Understanding The Dairy Cow

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Understanding the Dairy Cow

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Understanding the Dairy Cow
Third Edition
John Webster, MA, VetMB, PhD, DVM (Hon), MRCVS

Professor Emeritus of Animal Husbandry
School of Veterinary Science
University of Bristol
Bristol, UK
This edition first published 2020
© 2020 John Wiley & Sons Ltd
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Library of Congress Cataloging‐in‐Publication Data

Names: Webster, John, 1938– author.
Title: Understanding the dairy cow / John Webster, MA, VetMB, PhD,
MRCVS, Professor of Animal Husbandry, University of Bristol, School of
Verterinary Science.
Description: Third edition. | Hoboken, NJ : Wiley-Blackwell, 2020. |
Includes bibliographical references and index.
Identifiers: LCCN 2020006388 (print) | LCCN 2020006389 (ebook) | ISBN
9781119550228 (paperback) | ISBN 9781119550235 (adobe pdf) | ISBN
9781119550242 (epub)
Subjects: LCSH: Dairy cattle. | Cows.
Classification: LCC SF208 .W4 1987 (print) | LCC SF208 (ebook) | DDC
636.2–dc23
LC record available at https://lccn.loc.gov/2020006388
LC ebook record available at https://lccn.loc.gov/2020006389
Cover Design: Wiley
Cover Image: © TonyV3112/Shutterstock
Set in 10/13pt STIXTwoText by SPi Global, Pondicherry, India
10 9 8 7 6 5 4 3 2 1
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‘The cow, crunching with depressed head, surpasses any statue…they are so placid and
self‐contained. I stand and look at them long and long.
Walt Whitman
‘Song of Myself’
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Contents
Acknowledgements xiii
Preface to the Third Edition xiv
About the Companion Website xvi
Part I How the Cow Works 1
1 Introduction – The Dairy Cow of Today 3

Milk as Food 6
Nutrient Supply 7
Healthy Digestion 8
Taste and Appetite 9
Do no Harm 9
Biological Efficiency of Milk Production 10
Milk Production: Species and Breed Comparisons 11
Efficiency of Feed Conversion to Milk, Eggs and Meat: Competitive
and Complementary Feeds 12
Behaviour and Welfare 14
2 Digestion and Metabolism 18

Structure of the Digestive Tract 18
Eating and Rumination 22
Grazing 22
Salivation 23
Rumen Movements 23
Rumination 25
Digestion 26
Fermentation of Carbohydrates in the Rumen 28
Utilization of Metabolizable Energy for Maintenance and Production 31
Digestion of Crude Protein 32
Microbial Protein Synthesis 35
Truly Absorbed Amino Nitrogen 37
Urea Recycling 38
Digestion of Lipids 38
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Absorption and Secretion of Minerals 39

Calcium Exchange 41
A
ppetite and Food Intake 42
3 Reproduction and Lactation 45

A natomy of the Female Reproductive Tract 45
F ollicle Development and Ovulation 45
The Oestrus Cycle 49
Puberty 49
F ertilisation 50
Pregnancy 51
Placental Transfer and Foetal Nutrition 53
Parturition 53
Dystocia 55
Lactation 56
Anatomy of the Udder 56
Milk Yield 58
Extended Lactations 59
Hormonal Control of Lactation 60
Reproduction in the Male 61
4 Environment, Behaviour and Welfare 64

Environmental Needs 64
B ehaviour 65
Physical Comfort 66
T hermal Comfort 68
Sensible Heat Loss 68
Evaporative Heat Loss 69
Metabolic Heat Production 71
C limate, Production and Welfare 73
Tropical Climates 73
Cold Climates 74
Security and Social Behaviour 74
Sexual and Maternal Behaviour 75
Behaviour as an Indicator of Welfare 76
Part II Feeding the Dairy Cow 77
5 Nutrition: Supply and Demand 79

N utrient Requirements and Responses 81
N utrient Allowances for the Lactating Cow 84
Mineral Requirements 88
Nutritive Value of Feeds 90
Ration Formulation 93
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Prediction of Food Intake 93

A ssessment of an Existing Ration 94
F eeding Plans for Dairy Cows 95
Inputs 95
Outputs 96
Allowances for Growing Heifers 97
6 Feeds and Feeding Strategies 99

Pasture 100
Grazing Strategies 102
Legumes 104
Grass Silage 104
Dry Matter 105
Metabolisable Energy 106
Protein 106
Silage Additives 107
Hay 107
Straw 108
Ensiled Whole-crop Cereals 108
Other Green Feeds 109
R oot Crops 109
Cereals 109
By-products 111
Oilseed Cakes and Meals 111
M iscellaneous By-products 113
Sugar Beet Pulp 113
Maize Gluten 113
Brewers’ and Distillers’ Grains 114
Wheat Bran 114
Balancing Forages and Concentrates 114
Feeding Strategies 117
Feeding to Yield 117
Total Mixed Rations and Flat Rate Feeding 119
7 Feeding Problems and Metabolic Diseases 121

F eeding Problems 123
Rumen Acidosis 123
Abomasal Disorders 125
Bloat 126
Metabolic Disorders 127
Ketosis 127
Prevention and Treatment 129
Parturient Hypocalcaemia (‘Milk Fever’) 130
The Downer Cow 132
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Hypomagnesaemic Tetany (Grass Staggers) 133

Other Mineral Deficiencies 136
Phosphorus 136
Copper and Molybdenum 137
Cobalt 138
Selenium 138
V
itamin Deficiencies 139
Vitamin A 139
Vitamin D 140
Vitamin E 140
Last Words on Minerals and Vitamins 141
Part III Housing Health and Management 143
8 Healthy and Humane Housing and Handling 145

Accommodation 145
The Cow House 146
Cubicle Design 150
The Cubicle Bed 153
Passageways 154
Calving and Isolation Boxes 154
Heifer Yards 156
Handling Facilities 156
Lameness 157
Conditions that Cause Lameness 159
Sole Haemorrhage and Sole Ulcers 159
White Line Disease 161
Digital Dermatitis 161
Interdigital Necrobacillosis ‘Foul’ 162
Aseptic Laminitis, ‘Founder’ 162
Risk Factors for Lameness 162
T
ransport and Slaughter 164
Loading and Unloading 164
The Journey 165
A Gentle Death 166
9 Milking and Mastitis 168

The Milking Machine 171
T
he Milking Parlour 174
Hygiene in the Milking Parlour 174
M
astitis 175
Indicators of Mastitis 176
Contagious Mastitis 177
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Environmental Mastitis 178

Summer Mastitis 180
Dry Cow Therapy 181
10 Miscellaneous Maladies 182

Signs of Disease 183
Sudden Death 183
Drooling 185
Abdominal Symptoms 186
Nervous Symptoms 187
Fever 187
Inappetence and Anorexia 188
Notifiable Diseases 189
Bovine Tuberculosis 191
Foot and Mouth Disease 192
ther Infectious Diseases 193
O
Bovine Viral Diarrhoea (BVD) 193
Johne’s Disease 194
Salmonellosis 194
Leptospirosis 195
Parasitic Diseases 195
Part IV Breeding and Fertility 197
11 Breeding 199
S election Criteria 202
Genomic Selection 206
Sexed Semen 206
Cow Selection 207
Beef Bulls 209
12 Fertility 211
Fertility Management 212
Behaviour at Oestrus 212
Aids to Oestrus Detection 213
Synchronisation of Oestrus 216
Time of Insemination 217
Pregnancy Diagnosis 217
Rebreeding 219
Infertility 219
Ovarian Dysfunction 220
Uterine Disorders 221
Retained Placenta 221
Endometritis 222
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Early Foetal Death 222

Abortion 223
Nutrition and Infertility 223
Condition Score at Calving? 225
Condition Score at the Time for Rebreeding? 225
Milk Yields in Early and Mid-lactation? 225
How Well Does Nutrient Supply Match Requirements? 226
Transition Management 226
Part V Cows, People and the Environment 229
13 Cows, People and the Living Environment 231

Most of Those who can Consume Too Much Meat and Milk 232
Food We Could Eat is Fed to Animals While the Poor Grow Hungry 233
Intensive Livestock Production is Incompatible with Animal Welfare 233
Livestock’s Long Shadow is Destroying the Planet 235
Methane Production and Climate Change 237
Pollution from Dairy Units 238
A lternative Husbandry Systems 240
Organic Dairy Farming 240
Traditional and Village Systems 241
Fair Play for Cows, People and the Planet 242
Herd Health and Welfare 242
Herd Health Management 243
Animal Welfare: Quality Assurance and Quality Control 243
Further Reading 247

Index 252
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A
cknowledgements
I thank the following for permission to reproduce illustrations: Geoffrey Pearson,

Figure 2.3; The Scottish Farm Business Investigation Unit, Figure 8.1; The Institute
for Food Research, Reading, Figures 8.1 and 8.2; Martha d’Andrade, Figure 13.2.
The wisdom of any group with shared interests and enthusiasms is so much
greater than the sum of its parts. I owe an immense debt of gratitude to all my spe-
cial friends and colleagues on farms, in the veterinary profession and academe who
share my fascination with the dairy cow. Among so many I give special mention to
Nick Bell, Geoff Davies, Richard Dewhurst, Clive Snell and Becky Whay. Finally, I
must once again thank Nick Jeanes, who contributed the best of the illustrations.
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Preface to the Third Edition
The mediaeval expression ‘milch cow’ is, in modern parlance, variously used to
describe a cow kept for milk production and an everlasting source of easy money. It
is not hard to see how this second definition has come about. Since the earliest days
of agriculture, the cow has served humankind as a regular, reliable source of excel-
lent sustenance, in many different physical and social environments and from
almost any mixture of feeds that we can provide or that she can forage for herself.
Her value comes from her infinite ability to adapt. At the time when the first edition
of ‘Understanding the Dairy Cow’ (UDC) was published in 1987, most dairy farm-
ers in the UK fed their cows largely from pasture and other home‐grown crops, the
milk lorry took it away and regular cheques arrived in the post. It was all so simple.
The subsequent 30+ years have witnessed a roller‐coaster ride of change. The impo-
sition then removal of quotas on milk production. The explosive increases in indi-
vidual cow yields, achieved by a combination of genetic selection and radical
changes in nutrition. Our greater concern about the environmental impact of farm-
ing in general and ruminants in particular. Our greater concern, expressed through
our buying habits, about farm animal welfare and the potential risks attached to the
consumption of food from animals. The circumstances in which the dairy cow may
find herself are many and varied but a cow is still a cow. For this reason UDC, in its
successive editions, has never taken the form of an instruction manual on dairy cow
management but an examination of the fundamental principles of physiology,
health and behaviour that govern both her capacity to produce milk and also give
proper attention to her welfare in all circumstances; intensive or extensive, high‐
tech or organic.
This third edition is, in effect, is a complete rewrite with over half the material
radically updated or entirely new. It reflects the major shift in dairy production
away from family farms with 100 cows or less, each producing modest amounts of
milk largely from their own resources, to very large production units, with per-
haps 1000 cows, housed throughout lactation, producing very large quantities of
milk (and excrement) from feed tractored to them from near and far. It considers
in detail the impact of these changes on cow health and welfare, and their envi-
ronmental impact in terms of methane production and nitrogen pollution. It also
Preface to the Third Edition xv
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acknowledges that dairy farmers can no longer operate on the simplistic assump-
tion that while they continue to produce milk, the people will continue to buy it.
Consumers and retailers now demand quality assurance as to production stand-
ards with regard to environmental quality, sustainability and animal welfare. All
these things receive my attention.
There are some changes in the presentation. I have decided to include no refer-
ences to specific papers and reviews within the text. If I were to give proper credit
to the good scientific and technical publications that underpin the evidence I pre-
sent in this book, the list of publications would run into thousands. If I were to be
selective, I would be rightly accused of leaving too many good papers out. This
book has been written for those actively involved with dairy cows and those uni-
versity and college students beginning their education in these matters. It is not
really intended for postgraduates and research workers – although I would like to
think they might enjoy it and learn something. The list of papers and websites for
further reading, which appears at the end of the text, provides a lead into the lit-
erature for those who wish to delve deeper. I would add that one of the incentives
for me to prepare this new edition, and one of the reasons I felt I could achieve it,
has been the recent publication of a multi‐author, high‐science (expensive) book
‘Achieving sustainable production of milk: Vol 3. Dairy Herd Management and
Welfare’. I was invited to edit this book and, in the process, learned a lot.
Finally, I have acknowledged the need to conform to public demand for gender
neutrality. Farmers and vets are no longer referred to simply as ‘he’. Stockmen have
become herders or cowherds. I draw the line at emasculating that excellent word
‘husbandry’.
Achieving Sustainable Production of Milk Vol 3 Dairy Herd Management and Welfare
2017 ed. John Webster, Burleigh Dodds Science Publishing.
xvi
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About the Companion Website
Don’t forget to visit the companion website for this book:

www.wiley.com/go/webster‐dairy‐cow
The website contains downloadable figures from the book.

1
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Part I
How the Cow Works

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3
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Introduction – The Dairy Cow of Today
Understanding the dairy cow is a matter of heart and mind. We need to consider her
scientifically as a complex and elegant biological instrument to provide us with
milk, the nearest thing in nature to a complete food. Equally, we need to recognise
her as a sentient (and highly engaging) creature who deserves a reasonable quality
of life and, at the end, a gentle death. In both senses of the word this understanding
is not static. The more we study the workings of the dairy cow, the more we can
exploit her capacity to produce food for human consumption from milk, butter,
yoghurt and a dazzling variety of cheeses. The more we study her health, behav-
ioural and environmental requirements, the better we can ensure her welfare.
The cow was one of the first animals to be domesticated for human use and has
come a very long way since then. The traditional role of the family cow was to pro-
vide milk, work, fertiliser, fuel, clothing and the occasional fatted calf, while sus-
tained by fibrous feeds that the family could not digest for themselves, usually from
land that the family did not own. The modern dairy cow, typified by the Holstein
breed, is a very different creature: bred, fed and managed to produce as much milk
as possible within intensive, highly mechanised dairy units. Meat production has
become a relatively minor consideration, with calves destined for beef or veal sent,
more often than not, off farm to other specialist rearing units. Other roles for the
milch cow have disappeared altogether. The modern Holstein is most unlikely to be
harnessed to a plough! Most of this change has taken place in the last 80 years since
the industrialisation and mechanisation of agriculture made it more convenient to
bring the feed to the cows than expect them to forage for themselves on a year‐round
basis. This has had a profound effect on the types of cow that we have bred to suit our
current purpose. Consider the four pictures in Figure 1.1. All illustrate top quality
cows from breeds in use today. The Dairy Shorthorn (Figure 1.1a), now something of
a rare breed, has the traditional, functional shape of a dual‐purpose cow bred to pro-
duce milk and beef, primarily from grazed and conserved pasture. In the second half
of the 20th Century this breed was largely replaced in the UK by the British Friesian
(Figure 1.1b), which, when managed essentially within a pastoral system but given
more concentrate, was able to produce more income from the sale of milk (with beef
Understanding the Dairy Cow, Third Edition. John Webster.

© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/webster-dairy-cow
4 Introduction – The Dairy Cow of Today
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(a) (b)
(c) (d)
Figure 1.1 Shapes of dairy cows. (a) Dairy Shorthorn, (b) British Friesian, (c) American
Holstein, (d) Jersey.
as a good secondary enterprise). The two cows are rather similar in appearance
(phenotype). Both have deep bodies, containing a large rumen able to digest large
quantities of forage. Both also carry a substantial amount of muscle (and fat when
well fed) which enables them to sustain health and production at times when the
quantity and quality of feed may be in relatively short supply. This trait is, obviously,
consistent with the potential to produce good beef. These two breeds may be said to
be at the dairy‐type end of dual‐purpose (milk and beef) cows.
The modern Holstein, however, is a very different creature (Figure 1.1c). Not only
does she have a conspicuously larger udder, she is bigger framed, much more rhom-
boid in shape and carries much less muscle. This phenotype is the consequence of
a breeding policy designed to ensure the production of as much milk as possible
from individual cows spending most of their adult life in barns on a diet of rich
feed. The fourth picture is of a Jersey cow (Figure 1.1d), much smaller and daintier
than the Holstein, but essentially similar in shape and conformation. These breeds
are both examples of the extreme dairy type.
This book will explore our understanding of the physiology, behaviour, feeding and
breeding of the modern dairy cow mostly within the context of specialist, intensive
systems of dairy production. There are several good textbooks on dairy farming (see
section on Further Reading) and the information given in these is constantly aug-
mented and brought up to date by booklets from the advisory services: in the UK, the
Agricultural Development and Advisory Service (ADAS), the Milk Marketing Board
Introduction – The Dairy Cow of Today 5
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(MMB) and a number of private enterprises (e.g. GENUS, etc.). This book is not
intended to compete with these excellent sources of information but to complement
them. It is intended for those who wish to enrich their concern for the dairy cow with
better understanding based on sound evidence. It is primarily addressed to students
in agriculture and veterinary science but will, I hope, be of interest and value to farm-
ers, stockpersons (herders), those supporting the dairy industry as feed advisors and
in other agricultural support trades; also for those with no direct contact with the
dairy industry but that have real concerns for the welfare of farm animals and the
environment.
If we wish to achieve this better understanding, we have no option but to take a
deep breath and plunge into the principles of nutrition, physiology, genetics, animal
health and behaviour. This poses a different set of problems. Most textbooks and
scientific papers that deal with the workings of the cow, i.e. the physiology of diges-
tion, reproduction, lactation etc. are written by scientists (such as myself) who have
spent most or all their working lives in academic research. They tend to carry a
degree of complexity that may be necessary for those directly involved in agricul-
ture or veterinary science, but which are prone to tell the farmer, student or advisor
rather more than they actually want (or need) to know. Publications of this sort that
are full of information important to the fundamental scientist may provoke from
the farmer, non‐specialist student or concerned member of the general public, the
question ‘gee whiz, but so what?’. They are of interest to the microbiologist, for
example to identify the thousands of species of microorganisms that inhabit the
rumen and fundamental information of this sort has undoubtedly contributed
much to (e.g.) the development of feed additives, and current efforts to restrict pro-
duction of methane, a significant contributor to climate change. Similarly, they are
of interest to the reproductive physiologist to investigate in ever greater depth the
cascade of hormones that regulate sexual function and such research has led to
major innovations in the practical control of reproduction. However, knowing the
names and specific biochemistry of the individual microorganisms in the rumen, or
all the specific hormones involved in reproduction, is not really of much practical
use to the dairy farmer. My aim in this book is therefore to concentrate on those
aspects of cow function in health and disease that are of economic or welfare impor-
tance and amenable to improvement through action on the farm. These will be
presented in sufficient detail to convey a basic understanding – but no more.
Part I: How the Cow Works deals with the physiology of digestion and metabo-
lism, reproduction and lactation, together with the science of animal behaviour in
the context of welfare and adaptation to the environment. True scientists may find
this section rather simplistic, although it is undoubtedly more complex that that
found in most textbooks of husbandry and management. It assumes no more than
a good general knowledge of chemistry and biology and is, I hope, largely self‐
explanatory. Recommendations for further reading are given at the end of the book.
Parts II–IV deal respectively with feeding, breeding and fertility, housing, and
health and welfare. In each case husbandry practices are evaluated critically in
the context of the physiology, behaviour and welfare of the cow. This is not an
instruction manual that says ‘do this, do that’. It assumes that the reader has
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r easonable practical knowledge of dairy cow management and addresses the

question ‘when I do this, or if I do this, how will the cow respond?’.
Part V goes beyond simple consideration of how the cow works, behaves and responds
to various inputs and management practices to examine important current themes
within the broad context of cows, humanity and the living environment. When the first
edition of ‘Understanding the Dairy Cow’ was published in 1987, the objectives of dairy
farming for most producers were simple: to produce wholesome milk in large quantities
as effectively and efficiently as possible, in the confident assumption that it would all sell
at a fair price and the consumer would not ask too many questions. Since then, times
have changed. Relatively affluent consumers with far greater access to information,
more‐or‐less supported by evidence, have become much choosier in their food selection
and buying habits. Those who continue to buy milk (omnivores and lacto‐vegetarians)
may select low‐fat, lactose‐free, or organic options for reasons usually related to anxiety
about personal health. Many consumers, including vegans, express concerns about cow
welfare and the impact of cattle production on the living environment. These are valid
concerns and it is in the interest of both dairy cows and dairy farmers that they are given
proper attention. Part V considers environmental issues: environmental challenges and
factors relating to sustainability and quality of life in intensive and pastoral systems. It
examines what is meant by good husbandry in the context of practical ethics and public
opinion then explores how these aims may be achieved through the establishment, vali-
dation and promotion of systems that best reconcile the occasionally conflicting demands
of biological and economic efficiency with the need to ensure healthy and reasonably
happy lives for both the cows and the farmers.
I say again, this is a book about cows. It is not a treatise on dairy farming. The suc-
cess or otherwise of dairy farming in general and individual systems in particular is
heavily influenced by non‐biological issues of economics, politics, market forces and
fashion. Predictably, these things are unpredictable. However, the yield of nutrients
from the land and their conversion by cattle into milk and meat are governed by
fundamental, logical and essentially invariant laws of biology. In this book I shall
devote little space to the economics of dairy farming because they are so variable and
subject to so many factors outside the scope of my argument. The processes that
define the biology and behaviour of the dairy cow are complex, and we do not yet
fully comprehend any of them, but the more that we who are interested in dairy
cows and dairy farming can understand them the better we shall preserve and
develop our craft to meet the needs of the age and our long‐term responsibilities as
custodians of the land and the animals.
Milk as Food
The four essential qualities of a good diet are to:

1) Provide a correct balance of nutrients to meet our metabolic needs at all stages of life
2) Ensure healthy digestion
3) Satisfy taste and appetite
4) Do no harm.
Milk as Foo 7
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Nutrient Supply
The most important nutrient for all animals is energy. We tend to get more excited by
essential but quantitatively minor components of food such as minerals and vitamins
but our greatest need by far is for fuel to sustain the fire of life. The energy value of food
is measured in joules or calories (1 kcal = 4.2 kJ). This describes the amount of heat
liberated when that food is combusted completely in a bomb calorimeter. One gram of
wheat, for example, generates about 16.6 kJ of heat on combustion. Animals extract
energy from food by the processes of digestion and absorption, use it to meet metabolic
needs for maintenance, exercise and synthetic processes like growth and lactation and
produce heat in the process. After energy, the principal nutrients required, in decreas-
ing amounts, are amino acids from proteins, minerals and vitamins.
Table 1.1 lists the principal nutrient requirements for an adult doing moderate
exercise and a growing four‐year‐old child, and illustrates the extent to which these
can be met from whole milk alone. Table 1.2 illustrates how these requirements
would be met if man and boy were to subsist on a daily diet of 500 g of whole milk
and breakfast cereal. These tables make some important points that are too fre-
quently overlooked in many popular articles on human nutrition and dietetics. The
adult and child require, respectively, 12.6 and 6.4 MJ/day. The adult can meet this
need by consuming 800 g cereal plus 60 g of milk solids (total 860 g), the child needs
to consume 350 g cereal plus 60 g milk solids (total 410 g). Requirements for protein,
the second most important nutrient, are 87 g/day and 56 g/day, i.e. only 10% and
14% of the diet respectively. Absolute daily requirements for minerals and vitamins
are much smaller still. In other words, an adult requires about 90% of digestible
food as a source of energy (fuel), the child about 85%. The affluent are inclined to
Table 1.1 Contribution of 0.5 L cow’s milk per day to the daily nutrient requirements
of a four‐year‐old child and an adult doing moderate work.
Four‐year‐old child Adult
Requirement % from milk Requirement % from milk
Energy (kJ) 6400 25 12600 13

