextremely good at lambing!); (iii) to diagnoseand treat sick ewes and lambs; and (iv) toinvestigate and advise when flock problemsarise. It is also a good time to suggest flockhealth programmes for the future.

Maternal factors

Ewes do not withstand prolonged vagi-nal and uterine interference; a sick eweoften becomes a dead ewe!Uterine, cervical and vaginal tears arecommon following rough handling andinadequate lubrication.Clostridia' infections are common aftervaginal interference if vaccination is inad-equate and/or antibiotic not injected.Retention of the fetal membranes israrely a problem.

Fetal factors

Often there is more than one lamb -asorting out job - be patient. Remember

58 Chapter 6

how to differentiate front and back legsby feeling the direction of flexion ofjoints.Head and leg deflections are commonDo not pull legs until you have sortedthe head out.The head is the major cause ofobstruction and there is rarely suffi-cient room in the pelvis for the lamb'shead and legs plus your hand, so usea snare over the head to permittraction.Tight lambings can lead to fracturedribs, ruptured liver or intra-cranialhaemorrhage leading to rapid death,or if lamb survives, it often lies aboutand is very susceptible to hypother-mia. Good aftercare is needed.

Equipment

Ensure that you have the equipment listedbelow.

Gel hand disinfectant or soap andwaterLubricant (proprietary gel or liquid par-affin, petroleum jelly, soapflakes oreven lard will do in an emergency) andsmall handsDisposable arm-length polythene gloves(although these can tear or get in theway in difficult lambings)Snares (nylon cords with loops orplastic-coated wire - a clean piece ofbaler twine will do in an emergency)Injectable antibioticsA sharp knife.

History

Some pertinent questions are:Is the ewe at full term?How long has the ewe been lambing?The normal range is approximately:O change in temperament - 2-4 h;O cervical dilatation - 0.5-2 h; andO delivery - 0.5-2 h.Have any lambs been born or delivered?

Examination

Take special note of the following whenexamining the animal.

External inspection

Does the ewe look ill or exhausted?Are there signs of shepherd interfer-ence? Note bleeding and bruising.Presence or absence of lamb or mem-branes at vulva, strings attached to legsor head.Smell - putrefaction implies bad risk,little value and indicates embryotomyrather than caesarean.Udder - may indicate prematurity, mas-titis, lack of colostrum.

Internal examination

EWE

Note the size and shape of the pelvis.Observe any damage to the vagina andthe degree of dryness.Consider the extent of softening and dil-atation of the cervix. If the cervix is notfully dilated, particularly if unrupturedmembranes are palpable, re-examine inabout half an hour, rather than risk man-ual dilation. It may just be too early. Becareful if attempting to dilate - tearingand haemorrhage may result.

LAMBS

Are they dead or alive? (It is not alwayseasy to be certain; assume alive if notsure).How many? A jumble of legs and headsimplies at least two, probably more.Presentation - anterior? posterior? trans-verse? Breech suggests either large singleor triplets (lack of space in the uterus).Ankylosed joints may indicate otherdeformities.

Delivery

Aim to complete delivery within 15 minor make a quick decision about doingcaesarean.

The Periparturient Ewe 59

Consider giving an epidural - thismakes things more comfortable for theewe and easier for you.Lubrication is very important - useplenty. Filling the uterus with warmwater may help in a difficult dry case.Raising the ewe's hind end (but care-fully and not for too long) can help toavoid straining and allow repulsion of alamb.Where the uterus is contracted down,consider giving clenbuterol. This is notlicensed for sheep, but can make a dif-ficult case easier. (Note: In the UK pro-viding a drug is licensed for afood-producing species it can be usedfor another species under the so-called`cascade' system if no suitable drug islicensed.)

Anterior presentation

HEAD ONLY It is common for only a swol-len head to be presented outside the vulva,with both front legs retained.

If the head is not swollen, put a snareon, then carefully replace, find the legs,then deliver normally.If the lamb is dead (no suck or blinkreflex) then decapitate. If uncertain,treat as if alive.If the lamb is alive, lubricate well andinsert a small hand beside the headand neck and try to find a limb andextend it. It is often then possible inewes (but not ewe lambs) to withdrawthe lamb with only one limb extended -twisting the lamb while pulling willhelp to prevent the shoulder becominglocked.When the lamb is large or ewe is tight,get one leg up, put a rope on, replace,and repeat with the other leg beforeusing both ropes to pull both legs.

HEAD AND NECK DEFLECTIONS These are com-mon and often made worse by pulling onthe legs, expecting the head to follow. Thehead is the main bulk, so put a loop on thehead first, then straighten the head, andthen find the correct legs before pulling.

Posterior presentation

Large lambs in posterior presentation arevery vulnerable to hypoxia and to physicaldamage such as broken ribs. Provided bothhind limbs and tail are present, withdrawwith gentle traction. Be aware of the possi-bility of stifles locking under the pelvicbrim - lift and extend the legs beforepulling.

Breech presentations

It takes a good shepherd to spot a breechpresentation early; often the only sign iswetness down the back of the udder (indi-cating rupture of membranes). Gently repelthe lamb and search for the hind legs, thenbring them up one at a time into the pelvisby flexing/extending the limb joints.

Embryotomy

For ewes with dead smelly lambs, this is abetter option than a caesarean as the sur-vival rate is only 50% compared with eweswith live or freshly dead lambs.

For known dead lambs: with a swollenhead, decapitate; for other anterior presen-tations, find a front leg and pull so you cancut around the skin above the kneeOUTSIDE the vulva with a sharp knife,then use your fingers to undermine the skinand break down the muscles holding theshoulder blade to the chest. Both forelegscan be removed leaving the head to pull.The more decomposed the lamb, the easierit is. Remove any detached membranes andgeneral debris.

Caesarean operation

Indications for a caesarean are listed below.

Non-dilatation of the cervix (ringwomb)after one or two examinations at app-roximately half-hour intervals.Fetal oversize.Large (valuable) lamb in posterior/breech presentation.

60 Chapter 6

Irreversible malpresentation.Deformities.Uterine torsion (very rare - try 'unroll-ing' first).PT - rarely get viable lambs.

The operation is relatively quick and easy,compared with other species, and needsto be considered early in the proceedingsrather than too late! The site is the left flank,with anaesthesia by local infiltration, inver-ted L block or paravertebral injection.

Para vertebral anaesthesia

This is easy and satisfying to perform inlean ewes, but can be difficult in fat ani-mals. The technique is as in cows: (i) pre-pare the skin over the posterior thoracic andlumbar transverse processes; (ii) identifythe first lumbar vertebra; (iii) then inject1-2 ml 2% local anaesthetic subcutaneouslyand into the muscle about halfway betweenthe midline and the end of the process; and(iv) then 'walk' the needle off the front edgeof the transverse process to catch T13 andinject 3-5 ml just below the level of theprocess. Repeat off the posterior edge of L1,then the posterior edges of L2 and L3.Another option is a sacrococcygeal epiduralinjection of 0.25 ml 2% xylazine, but thisrequires about an hour to take effect.

Caesarean technique

1. Make an incision in the centre of the leftflank, being careful not to cut too deep, acci-dently cutting into the rumen - the abdomi-nal wall can be surprisingly thin.2. Palpate the uterus, identify the extremityof the lamb and carefully exteriorize, hold-ing it through the uterine wall.3. Incise over the extremity along the greatercurvature.4. Grasp the lamb and remove.5. Check the uterus for more lambs - it cansometimes be difficult to reach a lamb in theother uterine horn - feel down towards thecervix before 'turning the corner' and enter-ing the far horn. Remove any remaininglambs carefully.

6. Remove the fetal membranes if they aredetached, trim and leave in situ if stillattached.7. Repair the uterus with an inverting suturemaking sure no membranes protrude.8. Replace the uterus in the normal position.9. Suture the flank incision in two or threelayers.

The survival rate of a ewe undergoing acaesarean with live or freshly dead lambsshould be high.

After delivery

Revive the lamb: (i) clear the mouth andnose; and (ii) stimulate breathing (doxa-pram drops are often used). For an hypoxiclamb, consider giving 10 ml of 8.4% sodiumbicarbonate solution intravenously toreverse respiratory acidosis. A stomachtube can be used to inflate the lungs bypositioning it in the pharynx and blockingoff the oesophagus and nose. Once the lambis breathing, return it to the dam quickly forlicking.

Finally carry out the following:

Re-examine for:the presence of other lamb(s)both internally and by ballotting(it doesn't do your reputation anygood to miss a lamb!);

. damage - tearing, haemorrhage; and

. membranes - remove gently ifdetached.

Give a LA antibiotic injection.Consider giving NSAID, particularly if theewe is bruised or toxic (this is not licensedfor sheep, but nothing suitable is).Check the udder - milk off some colos-trum and give it to the lamb(s) using astomach tube; if there is none, give asubstitute.Check and treat the lamb's navel withtincture of iodine spray or antibioticaerosol.Check for defects such as entropion -correct immediately by everting theaffected eyelid(s).

7

Newborn Lambs

Lamb Mortality

Many farmers accept that up to 15% of alllambs are either dead when born or diewithin the first few days of life (occasion-ally these losses rise to 50%, e.g. in abortion`storms' or in unexpected severe weatherconditions). This means that in a flock of1000 lowland ewes anticipating 1800 lambs,over 250 lambs may be lost in the perinatalperiod (0-10 days).

As a bench mark, losses of:

5% or less indicate excellent management.8% indicates above-average management.10% is still better than average achieved,but is open to some improvement.15% is average, with definite room forimprovement.20% or more is too high, indicatingvery poor management or exceptionalcircumstances.

In an average flock with losses of15%, perinatal losses can be split roughlyinto:

Pre-partum stillbirths (including abor-tions) - 2%. These could be due touterine infections such as Toxoplasma,Salmonella, Campylobacter, enzooticabortion, Border disease, plus TBF,pregnancy toxaemia and swayback.

Parturient stillbirths (dystocias) - 5%. Ifthe losses are due mainly to lambingproblems, then the quality and quantityof the workforce needs looking at, andalso the age, breeding and feeding(e.g. large singles, and ewe lambs thatare CS 4 and crossed with a Texel ram!).Post-partum mortality - 8%. Thisincludes some that were said to be borndead, but actually died soon after birthand losses from neonatal diseases (seeTable 7.1).

It is important to try and split lamb deathsinto these three groups by fresh post-mortemexamination (PME), in order to apply sensi-ble control measures.

Post-mortem Featuresin Newly Born Lambs

Decomposition - indicates pre-partumdeath.Clouding of the cornea indicates pre-partum death.Weight - singles should be 4.5 kg, twins3.5 kg (but allow for breed variations).Excessive weight suggests dystocia,underweight suggests a pre-partumproblem (e.g. feeding of ewe or uterineinfection, or large litter size).

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 61

62 Chapter 7

Table 7.1. Common diseases of neonatal lambs.

Route of infection Organism Disease

Oral

Navel (also probably blood-borne)

Castration and docking wounds

C. perfringens type BEscherichia coli (non-specific strains)E. coli (enterotoxigenic strains)S. ser. Typhimurium and S. ser. DublinCryptosporidium parvumRotavi rusParapox virusStreptococcus dysgalactiae

Strep. dysgalactiaeE. coli, Arcanobacterium pyogenesFusobacterium necrophorum,

Staphlococcus aureusErysipelothrix rhusiopathiae

C. tetani

Lamb dysenteryWatery mouthColiform diarrhoeaSalmonellosisCryptosporidiosisViral diarrhoeaOrfJoint ill

Joint illJoint ill, meningitisJoint ill, navel ill

Joint ill, but morecommonly, insidiousdevelopment ofpolyarthritis

Tetanus

Umbilical vessels - thrombus indicatesthat death is post-partum. In lambsdying immediately before or duringparturition, the end of the artery issharply pointed (because of contrac-tion of the arterial wall), but if deathoccurred some time pre-partum, theruptured end is square. If the end isshrivelled, death is at least some hourspost-partum.Lung aeration indicates post-partumdeath (check to see if a piece of the lungfloats or sinks in water).Presence of food in the stomach indi-cates post-partum death but does notrule out hypothermia if a stomach tubewas used to feed shortly before death.Unclotted milk suggests recent feedingprobably by stomach tube.Subcutaneous oedema of distal parts ofthe legs, tail or head indicates dystociaor hypothermia.Hepatic rupture, thoracic, abdominalor meningeal haemorrhage (open upcranium and spinal canal to check)indicate dystocia.Well-nourished lambs are born withbrown fat reserves which support them

during the first few days of life. Instarvation, as the fat is metabolized,it is replaced by soft, red gelatinoustissue - look particularly around thekidneys and heart.Wear on feet indicates the lamb haslived for a few hours.

Checking for the presence or absenceof the above features should enable you todecide if deaths are occurring mainly inone category. That is, if the deaths aremainly pre-partum, look for causes of deathin utero; if at birth, then the shepherd'svigilance and availability may be inade-quate; if after birth, then the lambs haveprobably not sucked adequately and havebecome cold.

Lamb Survival

As a general rule, lambs survive if theyare of average birthweight, are kept warmand receive adequate colostrum, whereasthose that are small, cold and fail toobtain adequate colostrum, die (Figs 7.1and 7.2).

Newborn Lambs 63

Fig. 7.1. A good feed of colostrum provides energy to protect against hypothermia as well as supplying antibodies.

Fig. 7.2. Triplets need special care to make sure they get sufficient colostrum.

Colostrum Store 200-250ml colostrum/kg in the first 24h;this is to satisfy energy demands and will

Provision of adequate colostrum is crucial provide plenty of IgG if the ewe has beento maximizing lamb survival. Lambs need correctly vaccinated.

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Ewe colostrum

This is by far and away the best for a colos-trum store. It can be stored in a freezer forat least a year, so surplus can be availablefor the next season. Although it seems a bitof a nuisance to have to milk sheep in themidst of a hectic lambing period, it is wellworth taking any surplus from milky ewes.Oxytocin (1 ml intramuscularly) can begiven to help letdown. The only drawbackwith using pooled colostrum is the possi-bility of disease transmission (e.g. MV,Johne's disease). This is not a problemin commercial flocks producing fin-ished lambs, but needs considering in abreeding flock.

Cow colostrum

Cow colostrum is quite often used as areplacement for ewe colostrum. If goodquality material is used (the first milkingand before the calf is allowed to suck), it isan adequate substitute food (though lessenergy dense than ewe colostrum) and mostlambs tolerate it. To provide clostridial pro-tection with cow colostrum it is suggestedthat the cow can be vaccinated with sheep8-in-1 vaccine (10 ml 3 months before calv-ing and again at 1 month and 2 weeks beforecalving). If 100 ml of the subsequent colos-trum (given by bottle or stomach tube) isgiven soon after birth, it should provideprotection to the lamb for at least 3 months.

Anaemia caused by feedingcow colostrum

It is now known that some cows produce afactor in their colostrum which, as a resultof an immunological reaction in somelambs, leads to the rapid removal of therecipient lamb's red blood cells togetherwith the precursors in the bone marrow.This causes lambs of about 10-14 days oldto become suddenly weak and to stop suck-ing; they show extreme pallor (PCV <0.10)and they urgently require a whole-blood

transfusion. This is most economically andconveniently supplied by taking bloodfrom a ewe in a large syringe containing adrop of heparin, and giving it intraperito-neally (10 ml/kg) as for a glucose injection.Valuable pedigree lambs may be given anorthodox transfusion. Corticosteroid andantibiotic injections are also indicated bothto these lambs and to other lambs whichmay have received that batch of colostrum.A response is expected within a day,although some die and reveal very wateryblood and creamy white bone marrowon PME.

It is important (although seldom prac-tised!) to identify sources of colostrum, sothat donating cows can be traced and prob-lem ones avoided in future. Alternatively,mix colostrum from several cows beforefeeding to lambs to reduce the possibilityof this problem occurring.

Goat colostrum

Colostrum from goats is safer than fromcows; it is very similar to ewes' in composi-tion and antibody content, if the goats havereceived clostridial vaccines. The only thingto watch is that it comes from caprine arthri-tis encephalitis (CAE)-accredited herds, cer-tainly for flocks producing breeding stock,as this is a disease closely related to MV. Forfinished lamb producers only, this is not socrucial, as lambs will be long gone beforethere is any possible danger of diseasedeveloping.

Commercial colostrumsubstitutes

These are widely available and popular, butexpensive and often relatively poor in bothenergy and antibody content when com-pared with ewe colostrum. However, it can-not be denied that they are handy to haveavailable, and certainly better than nothing.They are most effectively used to 'extend' alimited amount of ewe colostrum so thatlambs get some of each.

Newborn Lambs 65

Commercial milk powders

These are fine for lambs of 1 day or older,but are not a substitute for colostrum.

Feeding by Stomach Tube

Lubricate the tube by dipping in colostrum,then introduce it into the lamb's mouth andpush gently. In most cases the tube will enterthe oesophagus and can then be advancedinto the stomach. If inexperienced, check thelength against the position of the lamb'sstomach first and mark at the appropriatepoint. It is possible to check that the tube isnot in the trachea by carefully watching theneck as the tube is passed and seeing or feel-ing it as it passes down inside the oesopha-gus. You can then be confident in givingcolostrum or milk (one x 50 m1 syringe for asmall lamb, two x 50 m1 for a medium lamband three x 50m1 for a large lamb). This is aquick and easy method of ensuring that weaklambs or multiple births get a good start anddo not quickly succumb to hypothermia.

Early Post-partum Problems

It is worth remembering that early problemsare often an expression of pre-partum distur-bances, for example: (i) so-called soft lambsmay indicate enzootic abortion; (ii) hairy shak-ers indicate Border disease; and (iii) ataxia/paresis/recumbency may indicate daft lambdisease, swayback or nutritional myopathy.

However, the main culprit is often inad-equate feeding of the ewe in late pregnancy,which leads to:

Short gestations, giving small weaklambs with poor protective fleeces andfew brown fat reserves. Such lambsbecome hypothermic very quickly.They require a bit of luck with theweather, and an observant shepherd, ifthey are to survive.Poor mothering, too little colostrum andmilk, leading to a vicious circle endingin hypoglycaemia and hypothermia.Surviving lambs are more susceptible to

post-partum infectionreduced colostrum intaSpecific deficienciesselenium leading tonutritional myopathy.

In common with all other species,lambs are exposed to a variety of post-partum infections introduced orally, via thenavel, or via docking and castration wounds.These infections produce a variety of clini-cal signs such as:

hyperexcitability, tremors, opistho-tonus, convulsions, nystagmus;dull, sleepy, weak, recumbency, coma;salivation;atony of gut, with abdominal disten-sion and no faeces;scour;navel ill;joint ill;ataxia/paresis; andscabby lips and proliferative sores ongums and tongues.

However, farmers (and sometimes vets!) areinclined to place too much significance onthe pathogens that cause these infectionsand therefore on therapy with antibioticsand other drugs. Actually, the main prob-lem more often stems from: (i) the presenceof susceptible lambs; (ii) lack of colostrum;(iii) a heavy weight of infection because ofdirty conditions, instruments and hands; aswell as (iv) inadequate observation, isola-tion and treatment of individual cases.Therefore prevention is paramount withgood forward planning, attention to detailand continual close observation.

It is worth repeating that lambs gener-ally survive if they are average birthweight,kept warm and receive adequate colostrum,whereas those that are small, cold and failto obtain adequate colostrum, die.

because of theke.of copper andswayback and

Investigation of a Perinatal Problem

It needs time and thought and shouldinclude: (i) history; (ii) farm observations;(iii) clinical examinations; and (iv) labora-tory examinations.

66 Chapter 7

History

Numbers involved (size of problem).Problems in previous years.Purchases and related incidence of dis-ease (is the problem confined to onegroup? e.g. replacement ewe lambs).Breeding and lambing dates.Weather conditions throughout pregnancy.Feeding of ewes, vaccination and dos-ings (e.g. copper, fluke).Farmer's account of mortality, clinicalsigns/treatment.

Farm observations

Cleanliness.Drugs and instruments.Shelter, isolation and warmth.Feed available including colostrum (doyour observations agree with the farmstory?).Shepherding quantity and quality.

Clinical examinations

Ewes - age, CS, udders.Weak lambs - age, size, litter size, clini-cal signs, castration/docking.

Laboratory examinations

Submit plenty of fresh material (includingfetal membranes). It may include pairedblood samples from marked ewes for EAE,Toxoplasma and BDV, plus blood biochem-istry (copper and glutathione peroxidise(GSHPx); gammaglutamyl transferase (GGT)and BOHB from ewes yet to lamb). If possi-ble, submit whole carcasses of lambs ratherthan 'bits'.

Some Specific Post-partum Problems

These include: (i) hypothermia; (ii) waterymouth; and (iii) neonatal diarrhoea/scours.

Hypothermia

This occurs when heat loss is greater thanheat production and is indicated by a bodytemperature lower than the normal:

39-40°C (102-104°F) is normal.37-39°C (99-102°F) is mildlyhypothermic.Below 37°C (<99°F) is severelyhypothermic.

Newborn lambs (<5h old) which arestill wet suffer from exposure (high rate ofheat loss); they usually have some brown fatreserves left and will respond to drying,warming, then feeding, by stomach tube ifnecessary.

Slightly older lambs (>12 h old) sufferfrom starvation (low rate of heat produc-tion). They have no brown fat stores left; ifwarmed without being given energy, theywill develop hypoglycaemic fits and die.Energy can be supplied as follows:

If the lamb can hold its head up, feed itby stomach tube, then warm, thenre-feed.If the lamb cannot hold its head up, it isdangerous to feed (will probably regur-gitate, inhale and die). Give an intra-peritoneal injection of glucose beforewarming the lamb.

Technique for intraperitonealglucose injection

Use 10 ml/kg of warm 20% glucose/dextrose solution (if using 40% solu-tion, use an equal volume of freshlyboiled water to dilute and to bring it tobody temperature).Holding the lamb by the front legs and,using a 19G x 1" needle directed back-wards at 45°, inject it into the abdomi-nal cavity just below and to one side ofthe navel (see Fig. 7.3).

Then put the lamb to warm, preferablyin a warming box with a fan heater underwire mesh. An infrared lamp can be usedbut great care must be taken to avoid over-heating the lamb. When the lamb's tempera-ture has returned to almost normal and it is

Newborn Lambs 67

The correct site is about 1.5 cm to the side and2.5 cm behind the navel. This avoids the prepuceand penis of a male lamb. Use a 19G x 1" needledirected backwards towards the opposite hip.

Fig. 7.3. The intraperitoneal injection site.

conscious and able to swallow, feed150-200 ml colostrum via a bottle or stom-ach tube and return it to the ewe as soon asit is able to suck the ewe vigorously. If thelamb is one of twins, remove the other fromthe ewe and return them together whenready. If it cannot be returned to its mother,it will need to be reared artificially or moth-ered on to another ewe.

Note: Do not give an intraperitonealinjection to a lamb with scour or waterymouth.

Watery mouth (slavers, rattle belly)

These are common terms used to describe acondition which affects very young lambs(up to 3 days old). The condition is charac-terized by the following:

Lambs rapidly become dull and weak,look miserable and don't get up, andthey become unwilling to suck.They have cold, wet lips and muzzlesfrom drooling saliva (but note that ter-minally ill lambs dying of other causesoften drool saliva).

No faeces (meconium) are visible andthe tail is dry.The temperature is at first normal, buthypothermia follows.The abdomen is relaxed at first andlooks full, but later there is tympanyand tenseness which causes 'rattling'when tapped or shaken, and the dis-tension may cause distressedbreathing.Without treatment, they usually diewithin the day, but some live longenough to develop scouring and evenjoint ill, just to complicate thepicture!The incidence can be frighteningly high(>20%), and is most common in twinsor triplets from ewes with CS <3 andlambed indoors.

Cause

Watery mouth is an endotoxaemia whichdevelops when lambs swallow a lot of bac-teria (E. coli from a contaminated environ-ment) before they have sucked colostrum.The bacteria are not destroyed in theabomasum (pH is 7 after birth and thereare no colostral antibodies there to dealwith them), so they pass to the gut, multiplyand die, producing endotoxin. This isabsorbed into the portal circulation, passesto the liver, which has limited capability todetoxify, so reaches the general circulationresulting in endotoxic shock. One earlyeffect is slowing of gut movements with anaccumulation of saliva and gas giving thebloated rattling effect.

Treatment (has to be early)

Antibiotic injection (broad spectrum),repeated daily.Oral antibiotic against E. coli (usually a`pump' dispenser product).50 ml of glucose/electrolyte solutionadministered by stomach tube, repeatedevery few hours and increased if thelamb is not sucking the ewe. Do notfeed milk until recovering.A small dose of NSAID such as flunixin(anti-endotoxin).

68 Chapter 7

Warm soapy-water enema (10 -20m1administered via a cut-down stomachtube).Leave the ewe and lamb(s) together ifpossible, and keep warm.

Control

Make sure lambs get plenty of colostrumearly (within minutes, not hours):

Feed the ewes well so that CS is atleast 3.

Use a stomach tube to feed colostrumquickly to at-risk lambs (weak lambs,triplets, etc.).Ensure good bonding (avoid moving aewe and her lambs too soon afterbirth).Ensure the lamb(s) suck well (avoidearly castration and have goodshepherding).

Reduce the weight of infection:

By keeping things as clean as possible -bedding, pens and udders.At birth, oral dose lambs with a suitableantibiotic. This should only be done ifother methods fail as there is the possi-bility it will it lead to an increase inantibiotic-resistant bacteria in the longterm.

Check for iodine deficiency in the ewes asthere is a suggestion that this may predis-pose to the problem.

Neonatal diarrhoea/scours

While individual scouring lambs can bedealt with without resort to laboratory diag-nosis, it is important in an outbreak or inany flock with a persistent problem withscouring lambs to establish, if possible, ifthere is one dominating causal organism.To do this requires submitting up to ten fae-ces samples (not swabs), as well as any ter-minally ill untreated lambs and/or freshcarcasses. This should provide sufficientinformation to prescribe appropriate treat-ment and control measures. Commoncauses are:

Lamb dysentery - antiserum is nolonger available; vaccinate any ewesremaining to lamb and, for the next sea-son, implement a proper ewe vaccina-tion policy.Salmonellosis - there is special adviceabout the risk of spread to other spe-cies, including zoonotic potential.E. coli - use antibiotic sensitivity testingto establish the appropriate treatment,administer oral rehydration therapy andensure there is adequate colostrumintake for the remainder of lambs yet tobe born. A vaccine used to be availablebut is no longer sold in the UK.Rotavirus - it may be worth consider-ing giving all lambs soon after birth50 ml colostrum from cows vaccinatedwith rotavirus vaccine.Cryptosporidia - you will have to rely onnon-specific measures (clean pens, dis-infection, good colostrum intake, etc.).

In general, it is vital to provide isolation,warmth and plenty of fluids/electrolytes andwhen in doubt about the causal organism, toinitiate antibiotic treatment aimed at E. coil.

Treatment of lambs with other infectionssuch as navel ill, joint ill, meningitis,

spinal abscess

Provide vigorous and prolonged (7-14 days)systemic treatment with high-dose, twicedaily broad-spectrum antibiotic. NSAIDsuch as flunixin may help. Use local treat-ment to clean up navel, joint lavage, etc.where necessary.

A decision should always be taken aboutthe likely outcome of sick lamb cases. Ifthe outlook or welfare is poor, the lambshould be humanely destroyed ratherthan being allowed a lingering death.

General Measures to Control LambMortality

Do not try to lamb outdoors at inappro-priate times of the year and be prepared

Newborn Lambs 69

for bad weather even during normaloutdoor lambing times.In large flocks, plan a break in the lamb-ing sequence (batch lambing) to allowcleaning out of the buildings and lamb-ing pens and recovery time forshepherds.Observe a high standard ofcleanliness - instruments, hands,bedding and disposal of fetal mem-branes/carcasses. Change lambingpens/areas (even re-strawing of thearea is helpful) and turn out if theweather allows.Make sure lambs get adequate colos-trum quickly. Ensure there is a goodsupply of frozen colostrum or a goodcommercial substitute.Provide adequate shelter (even a zig-zag of straw bales in the field ishelpful).Reduce stocking density in pens orheavily-used lambing fields.Spray navels with tincture of iodine.Ensure early detection and isolation ofsick lambs.Cull ewes that are thin and have faultyteeth and/or udders; and feed the othersproperly.Review the future policy for vaccination,feeding and the provision of copper andselenium.

Neurological Problems

In addition to the central nervous system(CNS) diseases of young lambs which mayfollow any post-partum bacteraemia orsepticaemia, there are three specific con-ditions which originate pre-partum:(i) swayback; (ii) Border disease; and(iii) daft lamb disease. These need differ-entiation and while at first the clinicalsigns may appear non-specific or confus-ing, careful history-taking and clinicalexamination should give you the confi-dence to arrive at a provisional diagnosis;this usually needs biochemical and histo-logical support before flock control meas-ures are introduced.

Some questions of history

Ask the farmer to describe the clinicalsigns.When did the signs first show (at birth,1 week or older, etc.)?How many cases have there been so farthis season?How many normal lambs are there?How many have died?Do any get better? With or withouttreatment?Are the affected lambs out of one par-ticular batch of ewes?Are they single lambs?Has the farmer 'done anything' to themrecently (e.g. changed pasture, weaned,dock/castrate, inject/drench)?Has the farmer any cases which can beexamined today?Are the sheep exposed to ticks?Ask questions about the ewes - abortions,breeding, copper supplementation.

Swayback (enzootic ataxia)

This is one of the most important of themany CNS diseases of lambs, and is causedby faulty development and degeneration ofnervous tissue, particularly myelin sheaths,in the brain and spinal cord of lambs whosemothers had low copper concentrations inthe blood in the latter part of pregnancy.Rather than an absolute deficiency, thecause in the UK is usually an induced defi-ciency caused by an excess of molybdenum,sulfur and iron, although soils deficient incopper can be found in other parts of theworld.

It is very important to remember thatcopper still heads the list of poisons insheep, so copper supplementation shouldnever be given without a clinical reason,backed up with confirmatory tests. Notethat it is illegal to add copper to sheep feedsor minerals.

Diagnosis

Diagnosis is based on a combination of thehistory, clinical signs and laboratory tests.

70 Chapter 7

HISTORY

Swayback has been diagnosed clini-cally on the farm before.Copper has not been given to the ewesduring pregnancy.It has been a mild winter. This influ-ences the quality and quantity of thegrass, the amount of soil eaten (miner-als such as molybdenum, sulfur andiron ingested with soil 'lock up' cop-per) and the quantity of concentratesconsumed by the ewes (although nocopper is added there is inevitably a`background' concentration of copper).Housing greatly reduces the riskbecause ewes are prevented from ingest-ing soil and are fed concentrates.Forecasts of likelihood of swayback,based on weather, are published in thefarming and veterinary press.The grazing is lush. Improved, ferti-lized and reclaimed pastures with sin-gle-sward grasses and high molybdenumand sulfur levels are particularly likelyto give rise to swayback.

CLINICAL SIGNS Signs may be present atbirth, within a few days of birth or notappear until lambs are several weeks old.

Congenital - lambs at or within a fewdays of birth show varying degrees ofataxia, paresis and inability to stand.Some may be born dead, or die within afew hours. Some will be able to suck ifpermitted and most appear alert andaware. The signs are, at best, only sus-picious and can easily be confused withthe other CNS disturbances of younglambs. It has been shown that lambs inflocks suffering from subclinical cop-per deficiency (i.e. no obvious cases ofswayback) have increased lamb mortal-ity rates. The main differential diagno-sis for lambs of a few days to a fewweeks is spinal abscess and joint ill.Delayed - lambs a few weeks old, whichwere normal at birth, develop varyingdegrees of hind-leg weakness, ataxia(swayback) and paresis. The signs aremore obvious when the lamb is chasedabout and turns quickly. It looks like a

spinal rather than a brain condition andthe lambs can suck and graze normally;some will fatten because they learnhow to cope with the disability.Acute delayed - rapidly developingsigns in lambs a few weeks old whichdie within a few hours. This type isuncommon

Incidence

This will depend upon the control meas-ures adopted and the weather but it is com-mon for a swayback-prone farm to have afew years with very few cases, followed by acalamitous 'storm' (50%). Fortunately, theadvent of housing and safer copper supple-mentation has reduced these incidents.

Materialinclude:

Pathology

required for diagnosis should

Formalinized brains and brainstems.At least ten heparinised blood samples(green tubes) from pregnant ewes thathave not recently had supplementarycopper. Concentrations below 9 umo1/1suggest a copper deficiency problem.Liver samples if available - copper con-centrations below 80 mg/kg DM aresuspicious.Herbage analysis - the following are sus-picious: Cu - below 5 ppm DM, Mo -above 1 ppm DM, S - above 0.20% DM.

Treatment

Because swayback can be a progressive con-dition, it is worth treating those younglambs which are not too severely affectedwith a single injection of copper (no morethan 5 mg) in an attempt to stop the condi-tion getting worse, although no improve-ment should be expected. Badly affectedlambs should be euthanized.

Control

1. During an outbreak - all the remainingpregnant ewes (unless the breed is suscep-tible to copper toxicity, e.g. Texel) should

Newborn Lambs 71

be treated with a suitable copper prepara-tion, together with those healthy lambsalready born out of ewes not previouslydosed, in order to prevent delayedswayback.2. Next year - consider housing the ewesduring the last half of pregnancy, thusremoving them from the source of the prob-lem. If housing is not practicable, dose allewes in early pregnancy with copper (cap-sules containing copper oxide needles arethe safest) but also then remove other knownsources of copper such as licks or mineralsthat contain copper and proprietary cattleand pig concentrates.

If there is a problem of ill-thrift, poorquality fleece and multiple fractures inlambs due to copper deficiency, then thelambs also require dosing, but not beforeother causes have been eliminated and cop-per deficiency established.

COPPER PREPARATIONS

Beware of copper toxicity! Some breeds,especially continentals, are verysusceptible.Check very carefully for the recom-mended dose of particular product tobe used.

Injectable (copper heptonate) and oralpreparations (copper oxide) are available.The safest and arguably the most reliablepreparations are in the form of capsulescontaining copper oxide needles, deliv-ered orally by a plastic gun. Ewes aredosed once in mid-pregnancy and lambsas required when they are over 5 weeksold. A combined copper, selenium andcobalt oral soluble glass bolus is alsoavailable.

Short-acting drenches are sometimesused, but they require repeat dosing and risktoxicity. Copper sulfate on its own (1.0g in30 ml water) is still used prophylactically byfarmers, but it is a risky material to haveabout on sheep farms.

To avoid toxicity, either within hoursof injection or weeks after dosing:

Make sure copper is necessary.Reduce the dose in small sheep.

Remove any other obvious source ofcopper, particularly if the animals arehoused and fed concentrates.Treat ewes with care, and follow mak-ers' recommendations.

Individuals and breeds vary in suscep-tibility to copper deficiency and toxicity.For example: (i) Scottish Blackface andSwaledales are more prone to deficiency;(ii) Texels and other continental breeds areprone to toxicity; and (iii) the NorthRonaldsay, whose natural diet is seaweedwhich is very low in copper, is extremelysusceptible to toxicity, often succumbing ondiets which would be deficient to otherbreeds. A change in breed might be consid-ered, or an alteration in the lambing date, orspecial precautions for selected breeds, orcull those ewes that produce swaybacklambs (there is familial variation as well asbreed variation). Remember that high sul-fate and molybdenum levels in the diet areknown to decrease copper 'availability',hence the term 'conditioned' copper defi-ciency, and hence also the use of ammo-nium tetrathiomolybdate and sodiumsulfate in attempts to control chronic cop-per toxicity.

Border disease (hairy shakers)

This is a congenital disease, first reportedfrom the English-Welsh border counties butsince recognized throughout the world. It iscaused by infection with a pestivirus (BDV)serologically related to bovine viral diarrheavirus (BVDV). Antigenic differences can berecognized between BDV and BVDV, andsheep strains will infect cattle and viceversa, though it is unclear how much spreadoccurs between the two species under natu-ral conditions. Sheep which are immune toone strain are susceptible to the others.

Clinical picture

BDV infection produces a number of clini-cal signs, though they do not all occur inevery flock. One or more of the followingpictures may be seen:

72 Chapter 7

A number of lambs showing a typicallong hairy coat, some of which are alsoataxic with fine rhythmic tonic/cloniccontractions of skeletal muscles (`hairyshakers'). These signs are usually evi-dent at birth, although in the naturallylong-woolled breeds, the abnormalbirth coat is not obvious. The incidenceof Border disease lambs is variable but`storms' are reported. Gimmers producethe highest percentage of Border dis-ease lambs, indicating progressiveimmunity.Many affected lambs survive for a time,but their growth rate is poor and theyappear stunted with domed heads andlag behind the rest of the flock. In addi-tion, persistently infected lambs occur,many of which do not show the earlysigns, but some show chronic unthrifti-ness and scouring. Some survive tobreeding age, and though their fertilityis reduced, they can produce infectedlambs in successive pregnancies.Persistently infected rams can transmitvirus in semen.There is a high prevalence of barrenewes, abortions or even of just weaklambs. This means that the disease mayshow as an abortion and infertilityproblem rather than as a disease ofyoung lambs.

Pathogenesis

Infection of healthy non-pregnant sheepproduces no obvious clinical signs andgives rise to the production of neutral-izing antibodies and an immune sheep.It is 'antibody-positive, virus-negative'.