Protein (g) 56.0 30 87 20
Calcium (g) 1.0 60 0.8 75
Iron (mg) 7.5 2 12.0 1
Vitamin A (iu) 3000 30 5000 15
Vitamin D (iu) 400 2 – –
Vitamin C (mg) 15 70 20 50
Vitamin B
nicotinic acid (mg) 6.0 7 12 3
riboflavin (mg) 0.9 85 1.8 45
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Table 1.2 Meeting the energy and protein requirements of an adult and a
four‐year‐old child from a diet of milk and breakfast cereal.
Adult Child
Daily requirement: energy (kJ) 12600 6400

Protein (g) 87 56
Energy supplied by milk (60 g solids, kJ) 1600 1600
Energy required from cereal (kJ) 11000 4800
Cereal intake (g/day) 800 350
Protein yield from milk and cereal (g/day) 120 62
Protein balance (g/day) +33 +6
paranoia about calories but this is because we eat too much. For the hungry, calories
are the biggest need by far.
A balanced diet is one in which the nutrients match the specific requirements of the
consumer. Humans cannot live on a diet of bread and milk alone (not quite) because it
lacks some of the minor nutrients. However, as indicated above, milk and cereal can meet
not only energy but also protein requirements, even for growing children. When one looks
at the minor nutrients, milk becomes even more impressive (Table 1.1). Relative to its
capacity to provide energy, milk is rich in high quality protein, calcium, vitamin A and
vitamin C. The nutrients it lacks are iron, vitamin D and some of the B vitamins, e.g. nico-
tinic acid. In practice this only constitutes a problem for animals such as veal calves reared
on milk alone. As a food for human consumption therefore, cow’s milk is rich in almost
all the nutrients essential for life, especially essential nutrients such as high‐quality pro-
tein (well balanced with respect to essential amino acids), calcium and vitamin A, so can
provide an excellent balancer for low‐cost, high energy foods such as cereals.
Healthy Digestion
Most people who drink milk on a regular basis can digest it without difficulty. Some
individuals can suffer the consequences of lactose intolerance manifest by abdomi-
nal pain, bloating and diarrhoea. This is caused by a deficiency in the enzyme
lactase that divides the disaccharide, lactose into its constituent monosaccharides,
glucose and lactose. All healthy mammals must have lactase at birth to digest their
mother’s milk. If, after weaning, they drink no more milk the lactase enzyme is
down‐regulated so that if they suddenly consume milk as adults, they may experi-
ence discomfort. The real prevalence of lactose intolerance is difficult to gauge,
being confounded by individual differences in severity of symptoms, real and imag-
ined. It is certain that the prevalence of lactose intolerance is much higher some
Asian and African communities than in Western communities accustomed to
consuming dairy products throughout life. What is not certain is the extent to which
Milk as Foo 9
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this is genetic or environmental (i.e. no milk after weaning). In my youth, I was

taught that the reason Chinese and other oriental races were unable to tolerate milk
was genetic. This is clearly not the whole story. With increasing affluence, the
Chinese have developed a taste for milk products and lactose intolerance does not
appear to be a major problem. Maybe they just worry less. Those for whom lactose
intolerance is real can, of course, buy lactose‐free milk.
Taste and Appetite

Milk is the basis for a wide range of highly attractive products: butter, cream, ice cream,
yoghurt and an amazing array of cheeses, to appeal to the palate of the consumer and
increase the value of milk to the producer (and especially the middle‐man). To these we
may add products such as spreadable butter and anti‐cholesterol spreads in which milk
products are mixed with vegetable oils. There has been some interest among animal sci-
entists (if no one else) in manipulating the nutrition or genetics of cows to produce
healthier milk, e.g. richer in omega 3 fatty acids. This seems to me to be a pointless exer-
cise. The versatility of milk (as distinct from meat) derives from the fact that so many
tasty (and healthy) things can be done to it after it leaves the cow. As to concerns about
appetite, we do have a problem. Milk products, butter, cheese, ice cream, are just too nice.
Do no Harm
For many years our main concerns about milk and health were driven by medical claims
of associations between the consumption of animal fats and ill‐health, especially obesity,
cardiovascular diseases (CVDs), and to a lesser extent, cancers. Animal products contain-
ing significant amounts of fats can undoubtedly contribute to obesity, because fats are
energy rich and these products are tasty. Moreover, obesity is a confirmed risk factor for
many cancers. The problem here is one of quantity, not quality. There is good evidence
that increasing the ratio of unsaturated to saturated fatty acids in the diet reduces the risk
of CVD. The composition of milk fat is approximately 60% saturated, 30% monounsatu-
rated, 10% polyunsaturated. In oily fish such as trout, the composition is 30% saturated,
40% monounsaturated, 30% polyunsaturated. We must conclude that for those at risk of
CVD, it is wise to reduce the amount of saturated fat in the diet. However, new evidence
makes it even more clear that those who select low fat diets and, in compensation, increase
their sugar intake are putting themselves at greater risk of obesity and diabetes.
There are some differences between the composition of the milk protein casein in
cows and humans that may have consequences for human health. There are, in fact,
several milk caseins, as‐1, as‐2, β and K casein. Beta casein exists in two forms, A1
and A2 beta casein. Most Holstein and Friesian cows secrete A1 and A2 in roughly
equal proportion. Some cattle, most notably Guernseys (and most goats) secrete milk
that is about 80% A2, which is similar to human milk. There are some claims that A2
casein may be healthier, although this has not yet been substantiated by meta‐analy-
sis. There is no evidence to suggest a link between differences in A1:A2 ratios and
milk allergies. However, if there was significant evidence of health benefit from the
consumption of A2 milk, it would be possible to select from the high A2 cows within
the Holstein breed.
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Biological Efficiency of Milk Production
The primary source of energy for all food production is, of course, the Sun. The
theoretical maximum efficiency of capture of solar energy by plants is about 3%.
Actual efficiencies of capture by plants range from about, 0.3 to 0.7%. These effi-
ciencies are very low but that is not too serious a problem as solar energy is plentiful
and will be around for a very long time. Grasslands (a collective term to include
clovers and other grazed herbs) are potentially the most efficient of the feed crops
because they can be grazed and cropped many times per year and the whole crop
gets eaten.
Food production from animals is inevitably less efficient than that from plants
because much of the food eaten by animals is required to meet their own needs.
Animals consume feeds from a variety of sources. Figure 1.2 illustrates very simply
a typical cow diet consisting mainly of forage, cereal and a protein supplement,
soya. In ruminants, the two‐stage processes of digestion in the rumen and downstream
FOOD INTAKE
Cereal Forage Soya (etc)
Faeces Digestion & Fermentation Methane
DIGESTIBLE NUTRIENTS
Urine
AVAILABLE NUTRIENTS
Energy Protein Mins Vits
NUTRIENT REQUIREMENTS
Maintenance Work Production Reserves
HEAT MEAT
CO2 MILK
EGGS
Figure 1.2 Nutrient supply and requirement (from Webster 2013).

Biological Efficiency of Milk Productio 11
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yield digestible nutrients after losses as faeces and methane (see Chapter 2). The
metabolism of digestible nutrients to meet specific demands for available nutrients
to meet maintenance and production needs incurs further losses in the urine
(especially nitrogen).
The amount of available energy is termed metabolizable energy (ME) usually
measured in MJ where:
Metabolizable energy (MJ) = gross energy of feed – energy in faeces, urine

and methane.
The primary need for available nutrients is to support maintenance, the energy
and materials needed to support life in an animal neither gaining nor losing body
weight. Feed consumed in amounts greater than maintenance requirement is
available for conversion into animal products (milk, meat and eggs). At mainte-
nance, nearly all nutrients are used to provide ME and oxidised to produce heat
and CO2. For the farm animal reared to produce milk, eggs or meat, the require-
ments for protein, minerals and vitamins increase in relation to energy in propor-
tion to the level of production, usually expressed in relation to maintenance. At the
maintenance level of feeding the gross efficiency of conversion of animal feed into
animal product (food for humans) is zero. The greater the capacity of a farm ani-
mal to ingest, digest and metabolizable feed into the synthesis of milk, eggs or
meat, relative to the demands of maintenance, the greater will be the overall bio-
logical efficiency of production. All other things being equal, it follows that the
way to maximise the biological efficiency of a dairy enterprise will be to breed and
feed individual cows to produce as much milk as possible. However, as we shall
see, all other things are not equal.
Milk Production: Species and Breed Comparisons

Table 1.3 compares the yields and composition of milk from Holstein and Jersey cows,
a sow giving birth to fourteen piglets, a Labrador bitch with eight puppies and a human
mother with one child. The figures for cows have changed substantially since the pre-
vious edition was published in 1993. Then I gave the example of a typical Friesian cow
giving 31 L/day. The figure for a typical Holstein of today in an intensive unit is 60 L.
The classic approach to making comparisons between species differing greatly in size
is to express inputs and outputs in terms of ‘metabolic body size’, body weight to the
power 0.75 (W kg0.75). This exponent of body weight is universally accepted as that
which confers proportionality on measurements of energy exchanges. In more simple
language, the maintenance requirements of homeotherms for energy, when expressed
per kg0.75 are, as a first approximation, the same.
There are interesting differences between species in milk composition. The milk
of sows and bitches is especially rich in nutrients. This reflects the fact that they
give birth to large litters of small, immature offspring who need to grow quickly.
Human milk is low in protein and fat, high in lactose. While human babies are
extremely immature at birth compared with (say) a calf, they grow slowly. In the
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Table 1.3 Yield and composition of milk from different mammals.
Holstein cow Jersey cow Sow Bitch Woman
Body weight (kg) 700 420 240 26 60

0.75
Metabolic weight (kg ) 135 93 60 11.5 21.5
Number of offspring 1 1 14 8 1
Peak milk yield (L) 60 35 8.5 1.3 1.0
Composition of milk (g/L)
Protein 33 37 60 83 12
Fat 37 49 83 97 38
Lactose 45 46 52 41 70
Calcium 1.2 1.4 2.7 3.0 0.3
Phosphorus 0.9 1.0 1.6 2.0 0.2
0.75
Nutrient yield (kg /day)
Energy (kJ) 1300 1180 770 715 132
Protein (g) 11.0 12.5 8.4 9.4 0.6
second edition (1993) I calculated the milk energy yield of the Friesian cow pro-
ducing 31 L milk/day to be 745 kJ/kg0.75 per day, not significantly different from
that of the sow or bitch. Today it has risen to 1300 kJ/kg0.75 per day. At that time, I
wrote that the peak metabolic demands of lactation for the dairy cow were not
significantly greater than for the sow, or bitch and that the stress of lactation was
related more to the duration – nine months at least as against eight weeks or less.
Today the physiological demands on the high yielding dairy cow are in a class of
their own. I shall have much more to say about the metabolic and welfare implica-
tions of this in later chapters.
Efficiency of Feed Conversion to Milk, Eggs and Meat: Competitive

and Complementary Feeds
Milk and egg production appeal to vegetarians and to thrifty souls like myself
because they do not involve killing the animal to get at the food. Moreover, milk and
(unfertilised) eggs are not bits of animals, they are simply foods of the highest nutritional
value: the former to feed the growing calf from the time of its birth, the latter to feed
the fertilised embryo up to the time of hatching. Table 1.4 compares the efficiency
of conversion of feed energy (ME) and protein into hens’ eggs, cows’ milk, pork
meat from the offspring of sows giving birth to 22 piglets/year and beef from exten-
sively reared cow‐calf systems where the contribution of the breeding beef cow is
but one calf/year plus her own carcass at eventual slaughter.
Biological Efficiency of Milk Productio 13
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Table 1.4 Efficiency of energy and protein conversion in meat, milk and egg
production (from Webster 2013). For each system, efficiency is described by the ratio
of output to input, where output is defined by energy and protein in food for humans;
inputs are described in terms of total and ‘competitive’ intake of ME and protein,
where ‘competitive’ describes energy and protein from feed sources that could be fed
directly to humans.
Eggs Pork Milk Beef
Production unit 1 hen 22 pigs 1 cow 1 calf

Support unit 0.05 hens 1 sow 0.33 heifers 1 cow
Output/year (kg food) 15 1300 8000 200
MJ food energy 130 13000 28000 2500
kg protein 1.65 208 264 32
Input/year (MJ ME in total) 389 67038 67089 29850
MJ ‘competitive’ ME 351 53630 20127 10268
Input/year (kg protein in total) 5.2 818 946 361
kg ‘competitive’ protein 5.0 736 236 108
Efficiency
Food energy/total feed ME 0.33 0.19 0.42 0.08
Food energy/‘competitive’ feed ME 0.35 0.24 1.39 0.24
Food protein/total feed protein 0.32 0.25 0.28 0.09
Food protein/‘competitive’ feed protein 0.33 0.28 1.12 0.30
In each column the efficiency of conversion of feed energy and protein is expressed
in two ways:
●● Overall efficiency: food energy and protein (for human consumption) relative to
total feed energy and protein consumed by the animals (both the breeding and
slaughter generations).
●● Competitive efficiency: food energy and protein (for human consumption) relative
to animal consumption of ME and protein from ‘competitive’ feed sources (e.g. feeds
such as cereals that could have been fed directly to humans) as distinct from ‘com-
plementary’ feeds (grazing, forages and by‐products remaining after preparation of
food and drink for human consumption (e.g. maize gluten, brewers’ grains).
The overall efficiencies of ME conversion into eggs, pork, milk and beef are 0.33,
0.19, 0.42 and 0.08 respectively; for protein conversion they are 0.32, 0.25, 0.28 and
0.09. The reason why the efficiency of energy conversion to milk is greater than that
for egg production can be attributed to the fact that there has, to date, been no limit
to the ability of breeders to select cows to produce more and more milk per day,
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whereas hens are still restricted to the production of one egg per day. Both milk and
egg production are more efficient than the intensive production of pork meat: beef
production (by these measures) fails to achieve an efficiency of 10%.
When energy conversion is examined in terms of competitive efficiency the picture
changes. Here beef becomes as efficient as pork (or no less inefficient) and dairy
farming becomes very efficient indeed. In this example, based on a typical diet fed
to the cows amongst whom I live in the pasture‐rich South West of England approx-
imately 65% ME is complementary and the output of food energy for human con-
sumption is 39% greater than their demand for feed that we could eat ourselves.
This impressive performance is not necessarily restricted to pasture‐based systems.
High competitive efficiencies can be achieved in fully housed systems though
proper selection of complementary feeds.
Table 1.4 provides a powerful illustration of the danger of leaping to simplistic
conclusions as to the profligacy of feeding our limited resources to farm animals.
Even within these limited parameters of feed conversion, there is no simple
answer. When other factors such as environmental sustainability, fuel costs, pol-
lution, animal welfare and ethics are taken into account, our view of what’s best
becomes decidedly fuzzy.
Behaviour and Welfare
Cows are sentient animals. By my definition this means that they have ‘feelings that
matter’. They are motivated to behave in ways intended to meet their emotional need
to seek satisfaction and avoid suffering. Many of these emotions are primitive, such as
hunger, thirst, pain and fear. However, there is now convincing evidence that cows, in
common with other farm animals, can experience (and are motivated by) ‘higher’
sensations within the spectra of confidence–anxiety, hope–depression, pleasure–
grief. The sentient animal can interpret its physical and emotional state when under
challenge, choose an action within the range of options available to its phenotype and
remember how effective it was. Its memory of the success or otherwise of its response
will affect how it feels when next presented with a similar challenge. If it learns that
it can cope it will become less alarmed; it will habituate. If it learns that it cannot cope
with the stress, or the anticipation of stress, then it is likely to suffer.
Stress and suffering are not the same. Sentient animals are well equipped to
respond to environmental challenges (stress) in circumstances that permit them to
make an effective response. Animals suffer when they fail to cope (or have extreme
difficulty in coping) with stress. This can occur when:
●● The stress is too severe, too complex or too prolonged
●● The animal is prevented from taking effective action to relieve the stress.
A prime example of the first source of suffering is the dairy cow that fails to cope
with the intense, multiple, prolonged physiological demands of lactation. This
problem will be considered in depth in subsequent chapters. A classic example of
the second is the sow in the extreme confinement of a pregnancy stall.
Behaviour and Welfar 15
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Nutrition
Environment
Infection
Social contact
Management
Inputs
Scenario
DAIRY COW
WELFARE OUTCOME
Physiology Health Emotion
Indicators
Observations
Veterinary procedures
Measurements Records
Figure 1.3 Dairy cow welfare and the environment: inputs and indicators.
The welfare of a sentient animal may be considered as an integral measure of its overall
emotional state within a range from very good, through satisfactory, to very bad. The owner
of any domestic animal, whether farmed or pet, has a responsibility to provide conditions
that promote a sense of wellbeing, defined by a satisfactory (at least) quality of life consid-
ered in terms of the multiplicity of factors that can affect its welfare. This presents us with
a problem. Our interpretation of the emotional state of others can only be subjective. Since
I can never be sure how they are feeling, I am reluctant to speak with authority on the
mental state of the dairy cow. Nevertheless, we have no option but to try. Figure 1.3 illus-
trates the complexity of the challenges that determine the welfare state of a sentient animal
(here a cow) and the indicators by which we attempt to assess it. The inputs are nutrition,
the physical environment, management, social contact and the potential for infection and
disease. These, together, constitute a scenario that affects its welfare through impact on its
physiology, health and emotional state. We can build up a picture of the welfare of indi-
vidual cows, or the whole herd, by an appropriate choice of indicators. These should
include the following, all of which will be considered at greater length.
●● Welfare outcomes: observations and measurements of physical state (e.g. body
condition, lameness) and emotional state (e.g. abnormal behaviour patterns)
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●● Husbandry provisions: nutrition, housing, herd health programmes

●● Records: fertility, mastitis, lameness control (etc.).
In the minds of the general public, and even some scientists, the biggest welfare problems
for farm animals are directly linked to the industrialisation and intensification of live-
stock farming, mainly because these systems deny them the free expression of natural
behaviour. This was highlighted by the publication in 1965 of ‘Animal Machines’ by
Ruth Harrison, that drew public attention to the conditions of pigs, laying hens and veal
calves kept in the most extreme conditions of confinement. For these animals, denial of
natural behaviour was a paramount cause of bad welfare. The impact of her book led to
the establishment of the Brambell Committee (1965), who concluded that all farm ani-
mals should be provided with conditions that allowed them, without difficulty, to ‘stand
up, lie down, turn around, groom themselves and stretch their limbs’. These became
known as the ‘five freedoms’ and were undoubtedly a high priority recommendation for
the animals in these extreme systems. However, it should be clear from Figure 1.3 that
they left an awful lot out.
In 1963 the UK Farm Animal Welfare Council produced a much more compre-
hensive set of Five Freedoms and Provisions. These are:
●● Freedom from hunger and thirst – achieved by readily accessible fresh water and
a diet to maintain full health and vigour.
●● Freedom from discomfort – achieved by appropriate shelter with a dry, restful
lying area and temperature within an acceptable range of tolerance.
●● Freedom from pain, injury and disease – achieved by prevention or rapid diagno-
sis and treatment.
●● Freedom from fear – achieved by conditioning animals to their surroundings and
avoiding situations that cause stress.
Table 1.5 Abuses of the five freedoms that can arise through systematic failures
in the provision of good husbandry (from Webster 2010).
Hunger Nutrition fails to meet the metabolic demands of

lactation
Chronic discomfort Poorly designed cubicles, inadequate bedding
Pain and injury Claw disorders (sole ulcer, white line disease)
Damaged knees and hocks
Mastitis
Infectious disease Mastitis, digital dermatitis
Fear and stress Rough handling, bullying, separation from calf
Suppressed behaviour Zero grazing, inadequate rest time
Exhaustion Emaciation, infertility, forced culling
Behaviour and Welfar 17
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●● Freedom to express normal patterns of behaviour – achieved by the provision of

room to move, things to do and the company of their own kind.
These recommendations have stood the test of time. For a start, they are measures
of outcome, now recognised as the most direct approach to the assessment of animal
welfare. They are, moreover, not intended as a counsel of perfection but as a guide to
good husbandry: simple enough to be memorable but comprehensive enough to be
effective. Four of these five freedoms are freedoms from: something that meets with
general approval. The final freedom: ‘to express normal patterns of behaviour’ does
arouse some concern. What, for example, is normal behaviour and when does nor-
mal behaviour become unacceptable? Isaac Stern expressed this well in a human
context by pointing out that your freedom to swing your fist stops at the point of my
nose. If I could persuade FAWC to rewrite the fifth freedom, I would reduce it simply
to ‘freedom of choice’. Applying this principle to a dairy system would imply (e.g.)
freedom to select a preferred environment for rest and recreation, freedom to select,
and avoid, contact with certain individuals in their social environment.
When we consider the welfare of the dairy cow, it becomes clear that her most
severe problems are likely to be associated with physical stresses to her health and
physiology, rather than denial of behavioural expression (Table 1.5). Relative to most
farm animals she is most unlikely to suffer in consequence of having nothing to do
all day. On the contrary she is worked quite extraordinarily hard. The modern dairy
cow can cope in the short term with the intense metabolic demands involved in the
production of 60 L milk/day (or more), coupled with the demands of consuming and
digesting enough food to meet these demands. It is an inescapable fact, however, that
too many succumb too soon to the long‐term stresses of lactation, in particular, the
production diseases such as rumen acidosis, ketosis, environmental mastitis and
lameness that are, by definition, linked to the methods employed in the breeding,
feeding and housing of cows to produce large quantities of milk (i.e. our fault).
Table 1.5 introduces a problem not addressed by the five freedoms, namely that
of exhaustion arising from failure to cope, in the long term, with the exacting phys-
ical demands of lactation. For the dairy cow, exhaustion is probably the biggest
problem of all. It describes a cow broken down in body, and possibly in spirit,
through a combination of stresses associated with nutrition, housing, hygiene and
management, exacerbated in many cases by breeding programmes that have over-
emphasised productivity at the expense of robust good health. Too many infertile,
emaciated or chronically lame cows are culled prematurely because they are no
longer making a productive contribution to the enterprise. This is not only an
abuse of welfare but also a terrible waste since a dairy cow needs to complete at
least four lactations to recoup the cost of rearing her as a heifer until she delivers
her first calf and enters the milking herd. We cannot escape the fact that while
some welfare problems for dairy cows may arise from bad luck, most may be attrib-
uted to systematic failures of provision. Later chapters will look in detail at how
the individual production diseases affect the health and welfare of the individual
cows, and how these may best be addressed at the herd level through the implementation
of a herd health and welfare strategy.
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Digestion and Metabolism
Digestion is the process whereby food is broken down into substances that can be
absorbed across the cell lining of the gut. The nutrients made available by digestion
and absorption are then available for metabolism by the tissues of the body to meet
the needs of maintenance, work, growth, reproduction and lactation. The dairy cow
is a ruminant, which means, in the simplest terms, that prior to the true stomach, or
abomasum, she has a very large fermentation vat, the reticulo‐rumen, that contains
microorganisms able to break down the structural carbohydrates of plant cell walls
into simple organic compounds that can be absorbed across the rumen wall and used
for energy metabolism. The material that flows out of the rumen into the abomasum
consists of food that has escaped, or been released by fermentation, plus a rich source
of protein from microorganisms that have multiplied within the rumen. From the
abomasum onwards the digestive tract of the cow and the processes that take place
therein are similar to those in humans and other simple‐stomached animals
(Figure 2.1). It is the special structure and function of the rumen that has given the
dairy cow the capacity to produce so much good food for human consumption while
subsisting so largely on plant materials that are of no direct nutritive value to us.
Structure of the Digestive Tract
The cow is popularly assumed to have four stomachs: the reticulum, rumen, omasum
and abomasum. In practice, it is easier to consider only two functional compartments.
The first, consisting of the reticulum and rumen, provides a huge reservoir wherein feed,
saliva and other secretions are stirred and mixed in the presence of microorganisms. At
birth, the reticulo‐rumen is smaller than the true stomach or abomasum, which (as in
humans) is the primary site for the digestion of milk. As the calf begins to consume plant
material, the reticulo‐rumen grows in volume and acquires a mixed population of micro-
organisms capable of breaking down the fibre in cell walls. In the adult cow it occupies
the major part of the abdominal cavity, extending on the left side from the diaphragm to
the pelvic inlet (Figure 2.2). The inner surface of the reticulum has a ‘honeycomb’
appearance. The inner wall of the rumen is made up of thousands of visibly recognisable

Oe
OG
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reticulum rumen
RoO
omasum
abomasum
F
duodenum
P caecum
ICCJ
spiral
colon
jejunum
proximal
colon
rectum
Figure 2.1 The digestive tract of the cow. F = fundus, ICCJ = ileocaecocolic junction, Oe
= oesophagus, OG = oesophageal groove, P = pylorus, RoO = reticulo-omasal orifice.
13th rib
O CDS
CP
OG
ADS CVS
RoO
rumen
Rt
Figure 2.2 Location of the main structures of the rumen. ADS = anterior dorsal sac,
CDS = caudal dorsal sac, CVS = caudal ventral sac, CP = cranial pillar, O = oesophagus,
OG = oesophageal groove, Rt = reticulum, RoO = reticulo-omasal orifice.
20 Digestion and Metabolism
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finger‐like processes (papillae), the function of which is to maximise the surface area for
absorption of the end processes of ruminal fermentation (Figure 2.3(a)). The oesopha-
geal opening and the reticulo‐omasal orifice, which form respectively the entrance and
exit to the reticulo‐rumen, are sited close to one another and linked by the oesophageal
groove, the lips of which close when a young calf sucks milk, thereby creating a short cut
from the oesophagus to the abomasum. The relationship of the rumen to the rest of the
digestive tract is like a huge lake with a river running through one corner (see Figure 2.1),
a design particularly well suited to delaying the passage of feed down the main stream of
the gut to allow time for ruminal fermentation.
The approximate relative weights and volumes of the major organs of the digestive
tract are shown in Table 2.1. The dry weight of the digesta (gut contents) removed
from each portion of the gut provides a measure of volume. The percentage of total
(a)
(b)
Figure 2.3 (a) Visible papillae of the rumen wall. (b) Microscopic papillae of the
small intestine wall (scanning electron micrograph).
Structure of the Digestive Trac 21
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Table 2.1 Relative weights of portions of the gut and gut contents in an adult cow.
% total wet tissue in

% total dry digesta in gut gut wall
Reticulo‐rumen 66 44
Omasum 4 16
Abomasum 5 7
Small intestine 15 20
Large intestine 10 13
wet tissue in the gut wall describes the mass of each organ after removal of its
contents. The reticulo‐rumen is by far the largest and heaviest organ of the gut. The
‘third’ stomach, or omasum, more quaintly known as the bible or psaltery, is also set
aside from the mainstream of the gut, which takes a short route between the retic-
ulo‐omasal orifice and the opening of the abomasum (Figure 2.1). The body of the
omasum is made up of more than 100 leaves (hence psaltery) of epithelial tissue, so
that while the mass of the empty omasum is relatively large (16%), it contains only
about 4% of total digesta. This is packed between the leaves of epithelium and tends
to be very dry, suggesting that the main role of the omasum is the absorption of water
and substances in solution. The exact function of the omasum remains something of
an enigma. However, it can be removed surgically without any significant effect
on digestion, which suggests that, as enigmas go, it is not very important.
The abomasum has two distinct sections: the fundus, which is the main site for
secretion of hydrochloric acid and enzymes that operate in an acid medium, and
the pylorus, where material gathers before being projected by muscular contrac-
tion through the pyloric sphincter into the duodenum as a discrete bolus of
partially digested food. The pyloric sphincter acts as a valve regulating the flow of
material into the duodenum and small intestine.
The acidified digesta leaving the abomasum are neutralised in the duodenum, sub-
jected to further degradation by enzymes, and then pass on to the jejunum and ileum
that together make up the small intestine. The word ‘small’ is misleading. The vol-
ume of the contents of the small intestine is only about 15% of total digesta. However,
the epithelial lining of the small intestine is made up of millions of microscopic
papillae, which give it an enormous surface area relative to its mass (Figure 2.3(b).
The microenvironment around the cell surface of the small intestine is extremely
complex and metabolically active. It contains the epithelial cells that constitute the
major site for absorption of nutrients. It also contains a very high density of cells of
the immune system. These are best known in the context of defence against infection,
but their role is much greater than this. A primary function of the immune system is to
distinguish self from non‐self and act accordingly. Non‐self refers to any complex
molecule that is foreign to (i.e. not a home‐made constituent) of the animal body and
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is, in consequence, a potential antigen. The surface of the digestive tract is the site at
which the body is presented with the greatest exposure to foreign molecules that
range from the essential (nutrients) to the dangerous (pathogenic bacteria). A
prime function of the immune cells is to distinguish between the ‘good’ and ‘bad’
molecules (nutrients and pathogens); to tolerate the former and attack the latter.
Most food allergies result from failures of the immune cells to come to the right deci-
sion. The microenvironment around the papillae in the lumen of the intestine also
includes an enormous population of microorganisms, most of which are harmless
and indeed essential to the health and normal function of the gut through their abil-
ity to compete with potential pathogens. Establishment and maintenance of a
healthy microbial population in the small intestine is the basis of probiosis. The
rumen microbial population (the microbiome) may be thought of as the best of pro-
biotics. The word prebiosis has a different meaning and describes the principle of
feeding a diet designed to have a favourable impact on the microbiome.
The large intestine is made up of the caecum, another reservoir set aside from
the mainstream of the gut, and the colon. Despite its large volume, the contribu-
tion of the large intestine to digestion and absorption in the ruminant is relatively
small. It acts as a secondary site for microbial fermentation and for absorption of
water and substances in solution such as mineral salts. This contrasts with species
like the horse and the rabbit, where effectively all the fermentation of fibrous feeds
takes place in the hind gut. The epithelium of the large intestine does not contain
the high density of papillae present in the jejunum and ileum so its effective
surface area is, in fact, less than that of the small intestine.
Eating and Rumination
Grazing
The strategy of ruminants at pasture is to ingest food as quickly as possible, then retire
to recycle it at their leisure to be broken down further through comminution (chewing)
and salivation by the process of rumination. This behaviour is conspicuously different
from that of small‐stomached, hind‐gut fermenters such as the horse, who ingest
pasture for a longer duration at a slower rate. The grazing cow harvests grass with a
mowing action. The tongue swings across the pasture, pulling grass into the mouth
where it is cut off by the incisor teeth of the lower jaw against the dental pad (there
being no incisor teeth on the upper jaw). This action makes the cow a much less selec-
tive grazer than the horse, or even the sheep. It also puts the cow at a disadvantage
with respect to the horse and the sheep when the grass is short (below 50mm in
length). Cattle can extract more nutrients from pasture than horses through more
efficient digestion, which is an obvious economic advantage when they are grazed on
well managed pastures. However, horses and sheep are less susceptible to starvation
on overgrazed or drought‐affected pastures because they can graze right down to the
ground. Goats, of course, are even better, but one big reason for this is that they are
much more imaginative in their food selection.
Eating and Ruminatio 23
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When the pasture is relatively short, young and low in fibre it is swallowed almost
at once, with little chewing or ensalivation. The same applies to short‐cut silage.
Long hay is pulled into the mouth and chewed between the molar teeth until it is
reduced to a suitably small and moist bolus for swallowing. The upper jaw of the
cow is wider than the lower, which means that only one side of the molar teeth is
involved in chewing at any one time, which saves on wear and tear. Cereals and pel-
leted feeds are consumed very quickly, usually without chewing. When cows are fed
unrolled barley or corn (maize) it is common to see in the faeces grains that have
been swallowed whole and passed unchanged right through the gut.
Salivation
The cow, in common with all ruminants, salivates copiously and continually. The
rate of flow varies from about 60 ml/min at rest, increasing to 120ml/min during
eating and 150 ml/min during rumination. The amount of saliva secreted per day
is likely to exceed 140 litres (over 30 gallons). The amount secreted per minute dur-
ing eating and rumination is not much influenced by the dry matter and physical
form of the feed. However, the time spent eating and ruminating a dry, fibrous,
long‐stemmed feed like hay obviously greatly exceeds that spent eating the same
amount of nutrients as cereals or pelleted concentrates. The total quantity of saliva
secreted per day is thus very dependent on the physical form of the feed.
The saliva of ruminants contains sodium salts, sodium bicarbonate and phosphate, which
act to regulate the pH of the rumen and restrict the fall (increase in acidity) that would oth-
erwise result from the production of organic acids as the end‐products of fermentation.
All diets for ruminants should contain a sufficient quantity of long fibre (>10 cm) to
maintain the stability of rumen pH. For the high‐yielding dairy cow, this creates a con-
flict between the need to provide sufficient nutrients and the need to promote healthy
digestion. This is a major problem and will be considered in detail in Chapter 7.
Rumen Movements
The movements of the reticulo‐rumen are complex and elegant because they gov-
ern four quite distinct processes.
1) Mixing of rumen contents
2) Outflow through the reticulo‐omasal orifice
3) Regurgitation of feed for ruminating
4) Eructation of gases (belching).
Some of these movements are illustrated in Figure 2.4(a–e). The arrival of a bolus of
food stimulates a contraction of the reticulum that pushes the contents of the retic-
ulum into the anterior dorsal sac of the rumen (a). The liquid on top and solids floating
on that liquid pass into the main body of the rumen, the rest of the liquid and the
denser solids remaining in the anterior dorsal sac (b). The anterior dorsal sac then
contracts as the reticulum relaxes (c), allowing some material to return to the reticu-
lum and some to pass on into the omasum and abomasum through the reticulo‐omasal
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(a) Oe GC
GC
Ru
(b)
Rt
ADS
Rt
(c) Ru
ADS
Rt
RoO (d)
ADS
Rt
(e)
ADS
Rt
ADS
Figure 2.4 Movements of the reticulo-rumen. ADS = anterior dorsal sac, GC = gas cap
above rumen contents, Oe = oesophagus, Rt = reticulum, Ru = rumen, RoO = reticulu-
omasal orifice. (a) Bolus arrives at ADS, Rt starts to contract. (b) Rt fully contracted. (c)
Contraction of ADS, material forced through RoO. (d) Mixing contraction in main body
of rumen. (e) Belching contraction.
orifice. The wave of contraction then spreads to the main body of the rumen, stirring
the contents in a figure‐of‐eight movement (d). This series of contractions designed to
achieve mixing and outflow recurs at intervals of about 40–60 s during eating and
rumination, slowing to about 80–100 s when no material (feed and ruminated boluses)
is entering from the oesophagus. The time taken for material passing over the cranial
pillar to complete a cycle of the rumen is about one hour.
Eructation is achieved by a reverse contraction that originates in the caudo‐ven-
tral sac of the rumen and drives the gas cap above the rumen contents up towards
the opening of the oesophagus (e). Regurgitation of material from the rumen
involves an isolated contraction of the reticulum that forces the contents of the
reticulo‐rumen anterior to the cranial pillar up against the gastric opening of the
oesophagus, which is, at the same time, dilated by expanding the thorax, thus per-
mitting food material and fluid to be drawn up into the mouth.
Eating and Ruminatio 25
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The movements of the reticulum and anterior dorsal sac both control the rate of
outflow of rumen contents and sort out the solid material into that which passes into
the abomasum and that which is returned to the body of the rumen. Smaller and
denser particles pass out into the abomasum, lighter, less digested particles are returned
to the rumen for further chewing and fermentation. The rate of passage of material out
of the rumen depends therefore not only on the quantity of food consumed but also on
its composition. When a dry (non‐lactating) cow eats a maintenance ration consisting
entirely of forage, about 3% of rumen contents exit per hour through the reticulo‐
omasal orifice. Looked at another way, this means that the retention time for forage in
the rumen is about 33 h. A high yielding cow will consume about three times as much
food from a mixture of forage and concentrates of high nutrient density and small
particle size. In these circumstances the rate of passage out of the rumen will be about
6% and 10% per hour for forage and concentrates respectively, equivalent to mean
retention times of 16 and 10 h.
Rumination
Rumination, or ‘chewing the cud’ begins with the propulsion of rumen contents
into the mouth (Figure 2.4(e)). Most of the liquid is rapidly squeezed out and re‐
swallowed. The solids, which tend to be the longer, lighter, less digested material,
are chewed over at leisure. Cows tend to ruminate when totally relaxed and have
even been shown to do so when electroencephalographic (EEC) records show
them to be in a state of deep sleep. The function of rumination is to process food to
the point when it can escape the cycle of regurgitation and pass on to the aboma-
sum for further digestion. The time spent ruminating is governed by the amount of
time required to achieve this objective. A dry cow whose diet consists mostly of
long hay may ruminate for 8–10 h/day. A beef animal being fattened on a diet con-
sisting almost entirely of cereals and a milled or pelleted compound diet may only
ruminate for 30 min. The longer a cow ruminates the more saliva it secretes. The
rate of saliva flow is critical to the process of healthy digestion in the rumen. It
dilutes the rumen contents thereby accelerating outflow to the abomasum. The
buffers in saliva (mainly NaHCO3) are essential to healthy ruminal digestion
because they neutralise the organic acids produced by fermentation and thereby
reduce the risk of ruminal acidosis. Diets for high‐yielding cows containing large
amounts of cereals and pelleted compound feeds are rapidly fermented and con-
tain little material to stimulate rumination and thereby salivation. It is common
practice to incorporate sodium bicarbonate into such feeds in amounts as high as
500 g/day. A dairy cow given a diet containing sufficient long fibre to stimulate her
to ruminate for 8–10 h/day will transfer about 2000 g/day sodium bicarbonate to
the rumen via her saliva. Moreover, the sodium is recycled within the body and the
bicarbonate has come from carbon dioxide, the end‐product of respiration.
It makes more sense, on grounds of both health and economics, to give a cow
access to a diet that allows her to produce sufficient sodium bicarbonate for herself
at zero cost. I review the aetiology, prevention and treatment of this important
production disease in Chapter 7.
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Rumination is often described by those whose primary interest is in animal

behaviour and animal welfare as a vital ‘behavioural need’. It should be clear from
the above that it is a physiologically vital process, but it does not necessarily follow
that cows feel an emotional need to chew the cud and a sense of deprivation if this
is denied. Some beef cattle fed diets containing very little long fibre may exhibit a
form of ‘sham’ rumination, going through the motions of chewing without having
regurgitated any food. This tends to be short‐lasting and does not progress to pro-
longed, compulsive, stereotypic behaviour comparable to bar‐chewing in confined
sows or weaving in confined horses. I know of no convincing explanation for this
but from analogy with recent evidence on the aetiology of bar‐biting and wind‐
sucking in horses, I suggest that it may be a learned behaviour whose effect is to
increase saliva flow, buffer the rumen contents and thereby reduce abdominal dis-
comfort. Veal calves that are denied all access to solid feed and long fibre do spend
abnormally long periods in purposeless, stereotypic oral activity such as licking
and chewing their wooden crates. This abnormal behaviour probably results from
a complex pattern of behavioural and physiological deprivation, especially lack of
oral satisfaction and abdominal discomfort. Within UK and the EU it is now com-
pulsory to provide veal calves with access to long fibre.
Digestion
The capacity of a feed, or single constituent of a feed, to provide nutrients for

metabolism is determined, in the first instance by its digestibility. The conventional
approach to determine digestibility is to record input and faecal output in a feeding
trial in which animals are fed a fixed diet for a sufficient time to ensure equilibrium.
This produces a measure of apparent digestibility.
Apparent digestibility of N ( N in feed N in faeces) /(N in feed ).
In this simple equation, N can refer to dry matter (DM), organic matter (OM),
energy or protein. Routine digestibility trials have been enormously valuable in
assessing the value of feeds for simple‐stomached animals like pigs and chickens.
This approach is of limited value because it does not take account of the fact that
faeces contain not only undigested food but also endogenous material secreted into
the lumen of the gut. Measurement of true digestibility that takes endogenous faecal
losses into account is relatively difficult, and for the major constituents (DM, OM,
energy and protein) seldom necessary. Apparent digestibility trials have little value
as measures of the availability of minerals because they cannot account for the
extensive exchanges of minerals between gut and body tissue (q.v.).
Simple digestibility trials are of limited value in the evaluation of feeds for rumi-
nants. It is necessary to consider ruminant digestion in two separate stages: digestion
in and absorption from the rumen; and digestion and absorption of food and other
Digestio 27
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Energy UDE
Protein (&NPN) UDN
QFE SFE
NaHCO3
ry
iva
Sal d
n
gla
Microbiota
QDN SDN
NH3 VFA
urea
Liver
Figure 2.5 Digestion of energy and protein in the rumen (for full definition of
abbreviations see text).
materials leaving the rumen and entering the abomasum. Rumen microbes make
energy and protein available to their host, the cow, by fermenting that which they can
(principally carbohydrates including fibre) and incorporating organic nitrogen into
microbial protein that is washed out of the rumen from digestion downstream. It has
become conventional to consider feed energy and protein supply to ruminants within
four categories (Figure 2.5):
1) Material that is quickly fermented or degraded in the rumen. Material that is
rapidly fermented to energy‐yielding substances such as volatile fatty acids
(VFA) is termed quickly fermented energy (QFE). Organic nitrogenous material
that is rapidly degraded to ammonia is quickly degradable nitrogen (QDN).
2) Material that is slowly and incompletely fermented or degraded in the rumen is
termed SFE and SDN.
3) Material that is unfermented or degraded in the rumen is termed unfermentable
digestible energy (UDE) and undegradable digestible nitrogen (UDN).
4) The final fraction is that which is neither fermented or degraded in the rumen, nor
digested downstream. Since it does not contribute to energy or protein supply it requires
no code.
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Fermentation of Carbohydrates in the Rumen

Fermentation was described by Pasteur as ‘life without oxygen’. It describes the
anaerobic metabolism of energy sources by microorganisms to provide fuel to
support their own needs for maintenance, growth and multiplication. This
involves the addition of a high‐energy phosphate bond to adenosine diphos-
phate (ADP) to create adenosine triphosphate (ATP). the primary energy cur-
rency for all biological systems, whether single cells or complex plants and
animals. The microbial population of the rumen (the microbiota or microbi-
ome) is extremely diverse, consisting of bacteria, ciliated protozoa and anaero-
bic fungi. Special mention must be made of rumen archaea because of their
contribution to methanogenesis. These were formerly classified as bacteria but
are now considered as a separate domain.
For practical purposes carbohydrates may be considered as the only nutrients
that can be fermented in the absence of oxygen to yield significant amounts of
ATP to the microbes. Cell contents, i.e. sugars and starches are made up of sim-
ple monosaccharides with six carbon atoms called hexoses (e.g. glucose C6H12O6)
or pentoses (e.g. ribose C5H5O5). Disaccharides are made up of two monosaccha-
rides, e.g. sucrose (commonly called sugar) is glucose + fructose, lactose, the
disaccharide of milk, is glucose + galactose. Cell walls (SFE) are made up of cel-
lulose, hemicellulose, pectin and lignin. Cellulose and hemicellulose may be
considered as complex polymers of hexoses. Pectin is not strictly a polysaccha-
ride but is rapidly fermented so classified as SFE. Lignin is a phenolic polymer
but since it may, for practical purposes, be considered indigestible, its chemistry
need not concern us.
Sugars and starches in cell contents ferment rapidly and form the main constitu-
ents of QFE. The capacity of the microbiota to capture energy from carbohydrates
in the form of ATP from anaerobic metabolism (i.e. in the absence of oxygen) for
respiratory‐chain oxidative phosphorylation is low; most of the substrate energy
remains and is excreted by the organisms in the form of simple, volatile fatty acids
(VFA), principally acetic, propionic and butyric, containing respectively two, three
and four carbon atoms. These serve as the main source of digestible energy for the
host animal, namely the cow. In a healthy rumen environment (pH 6–7) these VFA
are present as sodium salts, the sodium arising from saliva and direct secretion of
fluids across the rumen wall (Figure 2.5). Effectively all the VFA are absorbed
across the rumen wall, which explains the need for the large surface area created
by the rumen papillae (Figure 2.3(a)). The structure and normal function of the
papillae are controlled by the rate of production of VFA (especially acetate) and its
consequences for rumen pH. The impact of this on digestive health is considered
further in Chapter 7.
The rate of fermentation of all sugars and most starches is rapid so that they are com-
pletely fermented to yield VFA. However, a few carbohydrate‐rich feeds such as maize
and tapioca contain starches that ferment more slowly and therefore incompletely in the
time available to them in the rumen, some material passing unchanged into the aboma-
sum, where it is available for acid digestion. Of course, if the plant cell walls in cereals are
Digestio 29
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not ruptured by the mechanical action of chewing or grain processing then the carbohy-
drates in the cell contents can escape both fermentation and acid digestion, which
explains why it is not uncommon to see whole barley or maize grains in cattle faeces.
The structure of plant cell walls is made up of a complex weave of cellulose, hemicel-
lulose and lignin. The degree of lignification increases with increasing maturity: the plant
gets more ‘woody’. The rate of microbial fermentation of cell walls to yield SFE is gov-
erned in part by the extent of mechanical breakdown, through chewing or processing, and
in part by the extent to which the fermentable cellulose and hemicellulose are bound to
indigestible lignin. The extent of fermentation of SFE is determined both by fermentation
rate and by retention time in the rumen. Cellulose and hemicellulose that pass out of the
rumen before they can be fermented cannot be broken down by acid digestion although
they will, of course, meet another population of microorganisms in the caecum and colon
where some further fermentation can take place (normally less than 10%). The digestion
of protein will be considered later. So far as the rumen microbiota are concerned, dietary
protein is a source of nitrogen for microbial protein synthesis but yields little energy as
ATP. Fats cannot be metabolised to yield ATP in the absence of oxygen. Indeed, fats in
ruminant diets can inhibit fermentation, slow down digestion and reduce appetite unless
they are covered in a protective coat that resists attack by microorganisms.
Most of the steps in the biochemical degradation of carbohydrates are of little
practical concern. The final stages, however, are of extreme importance in the
context of feed efficiency, milk quality and environmental impact. To keep it sim-
ple, we may assume that all carbohydrates are fermented via monosaccharides to
the three‐carbon compound, pyruvic acid. This stage may be described thus.
C6 H12 O6 2CH 3COCOOH 4H 2ADP to ATP .
One molecule of glucose has been converted to two molecules of pyruvic acid. This
has stored a small amount of energy for the microbiota as two molecules of ADP have
been converted to ATP. It has also accumulated four protons or hydrogen atoms (4H).
Pyruvic acid is then metabolised further to a mixture of VFA, principally acetic, pro-
pionic and butyric acid. The yield of ATP to the microbiota from fermentation to
acetate, propionate and butyrate is (approximately) 4.3, 4.0 and 3.0 ATP/mole glu-
cose: so far as they are concerned, acetate production is the most efficient process.
Acetate production : CH 3COCOOH H 2 O CH 3COOH CO2 2H 4.3 ATP

Propionate production : CH 3COCOOH 4H CH 3CH 2 COOH H 2 O 4 ATP
Butyrate production : 2 CH 3COCOOH CH 3 CH 3CH 2 COOH CO2 3 ATP .