Infection of pregnant ewes leads to asimilar course of events in the ewe, but thevirus crosses the placenta and leads to thevarious clinical pictures, depending onvirus strain and breed of sheep, but mostimportantly, on the stage of gestation:

Infection prior to 60 days, at a timewhen the fetus has no ability to mountan immunological response, will resultin fetal death in a high proportion ofcases, leading to resorption and barren

ewes or mummification and abortion.Virus strains vary in virulence andthese early infections may allow someinfected fetuses to survive with virus invirtually every organ. Infection of theCNS leads to myelin deficiency and`shaker' lambs and infection of the hairfollicles leads to 'hairy' lambs. Weak oreven apparently healthy infected lambsmay be produced. All these lambs willbe immunologically tolerant to BDVand 'antibody negative, virus positive'at birth, and although they will acquireantibody in the colostrum, this willwane and they will be 'virus positive',probably for life. These lambs are per-sistent carriers.If infection occurs after about 85 days,the fetus mounts an immunologicalresponse and destroys the virus. Mostwill be normal at birth and will be`antibody positive, virus negative', likethe dam.If infection occurs between 60 and85 days, when the fetus is becomingimmunologically competent, either ofthe above responses may occur witheither clinical outcome.

Epidemiology

Most flocks become infected by the pur-chase of persistently infected lambs asbreeding replacements. It has been sug-gested that, rarely, infection may be intro-duced by pestiviruses from other speciessuch as cattle, goats or deer, or even by acontaminated live vaccine.

Diagnosis

The following indicates the tissues neededfor laboratory confirmation of clinicaldiagnosis:

1. From 'hairy-shaker', weak, scouring lambsor suspect persistently infected sheep -clotted and heparinised blood (red and greentube) from live lambs for virus isolation andserology. In dead animals, virus can bedetected by immunofluorescence and virusisolation from fresh tissues put in transport

Newborn Lambs 73

medium (e.g. kidney, spleen, thyroid; brainand spinal cord in calcium formolsaline forhistology).2. From aborting or barren ewes - clottedand heparinised blood for virology andserology, and placenta for virus isolation.

Treatment and control

There is no treatment and there are dan-gers in attempting to support weak orhairy shaker lambs which will beexcreting virus.

Ideally, a closed flock should be main-tained or replacements obtained from aflock which is serologically negative(this may form part of a sheep healthscheme in the future). Maintainingreplacements as a separate flock fromtupping to lambing will enable moni-toring of lambing to be done.In a flock which has recently hadBorder disease for the first time, thesheep suspected of introducing theinfection may be identified as 'anti-body negative, virus positive' fromblood samples. They and their lambsshould be culled before the next tup-ping season.In an endemically infected flock, allbreeding ewes should be deliberatelyexposed to infection 2-3 months beforemating by housing in close contactwith persistently infected sheep for3-4 weeks.

A vaccine has been developed for BVDin cattle, so it may eventually be pro-duced for sheep.

Other congenital neurological problems

Several neurological diseases affectingnewborn or young lambs with a particularbreed association have been recognized

Hydrocephalus (Dandy Walker malfor-mation) has been seen in Suffolks - thiscauses dystocia so needs to be consid-ered if dealing with this breed.Sometimes the lamb's skull is so softthat it can be crushed, aiding delivery;sometimes a caesarean may be neces-sary. It is fatal.Daft lamb disease has been seen in sev-eral breeds - lambs are born with cere-bellar abnormalities such as headnodding, ataxia and tremors and, as thename suggests, may appear mentallystupid, having difficulty finding theewe's teat.Cerebellar abiotrophy has been seen inCharollais lambs - cerebellar signsappear during the first weeks of lifewith ongoing deterioration.

Affected lambs should be euthanizedand diagnosis may require PME and histo-logical examination of the brain. Breedingrecords should be carefully examined sincethese diseases are often familial.

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8

The Lactating Ewe

Ewes rearing twins almost invariably havean energy deficit in early lactation so willlose weight. This is not a problem, provid-ing they were in good condition at lambingand do not become extremely thin, as theywill regain body condition after weaning.Ewes rearing triplets usually need supple-mentary food, even if grass supply is good,and are prone to mastitis problems becauseof hungry lambs competing for the teats andcausing teat lesions (Fig. 8.1). These ewesshould be managed separately with lambcreep feed supplied so that the demand onthe ewe is reduced as soon as the lambs starteating.

Particular problems of the lactating eweare:

mastitis;teat lesions; andhypomagnesaemia.

Mastitis

Our knowledge of sheep mastitis still lags along way behind that of the disease in cattle.It mostly remains a sporadic problem, withan incidence of 4-5% in lowland flocks,lower in hill flocks. The sector where itis important is in dairy sheep, in whichknowledge about cattle mastitis can be

usefully applied. Research into mastitis indairy sheep in countries such as Greece,where they are an important part of agricul-ture, is advancing knowledge in this sector.

Mastitis in the non-dairy ewe is com-monly seen at three stages in the productioncycle and is usually irreversible:

1. Acute, often gangrenous, at peak lactation -may be fatal; if not, requires life-saving treat-ment, although one could argue about themerits of this, as the animal should be culledwhen recovered.2. Chronic, seen after weaning or at the pre-tupping examination; requires culling.3. Blind teat at lambing - this is same cate-gory as (2), but was not detected at that time.Also eventually requires culling but wouldrear a single lamb if the other half isnormal.

Organisms commonly involved are:

Staphylococcus aureus which is foundon the skin.Mannheimia (Pasteurella) haemolyticawhich is found in the nasopharynx ofhealthy lambs.

Singly or together, these bacteria cause 80%of cases (both acute and chronic forms) andinvade the udder via the teat canal espe-cially when the skin of the teat is damaged.Other bacteria sometimes found include

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76 Chapter 8

Fig. 8.1. Ewes at peak lactation are vulnerable to mastitis.

streptococci, E. colt, coagulase-negative sta-phylococci, with occasionally A. pyogenesand C. perfringens.

Other causes of mastitis include:

MV - this causes an indurative mastitis.Leptospira hardjo (sometimes alsocalled Leptospira interrogans serovarhardjo) has been associated with suddenmilk drop.Mycoplasma agalactiae is important inthe Mediterranean area, causing conta-gious agalactia, but this does not occurin northern Europe.

Acute mastitis

This occurs most commonly early in lacta-tion, when the ewe is at peak milk produc-tion, usually suckling twins. It is difficult toknow precisely what triggers an attack, butit may be associated with movement on tolush pasture, or a period of bad weather.Shorn or crutched ewes are particularlyvulnerable shortly after turnout, perhapsbecause the udder is exposed to chilling.Teat lesions caused by orf or staphylococci(staphylococcal dermatitis) also predisposeto mastitis.

The clinical picture is dramatic and typ-ical: the ewe is obviously ill with a swollen

udder (usually only one half), she walksstiffly and the lambs appear hungry. The teatand a portion of the udder skin often becomecyanotic and cold, and oedema extends alongthe region of the mammary vein. Death mayoccur within hours so the ewe may be sim-ply found dead. If the ewe survives, thenecrotic udder and, commonly, the skin andtissue surrounding the milk vein, slowlyslough off with an extensive loss of abdomi-nal skin, leaving tubes of mammary ductsand blood vessels exposed. Healing thentakes many weeks and the ewe loses muchcondition. It may be necessary to tie off andamputate these granulating tubes to speedhealing and also to take measures to avoidflystrike.

Treatment

Consider first whether treatment is justifiedon both welfare and economic grounds. Ifso, vigorous systemic treatment is indicatedimmediately, but the local pathologicalchange is often already irreversible. Give ahigh dose of broad-spectrum antibiotic,repeated twice daily until the ewe showsimprovement (a day or so) or dies. Fluids(1-21) given orally or intravenously and aNSAID are also indicated. Strip the secre-tion out of the gland each time the ewe istreated. Drainage may be aided by removal

The Lactating Ewe 77

of the teat if it is gangrenous. Intramammarytubes are an optional extra. Ensure the eweis comfortable and has tempting food andwater nearby. Her lambs will need to be fedwith milk replacer unless old enough tomanage on creep feed.

Control

Control is difficult as predisposing factorsare often not clear. There is evidence thatinfection does not arise from pre-existingsubclinical intramammary infection, butfrom opportunistic invasion shortly beforeclinical events; therefore dry ewe therapy(DET) is unlikely to be effective.

The incidence varies between seasons,perhaps because of changing managementand climate, but it is usually of the order of1%; this level usually makes the condition anuisance to the farmer and does not justifywhole-flock control measures.

Some suggestions are:

If the ewes are too thin (CS <3), con-sider increasing the feed and so ensureadequate milk for vigorous lambs.Attend to teat sores - pustules, orf andsucking wounds; this may mean antibi-otic injections and even weaning thelamb(s) if they are old enough.Avoid turning out in cold wet weatherand/or ensure shelter.Ensure there is clean, dry bedding atlambing (` squelch' test!).Ensure proper clostridial vaccination.There is no evidence that Pasteurellavaccination is protective against masti-tis. If orf is a problem, it is worth consid-ering vaccination, but it must be donenot less than 7 weeks pre-lambing.

Chronic mastitis

This is usually discovered before tupping ata time when the ewes are selected for breed-ing or culling (e.g. because ewes are too thin,have problem teeth, are barren, or have aknown disease). One half of the udder, lesscommonly both, is lumpy and distorted withpalpable fibrosis or chronic abscesses.

The flock prevalence varies between 1% and15%. If cases are not obvious at this time,they become apparent at lambing and prob-ably account for many of the ewes whichlamb-down with only one functional gland,and for the problem of neonatal disease thatthis leads to. It is uncertain when infectionoccurs, but it is assumed that it is at weaningtime, because LA antibiotic, introduced then,is known to reduce the disease incidence,very similar to the dairy cow story.

Control

This is difficult, but consider the following:

DET at weaning: this is a two-personjob and the teats need to be cleanedbefore infusion. It is not necessary toinsert the nozzle into the teat - just lineup as in heifers.It seems a reasonable idea to dip orspray teats with a commercial cow teatdip at the time of infusion.Place ewes on poor pasture at weaningand keep them well away from the soundand sight of their lambs, to reduce milkproduction. Do not restrict water intake.Mark cases for culling.

Teat Lesions

These commonly predispose to mastitis.Additionally, affected ewes may be reluc-tant to let their lambs suck, so may be acause of ill thriven or dead lambs.

The main causes are:

Staph. aureus; andorf.

Staphylococcal infection

This produces very painful ulcerated andswollen lesions at the base of the teat, prob-ably triggered by damage from the sharpincisors of lambs when sucking. It is crucialto treat these as soon as possible, otherwisethe consequences of mastitis and starvinglambs follow. Aggressive treatment with

78 Chapter 8

injectable antibiotic and NSAID, plus localapplication of antiseptic and local anaes-thetic gel helps. While at first sight removalof the lambs might seem a good idea, it is bet-ter to allow them to continue sucking (aidedby application of anaesthetic gel if available),restraining the ewe if necessary. This mayseem rather brutal but lambs are the mosteffective way of emptying milk from theudder and if recovery is speeded up by theabove treatments, it may be possible to havea good outcome for both ewe and lambs.

Orf infection

This is more of a problem, since the viralinfection has to run its course. It is oftencomplicated by lambs also having infection

on their mouths. Local and parenteral anti-biotics help to control secondary infection,but there is no quick cure. If this is a realproblem, for the future, vaccination of ewesbefore the last 7 weeks of pregnancy may beappropriate.

Hypomagnesaemia

As described elsewhere, this is most usuallyseen in ewes at peak lactation sucklingtwins (Fig. 8.2). The stress of lactation, com-bined with grazing low-fibre, rapidly-growing grass, often fertilized with nitrogen,trigger the disease. Most often, ewes arefound dead, but may sometimes be seen col-lapsed and in convulsions. See Chapter 6for treatment and control.

Fig. 8.2. Ewes suckling twins or triplets are particularly at risk of hypomagnesaemia.

9

Growing Lambs

A common complaint made by farmers isthat a significant number of the lambs arenot growing as rapidly as expected (Figs 9.1and 9.2). The growth rate of lambs on low-land farms being raised for slaughter shouldbe 250-300 g/day though single lambs andlambs being raised for sale as rams willmanage higher growth rates than these.Although in the UK it is rare for farmersproducing prime lambs for slaughter toweigh their lambs regularly and so thegrowth rates will not be known, these canbe estimated by looking at lamb sales dataand working out the times taken to achieveslaughter weight. For example, if we assumethat the lambs are born in March andslaughtered at around 40 kg live weight inJuly, the weight gain will be 300 g/daywhereas if they are sent for slaughter inSeptember, the weight gain will only be200g/day. Many lambs grow well untilsome specific incident occurs, the timing ofwhich will help in diagnosis. Althoughmany causes are possible, the most com-mon reasons for a significant proportion ofthe lamb crop being thin are coccidiosisand parasitic gastroenteritis (PGE) and insome areas, mineral deficiencies, particu-larly of cobalt, which also predisposes toparasitic problems. It is highly likely thatthe poor weight gain will also be associatedwith scouring.

Coccidiosis

The incidence of coccidiosis has increasedsteadily over the last 15 years in the UK, prob-ably due to increased intensity of production,and is recognized as a considerable hazard oflowland sheep production throughout theworld. Several species of Eimeria have beendescribed which are specific to sheep, andtheir pathogenicity differs considerably. Manyof them produce few if any clinical signs,whereas two species (Eimeria ovinoidalis andEimeria crandallis) may cause severe disease,characterized by diarrhoea, weight loss anddeath. It is a specialist task to identify thesespecies so oocyst counts do not usually dif-ferentiate the species involved.

History

The majority of outbreaks, which involve ahigh proportion of the lambs, occur in ani-mals of 4-8 weeks old which have beenhoused since birth, or grazed on constantly-used pasture at high stocking rates.

Clinical signs

The first signs are that the farmer may recog-nize that the lambs have lost 'bloom' and

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80 Chapter 9

Fig. 9.1. These Herdwick lambs look to be thriving well.

Fig. 9.2. These lambs at weaning are rather a mixed bunch and show quite a variation in size.

Growing Lambs 81

show an 'open' fleece. Some animals mayhave slight diarrhoea with soiling of the woolbelow the anus. These signs extend to con-siderable numbers of the flock and weightgains are reduced, followed by weight loss.Severe untreated cases proceed to extensivescouring, dehydration and death, which ininfections with E. ovinoidalis, occurs 14-21days after infection. Treated recovered lambsoften continue to make poor weight gainsdue to slow repair of the intestinal lesions,resulting in villous atrophy, with consequentmalabsorption of nutrients.

Epidemiology

The ewes act as a source of oocysts, andsporulation occurs in 2 or 3 days. Oocystsremain viable for up to a year. Infections arebuilt up by multiplication through lambsand it is often later batches of lambs whichshow clinical disease.

The peak incidence at 4-8 weeks of agewas believed to be due to the fact that onecycle had to take place in the lambs, taking2-3 weeks, in order to build up a heavy envi-ronmental contamination with oocysts.Disease was believed to result from the mul-tiplication of this second cycle in the intes-tine before an effective immunity haddeveloped. It is now known that lambs arenot susceptible to coccidial infections (withE. ovinoidalis, the most pathogenic species)very early in life and that susceptibilityincreases up to about 4 weeks of age. If heavyinfections are encountered early in life, clini-cal signs are not seen (due to passive transferof immunity), active immunity is stimulatedand the lambs are less likely to show clinicalsigns of coccidiosis at 4-8 weeks old. Afterthis age, most lambs have encountered infec-tion and develop a strong immunity thoughin exceptional circumstances, coccidiosismay occur in older lambs.

Diagnosis

This is based on clinical signs and history.Oocyst counts are not reliable since it is pos-sible to see clinical coccidiosis associated

with developing sexual stages, before peakoocyst production occurs, and counts of upto one million oocysts/g in a faecal samplecan be seen without clinical signs associatedwith the non-pathogenic species. It has beenstated that it is easier to arrive at a diagnosisof coccidiosis if you don't possess a micro-scope! Nevertheless, it is often helpful toexamine a number of faecal samples (say ten)when counts of over 100,000 oocysts/g insome samples, together with suggestive clini-cal signs and history, warrant treatment forcoccidiosis. In lambs out at grass, Nematodirusbattus infection should be considered sinceit occurs at almost the same time. It hasbeen shown that concurrent infection withE. ovinoidalis, E. crandallis and N. battuscauses a much more severe disease thanany of these by themselves.

Treatment

There are two products which are effectivein the treatment of clinical outbreaks of coc-cidiosis in lambs.

1. Diclazuril, which has been available for afew years, is formulated as an aqueous sus-pension given orally by drenching gun. Alllambs in the affected group should be givena single dose. The drug is effective againstall stages of the two pathogenic species ofcoccidia and under field conditions allowsthe development of immunity. It reducesoocyst excretion significantly. It has a zeromeat withdrawal period.2. Toltrazuril, which is a relatively newdrug, is formulated as an oral suspensiongiven by drenching gun as a single dose.The drug is effective against all stages ofthe two pathogenic species and allows thedevelopment of immunity. Although thedrug can be used to treat clinical coccidio-sis, it is recommended that in order toobtain maximum benefit, it should be givenbefore the onset of clinical signs and thus ismore suitable for prevention and control ofcoccidiosis. It markedly reduces oocystproduction. The meat withdrawal period is42 days but this is not usually of impor-tance unless early, light lamb production isplanned.

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Control

On many farms, it is known that coccidiosisoccurs on certain well-used pastures eachyear and toltrazuril and diclazuril may beused to prevent such outbreaks. All lambsshould be treated at the normal dose rate ataround 3 weeks of age and in conditions ofheavy challenge, the treatment could use-fully be repeated 3 weeks later.

Very occasionally, severe scouring hasfollowed diclazuril treatment which hasbeen shown to be associated with freezingof the aqueous suspension and the activeingredient coming out of suspension result-ing in under-dosing and a failure to controlthe coccidial parasites.

Parasitic Gastroenteritis (PGE)

PGE is the most important cause of thin,scouring lambs from as early as 2 months ofage up to about 1 year old in all sheep-producing countries of the world. Duringthe first year of life, a strong immunitydevelops to most worm species (Haemonchusis an exception) which not only means thatclinical signs are rarely, if ever, seen in olderewes but also means that sheep may ingestinfective larvae (L3, i.e. third-stage larvae)but the life cycle is not completed and eggcounts are very low for most of the year. Theimportant exceptions to this rule are theperiparturient rise in faecal egg count inewes and the frequent observation that adultrams may have high egg counts.

The important worms in lambs in theUK and northern Europe are Ostertagia spe-cies (in sheep, renamed Teladorsagia spp.)in the abomasum and Trichostrongylus andNematodirus species in the small intestine.Explosive outbreaks of Haemonchus infec-tion in the abomasum are seen in July andAugust following suitable weather condi-tions in lambs and ewes and a more chronicform of haemonchosis has been describedin periparturient ewes.

Haemonchus is the most importantworm in tropical and subtropical countriesand is of immense importance in the

southern hemisphere countries, includingAustralia, New Zealand, South Africa andthe countries of South America. It is theimportant nematode which above all oth-ers rapidly develops resistance toanthelmintic drugs.

Although Haemonchus is recognized asthe most important worm of warmer cli-mates and was thought to be of occasionalimportance only in southern England, it isnow found widely across the UK includingScotland, perhaps associated with climatechange.

Clinical signs

N. battus causes severe scouring, loss ofbloom, dehydration, loss in conditionand death in lambs, typically in Mayand June but increasingly in the autumnalso. Ewes are not affected and immu-nity develops rapidly in the lambs.Teladorsagia, Trichostrongylus andNematodirus filicollis contribute in dif-ferent proportions to PGE during therest of the year, usually commencing inJuly and continuing into the late winterwith chronic scouring and unthrifti-ness. Subclinical parasitism character-ized by reduced weight gains withoutsignificant scouring is also of great eco-nomic importance.Haemonchus, which differs from theother worms in being an active bloodsucker, leads to anaemia, loss in condi-tion and death, without scouring.

Life cycles and epidemiology

Nematodirus eggs, which can be distin-guished from those of other worms in thatthey are much larger and even distinguisha-ble between species, develop slowly withthe moults to the infective L3 stage occurringwithin the egg in a minimum of 2 months,even under favourable conditions. The typi-cal life history of N. battus involves only onegeneration every 12 months with the egg con-taining the L3 overwintering on the pasture.

Growing Lambs 83

After being exposed to a low temperatureover the winter, the L3 hatch when the tem-perature rises to above 10°C, thus resultingin a heavy pasture infestation over a shortperiod in the spring. An annual nematodiro-sis forecast is published in the UK by UKVET(available at: www.nadis.org.uk). If the masshatch is early (e.g. February/March), mostspring-born lambs will not ingest many L3,since the larvae will have died off before thelambs are consuming much grass. If, how-ever, there is a late winter and the masshatch does not occur until May, severe dis-ease is likely since the older lambs will beeating a considerable quantity of grass. Thecycle is essentially a lamb-to-lamb annualinfection. It should be noted that though thistypical life cycle is still important, N. battushas developed the ability to complete its lifecycle without the fall in temperature associ-ated with winter and is becoming an impor-tant cause of PGE in autumn This appearsto be due to the fact that hatching is morecomplex than was thought and it has beenshown that hatching is inhibited at an uppertemperature of around 18°C. Selection fac-tors such as climate change may be respon-sible for the increasing proportion ofN. battus eggs which are hatching in theautumn It also appears that different strainshave different hatching patterns which mayexplain differences in nematodirosis on dif-ferent farms.

With Teladorsagia and Trichostrongylus,the eggs, which are indistinguishable fromeach other (or from Haemonchus and anumber of other trichostrongylid worms oflittle pathogenicity), develop to a first-stagelarva (L1) which hatches. The L3 is the infec-tive stage and the time taken for an egg todevelop to L3 varies with the environmentaltemperature from as little as 2 weeks to aslong as 4 months. Eggs are produced for afew weeks by ewes of all ages around lamb-ing time and during lactation by the 'activa-tion' of inhibited fourth-stage larva (L4) inthe mucosa and by completion of the lifecycle in these ewes whose immune responsehas been reduced. In addition, eggs are pro-duced by lambs which ingest overwinteredL3. These factors result in the well-known`telescoping' of larval development so that

eggs passed in March-June all reach theinfective stage in July as the early eggs takemonths and the late eggs weeks to become L3.Infective larvae overwinter on the pasturequite happily but most die off rapidly dur-ing May and June. This larval peak in Julyonwards is the main challenge to lambswhich are nearing market weight at thistime and ingesting much grass as the ewe'smilk supply dries up.

Haemonchosis usually occurs whenthere has been a spell of very warm humidweather in July and August so that a highproportion of the enormous numbers of eggswhich are passed by Haemonchus femalesdevelop rapidly to the infective stage, inges-tion of which, together with a poorly devel-oped immune response to this worm, resultsin explosive outbreaks of disease.

Diagnosis

PGE should be suspected from the clinicalsigns and the history of a high proportion ofthe lambs being involved, and can usually beconfirmed by faecal egg counts on a numberof affected lambs. Egg counts are usually over1000 eggs/g of faeces though, with N. battusin particular, severe scouring can occur justbefore the worms become mature and pro-duce eggs. Haemonchus infections producehigh egg counts of 5-10,000 eggs/g. Wormcounts on dead or killed affected lambs inthe abomasum and the first 10m of the smallintestine will usually yield counts of 50,000Teladorsagia or Trichostrongylus or more,but many may be immature. Haemonchuscounts in the abomasum are generally around1000 or more.

Treatment

Early recognition of clinical signs and par-ticularly the use of faecal egg counts allowthe treatment of affected lambs before severelesions of villous atrophy have developedwhich can render treatment ineffective.Villous atrophy, resulting in continued clin-ical signs, can also result if the lambs are

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left on a heavily contaminated pasturewhich may cause the farmer to believe thatthis is due to anthelmintic resistance.

Anthelmintics for PGE

Although there are an enormous number ofproprietary anthelmintic drugs available tofarmers, which gives rise to confusion, theyfall into five main chemical groups: (i) ben-zimidazoles (BZ drugs); (ii) imidazothia-zoles and tetrahydropyrimidines (levamisoleand morantel, so these are known as LMdrugs); (iii) avermectins and milbemycins(macrocyclic lactones or ML drugs);(iv) amino-acetonitrile derivatives (AADs);and (v) spiroindoles. The groups are dis-cussed below with examples given of someof the individual drugs in each group forillustration. The first three groups were theonly anthelmintics for 25 years, untilrecently when two new anthelmintics weredescribed, each belonging to a new group. Itis probable that more drugs belonging tothese two groups will become available inthe future. It is important that the datasheets for each drug should be consultedsince they have important differences in:(i) the range of activity; (ii) residual action;and (iii) withdrawal periods for meatand milk.

BZ drugs

These are the oldest and most widelyused drugs for the treatment and con-trol of PGE.The first member, thiabendazole, nolonger available, was introduced in1961 and is the parent drug from whichthe large number of benzimidazoles hasbeen derived. They are known as 'whitedrenches'.All benzimidazoles (except triclaben-dazole - see fluke, Chapter 4) are effec-tive against all stages of the normal lifecycle of BZ-susceptible worms whichcause PGE (e.g. oxibendazole); some arealso effective against lungworms (e.g.mebendazole); and some are effectiveagainst inhibited fourth-stage larvae

(L4), involved in Type II ostertagosis(e.g. fenbendazole).They are available in a wide range offormulations including a drench sus-pension, feed pellets, feed block orpowders. Oral preparations containingcobalt and selenium also are available.Anthelmintic resistance is widespreadto benzimidazoles and resistance to onemeans that the worms will be resistantto all benzimidazoles so changing fromone white drench to a different one isnot useful, which is not always appre-ciated by farmers.

LM drugs

The major anthelmintic is levamisole,the 1-isomer of tetramisole. There aredozens of proprietary formulations.Levamisole is effective against all stagesof the life cycle of worms responsiblefor PGE, including inhibited larvae andagainst lungworm infection.Levamisole is available as feed granulesand as a solution, which may be givenorally or by subcutaneous (SC)injection.Morantel is a related drug, which iseffective against BZ-resistant nema-todes but its range of activity isnot wide.

ML drugs

Until 1996, the one anthelmintic in thisgroup was ivermectin. An injectable ororal preparation, it is effective againstall stages of worms causing PGE, includ-ing inhibited larvae, lungworm infec-tion and against sheep scab mites.Moxidectin is available as a drenchand an SC injection in sheep and iseffective against all stages of wormscausing PGE, including inhibited lar-vae, and against lungworm. The inject-able form is active against sheep scaband itch-mites (Psorergates). It hasa marked persistent effect, the 1%injectable solution possessing residualactivity against Teladorsagia andHaemonchus of 5 weeks. There is also

Growing Lambs 85

a 2% LA formulation which is activeagainst Teladorsagia and Haemonchusfor around 100 days but which has avery long withdrawal period exceeding100 days.Doramectin is available as an intramus-cular injection in sheep. It has a widerange of activity, including sheep scaband itch-mites and has residual activityof 3-6 weeks.

AA Ds

This is a novel class of drugs with theone marketed anthelmintic, monepan-tel. This drug acts by binding to a spe-cific receptor only found in nematodesand so possesses a high safety margin.It is available as an oral drench with aspecial gun.It kills all stages of all the importantworms and is particularly useful onfarms where resistance to the threeolder groups of anthelmintic has devel-oped. It has the advantage of a short(7 day) withdrawal period.

Spiroindoles

This is the most recently developedgroup of anthelmintics and at present,the one marketed anthelmintic is der-quantel. It has limited availability atpresent to New Zealand (but will doubt-less become more widely available) as acombination oral drench with abermec-tin, thus combining its unique mode ofactivity with the wide range of activityof an ML drug.It is highly effective against adults andL4 larvae of all important worms includ-ing nematodes which are resistant toother anthelmintic groups. In addition,it is active against lungworm, nasal bot-fly and itch-mite.

(Some other drugs, which are mainly usedagainst fluke infections, are also effectiveagainst the blood sucking nematode, H. con-tortus. Examples are closantel and nitrox-ynil. They have been used in worm-controlprogrammes against BZ-resistant strains ofH. contortus in Australasia.)

Control and anthelmintic drug resistance

Many species of nematodes have becomeresistant to one or more of the majoranthelmintic drug groups and surveys indi-cate that these strains are widespreadthroughout all sheep-producing countriesincluding the UK which must be taken intoaccount in formulating control programmes.The major nematodes involved are com-monly Haemonchus and Teladorsagia but, atpresent, rarely in Nematodirus, thoughresistant strains of this worm have recentlybeen recognized Recent surveys have foundwidespread BZ resistance, less widespreadresistance to levamisole and, on a smallnumber of farms, resistance to all three of theolder anthelmintic groups. It is recognizedthat many of the methods which were usedto control PGE selected for resistant wormsand a re-appraisal of control strategies hastaken place and given rise to recommenda-tions under a programme called SCOPS(Sustainable Control of Parasites of Sheep).

It is believed that all populations ofworms contain a small proportion of indi-viduals that are more resistant toanthelmintics than the rest and progressiveselection of these worms in preference to thesusceptible worms eventually results in apopulation which is largely resistant. Whilethis may take years, depending on the selec-tion pressure and the genetic basis of drugresistance, once established it is impossibleto reverse. The SCOPS programme seeks toreduce the selection pressures so that thepopulation of worms remains mainly sus-ceptible to anthelmintics. In particular, itemphasizes the importance of the parasitepopulation which is not subject to selectionpressure which is mainly the stages on thepasture. This population is said to be 'in ref-ugia'. The principle behind the SCOPS rec-ommendations is that this population shouldbe kept as large as possible so that parasiteswith resistant genes are regularly dilutedwith those with susceptible genes.

The traditional control schemes whichexert a strong selection pressure are:

The Weybridge 'dose and move' inJuly - in this, all lambs are dosed in July

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and moved to a clean pasture such asaftermath after hay or silage. Clearly, theworms remaining after the dose are theresistant population which results inthe clean pasture being contaminatedwith a resistant population only.The same is true for all 'dose-and-move-to-clean-grazing' programmes, includ-ing dosing housed ewes at lambing andputting on a clean pasture, such asmight be provided by rotational grazingwith cattle.Early-season dosing of ewes and lambswithin the pre-patent period or withdrugs possessing residual activity inorder to prevent the July peak of larvaldevelopment - this method is very effec-tive at exerting a strong selective pres-sure. It means that any worms which dodevelop are resistant so, as susceptibleoverwintered L3 die off, the (small) Julypeak consists solely of resistant worms.This is then built up over years to alargely resistant population.

The SCOPS programme seeks to maintain apopulation of L3 which are largely suscepti-ble, so that anthelmintics remain effectivefor when they are really needed. It shouldbe recognized that this means that wormswill not be as well controlled as ideal andsubclinical disease may occur. It is alsopossible that clinical parasitism will resultif the system is not monitored carefullywhich emphasizes the need to carry outperiodic egg counts to anticipate thispossibility.

The main features of the SCOPS pro-gramme (slightly amended) are as follows:

1. Avoid importing resistant worms withpurchased sheep by quarantine procedures.Treat all purchased sheep with full doses ofmonepantel and moxidectin, consecutivelybut not mixed, and keep the animals on aconcrete yard for 24h with food and water.Put the treated sheep on to a contaminatedpasture to allow a susceptible population todevelop. Do not put faeces produced duringthe holding period on pasture for a year.2. Test for resistance annually by the useof the Faecal Egg Count Reduction Test.

In principle, give anthelmintic to a groupand do egg counts 7-14 days later.3. Give anthelmintics effectively by check-ing the accuracy of the drenching gun,weigh sheep and dose for the heaviest.4. Use anthelmintics only when really neces-sary. For example, do not dose ewes at tup-ping as most ewes are immune. Since it hasbeen shown that dosing ewes at lambing onceand putting on dirty pasture, containing over-wintered L3 is no better than not dosing at allon the overall periparturient egg count, donot dose or dose only a proportion of theewes, such as those in poor condition.5. Choose anthelmintic thoughtfully. It isusually best not to use fluke-roundwormcombinations as the best times for dosingdiffer for the two groups of worms: use BZdrugs for nematodirosis in May-June asresistance is rare; use closantel if haemon-chosis is the problem.6. If using 'dose-and-move' strategies, leave10% of the lambs untreated so that resistanteggs are diluted with susceptible eggs.7. Never have goats on a sheep farm as theymetabolize anthelmintics rapidly, whichexposes worms to sublethal doses.8. Do faecal egg counts on six to ten sheepperiodically to check efficiency of the pro-gramme and anticipate any breakdown,thus allowing appropriate anthelmintictreatment. Appropriate times might be ewesaround lambing, and lambs around Juneand in September, but this needs modifica-tion on each farm. If egg counts are not beingmade regularly there is a real danger thatclinical PGE may occur.

Since this programme is complicated andeasy to get wrong, veterinary practitionersshould be involved in its formulation andmonitoring.

Immunity to worms has a high geneticinheritance and it is possible to select ramswhich will produce lambs which developimmunity to worms more rapidly. Ramswith EBVs for genetic resistance to wormsare becoming available.

Although many of the features of thisprogramme are not controversial, there arethose who disapprove of the basic recom-mendation of leaving a large population of

Growing Lambs 87

susceptible parasites in refugia and itscounter-intuitive rationale has been criti-cized as being difficult to explain and assess.It is clear that the successful dilution ofresistant parasites with additional suscepti-ble parasites means that the total parasiteburden is increased which may lead to theappearance of clinical PGE. It has been sug-gested that early-season treatment of eweswith a product such as moxidectin LA orivermectin capsules, which have a residualaction for Haemonchus of around 100 days,followed in the first year only by dosing thelambs and moving to clean pasture at wean-ing, reduces anthelmintic use and resist-ance is likely to be delayed for many years.The fact that there are now potentially fivedifferent groups of anthelmintic is encour-aging and reassuring.

One exciting development is theresearch at the Moredun Research Instituteon the isolation of antigens from the gutepithelium of Haemonchus and their useto stimulate protective immunity in lambs.This experimental work which hasextended over several years, is leading to afield trial of a recombinant vaccine and itis hoped it will lead to a commercial vac-cine soon.

Anthelmintics for cestode infections

Adult tape worms of the genus Moniezia areextremely common in young lambs andstrings of white segments are frequentlyseen in the faeces by farmers and blamed forany clinical signs which may be found atthe same time. There is little evidence thatthey exert any adverse effect on production.However, many BZ drugs (e.g. albendazole)are very effective against Moniezia.Praziquantel is also very effective and isincorporated into a mixed anthelminticwith moxidectin which kills cestodes andnematodes.

It should not be forgotten that sheepact as intermediate hosts for several ces-todes of the dog and that treatment of dogsshould form part of a sheep healthprogramme.

Cobalt Deficiency

Cobalt deficiency is the cause of 'pine' or`ill-thrift' in lambs, a condition which iswell recognized in all sheep-producingcountries of the world. The incidence ishighest in areas where soils are derivedfrom acid igneous rocks and where there arecoarse, sandy soils. In Scotland, cobalt defi-ciency is widely distributed but in England,the localities most likely to be deficient arein the limestone areas of the Pennines, theold red sandstone areas of Hereford,Shropshire and Worcester, Dartmoor andthe Greensands at the edge of the chalk insouth-east England. As well as these areaswhere cobalt deficiency is endemic, otherareas became cobalt deficient as a result offarming practices, such as liming andreseeding which have improved pasturesand in so doing, lowered the availablecobalt. A constant intake of cobalt is neededto allow rumen organisms to produce vita-min B12, and the disease caused by cobaltdeficiency is thus an induced vitamin B12deficiency.

Clinical signs

The typical disease is characterized by:

Loss of appetite.Reduced weight gains proceeding toweight loss and extreme emaciation.Lambs have a dry coat and a tight skin.Severe anaemia and lachrymation inthe terminal stages.

Subclinically, a marginal deficiency ofcobalt may be of considerable economicimportance since typical signs may not bepresent but weight gains may be reduced.PGE is often also present and its clinicaleffects are more serious, and copper defi-ciency may be a complicating fact in somecountries including Australia, NewZealand, South Africa and the USA butrarely in the UK. However, farmers tend tosuspect deficiency states with littleevidence so care should be taken overdiagnosis.

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The adult ewe may show signs of cobaltdeficiency in late pregnancy due to fattyliver, leading to perinatal mortality.

Diagnosis

History of farm and geographical area.Clinical findings.Response to treatment - this is oftenvery marked after cobalt administra-tion, but it should be noted that lambswith reduced appetite due to othercauses may also show a response todosing with cobalt.Laboratory confirmation.0 In the animal, by serum and liver

vitamin B12 concentration.0 In the food, by herbage and soil

cobalt concentration.

Treatment and prevention

There is no placental transfer of vitamin B12and only low concentrations in milk; lambsrequire colostrum for their first supply.

Possible methods of treatment and pre-vention include:

Cobalt boluses - the most effectivetreatment is to give each lamb, at about8 weeks of age (not before, because theyare too small to dose, and the rumen is

not fully developed) a cobalt pellet orbolus. The bolus consists of solubleglass containing cobalt, selenium andcopper and is effective for at least ayear, but it is expensive, and for fatten-ing lambs it may not be worth it, thoughit would be for lambs which are to bekept for breeding. Beware giving prod-ucts containing copper unless there is aproven need for it.Oral dosing with cobalt - a drench ofcobalt sulfate can be given to affectedlambs which will need to be repeatedevery 3 weeks.Cobalt supplementation in mineralmixture - it is unlikely that lambs willbe on concentrates but if so, the mineralmixture should contain sufficientcobalt to raise the whole feed to 0.11 mgCo/kg DM.Injection of vitamin B12 - this will dealrapidly with an immediate problem,but cost and the need for injectionsevery 3 weeks precludes this as a pre-ventive measure.Application of cobalt sulfate to grazingland - cobalt sulfate may be applied as aspray or as a granular top dressing at2.0 kg/ha. Dressing need only be repeatedevery 3 years (or 6 years if the deficiencyis only marginal) and only one-third ofthe grazing need be treated (at 6 kg/ha),since the sheep graze the treated stripselectively. The pasture should not betreated soon after liming.

10

Sudden Death

Sudden death or, more accurately, 'founddead' is a common problem in sheep keep-ing. Since the sheep flock is usually not ascarefully observed as a dairy herd, theactual death is rarely observed and mayhave taken place at any time since the lastinspection, so making an estimate of howrecently death occurred is important(freshness, appearance of eyes, smell,autolysis). It is useful to look at the pos-sible causes in relation to the age of thesheep affected and whether few or manyare involved. The rest of the group or flockshould be observed carefully to see if anymore sheep are showing early clinicalsigns of disease. PME is an importantdiagnostic tool but it should be remem-bered that autolytic changes occur rapidlydue to the insulating qualities of thefleece.

Some of the diseases which must beconsidered in the differential diagnosis ofsudden death (Figs 10.1 and 10.2) aredescribed in other parts of this book andwill only be briefly mentioned here.

Young Lambs

In young lambs up to about 4 weeks old, asmall number of deaths may be caused by:

accidents;starvation/exposure (e.g. where a ewedevelops unobserved mastitis or a lambbecomes mismothered);watery mouth where colostrum intakeis delayed or absent;abdominal catastrophe such as gastrictorsion; andlamb dysentery due to faults in vaccina-tion technique, individual ewes beingmissed or lack of colostrum intake.

If many lambs are involved, the mostlikely causes are:

hypothermia as a result of extremeweather conditions;lamb dysentery in a non-vaccinatedflock; andsepticaemia associated withM. haemolytica.

Growing Lambs

Up to about 6 months old, a small numberof deaths may be due to:

redgut (torsion of the mesentery)particularly if being artificially rearedor on ad libitum creep feed; anddosing-gun injuries if drenching iscarried out by an unskilled person.

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90 Chapter 10

Fig. 10.1. This well-grown lamb is ready to wean and will be vulnerable to clostridia! disease if not alreadyvaccinated.

Fig. 10.2. These weaned mule lambs should be protected against clostridia! diseases and pasteurellosis,both of which cause sudden death.

If many lambs are involved the mainpossibilities are:

pulpy kidney disease;braxy;acute abomasitis (Clostridium sordellii);

acute pneumonia due to M. haemolytica;septicaemia due to Pasteurella trehalosi;andmassive parasitic infections, particu-larly of Nematodirus, Haemonchus,

Sudden Death 91

coccidiosis or acute fasciolosis but multiply in a number of different sitesother lambs in the flock will be show- in the body.ing less acute signs.

Adult Sheep

In adult sheep, single or a few deaths maybe associated with:

accidents such as newly introducedrams fighting and fracturing the occipi-tal process of the axis;sheep in fat condition becoming cast ontheir backs (common); andperiparturient problems in lambingewes.

If many sheep are involved, the mostlikely causes are:

metabolic disorders, particularlyhypocalcaemia or hypomagnesaemia(see Chapter 6);clostridial diseases, especially blackdisease, struck, blackleg or acuteabomasitis;acute pneumonia associated withM. haemolytica;acute haemonchosis or fasciolosis; andtoxicity associated with copper, yew orrhododendron.

Clostridia! Diseases

Clostridial diseases have already been dis-cussed in Chapter 3 so it is worth referringto this chapter too.

Clostridia are ubiquitous in the envi-ronment, especially in soil, so sheep arepotentially always exposed to infection.The modern generation of farmers tends tobe unaware of the catastrophic losses fromthese diseases which occurred in the erabefore vaccines were available. The major-ity of these diseases (apart from tetanusand botulism) cause rapid death so sheepare usually found dead with few or no clin-ical signs having been observed. Clinicalsigns if seen and death are associated withthe production of powerful toxins by dif-ferent species or types of clostridia which

Diagnosis

This needs to be speedy if control is to beeffective. It is usually dependent uponobtaining from the farmer, accurate and rel-evant historical information (a trigger factoror other reason for the disease) supported,where possible, by a PME of fresh carcasses.It is important not to rely on PME alone, notleast because the material is often too decom-posed for useful interpretation. Further labo-ratory tests to identify the presence of specifictoxins may be required.

The information you need includes:

Did the sheep die 'suddenly' or was it`found dead'? (Time since lastinspection?)Has clostridial disease occurred on thefarm before?What has the farmer done to controlclostridial diseases? Have vaccinesbeen used? (If so, closely check whatand when and if individuals could havebeen missed or colostrum not providedto affected lambs.)Were there any obvious abnormal signs?(scouring, convulsions, stiffness).Is a particular age group affected? (notethe age ranges for the different clostrid-ial diseases).Has the farmer done anything to pre-cipitate or introduce the disease? (e.g.change to better pasture or more con-centrate fed/injected with dirty needlesor irritant material/used rubber rings).What season is it? (Spring grass predis-poses to pulpy kidney and struck, flukein winter links with black disease, frostin autumn precipitates braxy.)Are the affected sheep in good condi-tion? (Clostridial diseases often 'select'the greedy, fatter animals).

Treatment

This is rarely an option and is usually unre-warding even if the animal is seen alive.

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Control

Clostridial vaccines are so cheap, so availa-ble and so effective (though no vaccine isever guaranteed 100% effective) that it isnot unreasonable to expect very few lossesfrom these diseases. However, laboratoryreports continue to show that serious lossesstill occur and that these are usually due tomistakes in application, for example: (i)choosing the wrong vaccine combination;(ii) injecting at the wrong times; (iii) 'dirty'injections (slick and clean SC injectiontechnique is needed to avoid abscess forma-tion); or (iv) just not vaccinating at all. Thevet has a significant part to play in promot-ing a suitable vaccination schedule as partof a planned flock health programme.

The recipe for control contains threeingredients:

1. Avoid the predisposing factors: in prac-tice, this really means the control of fascio-losis, the use of sterile instruments andworking in clean, dry conditions with dry,clean sheep.2. Antibodies derived via vaccination andadequate colostrum. Antisera for lambsfrom unvaccinated ewes are no longeravailable.3. Antibiotic cover (LA antibiotic) followingtrauma (e.g. assisted lambing, dog bites).

Main clostridia! diseases

These can be grouped into diseases:(i) causing enterotoxaemia affecting thedigestive system, liver or kidneys (lambdysentery, pulpy kidney, braxy, struck, abo-masitis, black disease and bacilliary haemo-globinuria); (ii) causing muscle or soft tissuenecrosis (blackleg, big head); and (iii) affect-ing nerve function (tetanus, botulism).

Lamb dysentery

This is seen in young lambs, up to about3 weeks old, caused by C. perfringens typeB. A few lambs are found dead, often only afew days old, with older lambs being affectedlater in the outbreak. A few lambs may be

seen with signs of abdominal pain beforedeath, with a hunched-up appearance.Dysentery is not necessarily present butPME usually shows haemorrhages in theintestinal walls and haemorrhagic gut con-tents. As with many clostridial diseases, thelargest, best-fed lambs are often affected. Upto 25% of the lambs in the batch may die.

Pulpy kidney

This is the most common clostridial dis-ease and is caused by C. perfringens type D.It is seen especially in the best growinglambs of around 4-10 weeks old and instore lambs being finished in the autumnon good grass or in the winter, often beingfed concentrates. Rams may be affected,especially those on supplementary feedprior to mating. Most affected lambs arefound dead as it is peracute, but some mayshow ataxia and convulsions before death.PME shows typical softening of one or bothkidneys and yellowish fluid in the pericar-dium. A quick test is to check the urine forglucose.

Braxy

This is seen in autumn and winter in lambsor shearlings, often after eating frosty grass,and is caused by C. septicum. Affectedsheep are found dead or may show abdomi-nal pain or recumbency prior to death. PMEshows acute abomasitis.

Struck

This is seen most commonly in the UK inadult sheep in spring, caused by C. perfrin-gens type C. The disease often follows achange in diet and feeding of concentrates.Signs are the classic 'found dead' with oth-ers showing dullness and recumbency.Losses are usually low. PME shows haemor-rhagic enteritis and excess fluid in bodycavities.

Acute abomasitis

Abomasitis caused by C. sordellii is seenin growing lambs of 4-10 weeks old,almost always in housed creep-fed lambs.

Sudden Death 93

These bacteria also cause toxaemia in older the jaws and limbs. It is usually unrewardinglambs and adults. to treat. For more details see Chapter 14.

Black disease

Infectious necrotic hepatitis, or black dis-ease, caused by C. novyi type B is seen inadult sheep during the winter and is associ-ated with migrating immature liver flukes.These damage the liver and give rise to theconditions which allow the bacteria to mul-tiply. The classic dark haemorrhagic appear-ance of the liver gives the disease its name.

Bacillary haemoglobinuria

This disease is caused by C. haemolyticum(novyi type D) and affects the liver and kid-neys. The disease is sporadic and uncom-mon, occurring in adults in winter, alsooften associated with migrating liver flukes.Haemorrhage in the kidneys colours theurine dark red which may cause staining ofthe wool in the perineal area. Affected ani-mals may live long enough for jaundice todevelop.

Blackleg and big head

These diseases are caused by C. chauvoeiand C. novyi type A, respectively, (malig-nant oedema is similar but caused by otherclostridia). These diseases are associatedwith injuries and wounds which allow themultiplication of clostridia in the damagedtissues and are often called gas gangrenebecause of the typical necrosis and gas for-mation which quickly develop in theaffected area. The sites affected most com-monly are the muscles of the hind limbs,shearing wounds, uterus, pelvic and peri-nea' areas in recently lambed ewes and theheads of fighting rams.

Tetanus

Affected animals are usually seen alive andshow rigidity of muscles including those of

Botulism

This is occasionally seen in sheep whichhave come into contact with manure frompoultry sheds. The bacteria multiply indecaying carcasses, producing toxins which,when ingested, cause progressive muscleparalysis. So, unlike the other clostridialdiseases in which toxins are produced frombacteria within the body, in this case thetoxin is preformed. Signs include salivationand increasing flaccidity of muscles. It isusually fatal.

Systemic Pasteurellosis

This disease is a major killer of fatteninglambs in autumn, particularly followingweaning, transport or movement on toricher pasture and should always be at thetop of the list of possible diagnoses, alongwith pulpy kidney, when losses are experi-enced in this age group. For further detailssee Chapter 13.

Toxicity

A variety of poisons, both organic and inor-ganic, cause severe illness and death. Themost common are: (i) copper (usually a resultof feeding concentrates or minerals formu-lated for cattle); and (ii) plants such as yewand rhododendron (often in sudden wintryweather when grazing is inaccessible, orfrom garden waste thoughtlessly thrown intofields). Obvious indicators may be present -jaundice and dark-coloured urine in the caseof copper toxicity, or the presence of plantmaterial in the mouth or rumen in cases ofplant poisoning. Laboratory assistance maybe necessary to confirm diagnosis.

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11

Lameness

Lameness is so common in most flocks ofsheep that many farmers regard it as a 'factof life' and give it only irregular attention(Fig. 11.1). Apart from the discomfort to thesheep, the loss in production can be consid-erable (e.g. 0.5 kg/week in the fatteninglamb) and inadequate food intake by preg-nant and lactating ewes contributes to preg-nancy toxaemia and neonatal diseases. It istherefore one of the major welfare concernsin sheep farming in the UK and worldwide.The prevalence of lameness in a flock variesgreatly with: (i) climate; (ii) pasture; (iii) age;and (iv) intensification. For example over50% of lowland lambs can be lame withscald or footrot (FR) if the weather and pas-ture conditions are suitable, whereas theprevalence in hill flocks is nearly alwayslow; similarly, many lowland sheep may belame with soil balling, a condition whichrarely occurs in hill sheep.

Techniques

Paring feet

In general, too much 'routine' paring isdone, which may actually damage feet.The emphasis should be on routine inspec-tion, with feet being left well alone inmany cases. However, overgrowth with

cracking of horn is common. Paring veryovergrown or loose horn is a necessarypart of diagnosis and treatment (Fig. 11.2)but should be done carefully with a goodpair of sharp foot clippers. Paring shouldbe sufficient only to cut away very over-grown horn or to make a clinical diagno-sis. Recent work has shown that foot paringas a part of treating relatively early casesof FR delays healing. Great care must betaken not to cut too deeply into sensitivetissues. In particular, it is very easy to cuttoo deeply at the toe causing profusebleeding. This may lead to the formationof a toe granuloma which will never healunless treated correctly.

Remember, hoof paring should nevermake the feet bleed!

Anaesthesia of the foot

For amputation of the digit, removal ofgranulomas or interdigital fibromas, IVregional anaesthesia is the best technique,though a ring block around the cannon boneis also effective.

Intravenous (IV) regional anaesthesia

Clean and disinfect the distal leg and placea tourniquet around the leg above the knee

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 95

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Fig. 11.1. Lame sheep should be examined and treated as soon as reasonably possible.

Fig. 11.2. This foot is overgrown and misshapen and requires careful trimming to investigate the cause.

or hock. Identify a suitable vein distal to thetourniquet and inject up to 5m1 of localanaesthetic. Anaesthesia develops in about10 min. The tourniquet should not bereleased for 15 -20 min to avoid potentialtoxicity problems.

Ring block

The cannon bone of the affected leg iscleaned and prepared. Then 8-10 ml localanaesthetic is injected at sites aroundthe leg. Following this procedure the leg

sometimes swells at the site of injection,so it may be worth putting a firm bandageon for a day or two.

Causes of Lameness

The main causes are:

interdigital dermatitis (ID, scald);FR - classic separation and under-running of the sole and often the wallwith a characteristic foul smell; and

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contagious ovine digital dermatitis(CODD) - separation and detachment ofthe hoof capsule starting at the coro-nary band.

Other common causes are:

soil and grass accumulating betweenthe claws (soil balling);interdigital hyperplasia (sometimescalled a 'fibroma');granuloma caused by over-trimming orother injury, or associated with FR;white line problems:0 localized tracks in the white line

with pus formation; or0 generalized white line separation

with impaction of soil and debris(shelly hoof); and

infection and sepsis in the pedal joint.

Although, as in pigs and cattle, the footis the most common site for lameness, thereare a number of important conditions affect-ing other parts of the limbs, for example:

injury;joint ill - at various ages and with arange of causes;post-dipping lameness;strawberry footrot; andnutritional myopathy.

Common Foot Conditions

See Fig. 11.3 for the main diagnosticfeatures. Recent work on ID and FR hasoverturned the traditional view of themicrobiology of these conditions (see below)and it is now clear that they should be con-sidered part of the same disease process.Often at least two feet are involved at thesame time, leading, for example, to walkingon both knees with consequent rubbing andloss of hair over the carpal joints. Sheepwith FR or ID can run about and are not easyto catch in a field, and it is often difficult topick out individually affected sheep when agroup are penned together, without turningall the sheep up which is very hard workand time consuming, but probably cannotbe avoided if a lameness problem is to beadequately tackled.

I nterdigitial dermatitis (ID, scald)

Traditionally, this has been considered to becaused by Fusobacterium necrophorumalone, but it has now been shown thatD. nodosus can initiate the lesion followingdamage to the skin of the interdigital space.If not treated, it is likely to progress to FR ifvirulent strains are involved. The main fea-tures are:

The lesion is limited to the skin betweenthe claws.This looks moist and reddened or grey-ish white, often with loss of hair.It is common in growing lambs.It is often associated with long, wetgrass in warm weather.It can affect a large number of animalsand develops quickly (overnight).It may affect more than one foot.It is likely to progress to FR unless onlybenign strains of D. nodosus areinvolved.

Most flocks are vulnerable and it is dif-ficult or impossible to eradicate, althoughsome flocks which have eradicated FR alsoreport few cases of ID.

Footrot (FR)

This is a result of the primary action ofD. (Bacteroides) nodosus with E necrophorumas a complicating factor. These are both anaer-obes. D. nodosus invades the horn resulting inseparation of the sole beginning at the inter-digital skin/horn junction near the heel. Thedegree of horn separation and severity of FRdepends upon the strain of D. nodosusinvolved (there are at least 11 strains varyingfrom benign types which cause little under-running, to virulent very aggressive forms)and may be further aggravated by other sec-ondary organisms such as spirochaetes andcorynebacteria. The main features of the dis-ease and the causal organism are:

Separation and under-running of thehorn of the sole, starting from the inter-digital space, often spreading across thesole to affect the wall (degree dependson virulence).

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Interdigital dermatitis (ID) - interdigital lesion only

Footrot (FR) - starts at interdigital space,undermines sole outwards

CODD - starts at coronary band -undermines horn of hoof downwards

White line abscess - black mark in white line,pus tracks up to coronary band

Shelly hoof - pocket under detached hoof wall;abscess may track upwards

Pedal joint abscess - claw swollen, dischargingsinuses in interdigital space and above coronary band

Fig. 11.3. Diagnostic features of foot lesions.

A characteristic necrotic smell withdirty greyish cheese-like debris underthe horn.It often affects both claws and may affectmore than one foot.Most of the horn of affected claws maybecome detached, often remaining onlyattached near the toe.

D. nodosus only lives in sheep's feet -survival on pasture is less than 2 weeks.It may also be spread by deer and cattle,but these are not thought to be impor-tant vectors and infected sheep are theusual source of infection.It only spreads in warm, damp weather,therefore spread in hot, dry summers

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and in cold winter weather is muchreduced.It does spread in winter housing, espe-cially if pens are damp and inadequatelybedded.It is less common in hill sheep becauseof the low grazing density and theorganism does not survive well onpeaty soil.

If untreated, self-cure can occur but can takemany weeks and it is unacceptable to leaveanimals untreated in the hope this willoccur. There is little naturally inducedimmunity, re-infection is common and feetmay show more than one stage of the dis-ease. As the main causal organism onlylives in sheep's feet, it is possible to eradi-cate the disease and have a FR-free flock.This can be difficult to achieve as carrieranimals are common

Contagious ovine digitaldermatitis (CODD)

This disease, which is distinct in appear-ance from ID and FR, was first reported in1994 in the UK and called 'new virulentfootrot'. It became clear that it was a differ-ent clinical entity and subsequent workimplicates spirochaetes (Treponema spp.),similar to those found in digital dermatitisin cattle, hence the name. So far, forunknown reasons, it appears to be restrictedto the UK. It is a severe disease, the mainfeatures being:

The lesion starts at the coronary band,and is often bloody in appearance.It spreads down from the coronary bandrapidly detaching the horn capsule.There is no necrotic smell as with FR.There is loss of hair above the coronaryband.If not treated, the foot may sustain per-manent damage.

Nothing is currently known about: (i) sur-vival of the organism in the environment;(ii) whether animals become immune; or(iii) whether carriers exist.

Dealing with Flock Lameness

Diagnosis

It is essential to examine a representativesample of the group or flock to establishwhich conditions are present. It is commonto have cases of ID and FR, and some flocksnow have CODD as well. The under-runningthat results from FR infection and detach-ment of horn in CODD needs to be distin-guished from the very common simpleovergrowth of the outer wall and toe, whereno sensitive tissues are involved and thesheep are not lame, and from conditionsaffecting the white line. Trimming shouldonly be sufficient to remove obviously loosehorn and confirm diagnosis, but should notcause bleeding. Treatment(s) should bebased upon a thorough understanding of thediseases present and it is likely that a com-bination of measures will be required.Picking out and treating only obviouslylame individual animals will never get ontop of a flock problem.

Possible methods of treatment

A selection of treatments will be required inmost flocks, the choice depending on: (i) thetype of flock; (ii) management; and (iii) themain problems present. For flocks badlyaffected with FR and/or CODD, whole-flocktreatment with tilmicosin (vet-only admin-istration in the UK), has been described asbeing effective, but use of this type of antibi-otic on such a scale must be seriously ques-tioned and justified.

Vaccination

An effective vaccine is available for FR andmay be curative as well as preventive so isworth considering as part of a treatmentpackage, but is not effective against any otherfoot diseases. Diagnosis therefore needs to becertain. The vaccine is in an oily adjuvantand can produce lumps at the vaccinationsite. It is dangerous if accidentally self-injected; medical advice should be sought.

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An overall improvement is usually seen fol-lowing the first injection. Timing and fre-quency of subsequent injections depends onindividual flock situation and identificationof main risk periods.

Topical sprays

Various brands of antibiotic spray are avail-able which are effective for treating ID andshould be used in addition to injectables intreating FR. Treated sheep should not beimmediately released into wet grass whichwill simply wash off the spray!

Parenteral antibiotics

Injectable antibiotics are now the method ofchoice for treating FR and CODD. Theseshould be administered to all lame sheepand any others with lesions. As mentionedabove, whole-flock treatment with mac-rolides has been questioned on the groundsof the risk of the development of antibioticresistance. After successful treatment withantibiotics every effort must be made to fol-low treatment through to prevent resurgenceof infection at a future time.

Possibilities are:

Tilmicosin (which must only be admin-istered by a vet in the UK) is effectivefor both FR and CODD and has beenused successfully (although at consid-erable cost) as a whole-group or flockblitz treatment but note concernsexpressed above.Very recently, gamithromycin has beendescribed as being successful in whole-flock treatment for FR but, as this is notlicensed for sheep in the UK and othereffective antibiotics are licensed, its usehas to be questioned.LA oxytetracycline is effective againstFR and is currently the treatment ofchoice. There are mixed reports of itsefficacy in CODD.Penicillin/streptomycin combination attwice the recommended dose has beensuccessfully used for treating FR.Amoxycillin in combination with foot-bathing with chlortetracycline has hadreasonably good results in treatingCODD.

Following parenteral antibiotic treat-ment, there is usually a rapid improvementof the foot within a few days. If cases of FRhave been treated early, paring the foot hasbeen shown to delay healing, so definitelydo not pare. If foot lesions are long standing,with overgrowth and detachment of thehorn, some careful paring may be necessarybut do not carry this out until some daysafter antibiotic treatment when healing iswell under way. Recent work suggests thefoot may regain a reasonable shape eventu-ally without paring at all though there maybe some disagreement on this point.

Footbaths

Footbathing is appropriate for treating out-breaks of ID, also as a precaution after gath-ering for any procedures in handling pens,and before housing. However, facilitiesmust be good and the bathing must be car-ried out correctly. The trend is to buildlarger, wider footbaths in which a group ofsheep can be held for the required length oftime. The volume of chemical can bereduced by placing a specially designed matin the base. After leaving the bath, keep thesheep in a concrete drying pen for at least15 min

Forma lin is cheap but unpleasant toboth the shepherd and the sheep, aswell as very painful to sheep withsevere foot lesions. In some countriesits use is not allowed. The strengthused should never be more than 5%and 2-3% is adequate and effective fortreating ID. `Walk-through' formalin iseffective, but be careful of rushing ani-mals through as the solution can besplashed into eyes. Forma lin 'goes off'quite quickly especially when contami-nated by organic matter so fresh solu-tions are needed after a few days.Forma lin hardens the horn so shouldnot be used excessively.Zinc sulfate (10%) is usually very effec-tive for FR and is the preferred treatment.Stand-in times vary according to the for-mulation of the product. Penetrationmay be aided by addition of a detergent(surfactant). For ID treatment, a stand-in

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time of 2min is usually adequate. ForFR, up to 15 min or even longer may benecessary, usually repeated weekly,though daily treatment will speed up thecure rate. Zinc sulfate does not deterio-rate and is still effective when it appearsto be very dirty. It has no adverse effecton horn.Copper sulfate solution is also effec-tive, but the potential toxicity of copperfor sheep and the environment in gen-eral means that it is should be usedwith care, and disposed of safely.A product containing copper has beenwidely used in the successful FR eradi-cation campaign in Australia.Various proprietary preparations areavailable (often containing organicacids) through agricultural merchantsand these are favoured by some farm-ers. Check that data is available on effi-cacy before recommending.Antibiotic solutions are being increas-ingly used, particularly for CODD,which may be unresponsive to othertreatments. There is nothing licensedfor use in this way, therefore theseshould only be used if no other treat-ment is effective. Antibiotic footbathsare effective against scald and FR andfarmers will want to use them for treat-ing these diseases. The legal back-ground should be pointed out. Thosecommonly used are lincomycin/spec-tinomycin and tylosin, and chlortetra-cycline has also been used. The dilutionrate used is 1 g/1 water. For CODD, thishas been used as a hand spray to treatindividually affected animals andseems to be effective if repeated severaldays in succession, but obviously doesnot address a flock problem.

Control

Chronically lame sheep are a serious wel-fare problem. In the UK in 2011, a FarmAnimal Welfare Council report said that theextent of lameness was unacceptable andmust be reduced. Most shepherds routinelytrim and footbath, but there is often noplanned control and sheep and shepherd

live with FR. The more energetic the pro-gramme, the more effective is the control.For every lame sheep treated, there will beseveral others with less obvious disease.Frequent use of handling pens may actuallyincrease the spread, therefore these shouldbe cleaned frequently and all sheep foot-bathed every time they pass through thepens, even if for some other procedure.

For ID or mild FR - regular (weekly)footbathing in weak formalin (now notused in some countries because of pos-sible carcinogenic effect) or zinc sulfateshould be effective. In small flocks,spraying affected individuals with anti-biotic spray is effective.For FR where there is a severe or viru-lent form present, antibiotic injection isbecoming favoured rather than repeatedfootbathing because this is less timeand labour intensive. However, repeatedfootbathing in zinc sulfate (stand-intime at least 15 min for clinical cases)has been effectively used over manyyears. Vaccination is also helpful.Separation of infected and uninfectedanimals, with the infected group treatedseparately until cured, is likely to leadto a better outcome.For CODD only, tilmicosin injection, oramoxicillin injection combined withantibiotic footbathing may be the bestoptions.If CODD and FR are present, the abovetreatment for CODD will be effective forFR as well.

Having got lameness under control, it isthen crucial to: (i) carefully monitor the sit-uation; (ii) treat newly lame animals as soonas possible; and (iii) re-impose group orflock treatments if the incidence starts toincrease again.

Eradication of FR

FR has been eradicated in some flocks in theUK but the main area in which success hasbeen achieved is in Australia. In New SouthWales the number of properties with viru-lent FR has been reduced from 6000 to 15 asa result of the combined efforts of vets,

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farmers and other advisors. It has helpedthat there is much more of a willingness tocull affected animals or even whole flocksthan there is in the UK. It also helps thatthere are predictable weather patterns withlong, dry periods when the disease is nottransmitted.

FR has only recently been recognizedas a problem in Scandinavia and seriousattempts to control or eradicate are beingmade.

Eradication is a difficult and time-consuming exercise and by no means cer-tain. It certainly requires that the farmer beprepared to examine all feet, pare suffi-ciently to determine presence or absence ofinfection, separating clean and infectedsheep, and to treat everything that is infected.In Australia parenteral injection of antibi-otic is now favoured over footbathing duringthis phase. Persistent cases are culled.Eradication must include safeguards againstre-introduction and this means maintainingself-contained flocks (including adequatesheep fencing) or inspection and eradicationof infection in purchased sheep. Few flocksin the UK, particularly the large ones, canmanage all this. It is best to attempt it whenmost of the lambs have been marketed andold ewes culled, but before tupping. It is alsowise to choose a time when there are fewercases, brought about perhaps by a previousvaccination programme and in a period ofdry weather if possible.

Other Foot Lameness

White line lesions

There are two common types of white linelesion: (i) shelly hoof; and (ii) white lineabscess. Shelly hoof occurs when a pocketdevelops beneath the outer wall of one ormore claws. This then becomes impactedwith soil and grit. When the loose horn ispared away, a characteristic half-moon appear-ance of the wall results, with the underlyinglaminae visible. Lameness does not occuruntil the impacted soil is pushed into thedeeper sensitive laminae when pus forms.

The sheep then develops acute lamenesswhich is not relieved until the pus is eitherreleased by paring or bursts out after trackingup to the coronary band.

White line abscesses develop in smalldiscrete tracks in the white line which againcause acute lameness and can sometimes bevery difficult to locate, although the affecteddigit should be identifiable by pain responseand the presence of heat. Careful paringmay release pus.

For both types, if careful paring doesnot find pus, application of a poultice cov-ered with a polythene bag and bandaged,left on for a couple of days will soften thehorn and encourage bursting, or at leastmake re-examination easier. Treating withinjectable antibiotics may suppress but noteliminate infection, so may actually prolongthe duration, but it would probably take abrave person to withhold antibiotics from avaluable animal! Once the pus has beencleared, healing occurs leaving a loose pieceof horn which can be trimmed

Foot abscess (pedal joint sepsis)

Infection of the pedal joint is a serious con-dition which needs to be differentiated fromwhite line lesions. There is severe pain(10/10 lameness) with obvious swelling ofthe digit and pus bursts out at several sitesaround the coronary band. One theory isthat infection gains access from the inter-digital space, but this is not proven and it ispossible that infection may be blood-borne.Radiography will help to decide if the jointis involved, as will careful examinationwith a probe. For early cases, irrigating thejoint via a cannula inserted either through alateral coronary band sinus, or by drillingthrough the lateral hoof wall into the jointhas been described and may lead to a satis-factory result. Either of these forms of treat-ment should be carried out under regionalanaesthesia. If recovery is not rapid afterthis form of treatment, amputation, which isrelatively cheap and easy, should be consid-ered, and certainly immediately for caseswhere treatment has been very delayed.

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Amputation of a digit

This should be carried out under regionalanaesthesia as described previously. Cleanthe lower limb and shave the skin above thecoronary band. When anaesthesia has devel-oped, incise through the skin all the wayaround the affected claw about 0.5 cm abovethe coronary band. Take great care in theinterdigital space that the incision does notdamage the opposite claw. Then remove theclaw either by sawing through the lower endof P1 using an embryotomy wire, or disar-ticulate the joint between P1 and P2. Place anon-stick dressing over the wound, packwith cotton wool and bandage tightly. Coverwith waterproof tape. Then release the tour-niquet. The bandage can be removed 2-3 dayslater. Opinions vary about re-dressing - somepeople prefer to leave the wound open,others prefer to re-bandage for a bit longer.In any case, the animal should be kept inclean, dry conditions until healing hasoccurred. This takes about 3 weeks.

Interdigital hyperplasia ('fibromas')

Fibrous outgrowths in the interdigital space(mainly hind feet) are a feature of somebreeds. Lameness occurs only when theybecome ulcerated and infected. Frequentfootbathing maintains some control, but theworst cases require simple surgical removalunder local anaesthesia; this is not a job to bedone just before tupping time but should beidentified and carried out well in advance.

Toe granulomas

Most large flocks have a few sheep withstrawberry-like granulomas, usually at thetoe, often the result of over-paring, but alsofollowing injury or FR. Although loose hornwill grow over and partly hide the lesion,healing will never occur without radicaltreatment. Loose horn should be pared away(made easier if the foot is anaesthetized), thegranuloma cut off after application of a tour-niquet to the leg, and the base cauterized

(a calf disbudding iron is suitable).Alternatively, repeated application of anastringent such as copper sulfate or formalin(5%) may eventually work.

Post-dipping Lameness

This is caused by Erysipelothrix rhusio-pathiae which can invade broken skin. Atthe time of dipping, this organism, which ispresent in soil, can seriously contaminatethe dip solution and enter limb wounds sus-tained in the dipping process. The diseasehas also been reported in the absence of dip-ping, after sheep passed through verymuddy pens. Within a day or so, manysheep may be very lame with a local celluli-tis of the hairy parts of the limbs. Earlytreatment with penicillin is essential. Infuture, ensure that dip and/or handling pensare cleaned before use. Contaminated dipshould not be used after standing overnightespecially in warm weather.

Joint Infections

Young lambs up to 1 month - mainly lowland

Polysynovitis and arthritis, particularly ofthe stifle (soft, bulging and painful synoviain the patellar region), carpus and hockjoints, follow a septicaemia possibly frombacteria gaining entry via the navel, tonsilsor gut. The lambs appear miserable andcrouched with flexed joints and arched backand are reluctant to move about. The mostcommonly isolated organisms are:

Strept. dysgalactiae - this is becominga widespread problem, with source androute of infection not clear as it is foundin well-managed flocks with goodhygiene standards.Other opportunistic bacteria includingE. coil and A. pyogenes.

Control is not always easy as it is notalways obvious what is at fault. Navel treat-ment and lambing pen hygiene should bechecked - is the navel dipped or sprayed?

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How effectively? Is a contaminated dipbeing used? Is cow teat dip, which is emol-lient rather than astringent, being used? Iscolostrum intake adequate? Are hygieneprocedures such as tailing, docking and eartagging adequate? If all possible predispos-ing factors have been dealt with, injection oflambs with a single dose of antibiotic (peni-cillin should be adequate) as a preventivemeasure can be considered as a last resort.As the problem may not recur in futurelambing times, this should not become aprocedure carried out routinely each year.

There is some evidence that Strep. dys-galactiae can be found in the posteriorreproductive tract of ewes, so lambs maybecome infected during and immediatelyafter birth. Use of disposable gloves for han-dling lambing ewes and newborn lambsmay help to reduce spread of infection.

Lambs over 2 months - lowland

Stiff lambs/erysipelas arthritis

On some farms, a significant number of fat-tening lambs at grass show a stiff, stilted,short-striding walk or hopping run, appear-ing to be lame on more than one leg. Verycareful examination and palpation disclosessome synovial swelling, general thickeningand pain in some limb joints, particularlythe stifle, hock and carpus. Although prob-ably infected soon after birth, the conditionis insidious and often irreversible by thetime it is recognized. E. rhusiopathiae is themost common organism causing this chronicfibrinous synovitis and arthritis. Often theorganism cannot be isolated from the jointsbut a blood titre of 1/320 and over indicatesthis infection. Badly affected animals shouldbe killed on humane grounds, but it is worthtreating less severe cases for which penicil-lin should be effective. Such lame sheepneed housing so that more intensive treat-ment and feeding can be applied and wherethey do not have to walk far for food or shel-ter. Repeated penicillin treatment is advisa-ble. Vaccination is effective, but relies oncolostral transfer of antibodies, thereforevaccinating ewes in late pregnancy (as forclostridia) is necessary.

In the USA, polyarthritis in lambs hasbeen associated with Mycoplasma spp. and,in fattening lambs in feedlots, withChlamydophila infection.

Lambs up to 4 months - hill

Tick-bite pyaemia, following tick bites andstaphylococcal septicaemia is the usualcause (see Chapter 16).

Adult sheep

Joint infection as a result of injury may be aproblem in individual adult sheep, leadingto visible swelling of the affected joint(s).Early treatment with a prolonged course ofpenicillin is necessary if this is to be suc-cessful. Delay leads to irreversible jointdamage and welfare issues in affectedanimals.

A chronic degenerative arthritis of oneor more joints, particularly elbows, butsometimes shoulders, hips and stifles isquite often seen in elderly sheep. Elbowsshould be carefully examined for character-istic thickening and restricted flexion. Suchsheep become progressively more lame andthin and need very careful attention. Cullingshould be advised.

Vitamin E and Selenium Deficiency

Deficiency of either selenium or vitamin E,or both together, lead to problems affectingmuscle function variously known as whitemuscle disease, stiff lamb disease, nutri-tional myopathy or nutritional musculardystrophy. Many areas of the world (e.g.parts of northern Europe, Australia andNew Zealand) have soils low in seleniumcontent. Vitamin E content is high in freshgrass but falls in stored forage and grain, sodeficiencies can be made worse if home-produced diets are fed.

This is essentially a disease of younglambs which are growing fast. Predisposingfactors include: (i) feeding only home-grownfoods; (ii) adding preservatives to straw and

Lameness 105

cereals; and (iii) use of artificial fertilizerswith high nitrogen (N) and sulfate (SO4),promoting rapid grass growth. Selenium-responsive ill-thrift in lambs has beenreported in some countries as has early fetaldeath leading to barren ewes and theincreased susceptibility to disease becauseof reduced phagocytic activity.

Clinical signs

The usual picture is that thriving younglambs (50% occur at 0-30 days old and 25%at 30-60 days old) have just been turned outto fresh spring grass and within a few hoursor days of running around, a few are founddown and reluctant to get up; one or twomay also be found dead due to cardiac fail-ure. Those that are able to stand if forced toget up, take a few tottering steps, showingparticular stiffness in the shoulders, and liedown again, looking alert and not uncom-fortable. Some may show distressed respira-tion due to failure of respiratory or cardiacmuscles, and pneumonia is a secondaryrisk. This situation is, at first, easily con-fused with pulpy kidney, pasteurellosis,swayback, polyarthritis, spinal abscess andinjury.