Acetate production generates a further excess of two protons (2H); propionate

production requires four protons and butyrate production is neutral. The rumen
microbiota, in most normal circumstances include archaea that combine protons
with CO2 to produce methane gas, which is excreted to the environment both
through belching and in expired respiratory air.
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Table 2.2 Fate of 1000 kJ energy fermented in the rumen.
Hay 1000 Hay 500 Hay 200

Diet Cereal 0 Cereal 500 Cereal 800
Energy yield to cow (kJ)

acetate 448 395 322
propionate 150 260 393
butyrate 182 185 185
Total VFA 780 840 900
Energy yield to microbes (kJ) 70 60 50
Energy loss as methane (kJ) 150 100 50
Methane production : CO2 4H 2 CH 4 2H 2 O.
Table 2.2 illustrates examples of what can happen to 1000 kJ of energy fermented in
the rumen of a cow fed different mixtures of forage (mainly SFE from cell walls) and
cereals (mainly SFE from starch). In all cases the great majority of the fermented
energy (FE) is unavailable to the microbiota and absorbed by the cow in the form of
VFA (780–900 J/kJ FE). The amount of FE used by the microbiota for their own pur-
poses is very small (50–70 J/kJ FE). The ratio of acetate to propionate is highly depend-
ent on the balance between forage and concentrate (QFE and SFE). This has a big
effect on proton balance and therefore methane production. In this example, energy
loss as methane is 150 J/kJ FE, in a predominantly cereal diet it is only 50 J/kJ FE.
The first and longest recognised problem with methane production is that it repre-
sents a significant loss of potentially metabolizable energy to the cow. In the Table 2.2
example 15% of FE is lost with the forage diet, only 5% with the high cereal diet. The
more recently expressed concern derives from the fact that methane gas is a major
potential contributor to global warming, being approximately 20 times more potent a
greenhouse gas than carbon dioxide. It is an inconvenient fact that extensive systems,
involving a high input of grasses and forage are less environmentally friendly (by this
measure) than intensive systems with a higher inclusion of starch leading to a higher
yield of propionate relative to acetate. I shall consider the environmental impact of
methane further in Chapter 13. Propionate carries another benefit to the cow in that it
is glucogenic. Being a 3‐C unit, it can be used for production of glucose, which is an
essential substrate for metabolism but in short supply from ruminant digestion, where
most of the energy derives from VFAs. Acetate and butyrate are said to be ketogenic;
simple energy sources for ATP production or, if present in relative excess, further
metabolised to ketone bodies (e.g. acetone). When a ruminant needs more glucose that
it can get from pyruvate, it has to increase the oxidation of glucogenic amino acids,
which could otherwise have contributed to synthetic processes like growth and milk
Digestio 31
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production. Diets that do not generate a sufficiency of propionate therefore reduce the
efficiency of utilisation of dietary protein.
So why don’t we feed cows on diets that give rise to the highest possible molar ratio
of propionate to acetate? In theory, this would be one that generated an
acetate:propionate ration of 2:1, which would exactly balance 2 x 2 H production per
molecule of acetate to the 4 x 1 H requirement for propionate. In these circum-
stances, energy retention would be greatest and methane production zero. While this
may seem an ideal aim in the context of feed efficiency and environmental sustain-
ability, it is not compatible with the aim of healthy digestion. In the dairy cow it is
essential to feed a diet that includes sufficient structural, slowly fermented carbohy-
drate to ensure that fermentation to VFA proceeds at a steady, controlled rate and is
accompanied by a sufficient supply of buffers from saliva to maintain stable, weakly
acidic conditions in the rumen (pH > 6). Too rapid fermentation of cereals leads to
increasing acidity. In conditions where rumen pH < 5, large numbers of ‘normal’
microorganisms are destroyed and those that are favoured by low pH, e.g. lactoba-
cilli, predominate. This disturbance to the normal rumen population will, at the very
least, reduce appetite. More severe ruminal acidosis can lead to serious metabolic
disorders or even sudden death. In Chapter 7 I consider in more detail the problem
of ruminal acidosis, a major production disease for dairy cows given the large quan-
tities of high concentrate feeds deemed necessary to sustain high milk yields. I shall
also briefly review recent research designed to reduce the environmental impact of
methane production through manipulation of the rumen microbiota.
To summarise: most of the digestion of carbohydrate in ruminants involves
microbial fermentation to VFAs and most of this takes place in the rumen. A few
starches that escape fermentation can be broken down to monosaccharides by
enzymes released into the abomasum and duodenum. A small proportion of the
fibre that escapes fermentation in the rumen may be fermented in the caecum and
colon. Normally this accounts for less than 10% of energy supply.
Utilization of Metabolizable Energy for Maintenance and Production

As we have seen, the capacity of a diet to provide fuel for the work of the body (energy
metabolism) is defined as metabolizable energy (ME). The direct determination of the
metabolizability (ME/GE) of feeds for ruminants requires a feeding trial in which calorimetric
measurements are made of the energy contained in feed, faeces, urine and methane. Thus:
Metabolizable energy = gross energy in feed – (energy in faeces + urine +
methane).
It is, of course, unrealistic to conduct feeding trials for every mixed ration or
component of mixed rations so that a range of laboratory procedures has been
developed to estimate ME values. Since by far the largest nutrient requirement of
any animal is for ME, it is this that primarily determines the overall efficiency of
conversion of animal feed into saleable animal products like meat and milk.
Dietary ME must first meet the requirements of an animal for maintenance; the
metabolic processes necessary to sustain life at a constant body weight. The energy
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used for these essential processes is all dissipated as heat. In other words, for an
animal at maintenance, ME intake = heat production. This can be determined using
an animal calorimeter or from measurements of respiratory exchange (oxygen con-
sumption and carbon dioxide production). If ME intake is less than heat production
(IME < H) the animal must draw on its own energy reserves to provide fuel and will
lose weight. Initially these reserves will come from fat. This is an entirely normal
process for wild ruminants, accustomed to seasons of plenty and shortage (e.g. wet
season–dry season, summer–winter). If the deficit of ME becomes too severe or too
prolonged, the animal is forced to oxidise body proteins for fuel. In these circum-
stances, loss of weight and body condition becomes much more rapid, since the
energy contained in lean muscle is only 5 kJ/g compared with over 35 kJ/g in fat.
The metabolic processes involved in the metabolism of ME to provide fuel in the
form of ATP incur an energy cost, i.e. the net efficiency of utilisation of ME for
maintenance is less than 100%. For cows, the net efficiency (km) of utilization of ME
for maintenance (∆RE/∆ME) is approximately 0.7: the remainder (0.3) is described
as the heat increment of feeding. It follows that the heat production of a cow eating
a maintenance ration will be approximately 40% (1.0/0.7) greater than the basal
metabolic rate, i.e. H when feed intake is zero.
Figure 2.6 presents a simple picture of the factors that determine the efficiency of
utilization of ME for maintenance and production. Both ME intake and energy
retention (RE) are expressed relative to maintenance (Em). The limit to ME intake
for a lactating cow is taken as 4Em, for growth (beef) the limit is set at 3Em. Efficiency
is expressed in two ways: (1) net efficiency of utilization of increments of ME
(∆RE/∆ME) below and above maintenance (Figure 2.6(b)) and (2) gross efficiency
(RE/ME) of conversion of ME (Figure 2.6(a)), fed above maintenance into lactation
or growth (milk or beef). For the limited range of highly nutritious diets likely to be
fed to dairy cows, net efficiency for lactation (kl) may be assumed constant at about
0.7. Net efficiency for growth and fattening (kf ) cattle on a wider range of feeds of
more variable nutritive value can range from about 0.4 to 0.6. In the example shown
in Figure 2.6(b) it is 0.5.
For producers, gross efficiency is what really matters. Until ME intake exceeds
maintenance requirements, gross efficiency is zero. Above maintenance, gross
efficiency increases in a curvilinear fashion to a limit defined by the limit to
appetite. In Figure 2.6(a) gross efficiency for a dairy cow consuming ME at 4Em,
approaches 50%. For beef cattle, where the limit to appetite will be close to 3Em,
maximum gross efficiency is about 30%. This rather technical exposition should
make it clear why, all other things being equal, it is in the farmer’s interest to get
as much milk out of each individual cow as possible, However, as I have said
before and shall say again, all other things are not equal.
Digestion of Crude Protein

The specific role of dietary protein is to provide amino acids as building blocks for the
synthesis of proteins in the animal that eats that diet. Only some, such as lysine, threo-
nine, histidine, methionine and cystine, are essential, others can be manufactured in
Digestio 33
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(a) 0.6
0.4 Milk production

RE/ME
Beef production
0.2
1 2 3 4
ME intake (multiples of maintenance)
(b) 2
Milk production
RE
1
Beef production
1 2 3 4
ME intake (multiples of maintenance)
Figure 2.6 (a) Gross (RE/ME) and (b) net (∆RE/∆ME) efficiencies of conversion of
metabolizable energy (ME) to retained energy (RE) in milk and beef production.
the tissues of the body from these essentials. The main source of amino acids to the
cow is the population of microorganisms that pass out of the reticulo‐rumen and are
digested in the acid medium of the abomasum by pepsin, or in the neutral medium of the
duodenum by pancreatic proteases. Synthesis of protein by the rumen microbiota does not
necessarily require amino acids from true proteins as building blocks: many microorgan-
isms, in fact, preferentially use simpler nitrogenous compounds, principally ammonia (NH3).
The totality of nitrogenous compounds in a ruminant diet is defined as crude
protein.
This value is derived simply by measuring the nitrogen (N) concentration in feed dry
matter and multiplying it by 6.25 on the assumption that dietary protein contains 16%
N (1/6.25). This assumption is only approximate. Moreover, the term crude protein does
not distinguish between true protein and non‐protein nitrogen (NPN) sources such as
urea, which is a significant substrate for microbial protein synthesis. It also does not
distinguish nitrogenous compounds that are bound into the lignified portion of the cell
walls and thereby unavailable for degradation in the rumen or subsequent acid diges-
tion. This fraction is best described as acid‐detergent insoluble nitrogen (ADIN).
To understand protein digestion in the ruminant it is best to avoid use of the term
crude protein and simply describe all processes in terms of dietary N. The pathways
of digestion and metabolism of dietary N are illustrated in Figure 2.7. Dietary N
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Dietary crude protein N
NPN true protein ADIN
QDN SDN UDN
<0.1 ≤1.0
Microbial N
0.75 amino 0.25 nucleic
Recycled N
0.15
Truly absorbed amino N

ADIN
N increment
of feeding
N retained in
tissues & milk
Endogenous N N excretion
urine & faeces
Figure 2.7 Pathways of digestion and metabolism of dietary crude protein nitrogen
(N) (for full explanation of abbreviations see text).
c onsists of true protein, NPN and ADIN. The flow of dietary NPN into the rumen is
augmented by NPN recycled from the blood stream via saliva and directly across the
rumen wall (see Figure 2.5). Microorganisms attack nitrogenous compounds entering the
rumen, degrading them to simple amino acids and NH3 before incorporating them
into microbial protein. In normal circumstances at least 70% of microbial protein is syn-
thesised from NH3. There have been a few experiments to demonstrate that cows can
produce milk, at least for a while, on diets containing no true protein and therefore no
amino acids. These may be of scientific interest but they are of little practical signifi-
cance. The rumen microbiota undoubtedly require a small supply of essential amino
acids as building blocks for protein synthesis. When the diet contains only NPN they
obtain these amino acids by degrading endogenous protein sloughed from the walls
of the rumen. This cannot, of course, be maintained indefinitely.
The rate at which the rumen microbiota degrade dietary sources of organic N
depends on their chemistry and physical structure. NPN and water‐soluble true
proteins degrade rapidly and completely to NH3. This is quickly degradable nitrogen
Digestio 35
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(QDN, Figure 2.7). The remainder of the true protein fraction degrades more slowly
and is termed slowly degradable nitrogen (SDN). As with SFE, the extent of degrada-
tion depends on the rate of degradation and retention time in the rumen. Thus, as
feed intake increases and the rate of passage of material through the rumen increases
the proportion of true protein converted to SDN decreases. The fraction that escapes
degradation in the rumen, undegradable dietary nitrogen (UDN) consists of true pro-
tein that is available for digestion in the abomasum and duodenum and ADIN,
which is completely indigestible.
Microbial Protein Synthesis

The rate of synthesis of microbial protein is linked closely to the rate of fermenta-
tion of organic matter (principally carbohydrate). The maximum yield of microbial
protein N is approximately 50 g/kg FOM (fermented organic matter). The cow does
not have access to all the microbial protein synthesised in the rumen, only that
which passes out into the duodenum. However, all the VFAs produced by fermenta-
tion are absorbed directly across the rumen wall and thus available to the cow as a
source of ME. If there were no outflow from the rumen the supply of microbial
protein to the cow would be zero. The ratio of protein to energy supply is therefore
determined by the proportion of microbial protein leaving the rumen. For a cow on
a maintenance ration with a rumen outflow rate of 35 h−1 the yield of microbial
protein N will be about 20 g/kg FOM, or 40% of total microbial protein synthesis. A
high‐yielding cow consuming feed at 3 x maintenance may have an outflow rate of
8% per hour and a protein yield of 40 gN/kg FOM. These estimates are approximate
but crucial to our understanding of protein supply and demand in ruminants as will
be explained in due course.
The relative rates at which energy and protein sources are respectively fermented and
degraded depend on the relative proportions of the quickly and slowly degradable frac-
tions. This is illustrated by Figure 2.8, which shows what happens to concentrations of
NH3 and VFA in the rumen following meals of hay, grass silage or grass silage plus a
small amount of QFE from (e.g.) fodder beet. The meal of hay alone produces a slow,
relatively small, relatively well‐balanced increase in NH3 and VFA concentrations. In
these circumstances all the degraded N may be used in microbial protein synthesis, i.e.
the ratio of degradable N to microbial protein N is 1.0. When the cow eats silage only,
rates of fermentation and degradation get out of balance since silage contains a lot of
QDN but almost no QFE. Not all the NH3 produced by degradation of QDN can be
taken up by the microbiota. This ammonia crosses the rumen wall and enters the liver,
where it is converted to urea (Figure 2.5). Circulating urea can return to the rumen
across the wall and via saliva so that ammonia produced in excess of immediate require-
ment is not lost but can be recycled for later use. In theory, provided the total daily sup-
ply of degradable N does not exceed the capacity of the microbiota to ferment energy
sources then all degradable N could be converted to microbial N at an efficiency of
100%. This is not likely to occur in practice. When QDN greatly exceeds QFE, as in the
case of diets based entirely on silage (or even fresh, lush spring grass) blood urea
concentration rises. Since the kidney excretes urea in direct proportion to blood
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Figure 2.8 Relative rates of production

of ammonia (NH3) and volatile fatty
VFA acids (VFA) in the rumen of a dairy cow
NH3 after feeding. The units in the vertical
axis are arbitrary and intended only to
illustrate the balance between
carbohydrate fermentation and
degradation of nitrogenous compounds.
hay 2 4 6 8
NH3
VFA
silage 2 4 6 8
NH3
VFA
silage + concentrate 4 6 8
Time after feeding (hours)
c oncentration some dietary QDN must be lost. For practical purposes we may conclude
that when the supply of degradable N and FOM are in balance, then the efficiency of
conversion of SDN to microbial protein is 1.0. For QDN, efficiency is <1.0. For the
practical purposes of ration formulation, we assume a figure of 0.8.
The bottom graph in Figure 2.8 illustrates what happens when a silage diet is
accompanied by a sufficient source of QFE. In this case the increase in NH3 and
VFA are in better balance and the efficiency of capture of QDN is improved.
Moreover, increased concentrations of NH3 and urea in the blood are known to
Digestio 37
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depress appetite. It is important therefore to balance the supply of QFE and QDN to
achieve the intakes necessary to sustain high milk yields. In the simple example
shown in Figure 2.8 this has been achieved by feeding fodder beet to accompany
silage, a common practice among traditional dairy farmers. The practical snag with
this approach is that cows like fodder beet so much that they tend to eat it all first
before filling up on silage, which rather defeats the objective. These days the objec-
tive of promoting maximum possible feed intakes through a balanced supply of
quickly and slowly fermentable energy and degradable N is best achieved through
the formulation and presentation of total mixed rations (TMRs) about which I shall
have more to say in Chapter 6.
Truly Absorbed Amino Nitrogen

Microbes and undegraded dietary nitrogen (UDN) are digested in the aboma-
sum and duodenum. Total microbial N is made up of about 0.75 amino acids
and 0.25 nucleic acids. The latter do not contribute to protein synthesis. The
digestibility of microbial crude protein (true protein + nucleic acids) is taken
as 0.85. The efficiency of uptake of truly absorbed amino nitrogen (TAAN)
from microbial protein N is therefore 0.64 (0.85 x 0.75). UDN also contains
indigestible ADIN. The remainder is assumed to have a digestibility of 0.9.
Thus, digestible UDN is 0.9(UDN − ADIN) and assumed to consist entirely of
amino acids, Thus,
TAAN = 0.6 4 microbial N + 0.9(UDN ADIN).
So far, this says nothing about the quality of the amino acid supply. The quality, or
biological value (BV), of a dietary protein Is determined by the composition of its
amino acids relative to the amino acid requirements of the animal that eats it. The
biological value of dietary protein is of extreme importance in the formulation of
rations for simple‐stomached animals like pigs and poultry and this makes it eco-
nomically sensible to consider the dietary inclusion of specific amino acids such as
lysine. However, microbial protein has a high biological value for growth and lacta-
tion in cattle. In many circumstances, this means that feeds such as maize gluten,
which has a low BV, can make a major contribution to UDN supply. Some very high
yielding cows fed high concentrate rations with a high UDN:RDN ratio may benefit
from supplementation with individual amino acids.
Throughout this section I have used N rather than CP to describe the processes
involved in the supply of substrates for protein metabolism in ruminants because it
permits clear distinctions between QDN, SDN, NPN, ADIN and N in proteins and
nucleic acids. However, nutritionists, feed manufacturers and farmers have for so
long been used to thinking and working in units of crude protein that in Part II,
Feeding the Dairy Cow I shall have to do the same. The crude protein equivalent of
TAAN becomes metabolizable protein (MP). Similarly, the terms QDN, SDN and
UDN will become QDP, SDP and UDP.
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Urea Recycling
When rumen microbes degrade urea to ammonia and then incorporate the nitrogen
into protein they do not discriminate between urea of dietary origin and endoge-
nous urea recycled into the rumen via the saliva and across the rumen wall
(Figures 2.5 and 2.7). Endogenous urea many arise from:
1) Excess NH3 absorbed earlier from the rumen and converted to urea in the liver.
2) Urea arising from the breakdown of body protein, especially during periods of
undernutrition.
3) Urea produced during the conversion of truly absorbed amino N (TAAN) to milk
protein, defined in Figure 2.6 as the N increment of feeding.
Consider the case of a cow in the dry season in the tropics with nothing to eat but
mature standing hay, high in fibre and low in nitrogen. This diet will sustain neither
the maintenance requirements of the cow nor that of the rumen microbiota. In these
circumstances, the cow breaks down her own protein reserves in (especially) muscle
to provide energy. Urea produced as an end‐product of protein oxidation is not all lost,
as it would be in simple‐stomached animals like ourselves but recycled to the rumen
where it is reincorporated into microbial protein, digested and absorbed as amino
acids. The significance of this physiological recycling of urea is threefold:
1) It restores amino acids to a malnourished animal.
2) It restricts urea excretion and therefore loss of body water in urine (see Chapter 6).
3) It maintains the microbial population of the rumen.
A reduction in the microbial population arising from a lack of N will reduce the
fermentation rate. The retention time of fibrous feed will increase and appetite
will fall. Loss of appetite in an animal already barely able to extract sufficient ME
for maintenance will accelerate the rate at which it loses body condition and
increase the risk of starvation. In a strictly evolutionary sense, the most important
consequence of this urea cycle is this ability to use the end products of protein
oxidation to sustain the rumen microbiota and thereby sustain appetite for poor
quality feed. The high producing dairy cow will also derive a significant propor-
tion of her QDN for microbial protein synthesis from urea produced during the
synthesis of milk protein from TAAN. However, while it is a fact that urea and
other non‐protein sources of NPN can make a useful contribution to the diet of
low‐yielding dairy cows (e.g.) in tropical and village systems, it is not realistic to
consider the inclusion of urea in diets for high yielders. These ladies need the best
diet we can provide.
Digestion of Lipids
The lipids that we eat ourselves are mainly fats and oils. Fats, mostly of animal origin,
are esters of fatty acids and glycerol in which all the carbon bonds are saturated
with hydrogen atoms. The structure of stearic acids may be written, simply, as
CH3CH2(16)COOH. Oils are unsaturated, which means that one or more carbon atoms
Absorption and Secretion of Mineral 39
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in the fatty acid chain lack H atoms and are linked by double bonds. Thus, linoleic
acid, which has two double bonds (CH=CH) is written as CH3CH2(14)CH(2)COOH.
Vegetable oils from soya beans, sunflower seeds, etc. are made up almost entirely of
mono‐ and polyunsaturated fatty acids (PUFAs), which are subdivided into two
classes, omega‐3 and omega‐6 according to the position of the first double bond. In
cold‐blooded animals, like fish, fatty acids are mostly unsaturated. If not, the fats
would solidify and the fish would seize up. Fats and oils serve primarily as energy
sources although animals (including us) have absolute requirements for specific
essential fatty acids. These are PUFAs that we cannot synthesise for ourselves because
we lack the desaturase enzymes required for their production. Linoleic acid (e.g.) is
Ω‐6, α‐linolenic acid is Ω‐3. The role of these essential fatty acids in nutrition is fasci-
nating but outside the scope of this chapter.
The metabolism of fats and oils to provide energy as ATP can only take place in the
presence of oxygen. It cannot occur therefore in the anaerobic environment of the
rumen. Moreover, since fermentation of carbohydrates generates an excess of pro-
tons (H), unsaturated oils entering the rumen attract excess protons and so leave as
saturated fats. This is why fats in the milk of cows and the meat of beef and lamb are
highly saturated. The cow can digest fats post‐ruminally using lipases from the duo-
denum and pancreas. She can also satisfy her requirements for essential fatty acids
through digestion of lipids in microbial cell walls. A small amount of dietary fat (up
to about 5%) can pass through the rumen, becoming saturated in the process but
without effect on normal fermentation. If it is deemed expedient to feed diets con-
taining >5% fat to meet the energy requirements of the very high yielding cow then
the fat must be protected from microbial action – and they must be protected from
it – by coating the fat in a material that protects it from microbial attack. Protected
fats can make a significant contribution to ME supply for the cow but they do not
contribute to the energy supply of the microbes for protein synthesis. Thus, attempts
to increase milk yield by the inclusion of dietary fats to increase ME supply may fail
because they reduce the supply (relative to ME) of TAAN or metabolizable protein.
Absorption and Secretion of Minerals
The major minerals, sodium (Na), calcium (Ca), phosphorus (P) and magnesium
(Mg), and the minor elements such as iron, copper, cobalt, etc., are present within
the main constituents of a cow’s diet, which can, if necessary, be supplemented
with inorganic salts or suitable organic complexes. Some digestive processes may be
involved in releasing minerals from organic complexes but the main factor deter-
mining the net uptake of minerals from the gut is the balance between secretion
into and absorption across the intestinal epithelium. An example of sodium
exchanges in illustrated in Figure 2.9. The figures are, of course, subject to consider-
able variation according to the circumstances of the moment. The message con-
veyed by Figure 2.9 relates to the absolute rates of flow between the compartments
of the body. In this example the cow consumes 40g Na/day. The amount of Na
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rumen large
small intestine
intestine
40 540 600 20
salivary
gland
60
580
500
400
free pool
(ECF)
200 20
fixed pool excretion
(skeleton) (skin)
Figure 2.9 Secretion and absorption of sodium (Na, g/day) between the digestive
tract and the extracellular fluid (ECF).
entering the rumen from the saliva and across the rumen wall is 500 g/day, i.e. only
8% (40/500) of Na entering the rumen has come directly from the diet. 540 g/day
passes out of the rumen and a further 60 g enters the duodenum and jejunum. From
here on, net movement is from gut to body fluids. 580 g/day leaves the ileum and
large intestine, leaving only 20 g to exit in the faeces. These figures should make it
clear that it is meaningless to describe the exchanges of a mineral like sodium from
measures of apparent digestibility or availability. This approach, which would cal-
culate a value for apparent availability of 50% from the simple equation [(40 −
20)/40] clearly overlooks all the internal exchanges that really matter.
About two‐thirds of the sodium in the body is contained in the extra‐cellular fluid
(ECF). In Figure 2.7 this value is given as 400 g. The sodium ion is mainly responsible
for maintaining the osmotic pressure and thereby the volume of this freely exchange-
able fluid pool. The remainder, bound mostly in bone, can be released only slowly. This
compartment is the fixed pool (here 200 g). The amount of Na leaving the small intes-
tine per day (600 g) is 50% greater than the size of the freely available Na pool in the
ECF. This highly dynamic state of equilibrium will be upset if the absorption of Na
from the ileum and large intestine is compromised by diarrhoea. The scouring calf
Absorption and Secretion of Mineral 41
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(a)
food gut faeces