Diagnosis

Suspicion arises if there has been previ-ous evidence of selenium deficiency onthe farm and, in particular, if the flockis receiving little concentrate and novitamin/mineral supplement and alsoif a lot of roots and/or poor qualityroughage is being fed.The sudden onset in several otherwisehealthy-looking lambs (often the fastestgrowing) should point to this conditionand the absence of obvious signs ofinjury and arthritis should increase thesuspicion.Necropsy should eliminate pulpy kid-ney disease and pasteurellosis, butnote that the muscle lesions are bilat-eral and therefore no comparisons arepossible within the lamb and that if

there is cardiac involvement, the lungsmay look congested.If analysis of plasma and whole blood(green tubes) from affected lambs showplasma creative kinase (CK) levels ofover 1000 IU/1 this indicates severemuscle damage, but the blood must betaken very early, as concentrations dropin a few days; and whole blood GSHPxis often <1 unit/ml.If analysis of whole blood (green tubes)from ten apparently healthy contactsshow suspiciously low levels of GSHPx(i.e. <20units/m1).Inject with vitamin E and selenium andsee whether there is a response (it maytake a few days).

Treatment

Inject with vitamin E and selenium,and repeat the next day if there is notmuch improvement. Usually there is agood (diagnostic) response if caughtearly.Rest the affected lambs - bring inside.Consider giving an NSAID injection toaffected lambs - this can make themmore comfortable and speed recovery.

Prevention

Be careful if recommending products con-taining several trace elements, particularlythose containing copper as accidental cop-per poisoning may occur in copper-sensitivebreeds.

Ensure there are adequate levels of sele-nium and vitamin E in the diet of ewesin late pregnancy: avoid low seleniumfoods (e.g. turnips), and feeds whichreduce vitamin E concentrations (e.g.treated grain, spoilt hay, oil seeds).Ensure a dietary concentration of0.1 mg/kg DM for selenium and30-50mg/kg DM for vitamin E.Inject ewes in the third month ofpregnancy with a selenium/vitamin Epreparation.

106 Chapter 11

Short-term control in lambs can beachieved by injecting them at strategictimes, such as shortly before turnout orfolding on roots.Some anthelmintics contain addedcobalt and selenium. These might besufficient to help lambs with marginaldeficiencies in the short term.Long-term control can be provided bysupplementing with selenium by vari-ous methods including:0 An annual injection to lambs at

weaning and to pregnant ewes, of aLA barium-complex of selenium.

Dosing at strategic times (tupping,lambing, weaning) with a proprie-tary trace element product contain-ing selenium.

0 Dosing weaned lambs and eweswith LA selenium pellets - thesegive 3 years protection.

0 If multiple deficiencies of copper,cobalt and selenium, or zinc, cobaltand selenium occur (particularlyon upland farms), it is worth con-sidering use of soluble glass bolusescontaining these minerals. Thesegive about 6 months protection.

12

Skin and Wool

Although a number of specific conditionsaffect the skin and wool of sheep (seeTable 12.1), it must be remembered thatbecause the production of wool is an activeprocess, many systemic diseases will resultin local or generalized loss of wool (Figs 12.1and 12.2). In addition, primitive sheep shedthe fleece in early summer, a feature whichis still seen to a limited degree in somebreeds and crosses.

Disorders Associated with Pruritus

Correct diagnosis is very important. Mostoften, scab or lice is the cause but infectionwith both parasites is possible. Treatmentshould be appropriate for the diagnosis -incorrect treatment based upon farmerdiagnosis or assumptions without confir-mation of presence of the parasite, hasresulted in the development of resistanceto some of the available (ever-reducing)treatments. Always check for the latestinformation on drug use as availability,indications for use and withdrawal peri-ods may change.

The flock should be viewed from adistance to obtain some indication of theproportion of ewes showing signs of pruri-tus: (i) restlessness; (ii) stamping of feet;(iii) rubbing against posts; or (iv) nibbling or

biting at areas of the body. Individual affectedsheep should be examined to:

determine the areas affected;establish the nature of the lesionsincluding involvement of the skin;discover the location of visible parasites(use a hand lens); andtake specimens from active lesions forfurther examination.

Parasitic conditions

Sheep scab (psoroptic mange)and other mites

Sheep scab occurs in most sheep-keepingcountries, although North America andAustralasia are free of this disease. It was anotifiable disease in the UK for many yearsand was eradicated from the country bycompulsory dipping in 1952. Unfortunately,after years of freedom, sheep imported fromIreland in 1973 reintroduced the disease anddespite compulsory dipping regulationswhich exerted some control, outbreaks con-tinued to occur every year. In spite of a ris-ing number of outbreaks, control wasderegulated in 1992 although it is once againnotifiable in Scotland. Control is the respon-sibility of farmers. In Scotland, treatment orslaughter of infected sheep is compulsory.

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 107

108 Chapter 12

Table 12.1. Summary of conditions affecting skin and wool.

Condition Cause Pruritus Area affected

Non-infectiousNatural sheddingWool breakWool slipSunburnPhotosensitization

ParasiticSheep scabEar mitesFoot and scrotal mangeLice

KedsBlowfly strike

HeadflyInfections

Mycotic dermatitisStaphylococcal

dermatitisGaseous

lymphadenitisActinobacillosis

Fleece rotOrfStrawberry foot rotRingwormUlcerative

balanoposthitis/vulvitisScrapie

GeneticIllness, debilityWinter shearingLack of pigmentPhotodynamic plant, liver

damage

NoNoNoNoYes when healing

Neck, back, bellyBodyFlanksEarsFace, ears

Psoroptes ovis Intense BodyPsoroptes cuniculi Head shaking EarsChorioptes bovis Medium Lower legs, scrotumBovicola ovis Medium BodyLinognathus ovillus Slight HeadLinognathus pedalis Medium-severe LegsMelophagus ovinus Little BodyLucilia sericata Intense Breech, shoulderPhormia terrae-novaeHydrotaea irritans Intense Head, base of horns

Dermatophilus congolensis LittleStaphylococcus aureus Little

Corynebacteriumpseudotuberculosis

Actinobacillus lignieresi

Pseudomonas aeruginosaParapox virusD. congolensis and orfTrichophyton verrucosumStreptococcus zooepidemicus?

Spongiform encephalopathy

No

No

NoNoNoNoNo

Back, ears, nosePeriorbital, nose,

legs, teatsAbscesses in lymph

nodes esp. parotidHead and neck

abscessesBodyLipsLower legHeadPrepuce, vulva

Usually intense Tail, flanks, head

In other parts of the UK, owners of infectedsheep can be prosecuted under various wel-fare regulations if the sheep are judged to besuffering unnecessary pain or distress.Regulations introduced in 1977 allow localauthorities to take action where farmers donot, particularly on common grazing. It isalso illegal to sell infected animals otherthan direct for slaughter.

EPIDEMIOLOGY The disease is caused by anon-burrowing mite, Psoroptes ovis, whichis specific for sheep. It is highly contagious,and is usually spread by direct contact,often being introduced by the purchase ofinfected sheep, or spreads among sheep on

common grazing. The mite can also live forabout 16 days in pieces of scab or wool, onfences, etc. and can be spread by contami-nated shears or clothing.

The mites 'graze' on the skin surface,feeding on skin secretions. Rapidly extend-ing moist lesions develop from the pustulesat the feeding sites, the skin reaction beingdue to hypersensitivity to the mite excreta,rather than to the mites themselves. Sheepshow signs of extreme irritation with head-tossing, occasionally even developing epi-leptiform fits, and rub vigorously and nibbleat the affected areas which are particularlyover the shoulder and flanks. The fleecebecomes stained and matted with loose tags,

Skin and Wool 109

progressing to areas of wool loss and bleed-ing often extending, in neglected cases, tomost of the body. Severe infections result inmarked loss in condition and death.

Fig. 12.1. Wool growth is an active process, somebreeds such as this Wensleydale producing heavy,long fleeces.

The mites are capable of enormousmultiplication over a relatively short timewith maximum numbers occurring 6-12weeks after infection. It is now known thatthere are different strains, which vary invirulence. The disease is most active duringthe winter, though latent infections withsmall numbers of mites are common in thesummer, with a flare-up to typical diseasein autumn and winter.

DIAGNOSIS In typical outbreaks of sheepscab, when a high proportion of the flock isaffected and lesions are severe, diagnosis isstraightforward since the white mites canjust be seen with the naked eye. Whenmites are not so numerous, superficial skinscrapings should be taken from the edge ofthe lesion for microscopic examination(add 10% KOH to clear skin debris).Psoroptes has well-developed legs whichprotrude beyond the body, and the first twopairs of legs, in both male and female mites,end in bell-shaped suckers which havelong, segmented (the diagnostic feature)pedicels.

A number of other mites are found onsheep, including Chorioptes bovis, usuallyon the legs, scrotum or brisket (see later)and tyroglyphid or forage mites which canbe found all over the body and which,

Fig. 12.2. This Texel ewe has wool break following a difficult lambing.

110 Chapter 12

though they are non-parasitic, occasionallycause pruritus.

TREATMENT AND CONTROL Always check thelatest information as availability andinstructions for use may change. The rangeof available products has decreased as syn-thetic pyrethroid (SP) dips are no longerallowed to be used in the UK because oftheir severe effects on the environment(they are much more toxic to wildlife, espe-cially in watercourses, than are organophos-phates (OPs)). This leaves only:

Diazinon dip (an OP) - this will treat andprevent reinfection for about 4 weeks(the withdrawal period is 70 days). Fortreatment, sheep must be in the dip for1 min and must be completely submergedat least once.Injectable avermectin or milbemycin -there are four possible products. All havelong withdrawal periods (6-15 weeks).Remember these are also anthelminticsso how they integrate into worm controlmust be taken into account.

O Ivermectin - this has no residualaction therefore two treatments areneeded 7 days apart to make sureall the mites are killed. It has noprotective action.

O Moxidectin 1% - this can be usedfor protection (28 days) and treat-ment (two injections at a 10-dayinterval).

O Moxidectin 2% LA - this is admin-istered as a single injection fortreatment and protection for up to60 days.

O Doramectin - this is administeredas a single IM injection for treat-ment and control.

Pour-ons are not suitable for treatingscab as some mites are exposed to a suble-thal dose of chemical. Resistance to SPs hasalready been reported in the UK; this almostcertainly developed as a result of repeatedapplication of SP pour-ons.

Concern has been expressed over thetoxicity of OP compounds for those dippingthe sheep and this has brought about licens-ing of those who use them and, overall, a

reduction in routine dipping. Alternativesbeing used include showers, sprays and jetsto apply chemicals, but OP dips are notlicensed for use by any of these methodsand only dipping is effective for scab treat-ment. There are strict rules about safe dis-posal of dips.

Psoroptes otitis

A sub-strain of Psoroptes (probably cuniculi)appears to have become adapted to living inthe ears of sheep. Affected sheep show headshaking, often with a purulent dischargefrom the ears, and a number develop auralhaematomata. This infection can be presentin flocks with no classic scab, and does notappear to spread from the ears to the body.Diagnosis can be confirmed by examiningswabs or washings from the ears for mites.Treatment is by two doses of ivermectin ormoxidectin 1% injected 7-10 days apart, ora single injection of doramectin or moxidec-tin 2%.

Chorioptic mange (C. bovis)

These mites colonize mainly the scrotum oframs or the udder of ewes and the lowerlegs, and are becoming common in somebreeds. Affected animals show itching ofthe legs (e.g. rubbing against troughs or onfence wire). Affected rams show thickeningof the skin of the scrotum which maydecrease fertility. Mites live in small colo-nies and are most easily picked up by usinga tape strip, rather than a skin scraping. Themites are surface feeders of skin debris,therefore treatment by injectables is noteffective. Dipping with diazinon is the onlycurrent treatment option.

Sarcoptic mange (Sarcoptes scabei)

This is not present in the UK or northernEurope but may be a problem in countriesin the Middle East, Asia and Africa.

Lice and keds

There are two types of lice: (i) chewing,Bovicola (Damalinia) ovis; and (ii) sucking,Linognathus ovillus and Linognathus pedalis.The sheep ked, Melophagus ovinus, is a

Skin and Wool 111

wingless fly and has made something of acomeback since the reduction in dipping.The life cycle of these highly host-specificinsects is similar, with all stages on the sheep.Adults live for only a few days off the sheep.

Infestation with lice has become a sig-nificant problem in the UK since dippinghas become less common. Lice are a majorproblem in Australia where they adverselyaffect wool production (the most importantsheep product) and in New Zealand wherethey cause downgrading of skins (an impor-tant by-product of the meat lamb industry)with an abnormality called 'cockle' (alsoseen in the UK).

Clinical signs are similar to sheep scab,hence much confusion, with heavy infectionsleading to irritation involving a high propor-tion of the flock with resulting rubbing, nib-bling and damage to fleece. Populations arehighest in the winter months. Keds are largebrown insects and are easily seen but lice maybe difficult to see. A few staples of wool shouldbe clipped from the edge of a lesion and exam-ined in a bright light with a magnifying glassfor adults and eggs attached to the wool.

Lice and keds are mostly susceptible toinsecticidal drugs including diazinon (bydipping) and SPs (pour-on), although resist-ance to SPs is developing. Sucking lice andkeds (but not chewing lice) are susceptible tothe systemic endectocides (ivermectin, etc).Treatment is usually carried out in the autumnor winter. If infested sheep have a heavyfleece, it is better to treat after shearing.

Resistance to SPs is particularly a prob-lem in Australia. This develops if the chem-ical is not applied in sufficient amounts tothoroughly saturate the fleece, which occurscommonly when automatic jetting races areused rather than showers or dips. Insectgrowth regulators have been used as analternative but resistance has also devel-oped to these products.

Blowfly myiasis (flystrike)

Strike is a common condition seen through-out the summer months in the UK (andfound in many other parts of the world) inwhich larvae of Lucilia sericata (green bottlefly), Phormia terrae-novae (black blowfly)and Calliphora erythrocephala (bluebottle)

invade the skin under soiled fleece, result-ing in extreme discomfort and rapidly lead-ing to death. The most common areas whichare affected are: (i) around the breech associ-ated with soiling due to scouring; (ii) on theside of the body where fleece is contami-nated from FR lesions when the sheep liedown; and (iii) in various sites associatedwith wounds. Affected animals are restless,show vigorous wagging of the tail when thebreech is affected or biting at affected areasand are often separated from the flock. Thelarvae of the flies, which develop within afew days from the eggs laid in the moist con-taminated area, burrow into the skin andcause a foul-smelling wound. This extendsrapidly as a result of secondary strike. Withearly lesions a careful hunt has to be made tofind the maggots. It is important that flocksat risk should be examined at least once aday to detect early cases as affected animalsdie within a few days of the initial attack.

Affected areas should be clipped andthe maggots removed physically. An SPpour-on will kill the maggots and protect thearea against further strike. Since secondarybacterial infection is common, injections ofantibiotic are valuable and an NSAID injec-tion will also help.

CONTROL This is by application of a suit-able product in the early summer. Choicesare:

Diazinon dip (30 seconds in dip) willcontrol blowflies for about 8 weeks.SP (cypermethrin) pour-on will treatand protect for 8-10 weeks.Insect growth regulator pour-on - eithercyromazine which protects for 10 weeksor dicyclanil which protects for about8 or 16 weeks depending on the partic-ular product. Note that these productsdo not treat, therefore they must beapplied before the eggs are laid.

Control of the factors predisposing to strike,especially faecal soiling, is also criticallyimportant.

Screw worms

Fortunately northern Europe and Australiaand New Zealand are free of these flies which

112 Chapter 12

lay eggs in a similar manner to blowflies, butwhose larvae (screw worms) are very inva-sive and difficult to control. Australia ispotentially at risk because of their presencein New Guinea. They are a great problem inparts of South America but an eradicationprogramme using irradiated, sterile maleshas cleared them from the USA, Mexico andCentral America.

Headfly

This disease is caused by a non-biting mus-cid fly, Hydrotaea irritans, which swarmaround the heads of sheep, causing rubbingwhich leads to self-trauma. The flies thenfeed on the exudate of blood and lymph,which leads to further attacks. The area wherehorns and skin join is often the site of smallbreaks in the skin which probably explainswhy the condition is particularly importantin horned breeds, but any open wound isliable to attack. The disease is most commonin the North of England and south of Scotlandbut the fly occurs throughout the UK. Thewounds do not heal while the flies are activeand extensive lesions involving much of theskin of the head are produced. Loss in condi-tion and disfigurement of the skin occurs.

The flies are active from late June untilthe end of September on still, warm humiddays and there is only a single generation offlies each year. Non-feeding females rest intrees and can fly 0.5 km/day. Each femaleproduces one or two batches of about 30 eggswhich hatch to larvae in pasture soil (notdung) from September to May especiallynear woods. Pupae are found near the soilsurface from May to June. The flies can feedon a variety of animals; meal analysis showsthat about 80% feed on cattle.

Many methods of control have beentried; none is entirely successful, but the mosteffective method is the application to the topof the head and base of the horns of an SPpour-on (cypermethrin). In areas of high chal-lenge, the treatment will have to be repeatedat least every 6 weeks while flies are active.

Ticks

See Chapter 16.

Midge hypersensitivity

This has been seen affecting individuals orsignificant numbers in several breeds, par-ticularly those with black wool (Black WelshMountain) or black belly wool (Torddu). Itseems to resemble sweet itch in horses andis seen from early May to autumn, whilemidges are active. Affected animals showsevere itching and discomfort with thick-ened, scabby, often bleeding lesions on thehairy parts of the body, especially face, ears,ventral abdomen, udder and perineum.Control is by improving the habitat to makeit less attractive to midges (cut overgrowngrass) and application of an SP pour-onbefore midges become active.

Non-parasitic conditions

Scrapie

Scrapie should be suspected when an indi-vidual adult sheep begins to rub, nibble orsuck its fleece for no obvious reason, lead-ing to bilateral semi-bald patches on itsflanks, hind legs, bridge of the nose and topof the head. The skin and fleece appear nor-mal except for self-inflicted healing scabs.The irritation is increased by firm fingerrubbing of the back and itchy areas. Otherneurological signs are often present (andsometimes on their own) and there is aworsening over days/weeks. Scrapie is noti-fiable. For details see Chapter 14.

Disorders with Usually Littleor No Pruritus

Infectious

Orf (contagious pustular dermatitis,scabby mouth)

This disease, which occurs worldwide, is aconstant worry to sheep farmers as shownby the priority that they give it for furtherresearch. If it occurs around lambing, itthreatens to develop into an outbreak andspread to the teats of ewes, which in turn

Skin and Wool 113

can lead to difficulty for lambs to suck andmastitis developing in the ewe. Later in theyear, it can disrupt sales of fat or breedinganimals. Occasional cases also inexplicablydevelop extensive and persistent lesions.It is a zoonosis so there is a risk of spreadto shepherds, particularly those caring fororphan lambs; lesions on the fingers, face orneck are, at best, irritating and painful, andat worst there is a very marked reaction withlocal lymphatic involvement. Doctorsare often unfamiliar with this infection -sometimes the vet diagnoses it first!

Control measures are difficult and theepidemiology of the condition remainsunclear. However, while the appearanceand site of the lesions in and around themouth suggest a lot of discomfort and inter-ference with sucking and grazing, manylambs survive without problems, most casesself-cure in a few weeks and the incidencein most flocks remains low.

Orf is caused by a parapox virus whichsurvives in dry scabs, from year to yearindoors, but for shorter periods outside;small scabby lesions on the hairy areas ofthe face and limbs are also persistent sourcesof the virus; it is susceptible to iodophordisinfectants. It has a distinct shape andsize and is easily recognized by electronmicroscopy (EM), although it is morpholog-ically indistinguishable from the paravac-cinia (pseudo-cow pox) virus found in teatlesions of cattle. It has an affinity for hairyareas particularly at the weak junctionsbetween skin and mucosae (e.g. commis-sure of lips) but it requires some surfacedamage to allow invasion (e.g. splitting oflips, eruption of incisors, rough grazing andteat sores following vigorous sucking andincisor injury by hungry lambs).

The lesions are characteristic and diag-nostic, although when in doubt, unpreservedscabs should be sent to the lab for EM exam-ination. They start as raised red papuleswhich coalesce and in a few days proceedthrough vesicles and pustules to thick scabformations which are firmly attached towhat looks like exuberant granulation, andremoval causes haemorrhage. Secondarymixed bacterial infection is common andexaggerates the local response. The lesions

are often confined to the outside of the lipsand are sometimes barely noticeable, but inyoung lambs, granulomatous lesions mayoccur within the mouth, involving the gumsand sometimes the tongue. Despite theirappearance, the lesions do not appear tocause much distress unless particularly exu-berant and extensive, and while there maybe some lambs who fail to thrive, most willself-cure within 3-6 weeks. The situationbecomes much more serious, however, ifand when the lesions secondarily arise onthe teats of ewes (see Chapter 8).

TREATMENT Individual severe cases shouldbe separated to ensure proper nursing withdaily application of antibiotic to tackle sec-ondary bacterial infection. Ewes should beinspected for teat lesions and these shouldbe treated with antibiotic. Ointments con-taining local anaesthetic may allow lambsto carry on sucking until healing occurs; inextreme cases it may be necessary to weanand hand rear their lambs (easier said thandone as lambs will often refuse a bottle,plus the risk of frequent handling) and todry off the ewe following infusion of LAantibiotic. Where necessary, sheep shouldalso be removed from pastures that appearto be causing face or limb abrasions (e.g.thistles). Where possible, contaminatedpens should be cleaned out and disinfectedbefore re-use, and again at the end ofhousing.

PREVENTION Immunity following primaryinfection is incomplete and short-lived, per-haps only a few months, but subsequentinfections are likely to produce milderlesions which heal more rapidly. Immunityis largely cell mediated and althoughhumoral antibodies are produced, they arenot protective, and therefore neither iscolostrum.

A vaccine is available which consists oflive virus. It is applied by skin scarification,usually on the hairless area of the innerthigh. Its efficacy and timing is debatablebut it probably shortens the recovery time ifnot preventing infection. It is commonlyapplied to ewes in early or mid-pregnancy,especially to those which will be housed at

114 Chapter 12

lambing, in an attempt to reduce the weightof infection in carriers, and to protect theteats. It is sometimes applied to lambs in thesummer a few weeks before sale, in anattempt to avoid lip lesions and subsequentrefusal at markets. It is also sometimesapplied to young lambs in contact withinfections, or where there has been a previ-ous history of disease, and even to thosewith lesions, in an attempt to prevent orcontrol an outbreak; the consensus seems tobe that this should be a last rather than afirst resort. It certainly should not be usedon ewes within 7 weeks of lambing nor inflocks that have no history of the disease, asthe induced scabs are a source of furtherinfection. The vaccine, like the naturalinfection, needs to be handled with care. Itshould never be used in a flock without aprevious history of the disease.

Strawberry footrot

Occasionally lambs at pasture, often in wet,muddy and abrasive conditions, developorf-like granulomatous lesions on the skin ofthe lower limbs particularly around the cor-onary bands, making the lambs obviouslylame. The condition does not involve thefoot and has no resemblance to FR, but thegranulation tissue is likened to a strawberry.Orf virus particles can usually be isolatedfrom the scabs, but so also can Dermatophiluscongolensis, the organism more commonlyassociated with lumpy wool; it is uncertainwhich gets there first! Treatment should befor both, which means local dressing andsystemic antibiotic. The lambs need to beremoved to dry pasture or housed. Somecases are particularly persistent and exten-sive, like other forms of orf, and these requireeuthanasia.

Ulcerative balanoposthitis (pizzle rot)and ulcerative vulvitis

It is quite common to find a scabby ulcera-tive lesion at the junction of the skin andmucosa of the prepuce in rams and vulva inewes. Raw, bleeding tissue is exposed if thescabs are removed, rather like orf, but thelesion is ulcerative rather than proliferative

and it is unusual to find orf virus particles.In some cases in rams, the ulceration is con-fined to the glans penis and therefore goesunnoticed. The incidence can be quite highand is sometimes associated with tuppingtime, suggesting venereal transmission.

Most cases self-cure or remain as minorlesions and there is no interference withbreeding or fertility. However, occasionallythe lesions are extensive with swelling,superficial sepsis and necrosis; in rams thismay mean the involvement of both the glanspenis and the mucosa of the sheath whichbecomes noticeably pendulous; subsequentscar tissue may interfere with breeding.

The cause is still uncertain, althoughureaplasms or Streptococcus zooepidemi-cus have been found in some outbreaks.Antibiotic aerosol spray is adequate for mildcases, but the more severe ones require sys-temic antibiotic and frequent local dressingand irrigation.

Staphylococcal folliculitis

Small discrete pustules are often seenaround the lips, muzzles and under the tailsof very young lambs, and on the udders ofewes (mammary impetigo). The surround-ing skin is hyperaemic but not proliferativeas is orf and a crater is left when the pus-tules rupture, which heals quickly leaving awhite patch if the skin is pigmented.Treatment is rarely necessary although localdressing and antibiotics directed at thecausal organism, haemolytic coagulase pos-itive Staph. aureus, may occasionally bejustified.

Staphylococcal dermatitis (facialor periorbital dermatitis or exzema)

This is another variant of the skin lesionsassociated with Staph. aureus. Extensive,suppurating scabby lesions, which bleedeasily and have a deep ulcerated centre sur-rounded by a zone of hair loss, are seen overbony prominences such as the orbit, noseand lower legs. Sheep feeding at crowdedsites are usually affected, typically late-pregnant ewes being fed concentrates withinsufficient trough space, where they both

Skin and Wool 115

injure themselves and each other, and trans-mit the infection to one another. Removalfrom the source of the problems andtreatment with local dressing and antibiot-ics usually leads to rapid improvement,although serious and disfiguring complica-tions can arise from eye involvement andfrom scar tissue. In future, adequate troughspace must be provided (at least 45 cm perewe) and the food spread evenly and quicklyto minimize aggression or adopt floor feed-ing if this is practical.

Mycotic dermatitis (lumpy wool)

This condition occurs in many countriesand in many if not most flocks, but generallyas a low-grade self-limiting infection, and isof little consequence in the UK other thansome downgrading of the fleece. However,occasional outbreaks occur where the infec-tion becomes more active and extensive, andsecondary problems arise such as flystrike;treatment is then necessary.

The disease picture is an exudativedermatitis passing rapidly through thestages of hyperaemia, exudate and scab. Itis caused by an actinomycete D. congolen-sis which also infects other species (e.g.horses, cattle and occasionally humans)and can remain viable in dry scabs for manymonths. It induces only weak local immu-nity, all of which means that successive`attacks' are common and eradication is notan option.

The condition is often only noticedwhen a sheep is handled (e.g. being condi-tion scored) and on parting the fleece, bun-dles of wool fibres are seen matted togetherby rough scabs. These scabs originate fromthe skin and are carried up in the growingfleece, eventually working to the tips andbreaking off. The back and top sides ofsheep are most commonly affected as theseare the sites which get soaked followingheavy rain or dipping; fat, flat-backed, close-woolled sheep are the most susceptible,where the fleece acts as a sponge. Otherareas do get infected, appearing as scabs onthe ears, head, limbs, udder of ewes andscrotum of rams, and these are constantsources of re-infection elsewhere.

The distribution of the scabs and thegeneral lack of pruritus are usually suffi-ciently diagnostic but if there is doubt,impression smears should be made of skinexudate or scabs taken, preferably thoseclose to an active lesion, for laboratoryexamination.

Significant outbreaks usually followwet weather or dipping, but it can also fol-low shearing when skin wounds may admitinfection.

Sheep that need treatment should behoused and given either a 5-day course of aconventional dose or a single high dose(70 mg/kg) of penicillin and streptomycin;topical dressing with aluminium or zincsulfate may be justified to prevent furthersurface spread. Combined insecticidal andantimycotic dips are no longer available.

Other fleece problems

Fleece rot is caused by Pseudomonasaeruginosa leading to discoloration(green, brown or blue) of the wool.Pseudomonas infection has also beenassociated with severe fatal necroticdermatitis, probably induced as a resultof bad dipping practice.Canary stain is a permanent yellow col-oration of the wool.

Ringworm

This is not particularly common in sheep,perhaps because of lack of contact withother hosts such as cattle or because of theprotective fleece, but housed, shorn ewesoccasionally develop the condition, partic-ularly if housed in buildings also used bycattle. It has also been seen on the heads oframs. It is caused by the fungus Trichophytonverrucosum and on the hairy areas of headand face, it looks just like the condition incattle, but the infection in the woolly areasoften produces more obvious circular raisedplaques which eventually lift off, leavingthe more typical crusty skin beneath.

The condition usually has to run itscourse, waiting for immunity and turnout;topical iodine sprays may be useful but han-dle with care as the disease is a zoonosis!

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Caseous lymphadenitis(CLA, cheesy gland)

This disease, seen in many sheep-keepingcountries including Australasia, was firstidentified in the UK in 1990 in importedgoats. It spread to sheep and is present insome pedigree flocks producing terminalsires and is being seen increasingly in com-mercial flocks, usually introduced byinfected rams. There is also a real possibil-ity of spread via contaminated shearsand shearing equipment if these are notadequately disinfected between flocks.

The disease is caused by Corynebacteriumpseudotuberculosis and is seen as chronicabscesses in superficial lymph nodes. Theseoften burst producing greenish cheesy orputty-like pus. Abscesses repeatedly walloff, producing a characteristic 'onion-ring'appearance. Abscesses may also form ininternal organs especially the lung andmediastinum, causing chronic wasting, orsigns resulting from pressure on vital struc-tures from large internal abscesses.Confirmation of diagnosis is by identifica-tion of the organism from samples of pus.An important differential diagnosis is bovinetuberculosis (TB) which is widespread inparts of the UK. Fortunately sheep seem tobe relatively resistant to this although asmall number of flock outbreaks have beenreported.

Popliteal

EPIDEMIOLOGY In the UK, the mode ofspread and the lymph nodes most com-monly affected are rather different fromthose in Australia where the disease is com-mon. In both countries, discharging lymphnodes in the lung form a common source ofinfection.

In Australia, the disease spreads atmajor gathering times such as shearingand jetting or dipping. Entry of the dis-ease is via skin abrasions; hence bodylymph nodes such as the prefemoraland popliteal are commonly affected.In the UK, spread appears to take placemore commonly via the oral route -trough feeding facilitates the spreadfrom discharging lung abscesses, thushead lymph nodes, especially the parot-ids, are commonly infected. These aresituated just below the ears (see Fig. 12.3)and should always be carefully exam-ined during any ram examination, aswell as the main superficial nodes (sub-mandibular, prescapular, prefemoral,popliteal, supramammary). Infectionalso spreads directly from sheep tosheep from discharging abscesses.

TREATMENT Although the organism is sus-ceptible to antibiotics, the nature of theabscesses means successful treatment isunlikely. Treatment of superficial abscesses

Parotid

Precrural(prefemoral)

Fig. 12.3. Important superficial lymph nodes.

Submandibular

Prescapular

Skin and Wool 117

is of little use since inevitably other lymphnodes become infected and infected inter-nal nodes cannot be detected.

CONTROL Vaccination is widely used inAustralia and other countries (usually incombination with clostridial vaccine) andseems to be quite effective. The vaccine isprepared from the bacterial toxins. Thisvaccine is not generally available in theUK, but in certain circumstances can beimported under special licence from VMD.Autogenous vaccines made from killed bac-teria have been used in the UK and recentinformation is that they may provide moreprotection than the Australian vaccine. It ispossible that a new vaccine may becomeavailable in the UK in the reasonably nearfuture.

It is best to try to avoid introducinginfection into a flock by careful selection ofpurchased animals and quarantine. AnELISA test is available and has led to theintroduction of the CLA Monitoring Schemeoffered by SAC. Monitored groups have tobe isolated for at least 12 weeks, are subjectto two clinical examinations and two bloodtests. If clear, these animals can be sold as`CLA monitored status' giving buyers confi-dence that they are unlikely to be infected.

If infection gets into a flock, measuresto reduce spread include: (i) floor feedingrather than trough feeding; (ii) weaning oflambs as early as possible (`snatching' lambsat birth and artificial rearing in extremecases); and (iii) keeping age groups separate.Ram breeders may sell ram lambs ratherthan keeping them to shearlings and riskinfection. Blood testing using the ELISA testwith culling of positive animals has hadsome success in eradicating the diseasefrom some flocks but is expensive.

Actinobacillosis

The main differential diagnosis for CLA issporadic cases of actinobacillosis (`cruels')where abscesses occur along the lymphaticsin the head and neck region. These areresponsive to treatment (penicillin/strepto-mycin by injection for 5 days should beadequate).

Non-infectious

Wool break

A wool break usually follows any severe ill-ness or prolonged debilitating conditionincluding inadequate nutrition. It is mostmarked during pregnancy and lactation,particularly following pregnancy toxaemia,difficult lambing or acute mastitis. It is com-mon to see ewes, often in poor condition, inlate winter or spring patchily shedding theircomplete fleece and in the process lookingvery 'moth-eaten'. Underneath, the skin isnormal and providing the precipitating fac-tors are reversed, normal wool regrows.

Wool slip

This is an allied but specific condition fre-quently seen in housed, winter-shorn ewes.Here, there is patchy loss of wool mainlyconfined to the hind quarters and back,developing within a few weeks of shearing.It is thought to be related to the stress ofhousing, shearing and cold, resulting inraised blood cortisol concentrations. Theewes are not obviously adversely affectedbut it can lead to delay in turnout.

Sunburn

Occasional cases of sunburn follow expo-sure to bright sunlight, particularly inrecently shorn white-faced breeds. Markedskin erythema and oedema develop inexposed surfaces such as the ears, back andudder and necrosis with extensive scabsmay develop. Affected sheep need housingand if secondary infection is suspected (e.g.Dermatophilus) antibiotic therapy is indi-cated. Shade will be required in future.

Photosensitization (yellowses)

Bright sunlight can also induce photosensiti-zation if the white sheep have previouslybeen eating a photodynamic agent as found,for example, in St John's wort (Hypericumperforatum), or they have raised circulatingconcentrations of the photodynamic agentphytoporphyrin (a breakdown productof chlorophyll), which arises when liver

118 Chapter 12

function is impaired. This impaired liverfunction can be caused by a variety of factorsincluding copper toxicity, toxic plants andfungi, and some drugs, so the precise factor israrely discovered, particularly if only one ortwo sheep in a flock are involved. In northernEurope, the plant bog asphodel (Nartheciumossifragum), found growing on natural hill ormountain pasture, is widely associated withthe problem. In New Zealand, the condition,known as facial eczema, is caused by inges-tion of sporidesmin fungal spores.

The most noticeable feature is themarked oedema of the head and face

including the eyelids and ears, whichmakes the sheep look very 'droopy' andmiserable; other non-pigmented areas mayalso be affected and if severe enough, thereis necrosis and eventual sloughing, partic-ularly of the tips of the ears which thenlook 'cropped'.

Cases should be housed and carefullynursed. Blood samples for liver enzymeestimations may help to decide the prog-nosis. If cases continue in a flock, look atcopper blood concentrations, check fortoxic plants and investigate recenttreatments.

13

Respiratory Diseases

Several of these diseases (see Table 13.1) areinvolved in two important areas of loss:(i) sudden death; and (ii) thin adult sheep.In both cases PME is going to be an impor-tant part of the diagnostic process in addi-tion to clinical examination of any liveanimals. Recently, ultrasound examinationof the chest has been developed as an aid todiagnosis of lung lesions, although someexperience is required in obtaining andinterpreting images.

Pasteurellosis

Microbiologists seem to like reclassifyingbacteria at intervals, seemingly to confusestudents and clinicians! This is particularlythe case with bacteria commonly referred toas `Pasteurella spp.'. The bacteriumPasteurella haemolytica, which used to bedivided into two biotypes, was then splitinto two separate species, Mannheimiahaemolytica and Pasteurella trehalosi. Thelatter has more recently been reclassified asBibersteinia trehalosi. In this book, to avoidconfusion, we will continue to use P. ratherthan B. trehalosi and to refer to the diseasesby the term `pasteurellosis'. This group ofbacteria is a common and important causeof pneumonia and rapid or sudden death insheep.

As most sheep carry M. haemolytica inthe naso-pharynx or tonsils, the mere isola-tion of this organism in nasal swabs or atPME, does not establish the diagnosis; it isgenerally held that it requires some stressfactor or intercurrent disease to precipatepasteurellosis.

There are three different manifestationsof disease:

1. Septicaemia and rapid death in younglambs caused by M. haemolytica (a few daysto 3 months old) - affected lambs are usuallysimply found dead or profoundly depressedwith a high temperature and a PME isrequired to confirm diagnosis.2. Pneumonia in older lambs and adults,also caused by M. haemolytica, most com-monly in late spring and early summer(May-July) but also in store and fatteninglambs in the autumn and winter. Affectedanimals are febrile and depressed with nasaldischarge, coughing and laboured respira-tion. Some may survive but go on to developchronic disease with weight loss.3. Septicaemia and rapid death in the fatten-ing and store lamb (6-9 months old) in theautumn and winter caused by P. trehalosi(systemic pasteurellosis). The most commonfirst sign is one or two sheep found dead.A few others may appear very ill and sepa-rated from the rest and unwilling to be driven;they are usually febrile (over 40°C) and show

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120 Chapter 13

Table 13.1. Summary of main respiratory diseases.