30 29
4
(PTH,D3) –
+
5
+ free pool 1 urine

12g
2
fixed 2
pool
(skeleton)
(b)
food faeces
65 36
4
(PTH,D3) –– ++ 33
1 urine
+ free pool
12g
4
fixed 2 30 milk
pool
(skeleton)
Figure 2.10 Exchanges if calcium (Ca, g/day) (a) in a dry cow, (b) in early lactation. PTH
= parathyroid hormone, D3 = vitamin D3 or cholecalciferol.
rapidly becomes dehydrated not only because it loses water but also because failure to
reabsorb Na from the gut reduces the osmotic pressure and thereby the volume of the
ECF. Rehydration in an animal suffering from chronic diarrhoea requires not only
water but salt (NaCl) to sustain ECF volume and glucose necessary for the active
absorption of Na across the gut wall.
Calcium Exchange
Over 99% of body calcium (Ca) is contained within the mineralised skeleton
(bones). Only about 12 g is in the ECF or freely exchangeable pool. Figure 2.10,
keeping things as simple as possible, illustrates Ca exchanges (a) in a dry cow, (b)
in early lactation. The dry cow consumes 30g Ca/day and excretes 29 g/day in the
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faeces. 5 g/day are absorbed from the gut and 4 g/day returned. The balance
between absorption and excretion is controlled by parathyroid hormone (PTH)
and vitamin D3 [1,25 2(OH) cholecalciferol), which also acts as a hormone. When
the need for Ca is high these hormones increase absorption and decrease secretion
across the gut wall. When the need is low, as in the case of the dry cow, absorption
is low and most of the Ca is returned to the gut. In this dry cow, in exact Ca bal-
ance, 1 g/day is excreted in the urine.
At the onset of lactation, this balance is greatly disturbed because suddenly the
cow starts to secret large quantities of Ca into her milk. In Figure 2.10(b) the cow is
secreting 30 g Ca/day in 25 L of milk. Her intake of feed has increased, increasing Ca
intake to 65 g/day. PTH and Vit D3 are now very active, increasing net movement of
Ca from the gut to 27 g/day. They have also produced a small (2 g/day) net release of
Ca from bone. This cannot, of course, persist indefinitely. The amount of Ca in the
freely exchangeable ECF pool is 12 g. If this is not replaced, milk secretion would, in
theory, drain the ECF of Ca in 10 h. In practice, the cow would be long dead by then.
Everybody who knows cows knows of the problem of ‘milk fever’; collapse and
paralysis following calving progressing rapidly to death unless the cow is treated
with large quantities of calcium. Knowing the dynamic nature of Ca exchanges
helps us to understand why. In Chapter 7 I consider the practicalities of prevention
and treatment of disorders arising from acute and chronic deficiencies of the major
minerals, calcium, phosphorus (P), and magnesium (Mg), and with the trace ele-
ments. At this stage, all that needs to be said about the metabolism of the trace ele-
ments is that, in general, they are stored in the body in large amounts relative to daily
dietary intake and slowly excreted. Unlike Na, Ca and Mg therefore, problems of
deficiency tend to be slow in onset but problems of toxicity can occur if high dietary
intakes are maintained for prolonged periods.
Appetite and Food Intake
Decisions to eat and to stop eating are conscious processes. The physiological moti-
vation for the decision to eat arises from the sensation of hunger. The many specific
triggers for the sensation of hunger need not concern us here. For the lactating
dairy cow, it is sufficient to say that the sensation of hunger is driven primarily by
the metabolic needs for nutrients. In a sentient animal, decisions as to what to eat
and how much to eat are modulated by appetite, simply defined as a conscious
attraction for especially palatable foods. In the lactating dairy cow, the sensation of
hunger is driven primarily by the metabolic needs for nutrients. The decision to
stop eating, satiety, is also driven by a complex of instinctive and conscious factors
affecting, respectively, hunger and appetite. We may fail to finish a large plate of pie
and chips but still find room for an ice cream.
Most lactating dairy cows in most systems are required to produce as much
income as possible from the sale of milk and therefore expected to consume as
Appetite and Food Intak 43
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much as they can of a diet calculated to provide a plentiful supply of all the nutrients
required to meet the metabolic demands of lactation. A cow producing 50 L milk/
day requires over five times as much ME as that required to maintain a cow that is
dry and non‐pregnant. For protein and other elements of the diet the relative differ-
ence is even greater. The magnitude of this nutritional demand, far greater than
that imposed on any other class of the food animals stretches the capacity of the
digestive system to its limits. In chapter 1 I outlined the four essential features of a
healthy diet for any animal (including us). They are to: (1) provide a correct balance
of nutrients to meet our metabolic needs at all stages of life, (2) ensure healthy
digestion, (3) satisfy taste and appetite, (4) do no harm. An ideal diet for a cow at
peak lactation is one that ensures an adequate supply of nutrients without compro-
mising healthy digestion. It is the cow, however, that decides how much to eat and,
where possible, chooses how much to eat of the different components of the overall
ration.
The first physical limit to food intake in any animal is defined by the volume of
the upper digestive tract. This is particularly the case for ruminants who eat fibrous
feed that remains in the rumen for many hours. Since the volume of the rumen is
fixed (at least in the short term), intake is constrained by the rate at which material
leaves the rumen through the small reticulo‐omasal orifice. To illustrate a general
truth with an unlikely example: suppose a cow giving 30 L milk/day is offered only
ad libitum access to hay. While this yield persists, the metabolic needs of lactation
will greatly exceed the supply of nutrients from the gut, even though the cow is eat-
ing to the point of satiety determined by the limit to rumen fill. She is in the unfor-
tunate position of being simultaneously hungry (for nutrients) but full up (with
undigested feed). For most high‐yielding dairy cows fed a substantial proportion of
forage or other slowly digestible fibre, rumen fill is the major constraint to nutrient
intake and thereby milk yield. As lactation proceeds and milk yield declines, so it
becomes easier for the cow to meet her metabolic needs within the constraint
imposed by rumen volume, although in late pregnancy, the increasing size of the
uterus and developing foetus progressively reduces the space available to the rumen.
When gut fill is the first constraint to food intake, nutrient supply is determined by
the rate at which the feed is digested (largely by fermentation) in the rumen since an
increase in digestibility will both increase the concentration of metabolizable nutri-
ents and reduce rumen fill through an increase in digestion rate and reduction in
rumen retention time. The simplest solution to the question ‘how to maximise intake
of metabolizable nutrients?’ would therefore be to feed a diet that is both rich in nutri-
ents and rapidly digestible. Unfortunately, this approach fails to meet the criterion ‘do
no harm’. As indicated already, highly digestible, high starch diets ferment too rapidly
and lead to rumen acidosis. In its most severe form (e.g. after a cow breaks into a feed
store and gorges herself on grain) this can end in death. This may be a rare occur-
rence. However, millions of cows (world‐wide) are fed high energy, highly digestible
diets that challenge the stability of the rumen environment and induce a chronic
degree of rumen acidosis, commonly referred to as subclinical but often severe
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enough to compromise both production and welfare. The animal feed industry derives
a considerable income from the sale of feed additives that claim to ‘boost production’
through control of ‘subclinical’ rumen acidosis. They are, of course, not aids to
improved production but substances given to reduce the harm created by the feeding
of an unhealthy diet. I shall have more to say on this in Chapter 7.
The three most important criteria of a good diet for a lactating dairy cow are
therefore that it should provide a sufficient, balanced supply of nutrients, it should
promote healthy digestion and that it should do no harm. The fourth criterion, sat-
isfy taste and appetite, has a relatively minor impact since the metabolic hunger of
a healthy cow at peak lactation is so strong that in most circumstances it is likely to
overwhelm the more subtle nuances of appetite. However, there is good evidence
that cows have a strongly developed sense of what to eat, when to stop and what to
select. This is based in part on taste (e.g. the sweet taste of fodder beet) but perhaps
more on how the cow feels after the meal is over. Figure 2.8(b) provides one clear
illustration of this. The cow is eating grass silage as the sole feed. Fermentation rate
is slow but N degradation is rapid. In these circumstances there is considerable
absorption of NH3, taken up by the liver and converted to urea. Elevated concentra-
tions of both and urea in blood are known to inhibit appetite in ruminants. Elevated
blood urea concentration in humans is known to induce a sense of malaise (we feel
‘liverish’). It is only fair to assume that in the same circumstances, the cow feels the
same. This leads to the depressing but inescapable conclusion that a lactating dairy
cow with high nutrient demand given a ration containing a large proportion of
grass silage, high in QDN, is likely to feel simultaneously hungry, full up with indi-
gestible fibre, and sickened by urea. The design of healthy diets is not just a ques-
tion of productivity, it is a question of welfare.
While it is undoubtedly the case that food intake in a high‐yielding dairy cow
reflects a primitive physiological conflict between the metabolic needs of the mam-
mary gland and the physical and biochemical capacities of the digestive tract, it is
essential to remember that the final conscious choice as to what to eat and how
much to eat is in the mind of the cow. It is possible to stimulate appetite by the
introduction of highly palatable feed (e.g. fodder beet) or the novelty of a different
feed, perhaps in a midday meal. This approach has rather fallen out of favour with
the introduction of TMRs in which fibrous forages, starchy cereals and appropriate
supplements are combined in a mixer wagon and fed together to cows in yards. The
practice of feeding TMRs has undoubtedly contributed to the increased productiv-
ity of dairy cattle for the good reason that it promotes stable and balanced carbohy-
drate fermentation and N degradation in the rumen. It is quite fun, however, to
watch cows presented with a TMR, nosing through their feed and blowing aside the
less favoured components to get at the bits they like best. We cannot arrive at a full
understanding of the physiological processes of digestion and metabolism in the
dairy cow without knowing something of her psychology.
45
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Reproduction and Lactation
The dairy cow is an exploited mother. We manage her life to ensure that she grows
up to achieve puberty at the optimal time (for us), becomes pregnant and gives birth
at regular intervals, and produces large quantities of milk for about 80% of her adult
working life. All these processes are controlled by an elegant hierarchy of hor-
mones. This chapter will describe the structure, function and control of the mecha-
nisms of reproduction and lactation in just sufficient depth to enable us to
understand what is normal and how some of these normal mechanisms can be
manipulated in practice. Suggested further reading for those who wish to examine
the physiology and endocrinology in more detail is given at the end of the book.
Anatomy of the Female Reproductive Tract
The gross anatomy of the reproductive tract of the cow, and its relationship with other
body structures, are illustrated in Figure 3.1. The vagina lies over the public bone, which
forms the ventral (lower) border of the pelvic canal. The main body of the non‐pregnant
uterus appears when examined from the outside post mortem, or palpated via the rec-
tum to be about 150 mm long, but internally, is only 30–40 mm in length. The uterus is
largely made up of two horns. The inner surface of the uterus is studded with about one
hundred cotyledons, protuberances having a shape like leather buttons about 15 mm in
diameter in the non‐pregnant animal. They form the sites for attachment of the foetal
membranes of the developing calf during pregnancy. The oviducts, or Fallopian tubes,
are over 200 mm long and coil back towards the bones of the pelvic canal. The ovaries
are rugby‐ball shaped and about 40 x 25 mm in size in the non‐pregnant cow.
Follicle Development and Ovulation
Fertilisation, the fundamental act of reproduction, is achieved when a sperm carrying

the male gamete penetrates the female egg (ovum), fuses with the female gamete and
lays down the blueprint for creation of a new individual. What happens in both sexes

46 Reproduction and Lactation
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(a)
pelvic bones
rectum
cervix
vagina
horns of
uterus
ovary
vulva
pubic bone
oviduct
bladder
(b)
left horn of
cotyledons
uterus
oviduct
body of
uterus
ovary with
infundibulum ripe follicle
and fimbriae
opening of
vagina cervix
(opened)
urethral vulva (opened)

orifice
ventral commisure
clitoris of vulva
Figure 3.1 The reproductive organs of the cow.
before fertilisation is simply directed towards bringing the male and female gametes
together. What happens thereafter in the female is simply directed towards the main-
tenance and development of this new life. Parturition (in this case, calving) may be
the most momentous aspect of reproduction for the mother. So far as the offspring is
concerned, it represents little more than a somewhat hazardous change of environ-
ment and a switch from intravenous nutrition to feeding by mouth.
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primordial
oocyte
primary
follicle
PRE-PUBERTAL
granulosa DEVELOPMENT
cells antrum
adult
oocyte follicle
ADULT
FSH
DEVELOPMENT
degeneration
mature (atresia)
follicle
LH
Oestrogen
ovulation
Progesterone
Corpus Prostaglandin
luteum
degeneration
Figure 3.2 Follicular development within the ovary. FSH = follicle stimulating
hormone, LH = luteinising hormone.
The genetic material contained within every ovum released by a cow throughout her
life is formed and stored within the ovary very early in development, indeed long before
she herself has been born. These primordial oocytes, present at birth, acquire a coating
of specialised granulosa cells and develop during prepubertal life into adult follicles
(Figure 3.2) with the oocyte situated towards one side and the centre of the follicle (the
antrum) filled with follicular fluid. After puberty, gonadotrophic hormones from the
anterior pituitary gland act to mature the follicles in sequence, normally one at a time,
and so establish the rhythm of the oestrus cycle in the mature, non‐pregnant female.
Initially follicle stimulating hormone (FSH) causes one follicle to enlarge and mature so
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that, just prior to ovulation, it is a turgid, fluid‐filled structure distending the wall of the
ovary and about 20 mm in diameter. As the follicle enlarges, the granulosa cells secrete
increasing amounts of oestrogen, the hormone that induces the physiological and
behavioural changes associated with being in oestrus, on heat, or ‘bulling’. Actual rup-
ture of the ripe follicle and release of the ovum is induced by a rapid, large release of
luteinising hormone (LH) from the anterior pituitary gland (Figures 3.2 and 3.3). This
also initiates the reorganisation of the ruptured follicle into a new structure, the corpus
luteum or yellow body, with a new function: secretion of the hormone progesterone.
The number of ova released during adult life is far less than the number of primor-
dial oocytes present in the ovary at the time of birth. Most follicles do not develop to
the point of ovulation but degenerate (atresia, Figure 3.2). I know of no explanation
for this quirk of evolutionary development. It does mean that artificial stimulation
of the ovary with injections of gonadotropic hormones can induce the cow to release
far more ova than she would normally achieve in a lifetime. Induced multiple ovula-
tion with embryo transfer (MOET) has become a recognised technique in commer-
cial cattle breeding. It will be reviewed, somewhat critically, in Chapter 12.
DAYS OVARIAN EVENTS HORMONE SECRETION

Ant. Pituitary Sex Hormones
Prooestrus FSH
follicle ripens
Ogen
4 Oestrus LH
ovulation
CL forms
12 Pone
Dioestrus
16
20 CL regresses PGF
Prooestrus
24
Oestrus
ovulation
CL forms
increases in hormone concentration
Figure 3.3 The oestrous cycle of the cow. CL = corpus luteum, FSH = follicle
stimulating hormone, LH = luteinising hormone, Ogen = oestrogen, Pone =
progesterone, PGF = prostaglandin F2α.
Pubert 49
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The Oestrus Cycle
Oestrus describes the time when the cow is attractive to and attracted by the bull and
will therefore permit mating. The duration of oestrus ranges from about 10–30 hours
depending on season and body condition and, if the cow does not become pregnant,
recurs at intervals of about 21 (16–24) days. Since oestrus is the most obvious stage of
the cycle to the observer, it is usually taken as day 1. The illustration of the oestrus
cycle in Figure 3.3 begins three days earlier, at the beginning of pro‐oestrus. FSH from
the anterior pituitary stimulates (normally) one follicle to mature. The maturing fol-
licle secretes increasing amounts of oestrogen. After about two days the bull can
detect by smell and other sensations that the cow is coming on to heat. She will not
accept him at this time and he will probably not press his suit too strongly. There is
however good evidence that, having had a sniff, he will keep a mental diary of cows
likely to be worth a visit on the morrow.
The cow in oestrus will exhibit a range of behaviours and responses. In a modern
dairy herd, these will seldom involve the bull because he isn’t there. She is restless,
will vocalise and may make sexual overtures to other cows. More crucially, she will
stand to be mounted by other cows. Practical recognition of oestrus from behav-
ioural and other signs is covered in Chapter 12.
Ovulation, induced by the release of LH, usually occurs just after the end of ‘standing
heat’. It is therefore better to be slightly too late than too early when using artificial
insemination. The granulosa cells of the ruptured follicle immediately reduce their
secretion of oestrogen (although oestrogen secretion doesn’t stop, Figure 3.3). As the
corpus luteum develops it secretes an increasing amount of progesterone, the hormone
primarily responsible for the maintenance of pregnancy. The luteal phase of the cycle,
or dioestrus, lasts, on average 16 days (12–20). Thereafter, unless fertilisation has
occurred, the corpus luteum regresses and stops secreting progesterone. Current under-
standing is that this is brought about by the action of another hormone prostaglandin
(or, to be pedantic, prostaglandin F2α, or PGF2α) secreted from the lining of the non‐
pregnant uterus and carried directly to the ovary through a counter‐current structure in
the local blood supply. Prostaglandin has become a valuable drug in dairy cow manage-
ment and medicine. It is used to synchronise oestrus (for example in a group of heifers
intended for artificial insemination) by synchronising the termination of dioestrus and
bringing the animals on to heat within three days. It is also valuable in the treatment of
retained placenta (see Chapter 12).
Puberty
Puberty in the dairy heifer is defined by the time when she comes on heat and
ovulates for the first time. Increased activity from the pituitary gland prior to
puberty, in particular, pulsed secretion of LH, stimulates some follicles to luteinise
and secrete progesterone even though ovulation has not occurred. The ‘feedback’
on the pituitary from progesterone appears to further stimulate LH and FSH
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release to the point where they can induce sufficient follicular development to
achieve ovulation. Once triggered, oestrus cycles will then normally proceed in
sequence until the heifer is fertilised and becomes pregnant.
Factors affecting the onset of puberty are age, body weight and body condition. In
large breeds such as the Holstein‐Friesian, body weight at puberty is usually within
the range 250–280 kg. For small breeds such as the Jersey, the range is 160–180 kg. In
the first (1987) edition of this book I gave the average age at puberty for Friesian and
Jersey heifers at 13 and 12 months respectively. Today average ages at puberty for
large breeds in commercial herds are given as 9–11 months. This reflects more gener-
ous feeding during the growth period. Age per se has a relatively minor direct influ-
ence on puberty. It is more important that the heifer attains a size and a degree of
body fatness that will enable her to sustain a pregnancy and subsequent lactation.
For cattle, as for most mammals, the onset of oestrus cycling is most closely corre-
lated with body fat content.
While the trend has been to lower the age at puberty through improved nutrition,
there is clear evidence that things can be taken too far. Trials in which growth rates
in excess of 700 g/day (in large breeds) were induced by feeding large amounts of
concentrates (sometimes accompanied by the administration of anabolic steroids)
have proved conspicuously unsuccessful. The extremely fast growth was associated
with reduced development of secretory tissue in the mammary gland and, in conse-
quence, a significant and lasting reduction in milk production.
Fertilisation
The ovum or oocyte released from the Graafian follicle is directed by the fimbriae
into the oviduct (Figure 3.1). Passage down the oviduct normally takes about 90 h
and proceeds in a ‘to and fro’ fashion, as muscle contractions move fluids along
the oviduct alternately towards and away from the uterus. Sperm are usually
deposited in the anterior vagina and the outer portion of the cervix during natural
service. The artificial inseminator normally penetrates the cervix and deposits a
smaller quantity of sperm within the body of the uterus. The first sperm may
arrive in the upper oviduct within 2–3 hours of mating. Since, with natural ser-
vice, this usually occurs several hours before ovulation, the fastest travelling
sperm are in place and ready for the ovum before it arrives in the oviduct. This is
aided by movement of cilia in the walls of the oviduct. Prior to ovulation they beat
towards the ovary helping to move the sperm upwards. After ovulation, they move
towards the uterus.
‘To and fro’ contractions of muscle in the oviduct help to cluster large numbers of
sperm and the oocyte into the same region. Sperm undergo a maturation process
(capacitation) and are attracted towards the cells and the membrane (zona pellu-
cida) surrounding the ovum. A large number of sperm attack the zona pellucida
mechanically and chemically using the enzyme hyaluronidase. Finally, perhaps
Pregnanc 51
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12 h after ovulation and 24 h after insemination, one sperm penetrates the zona and
brings together the male and female gametes. As soon as this first penetration has
occurred, the zona pellucida almost instantly changes in character to block the
entry of more sperm; one of the most remarkable features in this entirely remark-
able process.
Pregnancy
The fertilised oocyte begins the process of cell division and differentiation as it
migrates from the oviduct to the uterus. The process of differentiation establishes the
cells of the embryo itself and the membranes that surround it, protect it and attach
it to the uterus. At this stage the developing embryo is called a blastocyst. Figure 3.4
(a)
E AC
AL
Ch
YS
E
(b) Ch
UW AC
YS
AL
UC
Co
(c)
Co
AC
E
AL
AL UC
Figure 3.4 Development of the calf, placenta and foetal membranes. (a) Blastocyst
pre-implantation at 20 days. (b) Implantation complete at 40 days. (c) Foetal
membranes complete at 100 days. AC = amniotic cavity, Ch = chorion, Co = cotyledons,
E = embryo, UC = umbilical cord, UW = uterine wall, YS = yolk sac.
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illustrates the early stage of formation of the two membranes and fluid‐filled cavities
(‘bags of water’) that surround the developing calf during pregnancy. The inner
amniotic cavity will eventually surround the calf foetus in a relatively dense, lubri-
cant, shock‐absorbing fluid formed from the calf’s urine and other secretions. A yolk
sac, containing nutrients to feed the embryo, is present in early development but
rapidly regresses (Figures 3.4a, b). The second cavity is created by enlargement of the
allantois, which acts as a reservoir for the excretory products of the developing foetus
and is the first ‘bag of waters’ to rupture at the time of calving. Very early in develop-
ment, the embryo must signal to its mother its presence in the uterus to prevent her
releasing prostaglandins, which would destroy the corpus luteum and abort the
pregnancy. The blastocyst appears to achieve this by secreting oestrogen within two
weeks of fertilisation.
Implantation, the close attachment of the foetal membranes to the uterine wall,
begins about 25 days after fertilisation and is complete by about 40 days. The outer
layer of foetal membranes, the chorion becomes attached to the cotyledons of the
uterine wall. These specialised points of attachment develop a rich blood supply
and there is some erosion of maternal tissue. The cotyledons are designed to facili-
tate exchange of nutrients between the maternal and foetal circulations but there is
no direct mixing of foetal and maternal blood. Foetal blood vessels develop in the
chorionic wall to carry blood between the foetus and the cotyledons via the umbili-
cal arteries and vein (Figure 3.4c). Implantation is a vulnerable stage of pregnancy.
If it fails, the cow will return to oestrus, having missed at least one cycle (and prob-
ably more).
Twinning is rare. In most cases two ova have been shed and fertilised. These are
dizygotic twins and no more or less alike than any two offspring from the same mother
and father. Monozygotic or identical twins occur vary rarely, less than one in a thou-
sand births, when a single ovum develops two embryos. Where the chorionic mem-
branes of the two developing embryos come into contact it is likely that the two sets
of foetal blood vessels will unite, so creating a common circulation for the two calves.
If both calves are of the same sex, as is the case for 50% of dizygous twins and 100% of
monozygous twins, this is no problem. However, when calves that are genetically
male and female share the same circulation, the sexual development of the female is
distorted. A female calf born to a male twin is called a Freemartin. The early develop-
ment of the reproductive organs in both male and female embryos is the same. At this
stage both possess a pair of Mullerian ducts. In the female these will develop into the
uterus, cervix and upper vagina. In the male embryo, the developing testis secretes an
anti‐Mullerian hormone (AMH) that causes the Mullerian ducts to atrophy. When
male and female embryos share the same circulations, the AMH inhibits the develop-
ment of the female reproductive tract to a degree that depends on the state of develop-
ment reached before the fusion of the two circulations. Very often the vulva and
external reproductive organs of the Freemartin appear to be normal (although the
clitoris may be enlarged) but parts or all of the cervix, uterus and ovaries are missing.
Needless to say, these animals are infertile.
Parturitio 53
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Placental Transfer and Foetal Nutrition