Organism Disease Main age group affected

BacteriaMannheimia haemolytica

Pasteurella trehalosiMycoplasma ovipneumoniaeArcanobacterium pyogenes

Internal parasitesDictyocaulus Maria

VirusesRetrovirus

Lentivi rus

SepticaemiaPneumonia (acute and chronic)Systemic pasteurellosisAtypical pneumoniaLaryngeal chondritis

Parasitic bronchitis, husk

Ovine pulmonaryadenocarcinoma

Maedi

Young lambsGrowing lambs, adultsGrowing lambs in autumnGrowing lambsAdults, especially heavily muscled

terminal sire breeds

Growing lambs

Adults over 2 years (occasionallyin growing lambs)

Adults over 2 years

increased respiratory rates. Some may havecrusted eyelids and nostrils and usually thereis some coughing in the group. About 10%may become affected in an outbreak.

Diagnosis

Necropsy of fresh carcasses if available.In the septicaemic and systemic forms,widespread petechiae and ecchymosesare usually present with varying degreesof pleurisy and lung pathology presentin all forms. Mannheimia/Pasteurellaneed to be isolated in large numbers toconfirm diagnosis and ask the labora-tory for serotyping to check against thevaccine serotypes.Try to find a predisposing reason forthe deaths or illness; in particular,with systemic pasteurellosis enquire ifthe group has been moved or handledin the last day or so, or if the weatherhas been noticeably different, forexample wet and windy (rain/wind-chill factor) or warm and still. Otherintercurrent infections such as parain-fluenza virus type 3 (PI3), Jaagsiekteand tick-borne fever may also predis-pose to clinical outbreaks of the pneu-monic form.Consider clostridial diseases as themain differential, in particular pulpykidney and braxy, and check on thevaccination history and dates.

Treatment and control

For young lambs, control is by vaccina-tion of ewes (for colostral antibodies) andearly vaccination of lambs - remember,colostral protection is short, only 2-4weeks. Also improve the ventilationof lambing sheds. Administer antibi-otics such as oxytetracycline or tilmy-cosin (not if under 15 kg) if animalsare seen alive.For older lambs and adults, controlis by vaccination before the riskperiod, and improve ventilation ifpoor housing is a trigger (Figs 13.1and 13.2). Administer antibiotics asabove in acute cases. Chronic casesmay not respond unless the courseis very prolonged and this may not beeconomic.Systemic pasteurellosis can be difficultto deal with and control:

Sometimes the group is large andinaccessible, which means the inci-dence is unsure, PME is delayedand there is a very real difficulty indeciding when to do something,that is whether to gather (whichmay make matters worse) and treat(all?). Often a number of deathsoccur over a period of days or weeksand then unaccountably cease.Rescue and isolate affected sheep -treat these and as many contacts asseem worthwhile. Tilmycosin is

Respiratory Diseases 121

1 1 1 1 1 1 1 1 1 1 1 1 I I I III HI

Fig. 13.1. This lambing shed has good ventilation reducing the risk of pneumonia.

very good for pneumonia but isnow vet-only administration, so ifyou are going to treat sick animalsyourself this might be the drug ofchoice. If the farmer has to treat,other drugs will have to be used, forexample LA oxytetracycline giventwice at a 4-day interval.Recommend vaccination - a deadvaccine is available, containingmost of the serotypes known tocause the disease, and requires twodoses at approximately a 4-weekinterval to provide useful protec-tion. If given to ewes in late preg-nancy it not only affords protectionto the ewes that spring, when theincidence of Mannheimia pneumo-nia is highest, but also to the lambsvia colostrum for the first 3-4 weeks

of life and so helps to cover the firstmajor risk period for this type ofsepticaemia (contrast with passiveclostridial protection which lasts12-16 weeks). To cover adequatelythe next few weeks and months,lambs need to be given two doses ofvaccine at a 4-week interval, start-ing 3 weeks after birth; there is evi-dence that any colostrum-derivedantibody does not interfere with theresponse to this early vaccination.

0 Look at the environmental condi-tions (e.g. wet, exposed, over-crowded, lush food) and considerproviding plenty of shelter or mov-ing the group, although the movingcould make matters worse.Consider giving LA oxytetracyclineimmediately before the period of

122 Chapter 13

Fig. 13.2. These fattening lambs are vulnerable to pneumonia if the ventilation of the housing is poor.

risk (e.g. on purchasing or movingstore lambs in the autumn).In the long term, avoid, if possi-ble, very exposed wet and windysites which induce stress andencourage the flock to crowd intosmall sheltered sites which, inturn, intensify the aerial spread ofpathogens. Also, avoid puttingstore lambs on lush grass in theautumn without considering vac-cination first.

The position regarding vaccination iscomplicated by combining this vaccinewith a clostridial vaccine to form a verypopular product which is considerablymore expensive than clostridial vaccinesalone. While such a combination is idealfor the vaccination of ewes, it matches theneeds of lambs less well because of the dis-parate length of protection by colostralantibodies for the two categories of disease.In practice, if this combination is to beused in flocks where there is a significantincidence of septicaemia and sudden

deaths in young lambs which is diagnosedas pasteurellosis, the normal lamb clostrid-ial vaccination schedule needs to bebrought forward to 1 and 2 months ratherthan the usual 3 and 4 months; alterna-tively Pasteurella and clostridial vaccinescan be given separately at appropriatetimes.

The pasteurellosis vaccine wasimproved a few years ago and is now moreeffective in the control of disease in thelater store and fattening lamb. Antigenicityof some serotypes involved in this form ofthe disease was improved by growing thebacteria in a very iron-depleted mediumwhich increased the expression of someimportant antigens on the surface of thebacteria.

Parasitic Pneumonia(Parasitic Bronchitis, Husk)

Although sheep are commonly infectedwith a number of nematodes which are

Respiratory Diseases 123

found in various parts of the respiratorysystem, the only species which is associatedwith clinical disease is Dictyocaulus filaria.It is found in the trachea and bronchi. Theheaviest pasture infections with infectivelarvae occur from September to November.These larvae can overwinter and act as asource of infection to the next season'slambs.

The disease is not as important clini-cally as 'husk' in cattle. This is probablybecause of the more frequent dosing oflambs for PGE, which, with most modernwormers, incidentally reduces the numberof worms in the lungs. (Note that morantelis not effective against lungworms.)However, the worm is common and cancause coughing and loss in condition inlambs in August-October. The lambsdevelop a strong immunity and few wormsare found in older sheep, although they canbe found in old or debilitated animals. Manylambs are sent to slaughter before the peakof infection.

Diagnosis

Diagnosis is based on clinical signs and sea-sonal incidence and can be confirmedby faecal examination for first-stage lar-vae by the Baermann apparatus. Faecesshould be fresh and D. filaria can be distin-guished from the larvae of other non-pathogenic worms in that they: (i) are long(500 pm); (ii) have a blunt tail; (iii) have acephalic knob; and (iv) contain refractilegranules.

Treatment and control

All the modern benzimidazoles, levamisoleand avermectins are effective againstD. filaria and can be used to treat clinicallyaffected lambs. Parasitic bronchitis isunlikely to occur where these drugs areused earlier in the year to control PGE butmorantel, although effective against stom-ach and intestinal worms, is not effectiveagainst D. filaria at the usual dose.

Atypical Pneumonia

This is an unsatisfactory name given to thetype of pneumonia which closely resemblesthat so commonly found in the fattening pigand housed calf. It is principally a diseaseproblem in the housed or densely stockedfattening or store lamb (3-12 months old)and associated with a variety of agents suchas Mycoplasma ovipneumoniae, PI3 andadenovirus. It is particularly common fol-lowing the mixing of lambs introduced fromthe market in autumn and winter.

Clinical signs

The disease is characterized by chroniccoughing, ocular and nasal discharges,and is usually afebrile, although the occa-sional acute pneumonic lamb arises whichis febrile, off-food, listless, and with obvi-ous respiratory distress; these cases areassociated with secondary M. haemolyticainfection. Affected lambs take severalweeks longer to reach slaughter weightand consume more food to do so.

Diagnosis

This is based on the clinical signs, environ-mental conditions and the pathology of lungs,which show collapsed areas in the lowerparts of the lung lobes at PME or slaughter.

Control

As for pigs and calves:

Supply more fresh air.Reduce numbers under one roof, and inany one group.Split groups according to age, size andorigin.Inject with LA oxytetracycline if ani-mals show signs of clinical illness.Consider pasteurellosis vaccination toprotect against additional diseasecaused by these pathogens.

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Slow Viral Pneumonias

Ovine pulmonary adenocarcinoma(OPA, sheep pulmonary adenomatosis,

SPA, driving sickness, Jaagsiekte)

Although this condition has caused worry-ing losses in some flocks, particularly ofScottish origin where the incidence can beup to 10%, it usually only causes sporadicdeaths, but its potential danger is illus-trated by the losses that occurred in Icelandin housed sheep. It is a contagious adeno-matous tumour of the lungs of sheep andpossibly goats, and thought to be caused bya B-type or D-type retrovirus, perhaps asso-ciated with a herpes virus, with an incuba-tion period of up to 3 years.

Clinical signs

The signs are of loss of condition andsevere respiratory distress, but withoutmuch coughing, in an individual adultsheep when driven. This respiratory embar-rassment, which sounds like 'bubbly por-ridge' on auscultation, increases overseveral weeks. Characteristically, if theewe is held with its head lowered (the`wheelbarrow' test), relatively large vol-umes (30-300ml) of clear mucous exudateflow from the nostrils; this fluid containsvirus so is infectious. There is no feverand the animal feeds up to the terminalstages when there is often fulminatingpasteurellosis.

Diagnosis

There is no serological test and diagnosis isbased on clinical signs (including the`wheelbarrow' test) and PME; the lungs mayweigh up to 4 kg (1.5 kg is normal) and showareas of grey tumour tissue with frothywhite fluid in the trachea and bronchi.Although the virus can be detected in labo-ratory tests, no commercial test is yet avail-able. Pasteurellosis may mask the presenceof OPA, so where significant losses of oldersheep occur from pasteurellosis, lungsshould be checked histologically for OPA.

Control

Take care in introducing new stock to unin-fected flocks. There should be promptslaughter of the obviously affected animals.Once a serological test becomes available,then monitoring and pre-clinical cullingbecomes a possibility. The disease has beeneliminated from a few flocks by removinglambs at birth and rearing them artificially inthe same way as used to produce maedi-freeanimals from infected flocks (see below).

Maedi-visna (MV, ovineprogressive pneumonia)

Maedi means 'air hunger', visna means`wasting'. Maedi is seen as a chronic pro-gressive pneumonia affecting sheep over3 years old and visna is the nervous form ofthe disease, again affecting older sheep.Both diseases are caused by a lentivirus,similar but not identical to that causingcaprine arthritis encephalitis in goats. Thevirus causes lesions in the lungs, CNS, jointsand udder. Maedi was first recognized inthe UK in 1978, having probably been intro-duced from the continent, where it wascommon, with imported stock. It does notoccur in Australia and New Zealand.

A number of flocks, mainly in EastAnglia and southern Scotland, have hadclinical cases, but because of the insidiousnature of the disease which takes 3-4 yearsfor clinical signs to develop, it is likely thatmany more flocks have subclinical infec-tion. In 1993, a random check on bloodsamples showed a seroprevalence of 0.4%,

which extrapolated to at least 70,000 sero-positive sheep then, more now. Economiclosses occur from premature culling ofinfected ewes and from reduced lambgrowth rates. Unless sheep farmers take thethreat from this disease seriously, it couldhave a major impact on the health of thenational flock in the foreseeable future.

Unlike OPA, diagnostic serological testscan be used to identify MV-free flocks andthis is applied in the SAC Premium Sheepand Goat Health Scheme. This has particu-lar application for the pedigree breeder,

Respiratory Diseases 125

especially those wishing to export sheep,but should be taken up more widely bycommercial breeders. A monitoring schemeaimed at commercial flocks has been intro-duced with less rigorous rules than theaccreditation scheme.

The disease is spread in two ways:

1. By coughing or sneezing infectivedroplets, which is important in housedsheep.2. Most importantly, by colostrum and milkfrom infected ewes, which contains thevirus.

Clinical signs

Maedi is seen as a chronic progressive pneu-monia affecting sheep over 3 years old andis invariably fatal. Affected sheep lose con-dition and lag behind when driven, withcharacteristic difficulty in breathing whichbecomes progressively worse over a periodof months.

Visna is the nervous form of the dis-ease, again affecting older sheep, in whichweight loss and vague, slowly progressiveneurological signs occur. One recognizablefeature may be the development of a unilat-eral conscious proprioceptive deficit of onehind limb, with dragging and scuffing ofthe toe progressing to paralysis of the hindlegs.

The virus also affects the udder causingan indurative lymphocytic mastitis which isnot always recognized because milk remainsnormal in appearance, but lambs fromaffected ewes have been shown to weigh3 kg less at weaning than those from healthyewes. Arthritis and vasculitis are other pos-sible components of the clinical picture.

Diagnosis

In the individual, this is based on clinicalsigns and PME. Serological tests such as theagar gel immunodiffusion test (AGID) andELISA are useful at the flock level, but falsenegative results, due to delay in antibodyproduction or immunosuppression, dooccur, which makes them less useful in theindividual animal.

Control

Slaughter affected animals.Do not breed from the offspring ofaffected ewes.Be careful about the source of ewecolostrum fed to lambs.Keep a young flock and only keepreplacements from the young ewes.Purchase from accredited flocks only.Join the SAC Premium Sheep and GoatHealth Scheme and eradicate by testand slaughter.

Because the infection is not passed tothe lamb before birth, it is possible (thoughdemanding) to obtain uninfected lambs froman infected flock by supervising lambing andimmediately removing lambs, certainlybefore sucking the ewe. Lambs are then givencolostrum substitute and reared artificially.

Laryngeal Chondritis

This acute obstructive upper respiratorycondition, seen most commonly in Texelsheep (and Belgian Blue cattle), is character-ized by severe dyspnoea with laryngeal stri-dor and is often fatal if not treated quickly.The laryngeal occlusion results from chronicsuppurative lesions (usually associated withArcanobacterium pyogenes) within the ary-tenoid cartilages, the etiology of which isunclear but is probably connected to thecharacteristic exaggerated anatomy of thebreed with its short, broad neck. Rams, ewesand growing lambs are all known to havebeen affected. No investigations have beenmade into any genetic predisposition, assome breeders are reluctant to admit to hav-ing had cases.

Treatment

These cases are often presented asemergencies.

Treat with a large dose of steroid,intravenously if possible, andbroad-spectrum antibiotic. Carry on

126 Chapter 13

with reduced doses for 5-7 days. Thisregimen alone may be adequate for lesssevere cases.If dyspnoea is severe, an emergency tra-cheostomy is necessary under localinfiltration anaesthesia. This usuallygives immediate relief, but good after-care is needed with the tube changedtwice daily initially, reducing to oncedaily if the tube remains clear of dis-charges. After the tracheostomy tubehas been in for 2-3 weeks, infection

may have subsided, so try leaving thetube out. If dyspnoea is still present, theonly remaining option is surgery to tryto remove the necrotic tissue from thelarynx.

The prognosis should always be guardedas recovered cases may subsequently relapse,sometimes just being found dead. Thinkabout the advisability of using recoveredanimals for future breeding even if they aresaid to be valuable.

14

Neurological Diseases

Neurological diseases of sheep are commonthroughout the world, often affecting indi-viduals but some can become a flock prob-lem. They are a notoriously difficult areain which to make a firm diagnosis onwhich to base a specific treatment.Indicators such as age, number involvedand speed of onset will help. In additionto a clinical examination, a full neurologi-cal examination should be carried out (forthe routine to follow see Appendix 2`Neurological Examination of Sheep'), butthis is not easy in a collapsed sheep! Theaim should be to localize signs to a spe-cific part of the CNS, or to decide thatsigns are generalized.

The main CNS 'syndromes' whichshould be identifiable are:

Cerebral - depression, blindness, cir-cling, proprioceptive deficits, head turn(e.g. cerebrocortical necrosis (CCN), PTand meningitis are diffuse diseases; gid,abscess and tumour are more likely tobe unilateral).Cerebellar - wide-based stance, highhead carriage, ataxia, dysmetria, inten-tion tremors, nystagmus (e.g. gid,Border disease, daft lamb).Vestibular - head tilt, circling, fallingor rolling, nystagmus, sometimes facialparalysis (e.g. inner and middle earinfection).

Ponto-medullary(brainstem)-depression,multiple cranial nerve deficits especiallyV, VII and VIII (e.g. listeriosis).Spinal cord - varying degrees of ataxia,paresis or spasticity dependingon location of lesion (e.g. fightinginjury, Texel `wobblers', spinal abscess,swayback).

Other adjuncts to diagnosis include: (i) col-lection of cerebrospinal fluid (CSF, usuallythe lumbosacral site will suffice); (ii) whitecell counts (total and differential);(iii) blood biochemistry; and (iv) enzymemeasurements.

Metabolic Diseases of Ewes (PT,Hypocalcaemia, Hypomagnesaemia)

See Chapter 6.

Scrapie

Scrapie occurs in most sheep-keeping coun-tries except Australia and New Zealand.This ancient disease of sheep (a transmissi-ble spongiform encephalopathy, TSE), withno proven risk to human health, has receivedmuch attention since the bovine spongiformencephalopathy (BSE) epidemic in cattle.

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128 Chapter 14

Originally there was a theory that BSE hadgot into cattle by feeding meat and bonemeal contaminated by the scrapie agent, butthis has been disproved; additionally BSEhas never been diagnosed in sheep.

Scrapie is notifiable and is being tack-led on an EU-wide basis with the aim ofeventual eradication. There is a lot of infor-mation online - here in this book there is asummary of the main features. See the website www.defra.gov.uk where the informa-tion is likely to be more up-to-date than thisbook can be.

In the last few years the number of diag-nosed cases in the UK has fallen to a verylow level, probably due, at least in part, tothe genotyping programme which has beenin place since 1991.

Classical scrapie

The disease

Scrapie is a chronic progressive degenera-tive TSE of adult sheep (and goats). The trueincidence is difficult to assess as there isprobably under-reporting and some casesmay not be recognized by the farmer.Usually just one or two cases have occurredfrom year to year in a flock and so the dis-ease has been of little importance to theaverage commercial sheep farmer produc-ing prime lambs, but for the pedigree breederwhere older sheep may be retained andwhere there has been a susceptible strain,the incidence could have been significant.The causal agent is thought to be a prionwhich causes an abnormal form of prionprotein to accumulate in various tissues,especially the brain. It is very resistant toheat, formalin and UV light. Specified offals,including brain, spinal cord and spleen ofsheep over 6 months of age are now dis-posed of by incineration to prevent possiblerecycling of infection and feeding ruminant-derived protein to sheep (and other animals)is now banned. The disease is probablytransmitted prenatally as well as laterally inthe lambing pens and fields (via fetal mem-branes), although the exact mechanism isnot clear.

Genetic background and NationalScrapie Plan (NSP)

It has long been recognized that there is agenetic susceptibility and much work hasbeen done on this in recent years. The NSPwas introduced in the UK to promote thebreeding of resistant sheep by genotyping.This has been done by taking a blood sam-ple, but some countries use small skin sam-ples instead. The sheep is given an electronicidentification by means of a rumen bolus atsampling.

Sheep have two copies of the PrP gene,which encodes for the production of PrP(prion) protein in the brain, each consist-ing of 256 amino acids. It is the productionof abnormal PrP protein that leads to thedevelopment of the disease. There are threesites (codons) on the gene which are sig-nificant in determining whether an animalis susceptible or resistant if it meets theinfection. These are 136, 154 and 171.There are five different alleles (seeTable 14.1) and 15 different genotypesdepending on which alleles are inheritedfrom each parent.

The genotype is written as ARR/ARR,ARR/AHQ, ARR/VRQ, etc. and sheep areclassed in five different categories (type 1,type 2, etc.) according to susceptibility.ARR/ARR is the most resistant type, VRQ/VRQ is highly susceptible. There is a breedvariation in which genotypes predominate;for example Suffolks, where resistant ramshave been selected for a number of years,are now mainly ARR/ARR. The Texel breedhas a more complicated mixture of geno-types with a smaller percentage of resistanttypes. In contrast, primitive breeds may

Table 14.1. Allelesa involved in resistance orsusceptibility to classical scrapie.

Codon

136

AAAAV

154

R

H

R

R

R

171

R

QH

QQ

'A, Alanine; R, arginine; H, histidine; Q, glutamine; V, valine.

Neurological Diseases 129

have few if any resistant genotypes (the 'wild'sheep genotype seems to be ARQ/ARQ).

The NSP has had a number of schemeswithin it but these have been closed exceptfor a monitoring scheme for flocks wishingto export breeding sheep. There is randomtesting of deadstock and carcasses and acompulsory scheme for flocks where casesof classical scrapie are confirmed.

Clinical signs

Clinical signs vary and are usually seen inanimals over 2 years of age. The most com-mon are shown below and may be presentsingly or in any combination:

A change in temperament or behaviour,sometimes the sheep appearing appre-hensive, wild and excitable. Some othercases just look dazed and depressedand don't appear to focus properly.The most common and obvious sign isirritation, with scratching, rubbing,sucking and nibbling the fleece in anadult sheep. It is often seen at first asrestlessness with the sheep dartingabout from place to place as if it hasbeen bitten, and turning to nibble any-where it can get at, as well as rubbingon posts and walls, etc. (watching acase one could imagine it feels like`prickly heat'). The rubbing leads to aloss of fleece or hair over any areawhich the sheep can get at, includingthe head and both sides of the flank andhind legs. A fine rough stubble is left,often with scabs. If one rubs the sheep,it responds by standing still and nib-bling its lips in apparent pleasure andrelief. (Note that this test is applicablefor all conditions causing pruritus andis not diagnostic of scrapie. If severalsheep are affected, remember the pos-sibility of external parasites!)Change in posture and gait - these usu-ally show incoordination, so that thesheep becomes awkward to catch andto examine, and it won't relax andallow its head to be held comfortably.Rams can be quite dangerous and thedifficulty in raising the head can sug-

gest a high cervical lesion (e.g. fromfighting).

If allowed to live, all these signs worsenover the weeks and sometimes months,and although there is sometimes a tempo-rary stasis or even remission; all animalsbecome progressively thinner and diesooner or later.

Diagnosis

The clinical signs are eventually diagnosticbut obviously primary skin conditions (e.g.sheep scab!) have to be ruled out. If in doubtnotify the local Animal Health Office whichwill arrange examination of the suspect ani-mal, with slaughter and laboratory testing ifthe disease is suspected. Diagnosis is byimmunohistochemistry or rapid immuno-chemistry, although definitive diagnosis isby brain histology looking for characteristiclesions (these differ between different TSEstrains, e.g. the lesion 'profiles' of BSE andclassical scrapie are different and distinc-tive). There is no diagnostic test currently inuse in the live animal, although promisingresults have been achieved by taking tinysamples of rectal mucosa immediately adja-cent to the anus, which contains lymphoidfollicles. These can then be subjected toimmunohistochemistry.

If scrapie is confirmed there is a com-pulsory scheme consisting of genotypingthe flock and culling of susceptible geno-types. In the case of atypical scrapie, theflock is just monitored for 2 years.

Atypical scrapie -a complication

Fairly recently, a small number of so-calledatypical scrapie cases have been identifiedas a result of surveillance in several coun-tries including the UK. Here, out of over100,000 samples tested, only about 80 werepositive. These differ from classical scrapieand BSE in current diagnostic tests and mayaffect only one or a small number of animals(usually over 5 years of age) within a flock.Most notably, some cases have had theresistant ARR genotype. The significance of

130 Chapter 14

atypical scrapie is unknown at present butrestrictions are not currently placed onflocks with just the odd case.

Listeriosis

This is a sporadic disease of sheep (andless commonly, cattle) seen in many coun-tries and in a number of forms. As encepha-litis is by far the most common presentation,the disease as a whole will be dealt with inthis chapter. The causal organism is com-monly excreted in faeces and milk byapparently normal animals and is foundwidely in soil.

Types of disease seen are:

encephalitis - by far the most commonand significant form;abortion;diarrhoea and septicaemia;a few reports of kerato-conjunctivitisand also mastitis; andsepticaemia and death in young lambs.

Encephalitic listeriosis

There has been an increase in reported inci-dents of listeriosis over the past 20 years inthe UK, and it is now one of the most com-mon causes of sporadic disease in individ-ual adult sheep. It is seen particularly in thelate winter months when silage is being fed.Poor quality, badly fermented (i.e. high pH)silage, particularly if it is contaminatedwith soil, and stored where air can get at it,can contain large numbers of Listeria mono-cytogenes. It is thought that the organismgains entry via any mouth lesions (e.g.changing teeth) and travels up the V cranialnerve to involve the nuclei of the V, VII andVIII cranial nerves in the brainstem (ponsand medulla). The central nervous formappears to have a longer incubation periodthan other forms, cases usually occurringabout 6 weeks after silage feeding starts.This is probably because the bacteria takesome time to travel up the nerves to thebrain. Thus, it is mainly a winter disease

with a peak incidence in February/March,when many ewes are pregnant.

Do not dismiss the possibility of thedisease if silage is not being fed as theorganisms are found in soil so couldoccur, for example, when sheep arebeing fed concentrates on the ground ifgrass cover is poor.

Clinical signs

The signs are variable but classically the ani-mal is very depressed and there is unilateralV, VII and sometimes VIII cranial nerveparalysis (Fig. 14.1). This shows as: (i) droop-ing ear, eyelid and lip (facial paralysis);(ii) loss of facial sensation; and (iii) paralysisof cheek muscles with consequent dribblingand difficulty in eating and drinking. If theVIII nerve is involved, there is aversion ofthe head, propulsive circling and fallingover on to one side. The animal is unable torespond to the menace test (also palpebraland corneal reflexes may be absent) which

Fig. 14.1. Encephalitic listeriosis causes facialparalysis so examine the head carefully - this sheepis normal.

Neurological Diseases 131

may mislead one into thinking that the eweis blind in that eye, and so confuse the con-dition with, for example, gid. Deteriorationusually occurs over just a few days, leadingto recumbency and death.

Diagnosis

The CNS form requires differentiating clini-cally particularly from:

Hypocalcaemia (always check a recum-bent ewe for facial paralysis beforeassuming it is hypocalcaemia).Middle and inner ear infection -confusion may arise because infectionspreading from the ear locally to involvethe facial nerve will produce classicalsigns of facial paralysis but without theextreme depression of listeriosis. Thesecases usually respond well to antibiot-ics and probably account for some sup-posedly 'cured' listeria cases!Other differentials are PT, gid, CCN andbrain abscess.

A CSF sample obtained from the lumbo-sacral space may help to differentiate. Brainhistology is necessary to confirm listeriosis;serology is not helpful.

If, as expected, silage is being fed, orwas fed some time during the last 6 weeks,examine it for signs of: (i) poor fermenta-tion; (ii) spoilage (mould); and (iii) soil con-tamination. Most silage contains someListeria, although very rotten silage may besterile. Be very careful when handling sus-pect material, including silage, particularlyif you are pregnant or unwell.

Treatment

Therapy for the CNS form can be disappoint-ing. The organism is sensitive to a widerange of antibiotics in vitro, but in spite ofintensive treatment, many cases fail torespond. Success is more likely if treatmentis early and vigorous; try crystalline penicil-lin, at least 10 mg/kg (one-quarter ofthe reconstituted vial) plus a high dose(1 mg/kg) of steroid given intravenously.Follow with procaine penicillin for 5 days.The common unilateral eye complications

of corneal ulceration and uveitis also requireprotection from further damage and intensivelocal therapy.

Control

Vaccines have been tried particularly inEastern Europe with equivocal results. Themain control is in reducing contaminationof silage.

SILAGE MAKING AND FEEDING Although a fewincidents do occur at pasture, particularlywhen soil is exposed by heavy grazing, mostfollow silage feeding. It is almost impossi-ble to avoid contamination by Listeria, soone must seek to avoid the conditions inwhich it multiplies.

Make high quality silage with a pH <5and a D value of >65%, with additiveswhere necessary. Avoid gross soil con-tamination (e.g. mole hills) by rollingand not cutting grass too short, so that ithas an ash content of <100 g/kg DM.Compact and completely seal the silageas soon as possible (the same day) andso avoid air getting into the sides andtops of clamps.With big bales make sure they aresecurely wrapped and do not get punc-tured when moved or stored.If there are persistent problems, try toavoid grazing sheep on fields fromwhich silage will be made later in theseason - grass may be contaminated ifsheep are passing Listeria in faeces.Avoid feeding poor quality silage,which can be seen and smelt on thetop or sides, as a layer or even in lumpsin the middle, or left over in thetroughs.Do not give more silage than can becleared in 48 h maximum. Clear awayuneaten silage before giving new.It is less risky to feed suspect silage tocattle.Live attenuated vaccines are availableon the continent, but there is argumentover their efficacy and they are not usedin the UK. Some argue they can makematters worse rather than better, since

132 Chapter 14

the disease may actually be an allergicresponse in a previously sensitizedanimal.

Other forms of listeriosis

The alimentary form often produces diar-rhoea and even brief general illness, and ifthe ewe is pregnant, abortion may follow aweek or so later, sometimes with retentionof fetal membranes and subsequent sys-temic illness, but usually not encephalitis.However, others in the flock may showcharacteristic neurological signs of encepha-litic listeriosis. Lambs may show septicae-mia. For diagnosis submit faeces, vaginaldischarges, fetuses and milk (if any) for cul-ture and paired blood samples for serology.

Coenurosis (Gid, Sturdy, Bendro)

Good anthelmintic drugs for dogs and morestrictly enforced legislation on carcass dis-posal has reduced the number of cases ofthis CNS disease in the UK. It does occur inmany other countries but not in Australiaand New Zealand. The causative agent isthe metacestode (larval) stage of the lifecycle of Taenia multiceps (Coenurus cere-bralis), a tapeworm occurring in the dog(Fig. 14.2). Dogs usually acquire the infec-tion either through scavenging dead sheep,or through being fed sheep heads obtainedfrom abattoirs (now illegal). Surveys in thepast have shown that about 5-10% of farmdogs in the UK were affected with the adulttapeworm and that they carried a meanworm burden of about ten adults. The adultcestode also occurs in the fox but the wormsseldom reach maturity and become gravid,so foxes should not be blamed until everypossible dog source of infection hasbeen considered. The metacestode is alsorecorded in cattle, goats, horses and deer,but at a much lower incidence than insheep, and, very rarely, in humans.

Once a sheep or lamb (pet lambs areoften most vulnerable as they may be kept inclose contact with dogs) has ingested the

Fig. 14.2. Dogs can transmit a number of diseasesto sheep including the tapeworm responsible forcausing coenurosis.

tapeworm eggs the larvae hatch and migratein the bloodstream throughout the body butcan only continue their development withinthe CNS. Over a period of 2-8 months, theCoenurus grows into a fluid-filled cyst con-taining around 100 scoleces. Multiple cystshave been thought to only occur occasion-ally in natural infections, possibly becausean established cyst inhibits the developmentof further cysts, but recent magnetic reso-nance imaging (MRI) investigation has shownsome animals do have more than one cyst.

Clinical signs

Acute coenurosis usually goes unnoticed.Some 2-4 weeks after a sheep has ingested alarge number of the tapeworm eggs, nervoussigns such as ataxia, blindness, muscle trem-ors, nystagmus, excitability and collapse maybe seen. Diagnosis is extremely difficult and isusually at PME where haemorrhagic tracts andmigrating parasites are found in the brain.

Neurological Diseases 133

The chronic form of the disease ismuch more frequently seen. The onset ofclinical signs is usually 3-8 months afterinfection. The affected animal shows a vari-ety of neurological deficits usually correlat-ing closely with the location of the cystwithin the CNS. About 80% of cysts arelocated in the cerebrum, 10% in the cere-bellum, 5% are multiple cysts in severallocations and the remainder is in the brain-stem and spinal cord. Differentials are otherspace-occupying lesions such as abscess ortumour.

Affected sheep are usually identifiedinitially by the farmer because of abnormalbehaviour such as standing apart or failingto respond to the dog. Neurological exami-nation should then reveal specific localiz-ing signs (see Table 14.2), although it isimportant to consider combinations of signsrather than relying too heavily on any onedeficit and if a farmer has become very goodat recognizing early behavioural abnormali-ties, other neurological signs may not bevery obvious. As the cyst develops, the clin-ical signs gradually increase in extent andseverity, progressing to recumbency anddeath (over days or weeks) if the cyst is notremoved surgically. Locating the cyst and

Table 14.2. Locating the cyst.

attempting surgical removal is an interest-ing clinical challenge, though rarely finan-cially viable. Use of MRI to locate will rarelybe justified.Note:

Head tilt is the head rotated but thenose pointing forward. The cyst is usu-ally on the side of the lower ear.Head aversion is the head rotated andturned to the side and usually down.The direction is not a good indicator tothe side affected.Circling may be indicated by a plait ofstraw wound round the leg on theinside of the circle. The diameter ofthe circle may indicate whether it is inthe right or left side of the brain anddepth of the cyst.Unilateral menace deficit indicates thatthe cyst is in the opposite cerebrumbecause approximately 90% opticaxons cross over; residual vision couldbe from the 10% that are in the nasalfield which do not cross over.Spontaneous nystagmus indicates ves-tibular involvement. Cerebellar nystag-mus is induced by eye movement and isan intention tremor of the eye muscles.

Indicator sign Possible location

Behaviour

Head position

Movement

PostureWheelbarrow and

hemiwalking tests

Vision

Eye movementEye position

DepressionExcitabilityTiltAversion (turn)RaisedHead tremorCircling - wideCircling - tight

Dysmetria (hypermetria)Wide-based stanceUnilateral deficit

Bilateral deficitUnilateral blindnessBilateral blindnessNystagmusStrabismus

Cerebrum (rostra!)Cerebrum (temporal)Cerebellum or vestibularCerebrumCerebellumCerebellumCerebrum (ipsilateral, superficial)Cerebrum (contralateral, lateral

ventricle or basal nucleus)CerebellumCerebellumCerebrum (contralateral)

CerebellumCerebrum (contralateral caudal)CerebellumCerebellum or vestibular nucleiBrainstem nuclei of CNs III,

IV and VI

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Differential diagnosis

Unless there is a flock history, usually thefurthest a diagnosis can go is of a space-occupying lesion. The disease usuallyoccurs sporadically, although occasionallyoutbreaks are seen. It is characterized by theslowly progressive development of CNSsigns in sheep over 4 months old (usually1-2 years old and very rarely over 3). Thechronic nature of the disease and the age ofaffected animals, together with a knownfarm incidence, will aid diagnosis. In addi-tion, the presence of skull softening at ornear the horn bud site, due to the intracra-nial pressure, is diagnostic but is not a reli-able guide to the localization of the cyst.

Key distinguishing features of otherneurological problems to be considered are:

Listeriosis is an acute disease (2-3days), with severe depression and facialparalysis, occurring as mini-outbreaksmainly in winter, and usually associ-ated with silage feeding.CCN is also an acute disease (1-3 days),resulting in staggering gait, abnormalhead position (star gazing), blindness,strabismus, tremors and fits, butresponds to early therapy withthiamine.Louping-ill is a febrile illness charac-terized by `leaping' movements andusually occurring as outbreaks amongyearlings in tick areas and in the tickseason (spring/autumn)Other conditions to be consideredinclude CNS abscess, tumour, sway-back, intracranial injury, scrapie, PT,hypocalcaemia and hypomagnesaemia.

A differential white cell count and ananalysis of CSF may aid diagnosis. Usually,the white cell picture is not altered by coen-urosis so that a neutrophilia or a 'crossover'will generally indicate another cause of theCNS signs (e.g. listeriosis or abscess) but thesechanges do not occur invariably. CSF sam-pling should be carried out with care in caseswhere a raised intracranial pressure is sus-pected (e.g. coenurosis); only 0.5 ml shouldbe taken from the lumbar cistern to avoid her-

niation of the cerebellum. In coenurosis, theCSF does not show any diagnostic changes;surprisingly, there is no eosinophilia.

Treatment

Lambs near killing weight should be sentfor slaughter. Surgical removal of the cystcan be attempted in breeding animals orthose too small for slaughter. With practice,the surgical success rate is as high as 80%.The operation should be carried out undergeneral anaesthesia. We have routinely usedpentobarbitone, but this is no longer availa-ble except for euthanasia, so induction fol-lowed by intubation and maintenance witha gaseous anaesthetic is the usual proce-dure. Anaesthesia can be induced with amixture of ketamine (300 mg /3m1) plusdiazepam (30 mg/6 ml) in the same syringe,given to effect. Prior to surgery, crystallinepenicillin (1.5 g) and dexamethasone (6 mg)should be given intravenously, although itmay be wise to omit the steroid when deal-ing with a pregnant ewe. A C-shaped skinincision is made just caudal to the horn budon the appropriate side (left or right cerebralcortex), or in the midline just rostral to thenuchal line (cerebellum). The skull is tre-phined (0.5-1.5 cm diameter) and a circularplate of bone removed.

Sometimes, the skull is so soft that scis-sors may be used. However, it is not safe toassume that the site of skull softening indi-cates the location of the cyst. The bone at thecerebellar site is at least 0.5 cm thick and maybleed. In trephining at the cerebellar site, it isimportant to avoid the transverse suture lineabout 1.5 cm rostral to the nuchal line, sincethis marks the position of the tentorium cer-ebelli and the transverse sinus and serioushaemorrhage could follow. The meninges arecut and reflected to expose the cerebrum,which will bulge due to increased intracra-nial pressure. If the cyst is lying superficially,the translucent pale grey wall may be visibleand should be immediately grasped withartery forceps. If the cyst is not visible, a 16gauge (16G) needle with cannula (e.g. horseIV catheter) is inserted. When the cyst is

Neurological Diseases 135

punctured, clear cyst fluid wells up the nee-dle. The needle is removed and a 20-50m1syringe is attached to the cannula and someof the fluid is withdrawn. Cerebral cysts aver-age 35m1 but may contain over 100 ml; cere-bellar cysts contain 10 -25 ml. Suction is usedto trap the pale grey cyst wall in the end ofthe cannula which is then elevated to allowthe pedicle of the cyst wall to be grasped withartery forceps. Gentle tension is then applieduntil the wall is removed, draining more fluidfrom the cyst if required. The depth of the tre-phine hole at the cerebellar site may reducethe angulation of the cannula, making it dif-ficult to grasp a cyst that is laterally situatedin the cerebellum. Only the skin incision issutured, and antibiotic cover is continued for2 more days; steroids may also be necessaryunless cyst removal was straightforward. Thesutures are removed in 10 days and the skullheals in about 1 month.

The results of surgery can be veryrewarding; uncomplicated cases usuallymake a good recovery within about a week,but excessive probing, haemorrhage andmultiple cysts lead to a poor prognosis (bet-ter to euthanize rather than allow to recoverfrom anaesthesia).

Control

Worm dogs with a drug which is effec-tive against cestodes, for example prazi-quantel at least as frequently as every3 months.Do not feed uncooked sheep heads todogs (now illegal).Dispose of sheep carcasses properly -burying is no longer legal in the UK.Avoid sheep grazing possibly heavilyinfected pasture, for example followingsheepdog trials or if used by hounds.

Other tapeworms with larvalstages in sheep

Dogs act as definitive hosts for several othertapeworms whose metacestode stage occursin sheep.

Taenia hydatigena is very common insheepdogs and the larval stage,Cysticercus tenuicollis, occurs on theserosal surface of the liver and in theomentum in about 50% of lambs. Heavyinfections are seen occasionally caus-ing sudden death in young, usually pet,lambs. The liver is full of haemorrhagictracts. Cysts cause some local condem-nation of livers.Taenia ovis has a larval stage in sheepmuscles and heavy infection may resultin carcass condemnation.Echinococcus granulosus, a minuteadult worm, gives rise to large hydatidcysts in livers and lungs, resulting incondemnation of offal. Clinical signsare not seen in sheep but hydatid dis-ease is an important zoonosis in sheep-rearing areas in central Wales,occasionally elsewhere in the UK andin many other sheep-keeping countries.Successful eradication schemes havebeen carried out in many countriesincluding Tasmania, New Zealand,Uruguay and Cyprus and one has beenstarted in Wales.

Regular treatment of sheepdogs should be acomponent of sheep health programmes.

Cerebrocortical Necrosis (CCN,Polioencephalomalacia, 'Brain Rot')

This is an acute central nervous disease,said to mainly affect lambs 2-6 monthsold (not under 2 months, as it requires afunctional rumen), but it also occurssometimes in adults. It usually occurssporadically and 'out of the blue' butthere are occasional outbreaks affecting asmall number of sheep, and lasting a fewweeks following a history of change infood or worm drenching. It is associatedwith a deficiency of thiamine, probablyinduced by the microbial (by e.g.Clostridium sporogenes and Bacillus thia-minolyticus) production of thiaminase inthe rumen, causing an initial generalizedcerebral oedema followed by pressurenecrosis.

136 Chapter 14

Clinical signs

After a short period (a few hours) of aloof-ness, dullness and wandering, often 'stargazing' (even circling), the sheep becomesincreasingly excitable (over another fewhours, even up to 2 days) developing trem-ors, staggering, recumbency, opisthotonusand galloping movements. Opisthotonus,bilateral blindness and bilateral strabismusall point towards a high possibility of thisdisease Animals may just be found dead;yet another cause of 'sudden death'. Theabove clinical signs should help to differen-tiate it from such conditions as pulpy kid-ney,listeriosis,gid,PTandhypomagnesaemia,but it requires some confidence to avoid a`mass medication' approach at the firstexamination.

Diagnosis

Clinical signs, especially opisthotonus,blindness and strabismus.Response to thiamine treatment.If the animal dies, PME shows bilateraldiscoloration of cortical gyri and brightwhite fluorescence under Wood's lampof the sliced cortex.Histology.Rumen contents for estimation of thia-minase activity.Faeces for increased thiaminase activ-ity, and blood samples for increasedpyruvate and decreased transketolaseactivity can give supportive informa-tion, but they need special samplingprocedures so contact the laboratoryfirst.

Treatment

Give 200-500 mg thiamine (vitamin B1) IV(slowly) and IM, repeat IM daily for a fewdays. If the case has been 'caught early' (i.e.before much irreversible necrosis) improve-ment can be expected within hours (notminutes), that is the sheep will be quieterand have fewer convulsions, and often there

is complete recovery within days, althoughvision often takes longer to return.

Control

It is reasonable to look at the diet and per-haps suggest changing it, for exampleremove from that field or take off that con-centrate or lick (e.g. molasses), but it is onlymaking a shaky guess. There is some evi-dence that the contacts may appear not to bethriving and show signs of scouring, so havea look at them too. They might be injectedwith 500 mg thiamine, but the incidencedoes not usually justify such intervention.

Tetanus

This disease, most commonly seen in youngor growing lambs, should not occur ifclostridial vaccination has been correctlycarried out, since the vaccine is highly effec-tive. It does, however, rely on passive trans-fer of antibodies via the colostrum, so thedisease can occur in vaccinated flocks wherecolostrum management has been poor. Italso needs to be remembered that passiveprotection only lasts 12-16 weeks, so lambsrequire active protection after this stage.Most lambs are at risk, since the causalorganism, Clostridium tetani, is widespreadin the environment in the form of very resist-ant spores. Routine procedures such as tail-ing and castration provide perfect sites forthe bacteria to multiply and to release thetoxins which cause the characteristic clini-cal signs. Adults are also at risk throughinjuries or associated with bad lambings.

Clinical signs

These should be easily recognized: (i) rigid-ity of muscles, with the affected animal inlateral recumbency with limbs stifflyextended, jaw tightly closed, tail and earsheld stiffly; (ii) spasm of the third eyelid;and (iii) in older animals, bloating of therumen since they are unable to eructate gas.

Neurological Diseases 137

Treatment

This is usually unrewarding - considera-tion should be given to euthanasia on diag-nosis. Penicillin is effective against thebacteria and antitoxin can be given to try to`mop up' free toxins; sedation to help relaxmuscles and good nursing may help, but theprognosis is always poor.

Prevention

Implementation of a comprehensiveclostridial vaccination policy for the flockincluding vaccination of rams, ewes beforelambing and lambs from 10-12 weeks.Remember that two injections 4-6 weeksapart are necessary to provide active immu-nity. The 7-, 8- and 10-in-1 clostridial vac-cines all provide tetanus coverage.

Other Neurological Disorders

Focal symmetrical encephalomalacia isassociated with C. perfringens type Denterotoxaemia, causing vague neuro-logical signs, recumbency and deathmainly in growing lambs.Rams commonly sustain fighting inju-ries, the results ranging from instantdeath, to concussion, to neck injuries.Wobbler syndrome in Texels - this is arecently-recognized problem, affecting

both males and females, which showsup in young adults and has the appear-ance of `wobbler' horses and dogs.Affected animals develop a progressiveataxia and swaying of the hind quar-ters. Radiographic investigations usingcontrast medium and PME have shownthe problem is usually between C6 andC7 vertebrae, where a fat pad protrudesinto the vertebral canal from above,pressing on the spinal cord. There maybe a familial tendency.'Kangaroo gait' affects ewes, usuallyduring lactation and is a neuropathy ofthe nerves supplying the forelimbs,especially the radial nerve. Affectedanimals have difficulty using their fore-limbs and, as the name suggests, have astrange gait resembling that of a kanga-roo. Surprisingly, most cases recoverafter a few weeks. Weaning may hastenthis. Until they recover they need gen-eral nursing care to make sure they areable to get sufficient to eat.Ryegrass staggers is occasionally seenin the UK and more commonly inAustralia and New Zealand where itcan be a serious flock problem. This isa mycotoxicosis (a toxin produced byan endophyte which is found in rye-grass), causing staggering and trem-ors. Affected animals may fall intoditches or streams and drown, or areattacked by predators. Recovery usu-ally occurs if removed from theaffected pasture.

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15

Eyes, Ears and Nose

Eye Diseases

Contagious ophthalmia (ovine infectiouskeratoconjunctivitis, pink eye, heather

blindness)

This is a very common disease of sheep'seyes worldwide. Usually, there is onlysuperficial irritation recognizable by:(i) conjunctivitis; (ii) scleral congestion; and(iii) excessive lachrymation, blinking andsome blepharospasm. Some cases, however,particularly adult sheep, show cornealinflammation with blood vessels and pan-nus spreading from the corneo-scleral mar-gin, and progressing to shallow cornealulceration and temporary blindness. Botheyes are usually affected but not alwayssimultaneously or to the same extent. Badlyaffected sheep can find it difficult to findfood and are accident prone.

Outbreaks often arise after movement,probably because Mycoplasma conjuncti-vae, the organism most commonly associ-ated with the disease in the UK, is spread byclose sheep-to-sheep contact rather than byvector or airborne transmission. It may alsobe introduced by 'carrier' animals, as manynormal animals carry the organism. Bacteriasuch as Branhamella ovis and Staph. aureusmay play a role in increasing the ocularreaction. Chlamydophila spp. have been

isolated from some outbreaks in the UK and,commonly, in New Zealand.

Without treatment, the duration of thedisease is very variable; if only the sclera isinvolved, complete resolution may occur ina day or so, but if the cornea is involved,inflammation may persist for 3 or 4 weeks.However, many carriers remain and relapsesand new infections are frequent, with theresult that the disease persists in the flock.

The disease causes discomfort andindividual cases certainly merit treatmentwhen there is obvious blepharospasm,which usually indicates corneal involve-ment. A single injection of suitable antibi-otic (e.g. oxytetracycline) is the mostpractical treatment, particularly if largenumbers of animals are affected. Topicalapplication of an ophthalmic antibioticpreparation may be appropriate for individ-ual cases but needs to be carried out severaltimes daily. Remember that Mycoplasma spp.are not susceptible to penicillin-based prod-ucts. Subconjunctival injection of antibioticmay be necessary for severe cases or evensuturing the third eyelid. Separation fromthe group may be necessary in order toensure proper care and treatment.

In an outbreak, it is worth consideringinjecting all the immediate contacts withoxytetracycline: this routine can also beapplied to all newly purchased sheep, for

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 139

140 Chapter 15

example rams, in order to reduce the risk ofimporting fresh strains of M. conjunctivaeinto the flock, but the effectiveness of thiscannot be guaranteed.

The frequent movement and mixing ofsheep are obvious hazards and should bekept to a minimum.

It is worth noting that this condition isvery different in its etiology, pathogenesisand severity from so-called 'New Forest'disease in cattle, and that some ocular prep-arations, for example the penicillins for usein cattle, are generally inappropriate forsheep as they are not effective againstMycoplasma spp., although they may havesome effect on secondary invaders.

Silage eye

Listeria monocytogenes may occasionallybe implicated in eye problems as in 'silageeye' in cattle, although this is uveitis/iritisrather than keratoconjunctivitis so shouldbe distinguishable clinically. Infection prob-ably gains entry to the eye as a result of thesheep burrowing their heads into silagewhen feeding so it is usually associatedwith big bales but may also occur if anysilage is not cleared away regularly(uncleared silage allows multiplication ofthe bacteria). Examination of the eye mayshow folding of the iris with inflammatorychanges progressing from the edges of thepupil accompanied by clumps of fibrinunderneath the cornea. Treatment is by sub-conjunctival injection of antibiotic (oxytet-racycline) together with a small amount ofsteroid.

Prevention can be attempted by:(i) avoiding contamination of silage withsoil; (ii) preventing damage to the wrappingof big bales; and (iii) providing only suffi-cient silage so that it is eaten within 2 days.

Bright blindness (clear blind, glass-eyed)

This is an irreversible blindness in adultsheep, mainly reported in flocks in the northof England, but occurring in hill flocks in

other areas. The condition affects both eyesequally and simultaneously. The retinashows progressive degeneration withatrophy of the rods and cones; the tapetalarteries and veins are narrowed and there isa marked green reflection from the tapetum.Ophthalmoscopic examination of the retinais easy because the pupils are dilated andthe cornea and lens are clear.

It is caused by a toxic factor in bracken,and may require several seasons of brackenconsumption before signs become apparent;it is therefore only seen in adult sheep. Theprevalence may be over 5% and usuallybecomes apparent in the autumn followingthe bracken growth season.

As the condition is slowly progressive,the sheep have time to adapt and the blind-ness may only become apparent when thesheep are driven or placed in strange sur-roundings. They are not unwell, appearingperhaps more alert than usual and are noteasy to catch. They are, however, moreprone to accident and to get lost. Theyrequire culling.

Entropion

Entropion (Fig. 15.1) is common in newbornlambs in the UK, involving one or bothlower eyelids. The incidence varies fromflock to flock but cases occur in many flocksand some receive inadequate attentionresulting in unnecessary discomfort and

Fig. 15.1. This Iamb has entropion which urgentlyneeds correcting.

Eyes, Ears and Nose 141

corneal damage. Eyes of any lambs showingocular discharge should be carefully exam-ined for entropion, before assuming it is aneye infection. Some flocks have a distress-ing number of severe cases and there issometimes good evidence to suggest a breedfactor, with a recessive gene involvement.Entropion can also occur in very thin adultsheep as a result of loss of the fat pad behindthe eye.

Treatment

In mild entropion the eyelid can be easilyeverted by finger pressure, particularly innewborn lambs. In flocks with an entro-pion problem, an 'eyelid' check shouldbe routine with correction done as neces-sary as soon as possible after birth.More severe cases, where the lowereyelid is turned in a lot causing blepha-rospasm, keratitis and corneal ulcera-tion, require more vigorous attention,such as:

SC injection of a liquid below themargin of the lid, after manual cor-rection, sufficient to produce a blebwhich everts the lid. Liquid paraf-fin is effective, but an antibioticpreparation (e.g. penicillin) is moresensible as this will also treat anyinfection that may have resulted.

. Placing a tuck in the skin below thelid with 14 or 16mm Michel's clips.

. Surgical correction as in dogs; asthe above methods usually workwell, this is rarely necessary.

Most cases that have not been correctedimmediately after birth merit antibioticeye ointment at the time, and if possi-ble for the next day or so to deal withany infection which has becomeestablished.

Control

Consider the breeding lines. Has a newram been used?Mark and record each case and don'tbreed from them. This is easier said thandone with bought-in animals, as casescorrected at birth are undetectable.

Other genetic defects

Occasionally lambs, particularly Texels, areborn with very small eyes (microphthalmia)or no eyes (anophthalmia). In some breedswith a gene for four horns (e.g. Jacob orHebridean) sheep have a defect in the uppereyelid which, if severe, can predispose toeye infections and blindness. Both condi-tions are likely to be inherited; thereforebreeding lines should be investigated.

Ear Problems

The ear may be involved in a number of differ-ent diseases (Fig. 15.2), but allowing the ears todroop is usually a general sign that a sheep isunwell. (However, note that normal ear posi-tion is very variable between breeds - contrastfor example, Suffolks with Border Leicestersfor extremes of normal appearance.)

Specific problems include:

Paralysis of (usually one) ear - see liste-riosis and middle ear infection (seeChapter 14).Rubbing and shaking, with haematomaformation -see Psoroptes ovis (cuniculi)infection (see Chapter 12).Scabbiness - sunburn, dermatophilus,orf, ringworm (see Chapter 12).Swelling of the ears and head - seephotosensitization (see Chapter 12) andbluetongue (see Chapter 17).

Fig. 15.2. This Zwarbles ewe has some damage toboth ears.

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Nose Problems Skin lesions around the nose

Nasal discharge

This is commonly seen in various types ofpneumonia such as pasteurellosis, atypical(Mycoplasma ovipneumoniae) pneumonia,in OPA and as a result of nasal hots.Regurgitation of saliva or rumen contentsmay be mistaken for that associated withpneumonia. Look carefully at the type andquantity of discharge:

Copious clear mucoid discharge, whichincreases in amount when the sheep'srear end is lifted (the 'wheelbarrowtest'), accompanied by weight loss indi-cates OPA.Dirty, possibly bloodstained, dischargeaccompanied by sneezing may indicatenasal hots.Serous discharge accompanied by raisedtemperature may indicate pasteurellosis.Serous discharge with coughing butwith little or no raised temperature mayindicate atypical pneumonia.Clear mucoid discharge (saliva) in acollapsed heavily pregnant or recentlylambed ewe may indicate hypocalcaemia.Green-coloured discharge with typicalsmell indicates regurgitated rumencontents.

The most common causes are infection withorf virus and staphylococcal infection of theskin. See Chapter 12.

Nasal bots

The fly Oestrus ovis, which lays larvaeinside the nostrils of sheep, is found world-wide but is rarely a serious problem in theUK. The larvae move into the sinuses wherethey develop over about 6 weeks, or muchlonger in winter, before the sheep sneezethem out on to the ground where they pupateand complete their life cycle. The adult fliescause a nuisance to the sheep and the larvaecause nasal discharge. Anthelmintics con-taining ivermectin, doramectin or moxidec-tin are effective so flocks using theseproducts for worm control will also havenasal bots controlled.

Enzootic nasal tumour

This is not a problem in the UK but may beseen in some other countries, for example insouthern Europe. It is caused by a retrovirussimilar to that causing OPA.

16

Ticks and Tick-borne Diseases

Sheep act as host for many ticks throughoutthe world, especially in tropical countriesand a number of species of tick are respon-sible for the transmission of many diseaseswhich will not be discussed here.

The Sheep Tick (Ixodes ricinus)

Hard ticks belonging to the genus Ixodes arethe most important in sheep and the specieswhich is found most commonly is I. ricinus,the so-called sheep tick, though it is nothost specific and will feed on many mam-malian and avian species. The tick is ofimportance in sheep, cattle, humans andgrouse but it is also found on hosts such asdeer and other wildlife.

I. ricinus has a wide geographical dis-tribution from the Atlas Mountains in NorthAfrica in the south to Iceland, Sweden andRussia in the north and it extends eastwardto Iran and westward to Ireland. It is foundextensively throughout central Europeincluding Austria, Switzerland, Poland andSlovenia. It is the common tick found onfarm animals including sheep in the UK.Other species of tick belonging to the genusIxodes occur in North America.

It has a three-host life cycle in whichless than 3 weeks of the 3-year cycle is spenton the host. Larvae and nymphs can feed

successfully on birds and small wildanimals, but the adult female needs a largeanimal host (sheep, cattle, deer) in order toproduce eggs. All stages of this tick willbecome attached to humans and may trans-mit Lyme disease and louping-ill. Since98% of the life cycle is spent off a host, thesuccess of the tick is very dependent on theexternal environment.

Geographical distribution in the UK

The ticks are dependent on suitable habi-tats for the stages off the host, which require100% humidity. They are found, therefore,mainly on rough hill grazing in Scotland,the Pennines, the Lake District, Wales,Devon and Cornwall and a few other smallareas. However, small populations of I. ricinusare successful in finding suitable but smallhabitats in other less typical regions suchas Richmond Park in London where theymay become attached to domestic pets andhumans as well as their usual deer host.The areas where ticks are found in largenumbers have an annual rainfall of over100 cm (40 inches). The vegetation isbracken, heather, rushes and coarse grassesand the number of ticks increase with thethickness of the vegetation mat (Figs 16.1and 16.2). Pasture improvement, involving

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144 Chapter 16

Fig. 16.1. Moorland with heather is a typical tick habitat.

Fig. 16.2. This type of vegetation is also likely to be a tick habitat.

Ticks and Tick-borne Diseases 145

drainage and re-seeding, renders conditionsunsuitable for ticks.

Seasonal distribution

In most areas, there is a tick rise (i.e. theticks climb up the vegetation and thusbecome available to passing hosts) in springand another in autumn, but the precise tim-ing varies from year to year, particularly thetime of appearance of the major populationin spring. This is always close to the mainlambing time, but may occur when lambsare plentiful or sparse, which will influencedisease occurrence.

Small numbers of I. ricinus can befound on sheep throughout the year and ina few areas (Northumberland and south-eastScotland) there is no autumn rise. Springrise and autumn rise ticks are differentpopulations.

Flock distribution

The number of licks found throughout the sea-son on sheep increases with the age (or size) ofthe sheep. In one count on a heavily infectedfarm, ewes had 400 adult females, yearlinghoggs 300 and lambs 50, together with aboutfive times as many nymphs as adults, and1000 limes more larvae than adults.

Sheep distribution

Ticks attach initially to the ears, nose, lipsand feet and they migrate to become attachedto the hairy parts with only small numbers inthe woolly areas. Adults migrate further thannymphs and larvae hardly migrate at all.

Importance

Ticks are responsible for irritation and a cer-tain amount of blood loss, particularly inyoung lambs (tick worry) and for thetransmission of: (i) tick-borne fever (TBF);

(ii) tick-bite pyaemia; (iii) louping-ill; and(iv) Lyme disease. The tick-transmitted dis-eases are more important than tick worrybecause heavy infestations are uncommonand the blood loss is over a period of someweeks, which allows for compensation,except in lambs. Grouse are especially sus-ceptible to louping-ill and vaccination ofsheep and treatment for ticks has been shownto reduce the infection and mortality in grouseon moors where they are living together.

Control

Tick control is often affected by improve-ment in grazing associated with increases instocking rate. It can be done by pastureimprovement and by chemical treatment ofsheep.

Pasture improvement

Many hill farmers drained and re-seeded therelatively low pastures bordering on the highhills in order to improve lambing percentageand live-weight gains in the lambs. This hada dramatic effect on tick populations.However, if some grazing is improved and isused for ewes late in pregnancy and early inlactation, a waning of immunity to tick-bornedisease (especially louping-ill) may result,followed by disease when the sheep are laterturned on to the tick-infested hill grazings.A similar problem may occur with sheepwhich are away-wintered on lowland pas-tures. Heather burning every5-7 years reducesbut does not eliminate tick populations.

Chemical treatment of sheep

Sheep can be treated for ticks by 'plunge-dips', `pour-ons' or `spot-ons'.

Plunge-dipping in a bath can only bedone with diazinon, an OP compound.There are strict regulations for OP com-pounds to reduce the likelihood of toxicityto the operators who must also be licensedafter taking an appropriate course. Dippinglambs can lead to mismothering so is usedless commonly since the advent of the otherproducts.

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Pour-ons' and `spot-ons' use cyper-methrin or deltamethrin (SP compounds)and are applied with a special gun along themidline from the shoulders back but avoid-ing the tail of lambs in order to prevent mis-mothering. The drug spreads over the skinsurface in the sebum and will control ticksfor up to 12 weeks in adults and 4-6 weeksin lambs. These `pour-ons' are particularlyuseful for lambs as mismothering oftenoccurs after dipping. Operators should wearprotective clothing with SP compounds.

Ewes are dipped to reduce the pastureinfestation in successive years and lambsare protected to try and reduce the numberof ticks which they pick up. It is recom-mended that all ewes should be treatedeither before lambing at the end of March orbeginning of April or preferably after lamb-ing before going to the fell. Lambs may betreated from 4 days old.

Sheep should be re-treated in autumn

Diseases Transmitted by Ticks

Tick-borne fever (TBF)

This is caused by a rickettsia, now calledAnaplasma phagocytophilum, formerlyEhrlichia (Cytoecetes) phagocytophila. A sim-ilar organism of close antigenic identity isfound in cattle. The organism is transmittedby the nymph and adult of I. ricinus andmost ticks are infected throughout the worldincluding the USA. It causes disease in anumber of hosts including humans whereit is responsible for human granulocyticehrlichiosis.

The rickettsiae invade the circulatingneutrophils and monocytes and results intheir destruction, thus causing a neutrope-nia. It is this feature, combined with pyrexia,which gives rise to clinical signs and pre-disposes the sheep to tick pyaemia andincreases the severity of louping-ill. Inexperimental studies, it has been shown toreduce the immune response to many anti-gens and infections such as pneumonia so itis possible that it predisposes to otherinfections in the field.

Clinical picture

Since most ticks are infected, lambs in a tickarea become infected early in life. The clini-cal signs are mild and are usually not noticed -the lambs may be listless, fail to suck andhave a temperature rise (up to 41°C) for afew days. There is some evidence that somestrains are more pathogenic than others.Organisms can be found by Giemsa stain ofa thin blood film Immunity then developsand is probably short-lived, but is reinforcedthroughout life, producing 'acclimatized'sheep. There are no antibodies to TBF in thecolostrum, so lambs become infected as soonas they encounter ticks. More severe signsare seen in adult sheep brought from a tick-free area. The high temperature which fol-lows exposure to ticks may result in abortionin pregnant ewes (unusual because the timeof year is usually wrong) and temporaryinfertility (for about 3 months) in rams. Thisis of considerable importance since rams areusually purchased at September/Octobersales and become infertile just at the timethat they are turned out with the ewes.

Control

The organism is susceptible to sulfonamidesand broad-spectrum antibiotics, but it ismore important to obtain satisfactory immu-nity in lambs and to produce acclimatizedsheep. Do not move non-immune rams orpregnant ewes into a tick area, at least dur-ing the breeding season.

Tick-bite pyaemia

This is a generalized infection with Staph.aureus, a normal skin commensal, of lambsof 2-16 weeks old associated with tickbites and usually predisposed by TBF.Neutropenic lambs have been shown to behighly susceptible to staphylococcal septi-caemia. The disease is either a septicaemiaresulting in death or the bacteria localize inmany organs, producing abscesses in joints,CNS, liver, lungs, etc. Lambs are rarelyinfected before 2 weeks of age, probablybecause the neutropenia from TBF is not

Ticks and Tick-borne Diseases 147

evident before this time and also becausetitres of staphylococcal antibodies derivedfrom the colostrum wane at about 2 weeks.

Clinical signs

These vary with the site of the abscesses andinclude: (i) lameness with painful enlargedjoints; (ii) paralysis of the hind legs due toan abscess in the spinal cord; (iii) signs ofmeningitis due to abscesses in the brain andmeninges; or (iv) unthriftiness due toabscesses in liver, lungs, kidneys, etc.

The septicaemic form shows in suddendeath. The disease occurs wherever I. ricinusis found and is of great economic importance.It has been shown that half the lamb lossesand virtually all the lameness in lambs on alick farm is associated with tick-bite pyaemia.

Treatment

Antibiotics (e.g. penicillin) are effectiveagainst the organism and if lambs are treatedearly, the clinical signs may regress and thelambs recover. Lambs with spinal abscessesor with multiple abscesses in the liver andlungs are unlikely to recover despite treat-ment and it has been suggested that penicil-lin only hastens the recovery of lambs whichwere likely to recover spontaneously.

Control

Tick control and control of TBF.Synthetic pyrethroids applied to 7-day-old lambs before putting on tick habi-tats will delay infection until they are4 weeks old, and disease is then muchless severe.LA penicillin or oxytetracycline havebeen employed prophylactically justprior to exposure to licks, when the lambsare sent with the ewes to the fell, butthese only last for a few days and are notlikely to influence disease significantly.

Louping-ill ('trembling')

This is a virus disease (flavivirus) which affectssheep and many other hosts, including cattle,

deer, man, dogs and red grouse. Typically,there is an initial viraemia about 2-6 days afterthe tick bite, during which there is a febrilereaction (42°C). The majority of acclimatizedsheep show few clinical signs and even sus-ceptible sheep will usually recover rapidly. Insome sheep, however, the virus invades theCNS and severe clinical signs and death fol-low. There is evidence that a primary TBFinfection at the same time increases the likeli-hood of invasion. The virus is transmittedstage to stage by I. ricinus and only about onein 1000 ticks is infected. Some lick areas haveno louping-ill virus present at all.

Clinical signs

Disease is seen in all ages of sheep from asearly as 2 days old (suggesting prenatal infec-tion) to aged ewes. Lambs are dependent oncolostral immunity for protection, which isstrongest when immune ewes are exposed tore-infection a few weeks before lambing.Changes in grazing practice may prevent thisnatural boost to the immunity of the ewesand many lambs may then become clinicallyaffected. Lambs may be found dead, but thetypical signs are those associated with CNSinvolvement and are variable in nature. Theyinclude: (i) resting the head on the ground;(ii) head pressing; and (iii) abnormal jerkygait (`leaping'), staggering, circling and paral-ysis. Fine tremors of the facial muscles andears, nystagmus and twitching or nibbling ofthe lips may be seen. The disease progresseswithin 1-4 days to coma and death, oftenassisted by predators.

Usually only a small proportion of theflock is affected, but outbreaks may beexplosive with a high mortality. Animalswhich have recovered from the viraemiahave a solid life-long immunity and specificantibody can be detected in their blood.

Diagnosis in a severe outbreak is usu-ally made on clinical grounds but CCN, lis-teriosis, swayback, gid or abscesses must beconsidered. There is a typical histology ofthe brain and virus can be recovered at thelaboratory by mouse inoculation. There is aserological test for antibody. The disease isparticularly important in red grouse whereabout 80% of infected birds die.

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Treatment and control

Treatment is not effective but careful nurs-ing indoors may save some cases.

The aim of control is to ensure thatewes are immune and that lambs are pro-tected passively. There is an inactivatedvaccine available which is a white oilyemulsion. Warming of the vaccine to bodytemperature facilitates injection. The rec-ommended procedure for ewes is that 1 mlshould be injected subcutaneously on theside of the neck between tupping and mid-pregnancy and not later than 1 month beforelambing with a boost every other year beforelambing. It may be necessary to protectewe-lamb replacements before the autumntick rise.

Lyme disease

This zoonotic infection is caused by the spi-rochaete Borrelia burgdorferi and is trans-mitted in the UK by I. ricinus. Serologicalstudies show that in Scottish sheep as manyas 40% of hoggs showed antibody, withonly small numbers of lambs and older ewesshowing significant antibody titres. No clin-ical signs were seen associated with thepositive serology though severe lamenesshas been described in 6-month-old lambs inNorway associated with high titres of anti-body and heavy tick infections.

It is possible that sheep act as a reser-voir of infection of Borrelia from whichticks become infected and thus transmit theinfection to more susceptible hosts like dogsand humans. It is an increasingly recog-nized disease of hill walkers as ticks easilybecome attached to humans often without itbeing realized.

Summary of Control Methods forTicks and Tick-borne Diseases

Possible control methods for ticks and thediseases they transmit are:

Dip ewes around lambing and in theautumn (and possibly in the summerbut this needs to be related to treatmentfor blowfly strike) to reduce tickpopulations.Apply `pour-on' or `spot-on' prepara-tions to lambs before returning them totick areas.Administer LA penicillin or oxytetra-cycline to lambs before returning to tickareas.Take special care over the introductionof new rams and ewes.Vaccinate ewes against louping-illevery other year and lambs before theautumn rise.Carry out heather burning of areas onthe fells on a 7-year rotation.

17

Notifiable Diseases and Diseases Exoticto the UK and Northern Europe

Notifiable Diseases

All sheep-rearing countries take measuresto avoid the introduction of serious diseasesand to control them in the event that theydo become introduced (Figs 17.1 and 17.2).These measures include the legal require-ment for owners of animals to report sheepshowing clinical signs associated with a listof notifiable diseases to government veteri-nary authorities. In addition, many coun-tries require the reporting of other nameddiseases which do occur in the country butfor which special measures are being takento control or eradicate the disease or whichare of particular importance, notably ofzoonotic potential.

Australia has an extensive list of 93notifiable diseases for all species of farmanimals and horses for the whole countryand in addition, individual states are per-mitted to include other diseases. Thisnational list contains around 20 diseasesof sheep including exotic diseases whichdo not occur in the country includingbluetongue, Brucella melitensis infection,contagious agalactia, EAE, FMD, MV, pestedes petits ruminants, Rift Valley fever,sheep pox, sheep scab and scrapie. It alsocontains diseases like ovine pulmonaryadenomatosis and paratuberculosis(Johne's disease) which do occur in some

states and which form part of an officialcontrol scheme.

In the UK, the list of notifiable diseasesincludes many of the exotic diseases in theAustralian list and like Australia, many ofthem have never been seen in the UK andone, sheep pox, was last seen in 1866. Thereis one endemic notifiable disease of sheepin the UK, namely scrapie, which is dis-cussed in Chapter 14. There are two notifi-able diseases of sheep which are notendemic but have been seen in recent yearsand which are of considerable significance -these are bluetongue and FMD which aresubject not only to UK national legislationbut also to EU measures. These two diseaseswill be discussed here and some of the moreimportant notifiable diseases which occurin some parts of the world but not in the UKor Australia will also be included in thischapter.

Foot and mouth disease (FMD)

The massive outbreak in the UK in 2001resulted in over six million animals beingslaughtered, around five million of whichwere sheep (this number does not includeyoung animals at foot, especially lambswhich were not recorded. An estimate oftheir number resulted in the often quoted

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150 Chapter 17

Fig. 1 7.1 . These sheep kept in the Mediterranean region may suffer from diseases that could potentiallyspread to other areas of Europe.

Fig. 17.2. Sheep specialists should have some knowledge of exotic diseases such as those that may affectthese sheep in South Africa.

figure of ten million animals being slaughteredand valued at around £4 billion).

The primary outbreak was in pigs butlarge numbers of sheep farms were affectedearly in the outbreak, associated with themovement of sheep via a market in theaffected area to many other areas of the UK,since there was a considerable delay inreporting disease on the pig farm.

Clinical signs

The disease is severe in young lambs withhigh mortality and in pregnant ewes, result-ing in abortion but many sheep do not showobvious clinical signs. Where clinical signsoccur, sudden, severe lameness, usually inmore than one leg, is the most obvious fea-ture but since lameness due to other causes

Notifiable Diseases and Exotic Diseases 151

is so common in sheep, it is easy to miss thesignificance of the lameness. Sheep liedown and are often unwilling to rise orstand in a crouching position.

Early lesions are blanching and separa-tion of the interdigital skin at the coronaryband occurs; after a day or two, the lesionsbecome ulcerative and granulomatous andare easily confused with early FR.

Mouth lesions are less obvious and thesheep may eat normally with no excessivesalivation as occurs in cattle. Blanching andseparation of the mucous membrane occurs,particularly on the dental pad and less often,on the tongue and ulceration occurs within1-2 days of the initial blister. The carefulexamination of the mouths of many sheepduring the outbreak led to the recognition ofmouth lesions that looked similar to FMD butwere due to other causes, probably associatedwith mechanical damage. Initially called`OMAGOD' (ovine mouth and gum obscuredisease) or idiopathic oral ulceration, theymade diagnosis difficult. A recent retrospec-tive study on stored samples has shown that23% of premises suspected of having FMDdid not actually have the disease. Since theaim was to kill the animals on a suspect farmwithin 24 h, this was often before viral confir-mation was possible which has led to thesearch for 'pen-side' tests for on-farm usewhich is showing some success.

If there is any doubt, ask the boss or theDivisional Veterinary Manager to examine thesheep and stay on the farm until they have.

Control

FMD virus has entered the UK in the past by:(i) imported carcasses from South America;(ii) wind from the continent of Europe; and(iii) escape from a laboratory which workedon the disease. It is also possible that scrapsof infected meat from ships or illegal importsmay bring this disease into the UK. Primarycases were often seen in swill-fed pigs andthis practice has now been banned. Carefulsurveillance of the FMD status of countriesfrom which meat is imported helps to reducethe risk associated with the meat industry.All countries in the EU fall into the highestinternational FMD status of FMD-free and no

country is allowed to use prophylactic vac-cination. In addition, the movement of ani-mals in the UK is now much more carefullyregulated which would reduce the risk ofrapid spread which occurred in 2001.

The control strategy relies on the rapidreporting of suspect animals by farmers andveterinary surgeons followed by diagnosisand typing of any FMD virus isolated. Allsusceptible animals on the infected premisesand on farms which are considered to be dan-gerous contacts are slaughtered. The EUdirective allows emergency vaccination alongwith the implementation of the slaughterpolicy but a decision to vaccinate can only bemade by the Government Secretary of Statefor Agriculture after a positive diagnosis hasbeen made. It is believed that this vaccinationpolicy, perhaps of a ring nature of susceptibleanimals on farms surrounding the infectedpremises, will limit the spread of the disease.Banks of vaccine and antigens from a range ofFMD strains are held in EU countries.

Bluetongue

Bluetongue is a viral infection caused bybluetongue virus (BTV) of ruminant animalswhich occurs widely in tropical and sub-tropical countries throughout the world.There are more than 20 serotypes of BTV,each of which is immunologically distinct.

In recent years, there have been manyoutbreaks in several Mediterranean coun-tries and it has been suggested that globalwarming has encouraged the northern andwestern spread of the insect vector, themidge Culicoides imicola. It is believed thatthe virus spread into Europe from Turkeyand North Africa and strains of serotypes 2,4, and 9 have been identified in south-eastEuropean countries.