The close arrangement of the blood vessels of the maternal and foetal circulatory
systems in the cotyledons of the placenta ensures the exchange of nutrients, water,
electrolytes and the respiratory gases between mother and offspring. Water, most
electrolytes, carbon dioxide and oxygen in solution pass freely between the two blood
streams by simple diffusion. The principal nutrients for the foetus, glucose and
amino acids, are actively transported by specific transport mechanisms. Water‐solu-
ble vitamins and some minerals such as iron and copper are also actively transported
to the foetus. There is almost no transfer of whole proteins or the fat‐soluble vita-
mins A, D and E. The calf is born lacking both immunoglobulins carrying antibodies
to infectious disease and is deficient in fat‐soluble vitamins. These are normally
acquired by drinking colostrum. In the case of immunoglobulins that are carried
within the blood (e.g. the IgG group), the transfer from colostrum to blood must
occur within the first hours of life while the epithelium is permeable to entire pro-
teins. Other immunoglobulins contained in colostrum and milk (the IgA group)
offer protection at the mucosal surface of the intestine and confer protection through-
out the time that calves are able to consume mother’s milk. This makes whole milk
a much better feed than the best commercial milk replacer, especially when the calf
stays with (or on the same farm as) its mother and is exposed to the same endemic
pathogens to which its mother has developed a measure of immunity.
Parturition
The average gestation length for a Holstein‐Friesian cow is nine months or, more
precisely, 281 days. Sire breed has a small effect on gestation length, which is
approximately 284 and 287 days for calves born from Holstein‐Friesian cows to
Charolais and Limousin bulls respectively. Gestation length has little effect on the
incidence of calving problems. The effect of bull size and shape with be considered
later.
The process of parturition (calving) appears to be triggered by the calf (which is
why bull selection influences gestation length). A signal from the calf brain stimu-
lates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary
gland, which in turn triggers the release of steroid hormones from the calf’s own
adrenal cortex. These corticosteroids cross into the maternal circulation and stimu-
late the placenta to produce PGF2α. This inhibits progesterone secretion, directly
stimulates uterine contractions and sets in motion the sequence of events that leads
up to calving. This fundamental knowledge has been eminently applicable: corti-
costeroids and PGF2α are both used on veterinary practice to initiate parturition.
Here I shall describe only the sequence of events in a normal calving. Detailed
description of the skills necessary for assisted calvings, what can be done by the
stock people and when to seek veterinary assistance, are beyond my brief but can be
found in the list of suggestions for further reading at the end of the book. In the last
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10 days before calving the cow’s udder becomes increasingly distended and milk
may indeed run from the teats, particularly if she continues to be with other cows
who are regularly being milked. The secretion from the udder changes in consist-
ency from a sticky, clear, honey‐like fluid to the normal rich colour and consistency
of the colostrum or first milk. About 24 h before calving the ligaments of the pelvic
canal relax under the influence of the hormone relaxin to increase the circumfer-
ence of the birth canal. This can be recognised by a loss of tension and ‘dropping‐in’
of the ligaments that run from the spinal column at the tail head to the pin bones
(Tuber ischii).
The first stage of parturition begins with contractions of the smooth muscle of
the uterus induced by the hormone oxytocin from the posterior pituitary. In a nor-
mal delivery, the front feet of the calf are pushed towards the cervix, stretching it
and sending back signals to the brain, which responds by increasing the force and
frequency of contractions. The cervix begins to dilate, releasing a thick, slimy sub-
stance that was the plug that blocked the birth canal during pregnancy. The cow
shows some signs of discomfort at this time; she is restless and may turn her head
round to look at her flank but she does not yet strain to expel the calf using her
abdominal muscles. The exact duration of the first stage of parturition is difficult to
assess because the onset is gradual. In cows, 4–6 h would be normal and 8–9 h not
excessive. Heifers may appear to be restless and in discomfort for 2–3 days before
calving.
The second stage of parturition begins when the pressure imposed by the calf
on the birth canal (cervix and vagina) causes sufficient pain to induce
labour – strong, controlled contractions of the abdominal muscles. The first foe-
tal (chorioallantoic) membrane usually appears as a bladder‐like protrusion
from the vulva, then ruptures, releasing copious quantities of allantoic
fluid – the first ‘bag of waters’. The calf is propelled, front feet first into the
vagina, still at this stage covered in the amniotic membrane. The front feet, cov-
ered in protective ‘golden slippers’, appear at the vulva while the head and
shoulders (the widest part of the calf) are still in, or just behind, the bones of
the pelvis (the narrowest section of the birth canal). It is normal for there to be
some delay at this stage while full relaxation of the birth canal takes place. The
cow may stand or lie down at this time according to how she feels.
When the head enters the vagina the cow usually lies down and completes the
expulsion process with a few massive abdominal contractions. The second (amni-
otic) foetal membrane may break as the calf is expelled. If not, the calf will nor-
mally struggle and break it successfully within a few seconds. If it doesn’t, it requires
assistance. The umbilical cord ruptures quickly and easily in response to move-
ments by calf and mother and the umbilical vessels recoil and contract elastically to
minimise loss of blood. I repeat, all the blood in the umbilical cord belongs to the
calf. Normally, stage two of parturition lasts 1–2 hours. As a general rule, if a cow
has been in second stage labour for 3 h without producing a calf, she should receive
veterinary or equally expert attention. This does not necessarily mean assistance.
She may not be ready, but only an expert can tell.
Parturitio 55
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The third stage of labour involves the expulsion of the afterbirth (placenta and
foetal membranes). In normal circumstances this occurs without difficulty within
1–6 h of calving. If left to herself, a beef cow will probably eat the afterbirth. This is
an obvious safety measure in the wild, since it makes the appearance of a new‐born
calf less obvious to predators. I know of no good reason to suppose that eating the
afterbirth has any important psychological or nutritional significance for the cow
and very occasionally it may cause her to choke. On balance, it is probably better to
take it away.
Dystocia
The main causes of dystocia in cattle are malpresentation and oversized calves. The
three most common causes of malpresentation are head first, hind legs first and
breech (bottom first). All these need to be corrected by pushing the calf back into
the uterus to be rearranged. In expert hands, accompanied probably by epidural
anaesthesia to prevent the cow straining against the operator as they sorts things
out, these problems can usually be resolved quite quickly. The problem of the over-
sized calf is inherently more difficult and more painful for the cow. This is not the
place to go into detail as to individual cases and decisions, such as when to elect for
Caesarean section. It is however, important to be aware of the extent to which the
risk of oversized calves can be reduced through sire selection and management
As a general rule, bigger bulls are likely to produce bigger calves at birth. This is
especially a problem for herds of beef suckler cows where, for sound commercial
reasons, it makes sense to mate relatively small, hardy cows (with relatively low
maintenance costs) with much larger bulls so as to produce animals in the slaugh-
ter generation that are significantly larger and meatier than their mothers. The
risk of dystocia resulting from oversized calves is significantly greater when the
condition of the cows is good to fat. In beef herds, it is considered good practice to
ensure that the cows are lean at calving time (condition score 2). This can some-
times be difficult for autumn‐calving cows after a summer of good grazing. These
days, a fat dairy cow is a rare sight, so this is less likely to be a problem.
In traditional dairy herds it has been common practice to run the heifers at pas-
ture with a Hereford or Aberdeen Angus bull, both relatively small compared with
bulls of the continental breeds like the Charolais. These amiable British breeds are
easy to manage and undoubtedly reduce the risk of dystocia in first‐calving heifers.
Increasingly however, dairy farmers are choosing to fertilise all, or nearly all, their
cows and heifers by artificial insemination using selected progeny‐tested bulls
from the dairy breeds. In Chapter 11 I consider in detail the criteria for bull selec-
tion. These include ease of calving. For cows that have a history of dystocia, the
farmer can select a bull with a good score for ease of calving; for cows that regu-
larly calve without difficulty, other traits directly related to profit from milk pro-
duction can be given greater emphasis. The increased use of sexed semen
(Chapter 11) has made it possible to increase the proportion of cows inseminated
by dairy bulls, since it reduces the production of low‐value Holstein‐Friesian male
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calves. At present, the success rate for inseminations with sexed semen is lower
than with untreated semen, the difference being greater for mature cows than for
heifers. Consequently, many farmers are choosing sexed semen from progeny‐
tested dairy bulls for their heifer calves, which makes it particularly important to
consider ease of calving when selecting bulls.
Selection for extreme muscle development in the hindquarters of beef breeds, most
conspicuously in the ‘double‐muscled’ Belgian Blue1, greatly increases the risk of
dystocia in cows of these beef breeds. The extreme development of the gluteal muscles
is accompanied by a reduction in the circumference of the pelvic canal, further increas-
ing the risk, so much so that in some strains of Belgian Blue cows parturition is rou-
tinely managed by premeditated Caesarean section. However, the risk of dystocia in
Holstein‐Friesian cows inseminated by Belgian Blue bulls is not significantly higher
than that for large Charolais bulls. The most important risk factor is the size and shape
of the pelvic canal. The incidence of dystocia in small Jersey cows inseminated by beef
bulls is not significantly higher than for Holstein‐Friesians. Although the circumfer-
ence of the pelvic canal may be less in Jerseys, they also tend to have a shorter pubic
bone (the base of the pelvic canal) and this appears to facilitate the passage of the calf.
Lactation
Anatomy of the Udder

The cow’s udder consists of four entirely separate mammary glands, or ‘quarters’,
each with its own system of secretory cells and ducts and with its own storage cis-
tern. Unless the udder is severely damaged there is no connection between the quar-
ters. The cells that secrete milk form a single layer around the alveoli, which are
microscopic sacs that empty into small and then major ducts (Figure 3.5). These
ducts lead to a series of cavities or sinuses that form a cistern or reservoir for milk.
Secretion of milk by the epithelial cells of the alveoli is a continuous process. Milk is
retained within the gland cisterns by sphincters at the top and bottom of the teat
canal. Normally, during suckling or artificial milking, only the milk contained within
the sinuses is actually expelled. However, the natural stimulus to milk ejection pro-
duced by the bunting and suckling of the calf or the conditioned stimulus to ejection
produced by the gentle and pleasant routine of a good milking parlour induce the
cow to secrete oxytocin. This causes specialised myoepithelial cells around the alveoli
to contract and expel milk into the duct system. This ‘let down’ mechanism is essen-
tial to ensure proper milk ejection, which is why it is so important to preserve a
gentle, undisturbed rhythm in the milking parlour.
The main constituent of milk is, of course, water. This ranges from about 850 g/kg
in Jersey milk to 870 g/kg in a typical Holstein‐Friesian. Other major constituents
1 ‘Double muscling’ is a misnomer. It actually describes extreme hypertrophy of the normal muscle
arrangement.
Lactatio 57
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myoepithelial
cells
secretory
cells
small
duct
major duct
arrangement
of alveoli
medial ligaments
lateral ligaments
glandular tissue
opening of
major duct
gland cistern
teat cistern
teat canal
Figure 3.5 Anatomy of the bovine udder.
are listed in Tables 1.1 and 1.2. The osmotic concentration of milk is, of necessity, the
same as that of plasma. Colostrum contains about 780 g/kg water. Relative to milk in
later lactation it has a higher concentration of protein (150 g/kg) because of the
immunoglobulins, is low in lactose and normal for fat. The osmotic concentration of
milk in the healthy udder is largely determined by the presence of lactose, the milk
carbohydrate. In practice, this means that the ratio of lactose to water is fixed within
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very narrow limits: it is fruitless to contemplate experiments designed to alter this

ratio, however attractive this may appear to the producer or consumer.
Lactose is synthesised in the alveolar cells exclusively from glucose. The main milk
protein is casein synthesised from amino acids in the mammary gland. The generic
name casein describes several different proteins (a‐s1, a‐s2, β and K caseins). The
various caseins are held together in distinct micelles, with the a‐s1, a‐s2, and β
caseins in the middle and the K caseins forming the outermost layer. These K caseins
carry a negative electrical charge. Repulsion between the charges keeps the micelles
separate. The casein micelles clot in the abomasum of the calf or in the presence of
enzymes such as pepsin and rennin, which separate the milk into curds and whey.
Casein is contained within the clot. The whey proteins, lactalbumin and lactoglobu-
lin are also synthesised, for the most part, in the alveolar epithelium.
Immunoglobulins, the immune proteins containing antibodies to infectious agents
and other antigens experienced by the cow are synthesised by specialised plasma
cells in the mammary gland and elsewhere, and transported whole in the blood
plasma to and through the alveolar epithelium into the milk and especially the
colostrum. The synthesis of milk proteins is metabolically closely linked to lactose
synthesis within any one genotype and is thus closely related to water secretion.
This means that, while it is theoretically possible to manipulate the protein concen-
tration of fat‐free milk by nutritional means, it is unlikely to be practicable. In other
words, if one wishes to feed to produce more milk protein one must be prepared to
accept more lactose and water as inevitable accompanists. If, for dietary or other
commercial reasons, one wishes to manipulate these things, it is more easily done
after the milk has left the cow. The (limited) potential to manipulate the composition
of fat‐free milk through genetic selection is considered in Chapter 11.
The lipid content of cow’s milk is predominantly true fat (triglycerides). The
two main fatty acids making up the triglycerides are palmitic acid (C15H31COOH),
which is fully saturated and oleic acid (C17H33COOH), which is monounsatu-
rated. The concentration of polyunsaturated fatty acids such as linoleic acid
(C17H31COOH) is low, unless rather bizarre diets are fed. Milk fats can be synthe-
sised from VFA, especially acetate produced by fermentation in the rumen or
from longer‐chain fatty acids arising either from the diet or from fat reserves in
the body. Fat synthesis in the mammary gland and its secretion in milk take
place independently of the synthesis and secretion of lactose, protein and water
so that ‘butterfat’ concentration in milk is sensitive to the quantity and composi-
tion of the diet.
Milk Yield
The quantity of milk produced is determined by the number of secretory cells in
the alveolar epithelium, which is under genetic control, and the supply of nutri-
ents both from the diet and from body reserves. This supply is regulated by hor-
monal control of the partition of nutrients between the mammary gland and
other body tissues such as fat. Genetic differences in the expression of the main
Lactatio 59
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hormones controlling the partition of nutrients explain the differences in

lactation yields of (e.g.) Holsteins and Herefords.
Average lactation yields for dairy cows in the UK have increased from about
6500 to 7500 L over the period 2000 to 2017. This increase can be attributed primar-
ily to selection for increased yield from progeny‐tested Holstein‐Friesian bulls. For
North American Holsteins, average yields are approximately 10 000 L. At time of
going to press the record is held at 35 450 L by a cow from Wisconsin. The higher
average yields of the North American Holsteins reflect both increased intensity of
selection for yield and the fact that the majority of the cows are housed throughout
lactation and fed rations with a high ratio of starch from cereals to digestible fibre
from pasture (often the highest they can get away with without incurring serious
digestive problems – see Part II). The UK figure of 7500 L reflects a system that
provides (as a very rough approximation) 50% of nutrients from fresh and con-
served pasture. In New Zealand, where systems are overwhelmingly pasture‐based,
current average yields are about 6500 L, although some herds produce well in
excess of this amount.
Milk yield rises to a peak in about the fifth week of lactation, persists for 3–4
weeks, then begins a slow decline. In a pasture‐based system, the shape of the lacta-
tion curve varies according to the season of calving. For an autumn‐calving herd,
the decline is interrupted when cows are turned out on to spring grass for reasons
that are both nutritional and hormonal. If the cow has been successfully insemi-
nated the hormonal changes associated with the progress of pregnancy will acceler-
ate the decline to the point when the cow can be dried off to prepare her for her next
calving. For systems that aim to produce calves at 12 month intervals, the standard
lactation length is taken as 305 days (implying insemination at 90 days), giving a dry
period of 60 days. Daily yields at peak lactation are likely to be between 0.5 and 0.6%
total yield. Thus, peak yield for a cow with a total lactation yield of 7500 should be
within the range 38–45 L/day. The rate of decline in yield after 90 days of lactation
should be 1.5–2.0% per week. If the decline is greater than this and total lactation
yield does not come up to expectation from peak yield then something is
amiss – probably nutrition. If the rate of decline after 80 days is less than 1% this
suggests that the cow may not be pregnant or peak yield isn’t what it might have
been.
The composition of milk (see Table 1.6) remains relatively constant throughout
lactation. There can be a decline in milk fat concentration when cows are turned
out on to spring pasture, which is low in digestible fibre, and there is invariably an
increase in concentration of fat (and, to a lesser extent, protein) when milk yields
are low towards the time of drying off.
Extended Lactations
Conventional wisdom dictates that the dairy cow should produce a calf a year. A 12
month calving interval has made good sense on many grounds. The reproductive appa-
ratus is given three months to recover from the previous pregnancy and parturition,
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the cow can be dried off and enjoy a rest period of two months prior to the next calving
and the demands of lactation can be matched to nutrient supply, (e.g. grass growth in
spring‐calving pastoral systems), or seasonal variations in milk prices (traditionally
achieved in the UK through autumn calving). When total lactation yields in pasture‐
based systems were 6000 L or less, daily yields by the beginning of the eighth month of
pregnancy, or 300 days into lactation, were likely to be in the region of 10–15 L/day (or
less) and drying‐off could proceed with little stress to the cow or risk of mastitis.
Today, there are a great number of dairy units in which cows with lactation yields
of 10 000 L or more are kept in barns where the food is brought to them throughout
the period of lactation. In these circumstances, there is no pressing case to argue for
a 12 month calving cycle and, in theory at least, several good reasons to consider
extending the calving interval perhaps to a limit of 18 months. The first, obvious
reason for extending lactations is that it seems crazy to dry off a cow after 10 months
when she is still giving over 30 L milk/day. The second, potentially far more impor-
tant reason is that the most stressful period in the life of a dairy cow is the time of
calving and the first six weeks of lactation, when risks of digestive disorders, lame-
ness and infectious disease are greatest. Other potential advantages include an
increased ratio of months in milk to months dry (e.g. 16:2 for an 18 month calving
interval compared with 10:2 for a 12 month interval) and a reduced number of sur-
plus, low‐value, male calves.
The practical implementation of the excellent theory of extended lactations has,
so far, met with mixed success. It was expected that fertility would be at least as
good as, or probably better, if insemination was delayed until (say) 8 months after
calving but some of the results have been disappointing. In these circumstances
cows that do not conceive to the first or second insemination are likely to lose
money. Planned extended lactations with 18‐month calving intervals may, in the
future, become common practice in large zero‐grazed herds. At present an average,
largely unplanned calving interval of about 14 months would seem to be the norm
for these units.
Hormonal Control of Lactation