In summer 2006, outbreaks of diseaseassociated with a sub-Saharan strain, BT8occurred in the Netherlands and Belgiumand spread to Germany and France. The ori-gin of this strain has not been proved.The inevitable spread to the UK occurred inSeptember 2007, when cases were seen inEast Anglia, believed to be explained by

152 Chapter 17

infected midges being blown across theNorth Sea. The disease spread to other partsof south and south-east England.

Bluetongue does not affect or infecthumans and so has no public healthsignificance.

Epidemiology

The virus is transmitted by species of bitingmidges of the genus Culicoides, some ofwhich are widespread in the UK. Directanimal-to-animal transmission does not occur.In temperate climates, the adult fly is notactive during the winter and clinical diseaseis seen only from July to December so it wasbelieved that the outbreaks on the continentwould die out during the winter. However,this did not prove to be the case and outbreaksin northern Europe were more numerous andmore virulent in summer 2007 than in 2006,and in 2008 there were over 30,000 outbreaksin the EU. It has been shown that bluetongueoverwinters in northern Europe more effec-tively than had been expected probably dueto a combination of: (i) animals maintaining aviraemia for a long time; (ii) the survival ofsome midge species; and (iii) the transplacen-tal transmission of the virus.

Clinical signs

Usually, cattle remain as carriers with fewsigns and the disease is more virulent insheep but in the 2007 Netherlands cases,cattle were also seriously affected. Mortalityin sheep can be as high as 70% but the sever-ity is dependent on the breed of sheep.

In sheep, the disease is characterized byfever up to 42°C that may last for several days.Increased respiration and hyperaemia andswelling of the lips, mucous linings of themouth and nose and eyelids are seen, accom-panied by salivation and frothing at themouth. Nasal discharges are common Thereis sometimes oedema of the head and neck.The tongue may be cyanotic, giving rise to thename bluetongue. Laminitis and inflamma-tion of the coronary band may result in lame-ness and reluctance to stand Animals losecondition rapidly, including muscle degener-ation. Infection during pregnancy may resultin abortions and congenital abnormalities.

PME shows typical haemorrhages inthe pulmonary artery.

Control

As the result of a successful vaccinationcampaign, the UK was granted bluetongue-free status in July 2011 which removed therestrictions on the export of cattle and sheepintroduced in 2007. BTV cases were onlyidentified in home-bred ruminants inEngland though a case in an imported cowfrom Germany was found in Scotland. Nocases were seen in Wales.

Control was based on vaccination withnew dead vaccines which became availablefrom May 2008, a remarkably rapid devel-opment by several drug companies. Theuse of vaccine was voluntary in England,with the farmer bearing the full cost but theScottish Parliament decided that vaccina-tion would be compulsory with the farmeronly paying half the cost. The vaccinationcampaign was so successful that a total ofonly 149 farms had infected animals andno cases have been seen since 2008. EUdirectives state that prophylactic vaccina-tion cannot be used in a bluetongue-freecountry but veterinary authorities andfarming organizations are seeking permis-sion to allow stock to be vaccinated if farm-ers wish.

A fall in the number of infectedpremises has been seen in other EU coun-tries though small numbers of cases due toserotypes other than BT8 are still being seenon the continent of Europe so constant vigilis needed.

Control in countries where the diseaseis endemic is by vaccination but the largenumber of serotypes makes this difficult.

Diseases Exotic to the UKand Northern Europe

This book is based primarily on sheep dis-eases experienced in the UK, much ofwhich also applies to sheep kept through-out northern Europe. Where appropriate,we have tried to indicate which of thosediseases are also important in other major

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sheep-keeping countries such as Australia,New Zealand and South Africa, and, to alesser extent, in North and South America.There are a number of serious diseases thatdo not occur in northern Europe that affectsheep in large areas such as theMediterranean region, Africa, the MiddleEast and the Far East, of which it is impor-tant that the complete sheep vet has anappreciation. Some of these require vectorsnot present in temperate countries, but oth-ers could potentially occur almost any-where as a result of uncontrolled or illegalanimal or animal product movements. Thissection briefly brings together some infor-mation on the most important of these.More information is available from websites such as:

www.oie.int - web site of the OIE (WorldOrganisation for Animal Health);www.fao.org/ag/againfo/themes/en/animal health.html - web site of theFAO (Food and Agriculture Organizationof the United Nations); andwww.ec.europa.eu/food/animal/diseases/adns/adns en.htm - web site of theEuropean Commission.

One extremely important disease,known for thousands of years, that has inthe past affected sheep as well as cattle, wasrinderpest (cattle plague, murrain) whichoccurred as epidemics in Great Britain inthe 18th and 19th centuries. The last epi-demic in 1865-1867 led to the setting up ofthe State Veterinary Service. In 2011, whilewriting this edition, it has been confirmedthat rinderpest has been the first animal dis-ease to be globally eradicated.

Peste des petits ruminants

This is caused by a member of the genusMorbillivirus, closely related to that causingrinderpest. The disease is found in Africa,the Middle East and eastwards toAfghanistan, Pakistan and India. Clinicalsigns include fever, catarrhal head dis-charges, necrotic stomatitis and diarrhoea,often with a high mortality rate. Control isby vaccination.

Rift Valley fever

This disease is caused by a member of thegenus Bunyavirus, which is transmitted bymosquitoes. It occurs in sub-Saharan Africaand more recently has spread into theArabian peninsula. Infection in younglambs leads to a high mortality rate whichcan also occur in adults, though some mayshow a milder illness. Signs are mostly non-specific but often include haemhorrhagicdischarges from body orifices. Control is byvaccination. This disease is a zoonosis.

Nairobi sheep disease

This is also caused by a member of the genusBunyavirus, transmitted by Rhipicephalusticks in East and Central Africa. It causessimilar signs to those seen in peste des pet-its ruminants, with high mortality rates.Control is by the use of acaricides to controlthe tick vector.

Akabane disease

This is caused by yet another member ofthe genus Bunyavirus, transmitted mainlyby Culicoides spp. midges. Disease hasoccurred mainly in Japan and Australiawhere fetal infection has been the mostcommon presentation, leading to congeni-tal birth defects such as arthrogryposis andhydranencephaly. Diagnosis is by serologyand vaccines have been developed but arenot widely used.

Sheep pox

This disease occurs in sheep and goats andis caused by a member of the genusCapripoxvirus. It occurs in Africa north ofthe equator, the Middle East and parts ofAsia and has spread on several occasionsinto southern Europe from Turkey. Spreadis by direct contact and aerosol. Clinicalsigns vary according to the breed of sheepand to the strain of virus and the mortality

154 Chapter 17

rate can be high. Affected animals developfever with swollen lymph nodes and mac-ules and ulcerating papules develop on theskin and mucous membranes. Internallythere are lung haemorrhages. Control inendemic areas is by the use of live, attenu-ated vaccine.

Rabies

This fatal disease, caused by a member ofthe genus Lyssavirus, occurs in areas suchas North Africa and the Near East wherestray dogs are a problem.

Anthrax

This bacterial disease, caused by thespore-forming Bacillus anthracis, is found

worldwide. In some countries such as partsof Africa it is endemic. In others, such as theUK, it occurs very occasionally, mostly incattle, though sheep can be potentiallyinfected. It causes sudden death, the mostcharacteristic signs being dark blood oozingfrom body orifices and an enlarged spleen.In endemic areas it is controlled byvaccination.

Brucella ovis

This causes epididymitis in rams. It doesnot occur in the UK but is common in manyother countries. See Chapter 2.

Brucella melitensis

This is an important cause of abortion andhuman disease (Malta fever) in theMediterranean region, Middle East, Indiaand parts of Africa.

18

Health Schemes

There are two major types of sheep healthschemes: (i) national (or regional); and(ii) individual farm schemes. The nationalschemes aim to produce a pool of sheepflocks of recognized health status withregard to certain specified diseases.Individual farm schemes are provided bypractising veterinary surgeons for their cli-ents and are 'tailor-made' for a particularflock.

National and Regional Health Schemes

As described in Chapter 17, most sheep-producing countries have a list of exoticnotifiable diseases, designed to preventtheir introduction into the country. Othernotifiable diseases endemic to the countrymay be subject to special control measuresif they are widespread and of considerableeconomic importance. In addition, certainother non-notifiable diseases may be of suchsignificance that organized voluntaryschemes are designed to improve their con-trol. All these diseases may be included innational or regional health schemes.

In Australia, for example, officialnational schemes are available to improvethe control of the notifiable endemicdiseases, paratuberculosis (Johne's disease)and pulmonary adenocarcinoma (Jaagsiekte)

and in addition, the State of New SouthWales made virulent FR notifiable andsubject to eradication schemes some 50years ago.

In the UK, a national health scheme isavailable for the control of scrapie, a notifi-able endemic disease whereas other endemicdiseases, including EAE and CLA, areincluded in the national health scheme butare not notifiable.

In Scotland, but not in the rest of theUK, statutory measures have been taken tohelp with the control of sheep scab whichrequires farmers to notify the veterinaryauthorities of any known or suspect cases ofsheep scab. It also allows inspectors torequire farmers to pay for veterinary help indiagnosis and to treat any infected sheepflocks. In addition it makes provision forthe control of infection which arises oncommon grazing or in markets.

Premium Sheep and GoatHealth Schemes

The Premium Sheep and Goat HealthSchemes are administered by SAC and arethe official UK sheep health schemes. Theyare all voluntary and aim at improving thehealth and welfare of sheep throughout theUK. The diseases covered are:

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 155

156 Chapter 18

MV.CLA.EAE.Scrapie.

Full details are available on the web sitewww. sac. ac.uk/consulting/services or con-tact as follows: Sheep and Goat HealthSchemes, PO Box 5557, Inverness, IV2 4YT.

The schemes offered are briefly out-lined here.

Maedi visna/caprine arthritis encephalitis(MV/CAE) accreditation

This certifies flocks free of MV (and the simi-lar disease CAE in goats) after passing twoqualifying blood tests, providing that stringentbiosecurity rules are observed, preventingcontact with non-scheme sheep. A propor-tion of the flock is tested every 2 years tomake sure that animals remain negative.

Caseous lymphadenitis (CLA) testing

This aims to identify infected animals at anearly stage before significant transmissionhas occurred. An ELISA test developed atthe Moredun Research Institute whichdetects antibody to C. pseudotuberculosisis used on all animals every 3 or 4 months.Positive animals are then removed fromthe flock by culling. This is obviously anexpensive method but has been shown tobe effective in producing a clean flock.Another use is to screen animals beforepurchase to prevent introduction of thedisease into a clean flock. Animals screenedby a combination of blood testing and clin-ical examination are available at a limitednumber of ram sales.

Enzootic abortion of ewes(EAE) accreditation

This aims to establish a register of flockswith a high health status based on freedomfrom EAE. It is of particular value in provid-ing EAE-free hallbred replacements for low-land farms from hill flocks which aremembers of the scheme. EAE monitoring isby examination of all abortions at the localSAC/VLA Centre, by serology on all aborting

and barren ewes and on a statistical sampleof the healthy ewes within 3 months oflambing. Testing is carried out annually andafter 1 clean year, the flock is designated asbeing `EAE supervised' and, after 2 years, as`EAE accredited' status and included on aregister. Every consignment of breedingstock from a certified flock is given a certifi-cate, the flock may be advertised as EAEaccredited and a premium can be expectedfrom purchasers for this status. Vaccinationof ewes cannot be used in scheme flocks dueto interference with the serological test.

Scrapie monitoring and genotyping

A monitoring scheme is available for breed-ers wishing to export sheep throughout theEU. This involves annual inspection of theflock and screening of brains from somedead or cull animals. A genotyping schemeis available for selecting breeding sheep of aresistant genetic makeup (see Chapter 14).

Individual Farm Health Schemes

Veterinary surgeons with their special knowl-edge of the epidemiology, control and theeconomic importance of disease have made aconsiderable contribution to the improvedwelfare and success of dairy, pig and poultryflock health and production throughout theworld. There are numerous studies on theadverse economic effects of conditions indairy cows like lameness, mastitis and infer-tility which show that the distinctive knowl-edge and expertise of the veterinaryprofession can be applied to improve thefinances of a farm as well as the health andwelfare of the cows. Planned health schemesand regular visits are a feature of the work ofdairy and pig specialist veterinary surgeonsbut although many attempts have been madeover a number of years, in the UK, thereseems to be reluctance on the part of somesheep farmers to use their veterinary sur-geons for this type of scheme. In Australiaand New Zealand and a few other countries,sheep veterinary specialists are able to workand make a living solely on sheep but this israrely true in the UK.

Health Schemes 157

There are many reasons for this lack oftake up. Long-term studies on the effect ofhealth programmes developed by and runwith veterinary supervision are needed todemonstrate whether the benefits aresignificantly greater than the costs. Somestudies on the costs of specific disease likelameness, fasciolosis and other parasiticdiseases are becoming available and show

that veterinary advice does give a goodbenefit-to-cost return.

A great opportunity exists for UKveterinary surgeons to be involved in theformulation of health programmes withfarmers (Figs 18.1 and 18.2) as these arerequired as part of the SFP scheme for theCAP of the EU. The Animal Health PlanningSystem (SAHPS) is a web-based scheme

Fig. 18.1. Health programmes are aimed at maximizing production and minimizing losses from disease in flocks.

Fig. 18.2. Owners of small hobby flocks such as this are often very keen to follow health plans andeconomics are usually not very important.

158 Chapter 18

developed by the SAC but available to vetsthroughout the UK (www.sahps.co.uk) andis now being used in nearly 800 flocks soshows signs of optimism on the part of bothvets and some enlightened sheep farmers.This web-based system has the advantage ofbeing updated continuously as newsbecomes available or new technical advancesare made. It produces a calendar of farmevents, analyses production and financialdata and allows comparison with dataobtained from other farmers which is help-ful for arriving at targets. Data is easy toupdate each year. It can be accessed any-where there is internet access, allows com-munication between farmer and veterinarysurgeon and contains links to useful infor-mation such as descriptions of specific dis-eases and drug withdrawal times. Anotherweb-based scheme is produced by WelshLamb and Beef Promotions Ltd at www.wlbp.co.uk and is provided for registeredmembers of its lamb, beef and dairy schemesand their veterinary surgeons. Other schemesmay be produced by groups or individualvets and others for more localized use.

Successful on-farm schemes often startin a modest way with reaction to a particulardisease event. If the control plan has a posi-tive outcome it may then lead on to a moredetailed discussion with the farmer and theproduction of a more comprehensive healthplan. However, experience has shown that itis usually best to concentrate on a limitednumber of diseases or issues at first, ratherthan going for a hugely complicated planconsisting of many pages of information andinstructions that may well lie in the officedrawer on the farm until the next visit.

All farms have unique features and soan individual health plan is needed foreach. The following is an account of schemeswhich we and others have used on UK com-mercial sheep farms.

Objective of farm health scheme

To produce, monitor and maintain a uniquehealth scheme for a particular farm, in thebelief that this will both decrease disease

and increase production and contribute tothe welfare of sheep in the flock.

The scheme

The scheme has three components:

1. A written health programme containingrecommendations for the control of expecteddiseases and to improve production andwelfare.2. Planned visits (three or four annually) tomonitor health and production.3. Reactions to events and advice on newadvances during the year, to keep the pro-gramme up to date.

Its success hinges on the degree of coopera-tion between the farmer and the practisingveterinary surgeon and other advisors, andrequires honest pooling of information.

Health programme

Prior to producing a health programme,information about some or all of the follow-ing aspects of the flock will need to beobtained:

objectives of the flock;breeds, numbers, age structure;pasture and grazing management (includ-ing possible fluke habitats);feeding plans (types, quality andquantity);housing availability and management;lambing management including labour;clinical diseases experienced in the past;laboratory findings (including PME) ifavailable; andproduction and financial data as available.

As a result of the first planned visit dur-ing which a full and open discussion shouldtake place, a programme, in the form of a diaryof important management events through theyear, together with brief information on dis-ease areas highlighted as being particularlyimportant, is tailor-made to suit the needs ofthe farm. It is based around the fixed dates ofthe sheep breeding cycle - the proposed datesfor tupping, housing, lambing and weaning. Itshould address some or all of the followingmajor areas, depending on the commitment

Health Schemes 159

and interest of the farmer involved and onthem having identified the areas of most con-cern in their flock. The document may rangefrom its most basic form of a simple calendarof important events to a sophisticated compu-terized web-based system.

Rams - examination and preparationfor tupping time; use of teaser rams orother control of breeding.Ewes - condition scoring and culling ifnot done previously.Breeding schedule - date rams go inwith ewes and date removed (to pro-duce a compact lambing period).Vaccination schedule - essential andoptional disease cover.Lameness -identification of major cause(s)and control.Ectoparasites - status and control.Roundworms-control including anthel-mintic use and awareness of resistance.Liver fluke - control if applicable.Trace elements - known deficienciesincluding tests if necessary.

Lamb mortality - main causes and control.Feeding plans.Health of farm dogs including worming.

Planned visits

Several visits will be needed in order toassess the application and usefulness of thehealth programme. In the first year, three orfour visits are recommended though in sub-sequent years, fewer visits and samples willbe required.

Reactions to events

It will be necessary to modify the originalhealth programme from time to time duringthe year, as a result of unexpected events orfollowing information obtained during andin between the planned visits. The pro-gramme will need amendment at the end ofeach year to incorporate new research, drugsand vaccines in the light of the experienceof the past year and any alteration in theaims of the farmer.

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Appendix 1

Clinical Examination

Systematic Examination of a Sick Sheep

Carry out the examination in the ordershown, examining in more detail wherenecessary. If signs indicate a neurological

problem, a full neurological examinationshould be carried out. Use of an ultrasoundscanner may be helpful particularly for thethorax and abdomen.

From a distance

Parameter Some possible findings

Grade of illnessDuration of illnessGeneral appearanceMobilityFeeding

ConditionFleeceFaecesRespirations (count)HeadEyes

Mild, severe, dyingAcute, chronicNormal, excited, depressedRecumbent, unwilling to move, lame, ataxic, circlingPoor appetite, off food, difficulty eating, quidding, ruminating, regularity of

jaw movements if eating or cuddingThin, fat (beware of fleece masking)Broken, patchy, rubbingLoose, scour, absentDistressed, very fast, deep, coughing, nasal dischargeHigh, low, turn, tilt, ear(s) drooping, dribblingBlinking, blepharospasm, discharge

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162 Appendix 1

On handling standing

Parameter Some possible findings

Condition score (CS)TemperaturePulse (femoral) and/or heart rateFleece and skinAge and teeth

Incisors

Mandibles and molars (feel through cheeks)

Lips and gums

CheeksNostrilsEyes

Menace and palpebral reflexesEyelidsConjunctivaScleraCornea and anterior chamberPupils and lens

EarsLymph nodesLarynxChest

Auscultate heartAuscultate lungsWheelbarrow testUltrasound chest

Abdomen (size, consistency, ballot, ultrasound).Right kidney may be palpable behind last rib

Rumen (palpate, feel contractions, listen)

Abomasum and intestines (listen, ballot)FaecesVulva and vagina (F)

Prepuce, penis, testes (M)Legs and joints

1-5 (emaciated, thin, fit, fat)Normal is 39-40°CStrong, weak, rapid (may be fear, recheck later)Wool break, itchy (rub test), ectoparasites, scabs, sores

Number of temporary/permanent, broken mouth,periodontal disease, apposition

Thickening of mandibles, lumps, dischargingsinuses, pain, sharp edges, irregularities,food impaction

Sores, scabs, smell breath, gum colour (may bepigmented), ulcers, dribbling, capillary refill time

Impacted food, paralysisMovement, dischargeDischargePresence/absenceEntropionAnaemia, toxaemiaVessels injected, jaundiceKeratitis, uveitisSize, symmetry, cataractPosition, paralysis, discharge, haematoma, mitesEnlargement, abscessesObstruction causing stridor

Rate and soundsAbnormal sounds, absence of soundsExcess fluid from lungsAbscesses, tumoursDistended, tucked up, gas, fluid, solid

Irregular or absent contractions, abnormalresonance, gas, abnormal consistency

Abnormal sounds, no sounds, gas, solidPellets, soft, scour, blood, smellDischarge, fetal membranes, smell, injury,

bruising, haemorrhageUrethral obstruction/rupture, orchitis, epididymitisStiff, pain, swelling, abrasion, muscle wasting

Clinical Examination 163

Tipped up, sitting comfortably with back against legs of examiner

Parameter Some possible findings

Abdomen (palpate, ballot)Udder (palpate udder and teat canal)

Feet (locate painful digit by manipulation andpressure if not obvious)

Joints (knees, elbows, hips, stifles, hocks)

Fluid, solid, fetusSwelling, mastitis, fibrosis, abscess, gangrene,

milk, colostrum, serum, blind teat, sores, scabsOvergrown/loose horn, interdigital lesions/growths/

foreign body, smell, under-running (wall or sole),swelling, cracks, coronary band lesions

Pain, stiffness, swelling (fluid/firm)

Samples

BloodUrine

Faeces

From jugular vein (tube type depends on tests needed)By occluding nostrils (`smothering) for a few moments or use catheter. Use

test stick, check colour, turbidity, protein, ketones, bloodUsually for internal parasites

Appendix 2

Neurological Examination of Sheep

By working through the following sequence, possible to localize any lesion/s to assist innoting down any abnormalities, it should be making a diagnosis.

Indicator Some possible abnormalities

BehaviourMental stateHead positionHead coordinationCranial nerves

Menace testPupil sizePupil symmetryPupillary light responseEye positionEye movementPalbebral reflexFacial sensationJaw toneFacial symmetryBalancePrehensionSwallowing

StanceGaitNeck sensation and movementForelimbs

Skin sensationMuscle toneProprioceptionWheelbarrow testHemiwalking testTriceps reflex

Wandering, circling, head pressing, fitsHyperexcited, depressed, stuporous, comatoseTurn, tilt, high/low carriage, star gazingJerkiness, intention tremors

Visual deficitDilated/constrictedAsymmetryAbsentStrabismusNystagmusAbsentAbsentSlackFacial paralysisLoss of balance, rollingDifficultyDrooling salivaWide basedAtaxia, hypo/hypermetriaStiffness, opisthotonus

Absent (where?)Flaccid, spasticPlacing reflex absentDifficulty right/left/bothDifficulty right/left/bothReduced/increased/absent

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician164 (A.C. Winter and M.J. Clarkson)

Neurological Examination of Sheep 165

Indicator Some possible abnormalities

Pedal reflex Reduced/increased/absentDeep pain sensation Absent

TrunkPanniculus reflex Absent (side? level?)

Hind limbsSkin sensation Absent (where?)Muscle tone Flaccid, spasticProprioception Placing reflex absentHemiwalking test Difficulty right/left/bothSway response Can push over (side?)Patellar reflex Reduced/increased/absentPedal reflex Reduced/increased/absentDeep pain sensation Absent

Tail/anusAnal reflex Absent, rectum distendedTail tone FlaccidBladder control Incontinence

Blindfold (each eye in turn, then both) then reasses balance and gait, repeat wheelbarrow and hemiwalking tests.

Appendix 3

Checklist for Examination of a Sick Lamb

Indicator Select applicable description

Age Minutes/hours/daysBirth Normal/assisted/difficult/caesareanLitter size 1/2/3/4/5Lamb size Normal/small/large (? kg)Ewe condition score 1/2/3/4/5Ewe age ? yearsColostrum intake Sucked unaided/sucked with help/not fed/not known/

tube fed (volume ? ml)Temperature Normal/hypothermic/pyrexic (?°C)Respiration Normal/slow/rapid/laboured (?/min?)Heart rate Normal/slow/rapid/murmur (?/min?)Demeanour Normal/depressed/comatose/fitsPosture and gait Normal/standing but weak/sitting/lateral recumbency/

ataxic/shaking/lameBirthcoat Normal/poor/hairy/pigmentedHead

Jaw Normal/abnormalSalivation ExcessiveEyes Normal/entropion/discharge/other abnormality

Chest Fractured ribsAbdomen Normal/empty/distended (gas/fluid?)Navel Wet/dry shrivelled/swollen/pusAnal area Atresia/meconium/scour/bloodLegs Normal/swollen joints/fracture/contracted tendonsCastration No/yes (When? How?)Tailing No/yes (When? How?)

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician166 (A.C. Winter and M.J. Clarkson)

Appendix 4

Professional Development

Specialist Societies

Most countries with a significant sheeppopulation have an organization with a spe-cialist interest in sheep, small ruminants orperhaps one combined with beef cattle, forwhich details will be available from countryor state veterinary organizations.

Sheep Veterinary Society (SVS)

This is a specialist division of the BritishVeterinary Association (BVA) and member-ship is open to all members of the veteri-nary profession (whether BVA members ornot) and others interested in sheep. TheSociety holds two meetings a year (nor-mally 2 or 3 days) in spring and autumnwhich include farm visits as well as lec-tures and discussion in a friendly atmos-phere. Membership is a 'must' for all whowish to keep up with developments insheep veterinary work. Every fourth year(alternating with the international meet-ing, see below) the Society holds a meetingin another European country (for examplemeetings have been held in Denmark,

Holland, Germany and Spain). Contact theSecretariat at:

Sheep Veterinary Society (www.sheepvetsoc.org.uk)

Moredun Research InstitutePent lands Science ParkBush LoanPenicuikMidlothianEH26 OPZUK

International Sheep VeterinaryCongresses and the International

Sheep Veterinary Association

International meetings for veterinarians inter-ested in sheep have been held every fourthyear for over 25 years, initiated by the SVS inthe UK. Meetings have been held in the UK,New Zealand, Australia, South Africa, Greeceand Norway. The International SheepVeterinary Association has been set up tofoster relationships between sheep veterinar-ians worldwide and to oversee decisionsregarding the sites for future internationalcongresses (www.intsheepvetassoc.org).

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168 Appendix 4

Specialist Qualifications for SheepVeterinarians

The Royal College of Veterinary Surgeons(RCVS)

The RCVS offers certificate and diplomalevel qualifications. The certificate (CertAVP) is modular and can include farm ani-mal and sheep modules. It is designed forvets in general practice who have more thanan average interest in sheep and are willingto study a little more widely. The diploma(DSHP) is the highest standard of examina-tion and requires determination and a realcommitment to achieve. Details of sylla-buses, regulations and fees are availablefrom:

RCVS (www.rcvs.org.uk)62-64 Horseferry RoadLondonSW1P 2AFUK

European College of Small Ruminant HealthManagement

This college is a member of the EuropeanBoard of Veterinary Specialities and isresponsible for approving residents andtraining establishments and for awardingthe DipECSRHM. Applicants with at least 7years relevant experience, publications andpresentations can apply for de facto diplo-mate status until June 2013. After that datethe diploma will only be achievable byexamination. Although this is a EuropeanCollege, several notable de facto diplomatesare from countries outside Europe, forexample New Zealand, South Africa andCanada. Details are on the web site www.ecsrhm.eu.

Many other countries have schemes forachieving specialist sheep veterinaryqualifications and information about thesewill be available from country or stateveterinary authorities or other local veteri-nary organizations.

Appendix 5

Revision Problems and Questions

These are intended to help test your under-standing of the sheep industry and thecommon problems and diseases associatedwith it. Please note that these are based onsheep farming in the UK and are not com-prehensive. The suggested answers (given inAppendix 6) may not be complete or correctin every situation but are designed to makereaders think about what concerns sheepfarmers, problem solving and the most likelypossibilities to consider first. Problems andsuggested solutions may differ in sheepfarming systems in other countries.

Question 1

You meet one of your sheep clients at thelocal agricultural show. He mentions he isin the market for some new Charollais ramsand there is a forthcoming sale includingrams with EBVs. He asks whether you thinkit is worth spending extra money on theseor whether just to buy the ones he likes thelook of as usual.

i. What does EBV mean?ii. What main traits make up the EBV of

terminal sires such as Charollais rams?iii. What are the potential advantages toyour client of using rams with above-averageEBVs?

Related questions

a. What are the main characteristics ofthe Charollais breed and what does it looklike?b. How far in advance of the breeding sea-son should rams be checked and what arethe most important checks?c. How long do sperm take to mature?d. Are the reproductive capabilities oframs affected by season in the same wayas ewes are?

Question 2

You are asked in late July to do a flockhealth plan for a new client who is keen toimprove the management of the flock of250 Lleyn ewes. One objective is to tightenup the spread of lambing which currentlystarts in the second week of February andlasts to the end of March. The owner wouldlike to get most of the lambing completed inFebruary.

i. What factors do you have to take intoaccount in planning for the coming breed-ing season?

ii. What possibilities are available?iii. What are the advantages and disadvan-tages of each in this situation?

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170 Appendix 5

Related questions

a. What are the particular attributes of theLleyn breed?b. What is the length of the oestrous cyclein sheep?c. What is the length of the oestrous cyclein goats?d. Which British breed of sheep will breednaturally throughout most of the year?e. Which type of British breed has the short-est breeding season?

Question 3

The college-educated son has just takenover from his traditional father on one ofyour practice farms. It is an upland farmwith a flock of about 500 Swaledale ewes,mostly purebred, with a few rams sold forbreeding but most females kept as replace-ments and castrated male lambs sold asstores. Draft ewes are sold after four breed-ing seasons. The son wants to move tobreeding Mules which will be kept andcrossed with Texels to produce primeslaughter lambs. Some redundant cattlesheds are available for housing and lamb-ing. Father didn't believe in wasting moneyon vaccines but the son wants to implementa proper health plan including vaccinationif justifiable.

i. What aspects of flock managementwould you take into account in determin-ing your recommendations?ii. Would you recommend the use of anyvaccines and why?iii. If so, draw up a vaccination schedulefor the first year, starting in September orjustify your advice not to use vaccines.

Related questions

a. What type of sheep is a Swaledale andwhat does it look like?b. What is a draft ewe?c. How is a Mule produced and what are itsmain attributes?

d. What type of sheep is a Texel and whatdoes it look like?e. At what age and weight would you expectTexel cross Mule lambs to be ready forslaughter?

Question 4

You are carrying out a fertility visit to oneof your dairy farm clients who also has alowland flock of about 300 Mule ewes. Atthe conclusion of the visit, he says that heis worried because he seems to have a lotof thin ewes which are due to lamb in 8weeks' time.

i. What would you do and what are themost likely causes?ii. What dangers are associated with thissituation?

Related questions

a. What adverse consequences are likelyfor a flock of ewes with a low conditionscore (CS) at tupping?b. What is the most likely age for a lowlandewe which has one pair of broad (perma-nent) incisors in September?c. Do sheep develop protective immunityto liver fluke infection?d. Name two pneumonic conditions whichlead to thinness in old sheep.e. Name three diseases which might beassociated with liver flukes.

Question 5

One of your sheep clients phones in a panicas he has had eight abortions last week andsix abortions today.

i. What immediate actions would youtake?ii. Are there any dangers for himself andparticularly his wife, who is expecting theirfirst child in 5 months?

Revision Problems and Questions 171

Related questions

a. What effects other than abortion may yousee in a flock with enzootic abortion?b. Can you detect ewes latently infected withChlamydophila abortus by serological tests?c. What happens if a susceptible ewebecomes infected with Toxoplasma in thefirst 60 days of gestation?d. How is Campylobacter introduced into aclean flock?e. Name two causes of abortion in whichmummified fetuses are a feature.

Question 6

One of your clients contacts you about hisflock of 250 Welsh Halfbred ewes which hehoused 5 days ago in four pens. They aredue to start lambing in about 6 weeks andhave not been scanned. While out at grassthey were supplied with molasses bucketsand with some hay of which they did noteat much, which the farmer was not worriedabout as he thought the sheep looked well.He housed them in a bit of a rush as badweather was forecast. Their diet now con-sists of big bales of silage and 450 g pur-chased concentrate nuts per head fed oncedaily in troughs. Now two or three sheep ineach pen have become recumbent and oth-ers look dull and are off their food.

i. What are your initial thoughts about themost likely disease problems that might beinvolved?ii. Which factors in the management

described may be responsible?iii. How would you proceed to investigatethe problem?iv. What actions would you take to start totackle the problem?

Related questions

a. How is a Welsh Halfbred produced?b. What is their main role?c. When are crucial times to carry out con-dition scoring?

d. When is the best time to scan pregnantsheep?e. What is the normal gestation length forsheep?

Question 7

One of your clients in northern England isproposing to change from indoor lambing aflock of 400 crossbred ewes (producing 1.6lambs reared per ewe) in February to out-door lambing in March as there have beenproblems with coccidiosis and joint ill inlambs born indoors.

i. What problems can be expected withoutdoor lambing?ii. What precautions can be taken to mini-mize these?

Related questions

a. How is lambing percentage defined?b. How much colostrum do lambs requirein the first 24 h of life and does this varybetween lambs born indoors andoutdoors?c. For how long is the intestine permeable tolarge protein molecules (immunoglobulins)?d. For how long, approximately, do colos-tral clostridial antibodies protect lambs?e. What is the most common bacterial causeof joint ill?

Question 8

The owner of a flock of approximately 50pedigree Suffolk ewes contacts you duringlambing time. Five of the mature ewes havelambed with only one teat functioning. Asthese all have twins it means that extra lambshave to be artificially reared. Your client real-izes that nothing can be done with these ewesbut wants to try to prevent the same thinghappening next year.

i. What is the most likely time that thesesheep are becoming infected?ii. What do you suggest?

172 Appendix 5

iii. Would your advice be any different for aflock of 400 commercial ewes with the sameproportion of ewes affected?

Related questions

a. Name the two most common bacteriaassociated with mastitis in ewes.b. What are the most likely sources ofinfection?c. What are some possible predisposingfactors?

Question 9

One of your clients has a limited number ofpens for housing lambing ewes so ewes andlambs are normally turned out within 24hof birth. This year, due to adverse weatherconditions towards the end of lambing,ewes and lambs had to be held indoors for7-10 days, in some cases. Now, about 3weeks after turnout, some of these lambs,especially the twins, are scouring and los-ing condition.

i. What are the possible causes and howwould you go about making a diagnosis?ii. For each of the conditions you identifywhat is the possible sequence of events?iii. Suggest how you would proceed in eachcase.

Related questions

a. What are the main anthelmintic groups?b. Which anthelmintic group is most likelyto have worm resistance to it?

Question 10

You are reviewing a flock health pro-gramme for one of your clients who has aflock of about 300 Swaledales, most ofwhich are crossed with Bluefaced Leicesterrams to produce Mule lambs. The plan

was originally drawn up by the clienthimself. Lambing time is March into earlyApril. The best female Mule lambs aresold as breeding animals in the autumnsales and the males (castrated) are sold formeat throughout the late summer andautumn. After weaning in August, thelambs are put on to silage aftermath inorder to get them into good condition forsale. The ewes are vaccinated withclostridial vaccine but the lambs are notvaccinated. Each year there are a fewdeaths in the lambs in the weeks follow-ing weaning.

i. What are the main health issues thatneed to be considered for these lambs fol-lowing weaning?ii. What would you suggest is included in the

health plan specifically aimed at this agegroup?

Related questions

a. What does a Bluefaced Leicester looklike?b. What are the breed's main attributes?c. What is meant by 'aftermath'?d. What are the advantages and disadvan-tages of castration of lambs?

Question 11

One of your clients, who has a flock ofabout 50 pedigree Suffolk ewes, asks youabout tackling an ongoing problem withfootrot (FR). The flock sells mainly yearlingrams as well as surplus females for breed-ing. Attempts to get rid of the problem inthe past have been based on vaccinationand footbathing, but the owner would pre-fer not to use vaccination as it has resultedin a few lumps developing at the vaccina-tion site.

i. What do you suggest should be the aimin this flock - control or eradication?ii. What management factors might influ-ence your decision?iii. What measures would your action planbe based around?

Revision Problems and Questions 173

Related questions

a. What bacteria are involved in causingFR?b. What are the main products used forfootbathing and what are the advantagesand disadvantages of each?c. Clinically, how does FR differ from con-tagious ovine digital dermatitis (CODD)?d. What bacteria are associated withCODD?

Question 12

One of your clients who does not use youmuch for sheep work contacts you a weekbefore lambing is due to start. Since housinghis sheep 6 weeks previously many have beenscratching and losing some wool. He is nowconcerned that the lambs will become affectedafter birth.

i. What would you do first?ii. What are the two most likely

diagnoses?iii. For each diagnosis what are the treat-ment options?iv. What are the particularly difficult issuespresented by this problem at this time?

Related questions

a. What is a common cause of wool losswithout pruritus in late pregnancy/earlylactation?b. What would be the approximate weightof a fleece from an adult Mule ewe?c. What is the name of the chalky whitehairs found in the fleeces of some sheep andwhy are they a problem when wool is beingprocessed?

Question 13

Your client has been building up a smallflock of pedigree Beltex sheep for the past 6years. He asks you to examine a ewe whichwas purchased about 2 years previously and

which he has treated for pneumonia twicein the last few weeks. She is still breathingrather fast and has lost some weight.

i. What particular techniques can you useto examine sheep with respiratory disease?ii. What are the main possibilities in this

case?iii. For each main diagnosis, how can youconfirm, what are the implications for therest of the flock and what measures can betaken?

Related questions

a. What are the particular characteristics ofBeltex sheep?b. What upper respiratory disease is some-times seen in short-necked, highly muscledbreeds?c. What is the cause of atypical pneumonia andin what age group is it most commonly seen?

Question 14

One of your clients has been feeding hay asthe source of forage for his flock of crossbredewes which are housed for 6-8 weeks beforelambing in February to early March. Hay isbecoming difficult to make and expensive tobuy so he proposes to change to making andfeeding big-bale silage. He is aware of certainproblems related to silage feeding and asksyour advice to minimize any risks.

i. What disease is particularly associatedwith silage feeding?ii. In which part of the brain are lesions

found?iii. What are the key factors in making andstoring silage to minimize the disease risk?iv. What nutritional problems can be asso-ciated with silage feeding?

Related questions

a. How do the organisms you have identi-fied in (i) gain access to the body to causeneurological disease?

174 Appendix 5

b. What other disease pictures can theycause?c. What are the most common types ofspace-occupying lesion found in sheep?d. If a sheep is showing neurological signsincluding depression, circling and blind-ness in the right eye, where is the lesionmost likely to be sited?

Question 15

A client calls in your surgery asking for eyeointment to treat his lambs (1-3 weeks old)as a number have runny eyes. He has justhad an outbreak of New Forest disease inhis beef cattle housed in adjacent buildingsand suspects the lambs have caught it fromthe cattle.

i. Do you agree with his diagnosis? Whatwould you want to do?ii. What possible causes of eye disease are

there in this age group of lambs?iii. If your suspicions are confirmed whattreatment and advice do you give?

Related questions

a. What is the cause of New Forest diseasein cattle?b. What is the commonest bacterial cause ofeye disease in adult sheep?c. Do sheep develop a good immunity tothis?

Question 16

You have new clients who have just movedin summer from a lowland smallholding to aNorth Wales upland farm with more land,some of which is rough grazing with heatherand bracken. They have taken over the smallexisting flock of crossbred sheep but havebrought their own small flock of rare breed

Greyfaced Dartmoor sheep with them. Theboundary is well fenced and there are severalsmall fields of improved pasture near to thefarm buildings.

i. Apart from the usual disease issues whenmixing sheep from different sources, whatis a major disease risk for the newly movedsheep in this particular environment?ii. How do you suggest this is managed?

Related questions

a. Is this environment suitable for GreyfacedDartmoors?b. Suggest some other minority breedswhich might be suitable for keeping in thisenvironment in this area, rather than theresident crossbreds.c. What disease of humans might occur inthis type of environment?d. What problems are associated with ani-mals eating bracken?

Question 17

On a training course on notifiable diseasesyou are asked to name diseases causinglesions on and around the mouths and feetof sheep which might be confused with footand mouth disease (FMD).

i. Name the most common and give theirmain diagnostic features.ii. What signs might make you suspect thatyou had a possible outbreak of FMD?

Related questions

a. How is the bluetongue virustransmitted?b. Name two diseases of sheep, neitheroccurring in the UK, caused by Brucellaspp.

Appendix 6

Suggested Answers

Please remember these are suggestions!They indicate the most common factors youmight consider but may not be the onlysolution - all cases are different.

Question 1

i. Estimated breeding value.ii. Weight at scanning (21 weeks), lumbar

muscle depth, lumbar fat depth.iii. To produce faster growing lambs whichshould be ready while finished lamb pricesare still high. To produce better, more valu-able lamb carcasses with more muscle inthe expensive joints such as leg and loinand less wasteful fat. It is estimated thatlambs from high index rams can earn anextra £2-5 each. For a flock of 400 cross-bred ewes producing 1.7 lambs per eweweaned, this could increase income by over£3000.

Answers to related questions

a. A medium-sized, hornless sheep with apinkish face, with or without light-colouredhair. It has a short, dense fleece. The headand bone are finer than Texels or Suffolksmaking lambing easier. The main disadvan-tage is that newborn lambs do not have

much wool so may be more prone to hypo-thermia in cold weather.b. About 8 weeks before putting with theewes - check particularly teeth, toes andtesticles.c. Six to seven weeks so if condition is notcorrect at pre-tupping examination fertilitymay still not be good by tupping time.d. Rams are affected by season - testiclesize is reduced during spring and early sum-mer but they do not become infertile andare usually willing to mate at any time ofyear.

Question 2

i. To start lambing in early February, ramsneed to be in with the ewes about 7September so there is only 5-6 weeks left.Are ewes and rams in good condition? -look at them, condition score and adviseaccordingly. Lleyn ewes should be capableof lambing in February. Are rams nearewes - if so, move well away.ii. Vasectomized rams, progestagen

sponges, melatonin implants (but not reallyenough time to organize this).iii. Melatonin - barely time this year.Vasectomized rams - if not on farm alreadywill need to acquire and prepare some. Justabout time providing suitable animals can

A.C. Winter and M.J. Clarkson 2012. A Handbook for the Sheep Clinician(A.C. Winter and M.J. Clarkson) 175

176 Appendix 6

be found (may not be easy at this time ofyear). Will cost a bit of money if need to buy(probably three for this size of flock), biose-curity risks, cost of surgery. Plenty of timeto use sponges but also involves costs andquestion as to whether pregnant mare serumgonadotrophin (PMSG) needed (probablynot in late August). One possibility this yearis to put rams in field adjacent to ewes (afterkeeping them well away till then) for 2weeks before letting in with ewes, but thisneeds really good fences. Suggest keepingsome of next year's ram lambs to vasect-omize for next season.

Answers to related questions

a. Similar production to Mules - prolific,milky. Advantage is being able to breedreplacements and keep closed flock.b. 16-17 days.c. 21 days.d. Dorset (horn or polled).e. Primitives such as Soay (only has two tothree cycles usually).

Question 3

i. Increased intensification, increasedvalue of lambs, grow faster than purebredsso may be more susceptible to clostridialdisease, housing may make pneumoniamore likely.ii. Recommend use of 8-in-1 clostridial

vaccine, possibly plus pasteurella vaccine,depending on quality of housing and farm-er's attitude to risk.iii. Start in September by giving first doseof clostridial or combined clostridial/pas-teurella vaccine to all sheep that are remain-ing on the farm. Include rams. Give seconddose 4-6 weeks later. Give third dose topregnant ewes 4-6 weeks before lambingdue. Could risk leaving second dose to pre-lambing one in view of no history of disease(is this correct? Enquire about history) andproviding farmer understands risk. Givefirst dose to all female lambs to be retainedby 10-12 weeks of age and give second dose

4 weeks later. Fast-growing lambs are likelyto be ready for slaughter by about 16 weeksso could take chance of not being vaccinated(colostral antibodies should just about coverfor clostridial disease) but this is a risk.Slower fattening lambs should be fully vac-cinated (two doses) but could use 4-in-1vaccine designed for this age group.

Answers to related questions

a. A blackfaced mountain sheep with awhite nose, horned.b. A hill ewe that has bred successfully forseveral years and is sold to a lower, lessharsh environment where she could breedsuccessfully for another couple of years.c. Sire is Bluefaced Leicester, dam is aSwaledale or Dalesbred (North of EnglandMule) or Welsh Mountain or Specklefacedewe (Welsh Mule). Mule ewes are prolific,milky and good mothers.d. White faced, hornless, very meatysheep. Short neck, wide shoulders andlarge muscular legs.e. Singles ready from about 12 weeks, twinsfrom about 16 weeks (depending on milksupply of ewes and quality of grass) but salescan go on throughout summer and autumnFinished weight can be estimated from:weight of adult Mule ewe (65-70 kg approx.)+ weight of adult Texel ram (85-95 kgapprox.) divided by 4, that is approximately36-38 kg, although some may be sold a bitlighter or heavier depending on trade andtime of year.

Question 4

i. It is probable that the ewes are still out atgrass so arrange to visit the farm when theewes have been penned. Condition score atleast 50 ewes and estimate the extent of theproblem. If there are over five ewes whichhave a condition score (CS) of 2 or below, itis likely to be caused by the food or liverfluke infection though it is possible thatmolar teeth are involved, especially if theewes are draft hill ewes and are thus over

Suggested Answers 177

4 years old. If the sheep are on grass, exam-ine the pasture for quantity as the quality ofgrass in January is likely to be low (if qualityis low, more quantity should be available).Carry out a clinical examination of two thinewes and take faeces samples for fluke eggsfrom five.ii. There are several possible serious conse-quences and it is important that the foodshould be improved immediately by giving0.25 kg of concentrate feed per sheep daily.The lambs are likely to be small, increasinglamb mortality and decreasing lamb growth,both of which will be exacerbated by theeffect that that the low condition has oncolostrum and milk quality and quantity. Inaddition, the ewes which have two or morefetuses are in danger of ketosis (twin-lambdisease).

Answers to related questions

a. The number of lambs born is likely to below as ovulation rate is influenced by con-dition and can be improved by ensuringthat ewes are in increasing body conditionduring the tupping period.b. The ewe is likely to be around 18 monthsof age as the first pair of permanent teetherupt at just over 1 year old and most low-land lambs are born in March.c. No, which means that in bad fluke years,ewes of all ages may die from acutefasciolosis.d. Maedi visna (MV) and ovine pulmonaryadenocarcinoma (OPA).e. Liver flukes may cause acute and chronicfasciolosis alone or predispose to blackdisease and bacillary haemoglobinuria.

Question 5

i. In order to ensure the best chance ofestablishing a rapid diagnosis, visit the farmimmediately, after telling the farmer to keepfetal membranes and any aborted fetuses foryou to examine. Examine any fetal mem-branes for signs of placentitis includinginter-cotyledonary thickening (enzootic

abortion of ewes, EAE) or necrotic foci onthe cotyledons (toxoplasmosis). Send mem-branes and aborted fetuses to diagnosticlaboratory. Keep good notes as litigationmay follow later. Indicate the steps whichhe might take to reduce transmission toother ewes by isolating aborted ewes, col-lecting and disposing of all fetal membranesand spreading clean straw in sheds. Discusspossible treatment of pregnant ewes when apositive diagnosis has been reached.Arrange to visit later to discuss long-termcontrol methods.ii. Advise on danger of zoonosis, especiallyof EAE and stress that his wife should notbe involved in any way with lambing orrearing lambs and that he should changeclothes when he comes home to avoidintroducing infectious agents. Treat as aninfectious disease and use disposablegloves and polythene bags and use goodbiosecurity before leaving the farm andcalling elsewhere.

Answers to related questions

a. You are likely to see weak lambs andewes with little milk over the course of anoutbreak.b. No, there is no serological response tothe organisms in the latent sites as this onlyoccurs after invasion of the placenta.c. If the rams have been removed, there maybe a high barren rate due to resorption ofearly fetuses or the ewes may return to theram if present.d. This is usually by purchased carrier ewesbut birds feeding around troughs in fieldsmay be responsible.e. Toxoplasmosis and Border disease.

Question 6

i. The main possibilities are hypocalcae-mia, pregnancy toxaemia, rumen acidosisand listeriosis.ii. The main issues are:

Probably were too thin for this stageof pregnancy - no CS checks done,

178 Appendix 6

hay may have been poor quality sonot palatable (check), molassesbuckets may have been insufficient.Rushing to house them - may haveprecipitated hypocalcaemia.Sudden change of diet so some maynot adapt quickly so intake reducedalso leading to possibility of preg-nancy toxaemia (PT).Groups too large so may not all getequal share of food leading to PT.Too much concentrate introducedtoo quickly and stronger ewes mayhave eaten more than their shareleading to acidosis.No scanning so probably someewes carrying multiples are toothin leading to PT.Unlikely to have condition scoredat housing so thin and fat ewestogether.Big-bale silage may be poor contrib-uting to reduced food intake andalso possibility of listeriosis (butpossibly a bit early for this).

iii. Visit to look at sheep, housing condi-tions and food supplied. Clinically examineaffected sheep looking for specific signssuch as scouring (rumen acidosis) or facialparalysis (listeriosis). Try test dose of Ca ifhypocalcaemia a possibility - they shouldrespond in minutes if this is the only prob-lem. Take bloods for Ca, Mg and betahy-droxybutyrate (BOHB) from affected andnormal animals. Condition score other ani-mals. Look at silage bales for quality andsigns of spoilage.iv. The action taken will depend on yourdiagnosis or diagnoses but, apart from treat-ing affected animals, is likely to includesplitting into smaller groups based on CS,possibly changing back to hay if good qual-ity is available, splitting concentrate feedinto at least two meals, floor feed if possi-ble. Animals should be stressed as little aspossible during handling procedures.

Answers to related questions

a. A Border Leicester ram on WelshMountain ewes.

b. Prime lamb mothers, similar to Mulesbut perhaps slightly less prolific.c. At least 1 month before tupping and 8-10weeks before lambing is due to prevent toomuch loss of weight. But handle wheneverpossible at more frequent intervals.d. Between 50 and 80 days of gestation.Earlier than 50 days means early preg-nancies are missed, later than 80 daysmakes accurately counting fetal numbersdifficult.e. 145-147 days.

Question 7

i. Outdoor lambing can be very successfulbut creates more work for the shepherd.It is very weather dependent and badweather can create a lot of problems forlambs, swapping existing problems forhypothermia.ii. Are there some sheltered fields near thefarm buildings available for lambing? If not,provide extra shelter (straw bales, hay racks,plastic netting, etc. are possibilities). Havesome hospital pens available in buildings.Make sure ewes are in good condition sohave plenty of milk and colostrum. Checkewes regularly between first light and dark.Number the lambs and ewes so lost lambscan be identified. Keep a look out for at-risklambs (small, triplets, slow to stand) andmake sure they get colostrum (tube feed forspeed). Don't castrate or tail too early. Ifweather is bad, especially wet, could still getjoint ill problems.

Answers to related questions

a. Number of lambs reared divided bynumber of ewes put to ram multiplied by100. Can also be expressed as for example1.6 lambs per ewe.b. 150-250 ml/kg. Outdoor born lambsrequire most, especially if weather is bad.c. 24 h maximum, but ability to pass throughintestine declines from about 12 h.d. 12-16 weeks.e. Streptococcus dysgalactiae.

Suggested Answers 179

Question 8

i. During lactation and/or immediatelyafter weaning.ii. Look at the management of weaning - are

lambs all removed at the same time? Is thenutrition plane of the ewes reduced to rap-idly cut milk production? Make a very care-ful examination of udders at and just afterweaning. Consider the use of intramammaryantibiotics as in drying off cows - this is prob-ably cost effective in this type of pedigreeflock. Disinfect the end of the teat and useone tube per teat (don't split them betweenboth teats as this can transfer infection). Noneed to insert nozzle - just appose with teatopening as in heifers.iii. It is uneconomic to suggest dry ewetherapy for a commercial flock so concen-trate on weaning management.

Answers to related questions

a. Staphylococcus aureus and Mannheimiahaemolytica.b. Staph. aureus lives on skin so is presenton the teats; M. haemolytica is found in thepharynx of lambs and can be transferred tothe udder while lambs are sucking.c. Presence of teat lesions - these oftenoccur as a result of trauma from lambs'sharp incisor teeth. They are particularlycommon where the milk supply of the eweis insufficient for lambs (thin ewe withtwins, ewe rearing triplets) as lambs com-pete for milk.

Question 9

i. Lack of milk in ewes; coccidiosis (verylikely); nematodirosis. Examine ewes andlambs. If any dead or dying lambs have post-mortem examination (PME) done. Faecessamples may not be very helpful as oocystnumbers can be misleading if non-patho-genic strains are present and may be noNematodirus eggs present as disease canoccur before prepatent period.

ii. Ewes may not have had sufficient foodand water during extended housing periodso milk supply reduced. In the case of coc-cidiosis the earlier lambs would multiplyoocysts massively without becoming dis-eased; later born lambs which were housedfor longer than usual could then pick uplarge numbers of oocysts from beddingdeveloping clinical disease about 3 weekslater. Nematodirosis is a possibility ifimprovement in weather has stimulatedmass hatching of larvae just as later lambswere turned out.iii. If it seems to be a milk supply problem,separate ewes with twins if possible, increaseconcentrates for ewes and supply creep feed.Coccidiosis may be involved in any case -use specific anticoccidial such as diclazurilor toltrazuril drench. If nematodirosis isdiagnosed most anthelmintics are effective.

Answers to related questions

a. 1- benzimidazole (BZ) drugs; 2 - levami-sole and morantel (LM) drugs; 3 - macrocy-cliclactones (ML) drugs; 4-amino-acetonitril ederivatives (AADs).b. Anthelmintic resistance is most commonto the BZ group although it has also beendetected to LM and ML group products. Inrare cases, resistance has been found to allthree groups in the same flock. AADs is anew drug group.

Question 10

i. They are not protected by vaccination(passive protection will have completelywaned). Losses could be due to pulpy kid-ney and/or systemic pasteurellosis. Alsoconsider the worm situation.ii. Need vaccination programme to be

started so first and second injections can becompleted before weaning. Definitely needclostridial protection. Pasteurella protec-tion is desirable as history suggests thiscould be implicated, so could use a com-bined vaccine. Correctly vaccinated ewe

180 Appendix 6

lambs will be more attractive to buyers(some sales specify they must be vaccinatedanyway). As silage aftermath may be 'safe'grazing, need to think of worm controlstrategy. Worming immediately beforeputting on new grass would have been donein the past, but you need to think of thepossibility of increasing the resistant wormpopulation. Action depends on the futureuse of the grass field - if it is to be used forcattle or arable you can worm and move. Ifit is to be grazed by sheep you may need toconsider developing a susceptible 'refugia'population.

Answers to related questions

a. A tall, long-bodied sheep with a short,curly, fine, lustrous fleece and a pronouncedroman nose and upright ears. Skin colour ofhead is blueish, hence the name, but oftencovered with short white (or sometimesbrownish) hairs.b. It is very prolific and passes this trait andmilkiness on to its female offspring(Mules).c. This is the fresh grass growth after acrop of hay or silage has been taken offit. Depending on management earlier inthe spring it may be classed as 'safe'grazing.d. Advantages are that it removes the diffi-culty of managing male lambs after sexualmaturity (this is at about 5 months). Slaughterlambs reach the correct stage of finish at anearlier age than entires. Advantages of notcastrating are improved welfare for animalsthemselves, lambs grow to heavier weightand carcasses are leaner at slaughter.Disadvantages of not castrating are man-agement of older males, may be slow tofatten later in year, possibility of unwantedpregnancies and welfare issues associatedwith these.

Question 11

i. It should be possible to eradicate footrot(FR) from this flock.

ii. Risks will be buying in rams (couldthey use Al?) and if they show sheep.Complications will include whether theyare prepared to sell chronically infected ornon-responsive animals.iii. Best tackled after weaning ewes.Examination of the feet of all sheep to seethe extent of the problem. Separate infectedanimals so they can be closely checked.Consider giving the whole flock antibiotictreatment (tilmicosin is probably best optionbut has to be vet administered; gamithromy-cM has been used very recently under cas-cade) - this is in case any slightly infectedfeet have been missed. Move on to pasturenot grazed for at least 3 weeks to be on thesafe side. Alternatively inject infected ani-mals only (but in a probably valuable flocksuch as this it would be worth doing all).Re-examine all animals 5-7 days after treat-ment. Consider what is to happen to thosewhich are still infected - preferably cull butthere may be resistance to this if they areseen as valuable. Remember that suscepti-bility to FR is heritable. Footbathing couldalso be incorporated as a 'belt-and-braces'approach. Must keep close check and exam-ine any lame sheep at first sign in case thisis a resurgence of FR.

Answers to related questions

a. Dichelobacternodosus initiates the disease.Fusobacterium necrophorum is a secondaryinvader.b. Zinc sulfate (10%) is the product of choice -as it is non-irritant, doesn't harden feet anddoesn't degrade. Disadvantage is stand-intime. Forma lin is unpleasant, potentiallycarcinogenic, hardens feet if used too fre-quently. Advantages are is cheap and walk-through. Copper-containing products areeffective but bear in mind risks of havingthis potentially toxic chemical around.c. FR lesion starts in the interdigital spaceand extends across the sole towards thewall. Contagious ovine digital dermatitis(CODD) lesion starts at the coronary bandand extends down the wall.d. Treponemes.

Suggested Answers 181

Question 12

i. Visit and examine a representative sam-ple of the ewes. Assess how pruritic thesheep are. Carefully examine the skin forlesions and parasites using a hand lens ifpossible. Take skin scrapings from the edgeof any lesions.ii. Lice and/or sheep scab.

iii. Only plunge-dipping in an organophos-phate (OP) dip will treat both parasites. Licecan be treated with synthetic pyrethroid(SP) pour-on. Scab can be treated with aninjectable such as doramectin ormoxidectin.iv. These are heavily pregnant ewes so it isnot appropriate to dip now. If the cause islice, applying an SP pour-on to heavilyfleeced sheep is a problem because of woolresidues and difficulty of getting sufficientconcentration at skin surface. Probably bestto leave treatment until after shearing whichshould be done at first opportunity then treatall, including lambs. If the cause is scab,these can survive off the sheep for 16 days sowill be in the environment to infect thenewborn lambs. Probably best to treat with along-acting (LA) moxidectin preparationimmediately (be aware of anthelminticeffects as well). Then treat whole flock aftershearing either with injectable or by dipping.Do not use SP pour-on if scab is implicated.

Answers to related questions

a. Wool break, caused by weakening orbreaking of wool fibres either as a result ofpoor nutrition or illness.b. 1.5-2 kg.c. This is called kemp and causes problemsin manufacturing because the fibres breakeasily and do not take dye.

Question 13

i. Listen with stethoscope, although thisdoes not tell you a great deal. Do a 'wheel-barrow' test to check for excessive fluid in

the airways. Use ultrasound to examine thechest (but requires some experience to carryout). Serology, depending on your possiblediagnosis.ii. Chronic pneumonia, possibly with a

lung abscess; OPA; maedi.iii. May be possible to pick up a lung abscesswith ultrasound. May respond to long treat-ment with antibiotic (weeks not days). Noreal implications for rest of flock but mightconsider vaccination against pasteurellosis.OPA can be diagnosed if excess fluid ispresent in the airways as demonstrated bythe wheelbarrow test. Ultrasound may behelpful if you are experienced in interpretingimage. No serological test is available. PMEis the ultimate diagnostic test. Serious impli-cations for rest of flock - may be othersinfected but not yet showing signs. Expensiveand time consuming but can remove lambsat birth and rear artificially away from rest ofthe flock to create an uninfected nucleus.Maedi can be confirmed by serology. Thisalso has implications for the rest of the flock.Can use serology to identify and removeother infected animals to eventually createan uninfected flock or remove lambs at birthas above.

Answers to related questions

a. Beltex are an extreme form of the Texel,with a small head, short neck and highlymuscled body, particularly the hind quarterswhich look more like those of pigs. They areused for crossing to produce meat lambs withtop quality carcass conformation.b. Laryngeal chondritis, obstruction of thelarynx resulting in difficulty breathing and,quite often, death.c. Mycoplasma ovipneumoniae, seen inhoused fattening lambs.

Question 14

i. Listeriosis.ii. In the brainstem.

iii. Preparation of the field - elimination ofmoles to reduce soil contamination; not

182 Appendix 6

cutting grass too low, again to reduce soilcontamination; thoroughly wrap bales toeliminate air; make sure bales are not dam-aged during transport; make sure wrappingis not damaged during storage.iv. If silage is too wet or too mature, sheepwill be physically unable to eat sufficient tosupply metabolizable energy (ME)requirement.

Answers to related questions

a. Thought to gain access through mouthinjury or tooth socket (young sheep chang-ing temporary teeth for permanents). Thentravel up trigeminal nerve to brainstemwhere they lead to micro-abscessformation.b. Abortion, diarrhoea, septicaemia.c. Abscess, tumour, coenurosis.d. Left cerebral hemisphere affecting visualcortex. About 90% of neurons cross over atthe optic chiasm so blindness occurs in theopposite eye from the lesion.

Question 15

i. Unlikely to be the same as the cattle.You would want to see some affected lambsto check.ii. Most likely cause is entropion. Hairs

rubbing on the eye surface cause lachryma-tion and keratitis if not treated quickly.Occasionally can get eye infections in younglambs without entropion but always check.iii. If it is entropion, show client how eye-lids should appear and advise checking alllambs after birth. Usually it is fairly easy tocorrect at this stage just by pulling downthe affected lid (always lower ones). Thosewith runny eyes and keratitis will needtreating, probably by injecting antibiotic(procaine penicillin) into the lower lid tostiffen it after correcting the position.Alternative is insertion of Michel clips totake 'tuck' in lower lid. Ask about whethera new ram has been used which might haveintroduced the problem, since there is agenetic component.

Answers to related questions

a. Moraxella bovis.b. Mycoplasma conjunctivae, sometimesChlamydophila.c. No, immunity is slow to develop so out-breaks can be prolonged and carrier sheepOccur.

Question 16

i. It is likely that there will be ticks in therough grazing areas. The newly introducedsheep will not be immune to tick-bornediseases.ii. If possible, keep the Greyfaced Dartmoorson the improved pasture through the firstautumn and winter until after lambing nextspring. If they are introduced to tick-infestedland around tupping time, fertility will bebadly affected if the sheep get tick-bornefever (TBF). If the ewes are introduced in latepregnancy and get infected they may abort. Iflouping-ill occurs in the area, the vaccinecan be used. Applying an SP pour-on to ewesand lambs on turnout will reduce the tickburden. Keep a close eye on lambs in casethey develop tick pyaemia - perhaps con-sider prophylactic antibiotic injections forlambs on turnout, although this will not pro-tect for very long. After the first year, lambswill become infected with TBF early in lifeand the flock will gradually becomeacclimatized.

Answers to related questions

a. Yes, the breed is quite hardy and has athick fleece so should be able to adapt.b. There are several interesting Welshminority breeds that are attractive, interest-ing to keep and relatively easy to manage.These are the Black Welsh Mountain, theTorddu and Torwen (Badger Faced) and theBalwen (black with a white blaze on theface, white on the lower legs and a whitetail tip).c. Lyme disease.d. Bracken can be poisonous (especially tocattle), can cause retinal atrophy (bright

Suggested Answers 183

blindness) and may be linked to tumourdevelopment (e.g. intestinal and bladder).

Question 17

i. Mouth lesions include traumatic ulcers(often on the central lower gum) which havea well-defined raised border and orf whichcauses vesicles and scabs on the lips. Footlesions include interdigital dermatitis (skinlooks damp and greyish but no vesicles), FRcan be confused with foot and mouth dis-ease (FMD) lesions several days old, CODD(haemorrhagic lesion at the coronary bandspreading downwards under the wall of theclaw, rarely affects all feet) and bluetongue

(inflammation around the coronary band ofall feet).ii. Sudden severe lameness of many sheep,some ill particularly pregnant ewes, deaths inyoung lambs. Erosions on dental pad, blanch-ing and separation of interdigital skin. Ask forhelp immediately from the Animal HealthOffice if you are suspicious of the possibility.

Answers to related questions

a. Culicoides spp. (midges).b. Brucella ovis causes epididymitis;Brucella melitensis causes abortion andmastitis in sheep and is a zoonosis causingMalta fever in man.

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Index

AAD see Amino-acetonitrilederivatives (AAD)

Abortion 38-47Actinobacillosis 117AI see Artificial insemination (AI)Akabane disease 153Amino-acetonitrile derivatives

(AAD) 85Amputation, digit 95Anaemia, lambs 64Anaesthesia

epidural 53foot 95-96paravertebral 60

Anthelmintics 84-87Anthrax 154Artificial insemination (AI) 14-15

Benzimidazole (BZ) drugs 84Black disease 18,19Blowfly myiasis (flystrike) 111Bluetongue 151-152Border disease 71-73Breeding, control of 9-11Brucella melitensis 154Brucella ovis 12-13,154

CAE see Caprine arthritis encephalitis (CAE)Caesarean technique 60Campylobacteriosis 45-46CAP see Common Agricultural Policy (CAP)Caprine arthritis encephalitis (CAE) 64Caseous lymphadenitis (CLA) 116-117,156CCN see Cerebrocortical necrosis (CCN)

Cerebrocortical necrosis (CCN) 135-136Cerebrospinal fluid (CSF) 131,134Chlamydophila abortus 20,38,

40-43Chorioptic mange (C. bovis) 110CLA see Caseous lymphadenitis (CLA)Clostridial diseases

acute abomasitis 92-93bacillary haemoglobinuria 93black disease 93blackleg and big head 93botulism 93braxy 92control measures 19-20,92diagnosis 91lamb dysentery 92pulpy kidney 92struck 92tetanus 93vaccination 17-19

Cobalt deficiency 87-88Coccidiosis 79-81CODD see Contagious ovine digital

dermatitis (CODD)Coenurosis 132-135Colostrum 62-64Common Agricultural Policy (CAP) 4Condition scoring 23-25Contagious ophthalmia 139-140Contagious ovine digital dermatitis

(CODD) 98-101Contagious pustular dermatitis 112-114Copper deficiency 69-71Copper toxicity 71,93Corynebacterium pseudotuberculosis 116CSF see Cerebrospinal fluid (CSF)

185

186 Index

Daft lamb disease 65,69,73 eradication 101Dry ewe therapy (DET) 77 treatment 99-101

EAE see Enzootic abortion of ewes (EAE)Ear diseases 141EBVs see Estimated breeding values (EBVs)Entropion 140-141Enzootic abortion of ewes (EAE)

accreditation 156disease 40-43vaccines 20

Epidural anaesthesia 53Erysipelas 20,104Estimated breeding values (EBVs) 15-16Exotic diseases, UK and Northern Europe

Akabane 153anthrax 154Nairobi sheep disease 153peste des petits ruminants 153rabies 154Rift Valley fever 153sheep pox 153-154

Eye diseasesbright blindness 140contagious ophthalmia 139-140entropion 140-141genetic defects 141

Fasciolosis 30-32Feeding management

assessing ration 25-26ewe 5-8lamb 8ram 4-5

Flavivirus 147Flock health schemes 155-159Flock lameness

control 101diagnosis 99treatment 100-101vaccination 99-100

Flystrike 111Foot and mouth disease

(FMD) 149-151Foot lameness

CODD 99-101FR 97-101ID 97,100interdigital hyperplasia 103pedal joint sepsis 102-103toe granulomas 103white line lesions 102

Footrot (FR)control 101diagnosis 97-99

Gammaglutamyl transferase(GGT) 66

Growing lambscobalt deficiency 87-88coccidiosis 79-81PGE 82-87

Headfly 112Health schemes, flock 155-159Housing 35-38Hypocalcaemia 52Hypomagnesaemia 52-53Hypothermia 66-67

Interdigitial dermatitis (ID) 97

Johne's disease 32-33

Lactating ewehypomagnesaemia 78mastitis 75-77teat lesions 77-78

Lambsanaemic 64colostrum and 63-64hypothermia 66-67intraperitoneal injection 66-67neurological problems 69-73stomach tubing 65watery mouth 67-68

Lambingdifficult, dealing with 58-59induction of 11

Lamenesscauses 96-97control 101diagnosis 97-99treatment 99-101foot conditions

CODD 99diagnostic features 97,98FR 97-99ID 97interdigital hyperplasia 103pedal joint sepsis 102-103toe granulomas 103white line lesions 102

joint infections 103-104post-dipping 103

Index 187

techniquesanaesthesia, foot 95-96paring feet 95

vitamin E and seleniumdeficiency 104-106

Laryngeal chondritis 125-126Lentivirus 124Levamisole and morantel (LM) drugs 84Lice and keds 110-111Listeriosis 130-132Louping ill 147-148Lyme disease 148

Macrocyclic lactone (ML) drugs 84-85Maedi-visna (MV) 124-125Maedi-visna/caprine arthritis encephalitis

(MV/CAE) accreditation 156Mastitis 75-77ME see Metabolizable energy (ME)Meat and Livestock Commission

(MLC) 15Melatonin 11Metabolic diseases

clinical diagnosis 50hypocalcaemia 52hypomagnesaemia 52-53PT/twin-lamb disease 50-52

Metabolizable energy (ME) 6Midge hypersensitivity 112MLC see Meat and Livestock

Commission (MLC)Molar tooth disease 29Multiple ovulation embryo transfer

(MOET) and AI 14-15Mycotic dermatitis (lumpy wool) 115MV see Mae di -visna (MV)

Nairobi sheep disease 153National and regional health

schemes 155-156National Scrapie Plan (NSP) 129-130National Sheep Association (NSA) 1Neurological diseases

CCN 135-136CNS syndromes 127coenurosis 132-135listeriosis 130-132metabolic diseases, ewes 127scrapie 127-130tetanus 136-137

Neurological examination 164-165Neurological problems, newborn lambs

border disease/hairy shakers 71-73congenital 73swayback/enzootic ataxia 69-71

Newborn lambscolostrum store

anaemia 64cow 64ewe 64goat 64milk powders 65

diseases 61,62,66-68feeding, stomach tube 65neurological problems 69-73post-mortem features 61-62specific post-partum problems

hypothermia 66neonatal diarrhoea/scours 68watery mouth 67-68

Nose, diseases of 142Notifiable diseases 149-151NSA see National Sheep Association (NSA)NSP see National Scrapie Plan (NSP)

Orf 78,112-114Ovine pulmonary adenocarcinoma

(OPA) 124

Parasitic conditions, skin and woolblowfly myiasis (flystrike) 111chorioptic mange (C. bovis) 110headfly 112lice and keds 110-111Psoroptes otitis 110sarcoptic mange (Sarcoptes scabei) 110screw worms 111-112sheep scab (psoroptic mange) 107-110ticks 112

Parasitic gastroenteritis (PGE)anthelmintics 84-85clinical signs 82control 85-87diagnosis 83life cycles and epidemiology 82-83SCOPS programme 86treatment 83-84

Paratuberculosis see Johne's diseasePasteurellosis 20,119-122Periodontal disease 28Periparturient ewe

abdominal muscle rupture 57metabolic diseases 49-53obstetrical problems 57-60prolapses 53-57

Peste des petits ruminants 153PGE see Parasitic gastroenteritis (PGE)Photosensitization 117-118PMSG see Pregnant mare's serum

gonadotrophin (PMSG)

188 Index

Pneumoniaatypical 123parasitic 122-123pasteurellosis 119-122slow viral 124-125

Pregnancy toxaemia (PT) 51-52Pregnant ewe

abortionadvice 40campylobacteriosis /vibriosis 45-46causes 38-39EAE 40-43Q fever/Coxiel la burnetii 47salmonellosis 46-47toxoplasmosis 43-45

housing 35-38prolapses 53-57ultrasound scanning 35

Pregnant mare's serum gonadotrophin(PMSG)

injection 9,15and progestogen sponges 10

Production, sheep industryfeeding management 4-8structure and economics 1-4

Professional developmentInternational Sheep Veterinary Congress

and Association 167specialist qualifications, sheep 168specialist societies 167

Progestogen sponges 10-11Prolapses

Buhner suture for 54,56epidural anaesthesia 53intestines 55post-lambing, cervix 55uterine 55,57vaginal 54-55

Psoroptes otitis 110Psoroptic mange (sheep scab) 107-110PT see Pregnancy toxaemia (PT)

Q fever 47

Rabies 154Ram examination 11-12Reproduction

AI and MOET 14-15breeding control 9-11lambing induction 11ram examination 11-13vasectomized rams 11

Respiratory diseaseslaryngeal chondritis 125-126pneumonia

atypical 123parasitic 122-123pasteurellosis 119-122slow viral 124-125

Rift Valley fever 153Ringworm 115

Salmonellosis 46-47Sarcoptic mange (Sarcoptes scabei) 110Schmallenberg Virus 47Scrapie

atypical scrapie 129-130classical scrapie 127-129NSP 128-129

Screw worms 111-112Selenium deficiency 104-106SFP see Single farm payment (SFP)Sheep pox 153-154Sheep scab 107-110Sheep tick 143-146Sheep Veterinary Society (SVS) 1,167Sick lamb, examination of 166Sick sheep, examination of 161-163Single farm payment (SFP) 4Skin and wool disorders

CLA 116-117mycotic dermatitis 115orf 112-114parasitic conditions 107-112photosensitization 117-118ringworm 115staphylococcal infections 114-115wool loss 117

Slow viral pneumoniasOPA 124MV 124-125

Staphylococcal dermatitis 114-115Strawberry footrot 114Sudden death

adult sheep 91clostridial diseases see Clostridial

diseasesgrowing lambs 89-91pasteurellosis 89,90,93PME 89toxicity 93young lambs 89

Sustainable control of parasites of sheep(SCOPS) programme 86

SVS see Sheep Veterinary Society (SVS)

TBF see Tick-borne fever (TBF)Teat lesions 77-78Teeth and ageing 27-28Tetanus 136-137

Index 189

Thin sheepChronic respiratory diseases 33,

124-125CLA 33,116-117condition scoring 23-25fasciolosis 30-32feed ration assessment 25-26Johne's disease/paratuberculosisteeth 27-30

Tick-borne fever (TBF) 146Ticks and tick-borne diseases

control methods 148diseases transmission

louping-ill 147Lyme disease 148tick-bite pyaemia 146-147tick-borne-fever 146

Toxicity 93Toxoplasmosis

disease 43-45vaccine 20

Twin-lamb disease 50-52

Ultrasound scanning 35Urolithiasis 13-14

Vaccinationabortion 20bluetongue 21

32-33 clostridial diseases 17-20erysipelas 20FR 20louping-ill 21orf 21pasteurellosis 10

Vasectomized ramsVeterinary Laboratories Agency (VLA) 39Veterinary Medicines Directorate (VMD) 33Vitamin E deficiency 104-106

Watery mouth 67-68White line lesions 102Wool break 117