The hormonal mechanisms for control of the development of mammary tissue dur-
ing late pregnancy and the synthesis of milk after the calf is born are complex and
beyond the scope of this book. I wish only to make three rather obvious but impor-
tant points:
1) To ensure proper mammary development and lactation all the hormone systems
of the body need to be in good order. The is no single or simple controller.
2) The optimal hormonal balance for pregnancy, mammary development and lac-
tation are not the same, thus the hormonal consequences of advancing preg-
nancy conflict with the hormonal stimulus to lactation.
3) There is competition between the mammary gland and other body tissues (mus-
cle and fat) for nutrients as this is under hormonal control.
Reproduction in the Mal 61
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The two hormones most responsible for controlling the partition of nutrients
between the mammary gland and other body tissues are insulin and growth hor-
mone or somatotropin. Very simply, insulin stimulates the net uptake of nutrients
into body tissues like muscle and fat and growth hormone stimulates their net
release from body tissue reserves into the circulation. In early lactation the cow
secretes relatively large amounts of growth hormone and small amounts of insulin
thus mobilising body reserves and directing them to milk‐synthesising cells in the
alveoli, thereby enabling her to ‘milk off her back’.
Synthetic bovine growth hormone, or somatotropin (BST), genetically engineered
in bacteria and administered to cattle by regular subcutaneous injections, can increase
milk yield by 5–30%, depending on circumstances. For most properly fed cattle in
good condition increases of 15–20% are to be expected. However, BST does not give
farmers something for nothing (beyond the price of the drug). Because it directs more
nutrients to milk synthesis it means the cow must eat more or lose condition. For the
high genetic merit dairy cow in early lactation, it is normal for the uptake of nutrients
by the mammary gland to exceed her capacity to eat, digest and absorb nutrients from
her food. Administration of BST in early lactation is likely to accelerate loss of body
condition and predispose to infertility. Increased hunger also increases the risk of
digestive disorders for cows fed high energy diets. Administration of BST after 100
days, if the cow is back in calf, nutrient supply has caught up with demand and body
condition is satisfactory, can produce a sustained increase in yield so that milk pro-
duction over the entire lactation may be elevated by 15%. The use of BST to increase
milk production has been prohibited in the European Union (and the UK), mainly,
although not explicitly, on grounds of animal welfare. While it is permitted in the
USA, the uptake has been much lower than that predicted by the manufactures or
feared by the consumers. Most dairy farmers appear to have concluded that their
cows are performing very satisfactorily without it and the gains do not justify the cost,
hassle and potential threat to cow welfare.
Reproduction in the Male
The role of the bull in the life of the average dairy cow is, at best, a brief and infre-
quent affair and in most cases his direct involvement has been usurped by the mid-
dle man in the form of the artificial inseminator. The reproductive tract of the bull
is illustrated in Figure 3.6. The testes are formed in the abdomen during foetal
development and descend through the inguinal canal into the scrotum before birth.
They contain seminiferous epithelium wherein the sperm are produced and inter-
stitial cells that produce the hormone testosterone. The hormones from the anterior
pituitary that control sexual function in the male are the same as in the female.
Follicle stimulating hormone (FSH) stimulates spermatogenesis and luteinising
hormone (LH, otherwise called ICSH, interstitial cell stimulating hormone) regu-
lates testosterone secretion. Puberty, as determined both by libido and the presence
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of mature sperm in the ejaculate, occurs at about 10 months of age although, as

with the female, this depends on growth rate.
Spermatozoa leave the seminiferous tubules at an immature stage and enter the
epididymis, where they are nourished by epididymal secretions and allowed to
mature over a period of about 10 days. The most obvious feature of maturation is
that they acquire motility, the ability to swim by moving their tail. There is a con-
tinuous movement of sperm through the epididymis and into the vas deferens or
spermatic cord. The quantity of sperm maturing in store outside the testis is about
5–6 x 1010, which is about 10 times daily sperm production. This maturation process
is essential for proper fertility; if a bull ejaculates too often not only will sperm num-
bers decrease, so too will their capacity to fertilise. During ejaculation spermatozoa
are propelled from the epididymis and vas deferens into the urethra, where the
ejaculate is augmented by secretions from a series of accessory glands that provide
a transport medium, a source of nutrients and buffers to offset the acidic end prod-
ucts of sperm metabolism and so prolong their active life.
The penis of the bull is a long, thin structure made up largely of fibroelastic tissue
that makes it firm even at rest. Normally it is retained within the prepuce by the
retractor penis muscle that folds it into a sigmoid (S‐shaped) flexure (Figure 3.6).
During sexual excitement sinuses within the penis become engorged with blood but
rectum
accessory glands
retractor
penis
sigmoid muscle
bladder flexure
vas deferens
penis (spermatic cord)
epididymis
testis
Figure 3.6 The reproductive organs of the bull.

Reproduction in the Mal 63
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erection is achieved mainly and very rapidly by relaxation of the retractor penis
muscle that allows the sigmoid flexure to straighten out. The long, thin structure
and simple erection mechanism of the bull’s penis make intromission simple and
rapid. Ejaculation usually occurs within 2–3 s of intromission with the tip of the
penis close to the vaginal end of the cervix. The quantity of semen ejaculated is only
about 5–8 ml but the sperm density is high (about six million sperm per millilitre).
Herders are well aware (or were, when herd bulls were commonplace) that dairy
bulls such as the Friesian are more difficult to handle than beef bulls such as the
Hereford. This reflects, in large part, differences in their life style. A Friesian bull
was likely to be isolated in an individual pen, whereas the Hereford bull may spend
most of his time with a harem of bulling heifers and pregnant cows. In these cir-
cumstances one might reasonably expect the Friesian bull to be less favourably dis-
posed to the world at large. However, there are real genetic differences between the
breeds in both physiology and behaviour. The Friesian produces more sperm than
the Hereford, is more quickly aroused and will copulate more often before exhaus-
tion. A Friesian bull might reasonably be expected to make about 20 mounts over a
period of 6 h before showing signs of sexual exhaustion and 80 mounts in 24 h is not
uncommon. However, as indicated earlier, after more than 10–12 natural services
per day, sperm count and fertility start to decrease.
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Environment, Behaviour and Welfare
The aims and responsibilities of farmers and herders are to seek optimal efficiency
of production within an environment that ensures comfort, hygiene and satisfac-
tion for the cows. This can be expressed in terms of the provisions necessary to
promote the five freedoms. The need to achieve freedom from hunger and thirst
will be considered at length in Part II: Feeding the Dairy Cow. Freedom from pain,
injury and disease will be covered in Part III: Housing, Health and Management.
This chapter will look at how the environment may affect the behaviour and physi-
ology of the cow and consider the implications for her welfare.
E
nvironmental Needs
The most important environmental needs of farm animals are summarised in

Table 4.1. All these criteria apply to the dairy cow, after clarification to take account
of the special features of her physique and temperament. For example, a suitable rest-
ing area for a somewhat clumsy animal with bony limbs and weighing over 600 kg
means a bed with sufficient ‘give’ to allow her to lie for long periods without incurring
discomfort or injury, sufficient space to change position (stand up and lie down) with-
out difficulty, and sufficient protection from risk of injury through the accidental or
deliberate actions of other cows in the herd. Her need for security includes security of
food and water supply (obviously), minimal risk of death, pain or injury from physical
contact with other animals, people or hazards such as fire and flood. Security also
implies freedom from fear of real threats, such as aggression, and perceived threats,
especially neophobia, or fear of the unknown. One of the most important criteria for
the welfare of both cow and farmer is biosecurity: protection against the importation
of infectious diseases such as bovine tuberculosis. This will be considered in Part III.
Good hygiene is essential, not only to reduce the risk of disease but also to ensure that
housed cows do not have to live in squalor.
The last environmental need listed in Table 4.1 is freedom of choice. In Chapter 1
I described this as ‘freedom to select a preferred environment for rest and recreation,

Behaviou 65
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Table 4.1 Major environmental requirements of farm animals (from Webster 1996).
Comfort, physical A suitable resting area

Space for freedom of movement, grooming, limb stretching, exercise
Comfort, thermal Neither too hot or too cold
Security Of food and water supply
From exposure to infection (biosecurity)
From death, pain or injury due to aggression, predation, fire,
flood (etc.)
From fear of aggression, predation and the unknown
Hygiene To reduce the risk of disease
To avoid the discomfort of squalor
Choice To permit coping behaviours
To allow animals to acquire security through experience and
adaptation to the normal sights and sounds of farm activity
freedom to select, and avoid, contact with certain individuals in their social environ-
ment’. The welfare of a sentient animal is determined by its ability to cope with
challenge (in this context, a more accurate definition than stress). Challenge can pro-
gress to stress and then to suffering if the cow discovers that it is unable to cope, either
because the stresses are too severe, too complex or too prolonged, or because the con-
straints of the environment make it impossible for her to carry out coping behaviour.
Freedom from fear is achieved not only by protection from obvious threats (e.g.
stray dogs) but also by creating an environment in which a growing animal can over-
come one of its greatest fears: neophobia, or fear of the unknown. In a secure, natural
environment the natural curiosity of a young calf will motivate it to explore while still
in the care of its mother, become familiar with its routines, sights and sounds, and
learns by experience that that these are things with which it can cope. In the FAWC
code, freedom from fear is achieved by achieved by conditioning animals to their sur-
roundings and avoiding situations that cause stress. The routines on a well‐managed
dairy farm are so familiar that milking cows should rarely experience fear. However,
male calves from dairy cows that were (and in many parts of the world, still are)
reared for white veal in individual crates, near total darkness and without experience
of the natural sights and sounds of farm activity, developed chronic anxiety and could
be panicked by almost any novelty, such as the sudden appearance of a cat in the barn.
B
ehaviour
Behaviour is what an animal does. Most of the behaviour of a dairy cow will appear
perfectly straightforward to a sympathetic observer although some of the subtler
features may escape the eye of all but the most experienced stockperson. Ethology,
66 Environment, Behaviour and Welfare
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or the science of animal behaviour, addresses the questions ‘what do animals do

and why’? The two main lines of investigation are:
Study of behaviour in a natural environment: How does an animal allocate its time
when it has freedom of choice? From this we can assess the extent to which different
‘unnatural’ environments, e.g. close confinement in intensive housing, may compro-
mise the expression of natural behaviour.
Motivation analysis: This approach is designed to identify preferences and aver-
sions, measure the strength of preferences and aversions (how much these things
matter) and determine behavioural priorities. In one study, heifers were given six or
nine hours uninterrupted lying time, then their preference for eating, social contact
or further lying time were recorded in the hours remaining. Despite other potential
attractions, the heifers showed an inelastic demand to lie down for 12–13 hours in
each 24 hour period. This observation has serious implications for the welfare of
high‐yielding dairy cows, obliged to stand eating for long periods to meet their met-
abolic demands and queue to be milked 2–3 times daily.
The actions of any animal may be innate, acquired or a combination of the two.
When the cow licks her calf after birth and the calf struggles to its feet and seeks the
teat, these actions are innate (i.e. unlearned and instinctive). The cow that trots to
the feed trough when she hears the tractor coming is performing an action that has
been entirely acquired by learning. The month‐old calf that runs across the field to
its mother and latches onto a teat is performing an innate action that has been rein-
forced by learning. The stimuli to innate and acquired behaviour are internal (hun-
ger, thirst, heat and cold), external (fear, security, companionship), or internal
reinforced by external – much sexual behaviour falls within this category. Most of
the natural behaviour of farm animals such as cattle is directed towards one or more
of the following objectives:
1) Maintenance of homeostasis: avoidance of hunger, thirst, thermal stress
2) Comfort and security: rest, grooming, avoidance of real or perceived threats
3) Education: investigation of the environment, learning to cope
4) Social intercourse: establishment of the social order – friends and foes
5) Genetic (Darwinian) fitness: sexual and maternal behaviour.
Most of the behaviour associated with the maintenance of homeostasis, eating,
drinking, urinating, defaecating, is too obvious to require comment. This chapter
deals with the needs of cattle to achieve comfort and security.
Physical Comfort
The most important source of physical comfort for a working dairy cow is a suitable
bed. On average dairy cows lie down for 10 h/day. Given that young, less hard
worked heifers are motivated to lie for 12–13 h, this suggests most lactating cows
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are not getting enough rest. It is critical therefore to ensure that they have easy
access to a resting area that provides sufficient space to lie down and lunge forward
in the process of rising to their feet, a cosy, secure bed that allows them rest for as
long as possible, uninterrupted by the demands of milking, the attention of other
cows, or the need to get up and change position to relieve discomfort. The design,
composition and management of lying areas for dairy cows will be discussed in
Chapter 8.
On a level surface, cows tend to lie more on their left‐hand side, about 65% of the
time in early pregnancy and increasing as pregnancy progresses, presumably to reduce
the pressure of the rumen on other contents of the abdomen, especially the gravid
uterus. However, they are (unsurprisingly) also motivated to adjust their comfort from
time to time In cubicle houses where lying accommodation is on a slope, they prefer to
lie with their legs pointing downhill because this makes it easier for them to stand up
and lie down. It has been argued that the floor of a cubicle house should be built on a
slope to encourage all the cows to lie the same way and so reduce the risk of injuries
such as tramped teats. This argument fails to understand the dairy cow.
Table 4.2 summarises observations of the behaviour of cows on two farms; one on
the level and one with a 4.2% (1 in 24) slope across the cubicles. All cubicles were bed-
ded with a small amount of straw, enough to reduce the risk of slipping but not enough
Table 4.2 Behaviour of Holstein/Friesian cows when housed on the left and right
side of two houses. On farm B the cows in the left cubicles had their feet [pointing
down the slope when they lay on their right side and vice versa.
Farm A Farm A Farm B Farm B
Slope across cubicles Level Level 4.2% 4.2%

Left side Right side
downhill downhill
Bedding Straw Straw + 20 Straw Straw
mm mat
Total occupancy (%) 47 82 60 58
Time, % total occupancy
Lying left side 38 38 5 66
Lying right side 19 35 74 8
Standing, four feet in 10 12 10 9
Standing, two feet in 33 15 11 17
Time, % total lying time
Lying left side 67 52 7 89
Lying right side 33 48 93
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for comfort. On farm A, cubicles on the right side of the building also had a 20 mm
thick layered mat. On farm B the left and right sides of the cubicles pointed downhill.
On farm B a slope of only 4.2% made over 90% of the cows lie on their right sides, with
their feet pointing downhill. On farm A, cows undoubtedly preferred the cubicles with
mats. When only chopped straw was provided as bedding, lying time was 67% left, 33%
right. When a 20 mm mat was provided, the cows showed no preference. The observa-
tion that cows showed no preference for left or right side on the more comfortable bed
suggests that when a cow shows a preference to lie on its left side it is to reduce the
abdominal discomfort resulting from lying on a hard surface. More precisely they are
displaying a relative aversion to lying on their right side. As with us when lying in bed,
they don’t lie on one side all the time because this would, in time, cause discomfort in
the limbs they are lying on and the harder the bed the sooner the onset of this discom-
fort. The cows on farm B, forced by the slope to lie on one side or the other nearly all
the time must therefore have experienced more discomfort than those on farm
A, which indicates that a lateral slope for cubicles is a bad thing.
In this trial carried out by two of my former students (Peter Creber and David
Warnes), cows in the less favoured cubicles were more inclined to stand with their
hind feet out of the cubicles and in the slurry passage. Peter and David quickly spot-
ted that they stood this way to give them a better start in the race to a more comfort-
able cubicle the moment one became available on the other side of the building.
Thermal Comfort
The optimal thermal environment for farm animals is conventionally defined as the
zone of ‘thermal neutrality’ wherein the animal can maintain normal body tem-
perature at negligible cost by balancing heat production in metabolism (Hp) against
heat loss to the environment (Hl). The heat balance equation in any circumstance
may be written as follows:
Hp Hs Hl Hn He . (4.1)
Heat exchange is conventionally measured in Watts (J/s) but units of MJ or kJ/kg W0.75
per day are generally more useful when calculating the effect of thermal stress on food
energy requirement.
Sensible Heat Loss

Hn describes loss of heat produced in metabolism by the ‘sensible’ (or Newtonian,
hence Hn) pathways of conduction, convection and radiation down temperature gra-
dients from the metabolically active tissues, first to the skin, principally by convection
through the blood vessels, and thence from the skin, through the coat to the environ-
ment by conduction (direct contact with other surfaces), convection through air
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c urrents and radiation. The cow can regulate heat loss to the skin surface to some
extent by changing position to alter the exposed surface area but mostly by vasocon-
striction or vasodilation of the superficial blood vessels. The dairy cow has a special
problem in cold environments because the udder is outside the body cavity and there-
fore particularly susceptible to heat loss especially when she lies on cold, uninsulated
floors. Local cooling of the udder reduces blood flow and can lead to a fall in milk
production because fewer nutrients are carried to the alveolar epithelium. It may
predispose the mammary gland to mastitis.
External insulation against sensible heat loss from the skin to the air is provided by
the hair coat and (mainly) the air trapped within it. While the cow is standing up,
most of the heat transfer is by convection and radiation. When she lies down much
heat is lost by conduction and the insulation of the surface on which she lies assumes
major importance. Cows of the traditional beef breeds wintered out of doors on a
hillside in Scotland or on the North American prairie have much thicker coats than
high‐yielding dairy cow housed indoors. The difference is partly genetic, partly envi-
ronmental. Hair growth is primarily controlled by day length, thus in autumn, the
growth rate increases to prepare the animal for winter. Hair shedding is however
sensitive to temperature, or more precisely, to the sensation of cold as perceived by the
cow. If she feels cold, shedding is delayed so the coat becomes thicker, rougher and
more insulating. If she feels warm or hot, the rate of shedding is increased and the
coat becomes short and glossy. Thus, the housed, well‐fed dairy cow has a short, sleek
coat not only because she is a Holstein or a Jersey but also because she feels comfort-
ably warm. On the other hand, the dairy cow that eats little, perhaps because she is
sick or food is not available, develops a long winter coat and retains it later into spring.
It is often said that the ‘poor doer’ is the last to lose its winter coat and this is why.
Environmental factors affecting external insulation are wind, rain or snow, and
sun. Wind, rain and snow all reduce insulation by disrupting the layer of warm air
trapped inside the coat. Sunshine creates a heat load on the animal to an extent that
depends on the intensity of solar radiation and how deeply this radiant heat can
penetrate the skin. A Hereford cow with a thick coat and pale skin may absorb 80%
of the heat from incoming solar radiation to a depth where it will be convected
round the body in the blood stream. This is useful when the sun shines in the winter
in the higher latitudes but a problem in the tropics. Tropical cattle such as the White
Fulani of West Africa (Figure 4.1a) have a glossy white coat over a black skin, which
is extremely effective at repelling solar radiation: about 40% reflects off the glossy
white coat, much of the rest is absorbed superficially on the superficial layers of
black skin and transmitted back to the environment by infra‐red radiation rather
than carried via the blood stream to the body core.
Evaporative Heat Loss

When cattle are feeling warm to hot, their main mechanism for maintaining homeo-
thermy is by regulating evaporative heat loss, through sweating and thermal panting.
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(a)
(b)
Figure 4.1 Cattle in the tropical mid-day sun. (a) Fulani (bos indicus) in Northern
Nigeria, (b) three-quarter Friesian cattle in the Egyptian desert.
The first and more efficient response is to sweat. It is, of course, not the production of
sweat but the evaporation of sweat that cools the animal so that if humidity is high, or
if the sweat is trapped in a long thick coat, the efficiency of this mechanism is impaired.
Tropical cattle (Bos indicus) have a greater capacity to sweat than European cattle (Bos
Taurus) and this, combined with a short, sleek coat that does not trap sweat gives them
far greater heat tolerance. Unlike humans, who become sodium depleted with pro-
longed sweating, cattle can regulate the proportion of sodium and potassium secreted
in the sweat glands. Since most plant feeds for ruminants are rich in potassium, this
Thermal Comfor 71
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mechanism enables them to sweat for prolonged periods without becoming deficient
in either mineral.
Thermal panting involves an increase in rate but decrease in depth of respira-
tion, the effect of which is to increase air movement across the heat exchanger
provided by the turbinate bones in the nose without altering the volume of air
passing through the lungs for pulmonary exchange of O2 and CO2. When a cow
feels cool or cold, she will breathe deeply at about 18–20 respirations per minute.
The hotter she feels, the more she will increase respiration rate up to a maximum
of about 189/min. Respiration rate is therefore a good, simple indicator of whether
she feels, cold, hot or comfortable. A rate of 30–60 indicates that she is thermally
comfortable. Above 60/min and she is beginning to feel hot. Thermal panting is a
second order response to the need to increase He. A Fulani cow in the sun at 35 °C
sweating copiously into a thin glossy coat may be able to maintain a normal deep
body temperature at a respiration rate below 40 min‐1. in the same circumstances
a Hereford cow with a thick body coat may be unable to avoid hyperthermia at a
respiration rate of 180/min.
Metabolic Heat Production

Within the zone of thermal neutrality, the rate of heat production is determined
entirely by the work it must do to meet the metabolic demand of maintenance,
activity and production (growth, pregnancy, lactation). As a first approximation,
the metabolic rate of adult homeotherms at maintenance is a constant function of
‘metabolic body size’ (W kg0.75). As previously illustrated in Chapter 1, the concept
of metabolic body size is conventionally used to permit comparisons between the
metabolic rates and food energy requirements of animals differing in body weight
both between and within species. Since Hn is also related to surface area, it follows
that there is little effect of body size on heat or cold tolerance.
When the effect of body size is taken into account by use of the denominator W
kg0.75 the main factor affecting the heat production of a dairy cow is her metaboliz-
able energy (ME) intake. Thus, a Friesian cow consuming enough ME to support a
yield of 35 L milk/day may produce 900 kJ/kg0.75 per day, compared with about 500
kJ/kg0.75 per day at maintenance. The cow that eats the most is the most sensitive to
heat and the least sensitive to cold. Figure 4.2 compares the heat exchanges of a
high‐yielding Friesian cow (Bos Taurus) with a Fulani cow (Bos indicus) at mainte-
nance. According to this calculation, the Friesian cow, by virtue of its high Hp, can
maintain thermal neutrality at all air temperatures between +25 and ‐20 °C. It
would be insensitive to conclude that the zone of thermal comfort, as perceived by
the cow, is this broad. She will undoubtedly experience discomfort if forced to lie on
very cold, uninsulated floors or exposed to draughts. However, the practical conclu-
sion to be drawn from this arithmetic is that high performance dairy cows are rarely
likely to be stressed by cold but are particularly susceptible to heat stress.
The Fulani cow, adapted to hot environments and poor quality feed, has a
lower thermoneutral Hp and a greater capacity to evaporate heat by sweating.
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1500 Friesian, Fulani,

peak lactation maintenance
1000
Hp Hp
500
local
(kJ/kg0.75day)
chilling optimal too hot

to udder too cold optimal
He
Heat exchange
He
500 Hn
Hn
1000
vasoconstricted vasodilated vasoconstricted vasodilated
–20 0 +20 +40 –20 0 +20 +40
Air temperature (°C)
Figure 4.2 Heat exchanges of Friesian and Fulani cattle. Hp = heat production, Hn = sensible heat loss, He = evaporative heat loss.
Climate, Production and Welfar 73
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She can tolerate air temperatures up to 40 °C with little adverse consequences

other than perhaps a slight fall in appetite. She is, of course, much more suscep-
tible to cold.
Climate, Production and Welfare
Tropical Climates
The susceptibility of dairy cattle to heat stress presents a big problem for dairy pro-
ducers and their cows in tropical and subtropical climates. The effect of high air
temperatures is exacerbated by conditions of high humidity, which reduces the
effectiveness of sweating and by high heat loads from solar radiation. When the
heat load exceeds the capacity of the cow to maintain homeothermy, body tempera-
ture rises. The cow is now under stress, appetite and production fall, welfare is
impaired and, if the stress persists, it can ultimately end in death. Fortunately, the
nights are usually cooler than the days. In hot, dry climates such as the deserts of
Israel, the Arab countries and southern California, total heat load can be reduced by
the simple provision of a sun shade (Figure 4.1b). Ideally, the shade should take the
form of a ‘breathing roof’ that permits heat and moisture from the cows to get out
but does not let the sun in. When the shaded area forms only part of the cattle lot
and the animals have the freedom to move in and out, the shelter should run east–
west, rather than north–south, since in tropical latitudes this provides protection
from direct sunlight for most of the day. A more expensive solution to the problem
of heat stress in these environments is to keep the cows in an air‐conditioned build-
ing. When relative humidity is low, this can be achieved simply and at relatively low
cost by sprinkling water to create a mist within the building. The latent heat of
evaporation of this mist cools the air without compromising the effectiveness of the
cows’ ability to regulate He by sweating.
Hot, humid climates present a greater problem because cattle cannot seek a less
humid spot and the effect may not get much less when the sun goes down. The sever-
ity of heat stress in these circumstances can be quantified in terms of a ‘temperature/
humidity index’, which takes into account both dry and wet‐bulb temperatures and
the length of time that the index exceeds the point above which the cows are unable
to maintain homeothermy and rectal temperature begins to rise. There is no simple
solution to this problem. Cows exposed to prolonged periods of high temperature and
humidity will have reduced appetite, milk production and fertility. Some have claimed
success in breeding dairy cows for increased resistance to heat stress. However, the
physics of heat exchange are inescapable. When the means for heat loss are stretched
to their limits, the only way to maintain homeothermy is to reduce heat production
and the only effective way to achieve this is through reduced ME intake and thereby
milk production.
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Cold Climates
We have seen that high performance dairy cows are extremely tolerant to low air
temperatures. Factors such as wind, rain and snow, which reduce external insula-
tion, obviously increase the severity of cold. So far as cow comfort is concerned, the
prime requirement of winter housing is to keep the cows out of the weather rather
than in the warm. When designing winter accommodation for milking cows it is
also important to ensure special protection for the udder from excessive heat loss in
draughty conditions when cows stand around before and after milking, or when
lying on poorly insulated or wet floors.
Security and Social Behaviour
The responsibility of the farmer to provide security of food supply, and minimal
risk of injury from badly designed or maintained fixtures and fittings (e.g. bro-
ken slats), is self‐evident. Biosecurity will be discussed in Part III. This section
considers the emotional need of cows to achieve, at least, freedom from fear and,
ideally, contentment. The development of cattle behaviour is driven by a balance
between curiosity and caution. Curiosity is a powerful motivating factor in young
animals as they seek to gain necessary information about their physical and
social environment. Young calves reared by their mothers in a natural outdoor
environment will, at first, seek to ensure their own security by the instinctive
mechanism of ‘hiding’ where left by their mothers in a perceived safe spot away
from the herd. As they grow and develop, these young calves will typically spend
a lot of time together, playing and investigating the environment apart from the
adult cows but close enough to run to mother in the event of any alarm. In these
circumstances they acquire security through experience. Artificially reared dairy
calves also acquire security through adaptation to the normal sights and sounds
of farm activity, including the behaviour of the farm staff. The routine of an
adult dairy cow is such that she is most unlikely to experience neophobia. The
intensity of her work load is such that she has little time for exploration or play.
After comfort, the prime motivation of most cows is for a quiet life.
Cattle are a herding species: they prefer to be in groups rather than in isola-
tion. This has evolved as an innate behaviour designed to protect the individual.
A cow on its own that encounters a pride of lions on the African plain has per-
haps an even chance of survival. In a herd of forty, the risk of death for an indi-
vidual cow is no worse than 1 in 40. Despite this instinct to achieve security
through being one of a herd, it is likely that when two cows, unknown to one
another, converge upon and compete for the same resource, e.g. feed or a good
bed, there is likely to be conflict. Cows fight either by pushing head to head, or
by making swinging, gouging or lifting movements with the head into the hind-
quarters or flank of their opponent. When cows have horns this can be painfully
effective. However, most conflicts are resolved fairly quickly when one cow
Sexual and Maternal Behaviou 75
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elects to submit. In unstable herds where cows have not established their place
in the social hierarchy, it is usually the larger cow (or the one with horns) who
wins. Thereafter each cow remembers its place. On subsequent encounters the
cow that deems itself to be inferior assumes a submissive position with its head
held low, the dominant cow acknowledges this and unless there is severe com-
petition, e.g. for trough space, both parties accept the status quo. Thereafter the
motivation of the adult cows to seek a quiet life ensures that most individuals
prefer to return to the same cubicle and queue quietly for the milking parlour.
In relatively small, stable herds older cows tend to assume dominance by virtue
of age, newly arrived heifers adopt a submissive attitude from the outset and main-
tain this respect for the older animal so long as both remain in the herd. It is how-
ever almost inevitable that some cows will bully some heifers or other new arrivals.
It is important therefore to ensure that they sort themselves out well before critical
times like calving and that heifers and other new arrivals are not prevented by other
cows from getting access to the food trough and to a resting area. A heifer that
calves for the first time at grass, immediately subjected to the strange environment
of a cubicle house, collecting yard and milking parlour, then experiences aggression
from older cows, can become very frightened and bewildered. She may be reluctant
to approach the feed fence or cubicles and stand, or worse, lie in the dunging pas-
sage for many hours. Not only is this bad for her welfare, it increases the risk of
many of the veterinary problems of early lactation, especially metabolic disorders,
environmental mastitis and lameness. Wherever possible, heifers should be intro-
duced to the physical and social environment of the adult herd some weeks before
they calve for the first time.
There is some evidence that cows can recognise and remember about 50–70
other cows as individuals. This implies that in stable herds of about this size each
cow remembers its place and aggression is minimised except when new heifers
arrive and are treated as strangers. In many commercial units of today, herd size
can range from over one hundred to one thousand animals. There have been sug-
gestions that aggression may be greater in larger herds but provided there is good
management and the accommodation is designed to provide adequate trough
space, resting space and freedom of movement, I am not aware of any evidence
to suggest that large herd sizes increase the risk of socially unacceptable behav-
iour. It may also be easier for a heifer to merge unnoticed into a larger herd.
Sexual and Maternal Behaviour
Sexual behaviour was described briefly in the previous chapter and I shall in
Chapter 12 return to the important practical matter of recognition of oestrus from
behavioural and physiological indicators. There is an obvious case for keeping the
calf with its mother for the first 24 hours to give it the opportunity to take in as
much colostrum as possible while the intestinal mucosa is open for the absorption
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of gamma globulins. Milk continues to confer mucosal immunological protection

from alpha globulins in the days after closure has occurred. It is undeniable that
mother’s milk is best and some farmers permit their calves to join and feed direct
from their mothers for 2–3 weeks – and very well the calves look. Only allowing the
calves access to their mothers twice daily is not such a big departure from normal
behaviour since calves are a hiding species. Nevertheless, total severance of the calf
from its mother is always a stress and I am convinced that the stress is greater when
they have been in contact for long enough to establish a firm bond. When ‘tis done,
it were well it were done quickly’.
Behaviour as an Indicator of Welfare
Animal behaviour can be a powerful indicator of animal welfare. Perhaps the most
important examples of this are the behavioural indicators of pain and disease that
can, to a practised eye, be the first signs of a developing problem. Loss of appetite is
commonly the first sign of incipient disease. Limping and reluctance to move are
clear signs of pain, most commonly associated with lameness but may be caused by
other painful conditions such as mastitis. Other behaviours can provide indicators
of a cow’s emotional state as she seeks to cope with life. They may be seen as on a
‘spectrum’ (a word much used by psychiatrists of the day) with high anxiety or apa-
thy (learned helplessness) at the negative extreme, pleasure (or perhaps happiness)
at the positive extreme, contentment in the middle. Signs of anxiety should be easy
to recognise. Signs of apathy include failure to groom or indulge in social contact
with other cows. Signs of pleasure are probably few and far between in housed
cows. However, I always enjoy watching the behaviour of dairy cows when first
turned out to spring grass. Their running, bucking and mock fighting are, to my
mind, clear signs that they still have the capacity to experience pleasure. If the
response of the cows to turnout is apathetic then something must be seriously
wrong.
77
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Part II
Feeding the Dairy Cow

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79
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Nutrition: Supply and Demand
The aim of nutrition science is to produce a correct ration, defined by quantity and
composition, that balances supply with demand for all essential nutrients. The aim of
the dairy producer is to achieve the best possible gross profit margin from the sale of milk
relative to the cost of feed. In areas of the world where grass has been the most productive
crop it has been the tradition to obtain the maximum possible contribution from
home‐grown fresh and conserved pasture (grasses and clovers), supplementing this
basic ration with a balanced supply of other conserved forages (e.g. maize silage), root
crops, cereals and compound feeds (dairy cake) to provide a sufficiency of all nutrients to
meet demand for maintenance and milk production at all stages of lactation.
In recent years, this traditional approach (which occupied most of this chapter in
the previous edition) has, to a large and increasing degree, become outmoded as a
result of the development of the modern Holstein, a cow bred to live in a barn and
produce a quantity of milk that stretches the limits of her capacity to supply the mam-
mary gland with nutrients and certainly far exceeds her capacity to provide these
nutrients from a diet arising primarily from pasture. Figure 5.1 illustrates the propor-
tion of grazed pasture in the annual diet of cows in different parts of the world and
compares it with estimates of operating expenses. The values for the contribution of
pasture to the diet are entirely realistic. The values for the costs of production can only
be approximations and the relationship should not be interpreted too strictly.
However, Figure 5.1 does make the clear distinction between pasture‐based, low
input: low output systems in (e.g.) Ireland and New Zealand and barn‐based, high
input:high output systems in the intensive Holstein dairy factories of North America.
Nutrition strategies vary, therefore, according to the circumstances of the system.
Where the system is predominantly pasture based, the aim will always be to obtain
the maximum possible nutrient supply from pasture and other home‐produced
feeds, supplemented at higher cost with cereals, proteins, minerals and vitamins to
achieve the optimal balance between supply and demand for nutrients consistent
with the genetic capacity of the cows for milk production. In the high‐performance
Holstein barns, the aim is conceptually simpler, though not so easy in practice:
namely to devise diets (typically total mixed rations) that encourage the cows to eat

80 Nutrition: Supply and Demand
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100
90
80
70
60
50
40
30
20
10
0
K
g
ed
nd
lia
y
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s
d
in
ar
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us
an
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al
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st
ho
Fr
en
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D
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et
ew
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N
Figure 5.1 Proportion of grazed pasture in the diet (dark columns, %) and approximate
costs of production (light columns, US cents per litre), adapted from Roche (2017).
as much as possible of a selection of feeds combined in a mixer wagon to provide a

nutritionally balanced diet containing the highest possible concentration of metab-
olizable energy (ME) consistent with healthy digestion.
The intensification of dairy farming has thrown up a new problem that poses a
major threat to sustainability. It is no longer possible to assume that increased produc-
tivity is automatically a good thing. Feeding strategies for dairy herds can no longer be
evaluated simply in terms of providing the nutrient requirements to meet their genetic
potential for milk production; they must also take into account the environmental
damage that can accrue from rations (and concentrations of cows) that lead to the
excessive production and dispersal of waste products, especially nitrogen and phos-
phorus. In the Netherlands legal limits for these pollutants are already subject to leg-
islation. These issues will be addressed in Chapter 13.
A comprehensive description of the nutrient requirements of the dairy cow and
the nutrient composition of feeds for the dairy cow is beyond the scope of this book
or the needs of all but the most specialist reader. These days, ration formulation is
usually left to specialist nutritionists armed with the most up‐to‐date computer pro-
grammes. It is, however, proper that farmers, agriculture students and veterinary
surgeons should have enough understanding of the basic principles of nutrition not
just to know what the professionals are talking about but also to be able to recognise
unprofessional quacks, snake‐oil salesmen and others of their like. They do exist!
Practical nutrition has four main themes:
1) Nutrient requirements: description and prediction of the amounts of specific
nutrients required for maintenance, growth, pregnancy and lactation.
2) Nutritive value of feedstuffs: description and prediction of the amount of available
nutrients per unit mass of feed, typically expressed per kilogram of dry matter (DM).
Nutrient Requirements and Response 81
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3) Formulation of rations so that the available nutrients provided by the feed mix-
ture closely match nutrient requirements at least cost, promote appetite and
healthy digestion, and minimise the risk of disorders of digestion and
metabolism.
4) Aid the diagnosis and treatment of disorders of digestion and metabolism
through precise evaluation of the balance between nutrient supply and demand.
Nutrient Requirements and Responses
The procedure for assessing the nutrient requirements of any farm animal for any
productive function is illustrated in Figure 5.2. In the case of the dairy cow, the first
step is to assume a target, e.g. 35 kg milk/day for a group within the herd or for indi-
vidual animals, based on past records. The nutritionist then constructs a list of
requirements for energy, protein, minerals and vitamins to meet the target and for-
mulates a ration that will meet these requirements within the constraints of appetite
(DM intake, kg/day). This may start with an assessment of the nutrients available
from feeds grown on the farm (fresh and conserved pasture, maize silage, root crops,
cereals) then calculate the requirement for bought‐in supplements (e.g. compound
Animal management Appetite Crop management
FOOD INTAKE NUTRITIVE VALUE
AVAILABLE NUTRIENTS
NUTRIENT REQUIREMENTS
maintenance growth pregnancy lactation
target performance
Figure 5.2 Factors affecting nutrient supply and requirement.

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concentrate cake). In intensive systems where cows are housed, when most or all
their lactation and feed requirements significantly exceed that which can be produced
on farm, the aim will be to formulate a ‘total mixed ration’ (TMR), where all the ingre-
dients are combined in a mixer wagon and presented to the cows at the feed face. This
is undoubtedly a sound strategy when feeding high yielding cows with high energy
requirements since the quickly fermentable starchy feeds and slowly fermentable
fibrous feeds are presented together, thereby helping to promote stable rumen fer-
mentation and healthy appetites. In fact, cows do tend to sift through the mix and eat
first the bits they like best but not (I think) to an extent that does them significant
harm. Whatever the feeding strategy, the primary aim is to balance supply and
demand of ME because energy is the nutrient required in greatest abundance and
therefore the most expensive to provide. The ration is then balanced for protein, min-
erals and vitamins. When all feeds, including those not currently in use, are properly
described in terms of nutritive value and cost (pounds per tonne) the nutritionist can
provide the farmer with options for a ‘least cost’ ration, i.e. one that will maintain cur-
rent income from milk sales while reducing the cost of feeding.
The ability of a ration to meet nutrient requirements is defined (obviously) by DM
intake and the nutritive value of the DM. These two things are closely related. The
nutritive value of a forage crop such as grass silage can vary greatly according to
harvesting methods and weather at the time of harvesting. Silage quality affects not
only the amount of available nutrients per kilogram DM consumed, it also has a
major effect on appetite, through variation in palatability and rumen retention
time. Quickly fermented starchy cereals provide a high concentration of ME per
kilogram of DM and are very palatable to cows that don’t know better but, if pre-
sented in excess, cause rumen acidosis, that will, at the least, lead to a fall in appe-
tite. These things will be considered in more detail in the next chapter. Food intake
can also be encouraged by good design, the provision of sufficient space at the feed
face and good management to ensure that mangers are cleaned regularly and the
available food is always fresh.
Having formulated and fed the ration, the next step is to assess performance from
milk records to see how well they compare with target predictions. If performance
appears to be unsatisfactory, the farmer and his nutritionist, veterinary advisor, or
preferably both, should proceed through the nutrients in sequence to discover
where supply appears not to meet demand and the extent to which this may be
attributable to the quality or quantity of the food eaten. In the wise words of Roger
Blowey, ‘common things occur commonly’: poor performance is far more often due
to a lack of the major nutrient, ME, than to deficiency of a trace mineral, especially
in the case of dairy cows who receive generous amounts of the minor nutrients in
compound feeds. Other manifestations of poor performance, e.g. infertility, can be
examined in the same way to discover the extent to which they may be nutritional
in origin.
The concept of feeding to requirement for specific nutrients is fundamentally
sound because it seeks to maximise the efficiency of conversion of animal feed
into animal product. However, it should not be interpreted too rigidly. Tables of
Nutrient Requirements and Response 83
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nutrient requirement and nutrient composition, e.g. from the UK Agricultural

Research Council (1980) and US National Research Council (2004) are no more
than fair approximations to requirement for the average cow and less certain esti-
mates of the composition of the feeds offered. Inevitably, some cows will perform
better and some worse than expected. This means that, even when performance
appears to be on target, there may well be scope for improvement through changes
to the ration that further increase production without compromise to long‐term
health. In the recent economic climate (2019) higher (healthy) production has
almost always meant more gross profit. At the time of the previous edition (1993)
milk quotas were in force throughout the European Community and the aim was
to minimise feed costs. In the future, it appears likely that milk production from
cows in large herds will be restricted by environmental constraints, especially in
respect to nitrogen and phosphorus excretion. One of the few certainties in the
uncertain science of economics is that things change. Our understanding of how
to feed the dairy cow must embrace these changing terms of reference.
Two limitations of the factorial approach to calculation of nutrient requirements
are that it considers nutrients in isolation and that it calculates the least amount of
each nutrient required to meet a specified requirement, e.g. 30 kg milk/day. This
defines the optimal biological efficiency of conversion of (say) food protein to milk
protein, which will also be close to the optimal yield of milk protein relative to
nitrogen excretion in faeces and urine. It does not address the possibility that
increasing protein intake in excess of requirement might increase milk yield further
and therefore make more money, even though the extra protein is used at a lower
biological efficiency.
Figure 5.3 presents a schematic illustration of the effect on milk protein yield of
increasing protein concentration in the diet. The three curves depict increases in
milk protein yield (100 g milk protein = 30 kg Holstein milk) in response to increas-
ing the crude protein (CP) concentration of the ration from 120–180 g/kg DM when
the ME concentration (M/D) is 9.5, 10.5 and 11.5 MJ ME/kg DM. Assuming all
animals consume the same quantity of DM then M/D determines intake of ME.
When M/D = 9.5 the cow shows a production response to increasing protein concen-
tration up to 135 g/kg. Thereafter further increases in protein produce no further
increase in yield because ME supply is now limiting production and the extra protein
is now being used as an energy source. As ME supply is increased the cow can respond
to further increments in CP to the point where a diet rich in ME (M/D = 11.5) produces
peak yields when crude protein concentration is 160 g/kg. This concentration is likely
to be greater than that calculated from the factorial method for calculating nutrient
requirement and will undoubtedly increase N losses in urine and faeces. Whether it is
justified in practice will depend on the financial benefit accruing from the increased
yield relative to the cost of increasing CP intake. It is also important to stress that this
theoretical argument based on CP intake has been greatly simplified in the interests of
clarity. The real efficiency of conversion and partition of dietary CP between milk pro-
tein production and N excretion will depend on the efficiency of digestion and absorp-
tion of dietary CP (true protein and NPN) as metabolizable protein (MP) and the
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1200
1000 11.5
Milk protein yield (g/day)
800
10.5
600 9.5
400
200
0
120 130 140 150 160 170 180 190
Crude protein concentration in diet (g/kg)
Figure 5.3 Milk protein yield in response to increasing dietary crude protein
concentration at different levels of energy intake as determined by the ME
concentration in the dry matter (M/D, MJME/kg DM).
balance of essential amino acids therein. Advanced, computer‐based ration formula-

tions should take these things into account.
Nutrient Allowances for the Lactating Cow
The aim of good nutrition is to supply cows with the nutrients they need to ensure
optimal physiological state at calving, optimal milk production, satisfactory body con-
dition and good health throughout lactation and pregnancy, plus the probability of
long productive lives through maintenance of high fertility. Figure 5.4 illustrates sim-
ply the annual sequence of events for a dairy cow on a grassland/mixed farm in the
UK, calving in October. Peak yield (here 35 kg/day) is achieved 40–50 days into her
lactation. If all is well, she will display her first return to oestrus (standing heat) about
5–7 weeks after calving. Insemination to this first standing heat is seldom practised
since it is seldom successful. Here she is successfully inseminated at day 90 of lacta-
tion, turned out to pasture in the spring and calves again exactly one year later. After
100 days, her milk production will decline at about 1.5–2.0% per week, although in this
pastoral system we would expect to see a recovery in yield on turn‐out in the spring. An
average rate of decline greater than 2%, whether or not accompanied by loss in body
condition, suggests something is wrong with the nutrition. In this system, geared to
coincide with the seasons, the cow is dried off after 10 months lactation to give her two
months rest before her next calving. The aim in traditional pastoral systems is to keep
calving interval as close to 12 months as possible, to coincide with the seasons. Autumn
calving, as illustrated in Figure 5.4, has been traditional where I live in South West
England to obtain maximum input from conserved forage crops (spring grass and
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40
30
Milk yield (kg/d)
20
peak spring next

10 yield service turnout calving
100 200 300
+25
Energy (MJ/d)
–25
650
Weight (kg)
600
550
20
DMI (kg/d)
spring
10 turnout
100 200 300

Days of lactation
Figure 5.4 The sequence of events during lactation for a Friesian cow calving in the
autumn, housed over winter and turned out to grass in spring.
maize (corn) silage) and benefit from seasonality in milk prices. Spring calving,
designed to obtain maximum yield of nutrients from grazed pasture, is the norm in
Ireland and New Zealand. Where high yielding Holsteins are housed throughout lacta-
tion and fed TMR from a forage wagon, seasonality of production is of little conse-
quence. Optimal lactation lengths for such cows will be discussed in Chapter 12.
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In Figure 5.4 appetite (DM intake) is 10 kg/day before calving, rising to 17 kg/day
by day 40 of lactation. During this period, it is normal for cows to lose weight and
body condition. Figure 5.4 shows the initial loss from the calf and other products of
conception followed by a further loss of 40 kg over the next 40 days as the cow
‘milks off her back’. A Holstein‐Friesian cow that loses more than 40 kg during this
time is not receiving enough nutrients, although her milk yield at this time may
well meet or exceed expectations. A cow that loses less than 20 kg during this time
is almost certainly not giving enough milk. It is normal therefore for the daily bal-
ance of energy and other nutrients to be negative in early lactation and reach equi-
librium at about 100 days. Thereafter nutrient balance must be positive to ensure
she recovers lost tissue reserves and to provide all the nutrient requirements for her
next calf.
The physiological capacity of the high‐yielding dairy cow to direct nutrients into
milk in early lactation nearly always exceeds her capacity to supply the mammary
gland with ME and MP within the constraints of appetite. Feeding the cow in the
first half of lactation is a matter of ensuring that the nutritive value of the ration, its
palatability and presentation are all such as to promote maximum nutrient supply.
From mid‐pregnancy onwards the aim must be to ensure that cows don’t eat too
much and get too fat. The special business of feeding cows in the transition period
between drying off and next calving will be considered in detail in subsequent
chapters.
The calculations and tables of nutrient allowances that follow are drawn from UK
and USA publications on the nutrient requirement of dairy cattle. In drawing up
these tables a distinction is made between nutrient requirement and allowance.
Requirement describes the amount of nutrient required to meet a stated level of
production in the average cow and does not take into account individual variation.
The farmer who feeds to meet the requirement of the average cow, by definition,
underfeeds approximately half the cows in the herd. An allowance is defined as
the amount required to ensure that nearly all the cows in the herd receive at least
their requirement. In most cases allowances are calculated by increasing require-
ment by 5%.
Tables 5.1 and 5.2 present published values for nutrient allowances taken, respec-
tively, from the UK Agricultural Research Council (1980) and the more recent US
National Research Council (NRC 2001). Table 5.1 is essentially the same as that
which appeared in the previous edition, which is OK since our estimates of require-
ment for maintenance and per unit of production have not significantly changed.
What has changed, of course, is the quantity of milk produced by day by individual,
high‐performance cows. Table 5.2 (taken from NRC 2001) gives estimates of abso-
lute requirements for net energy, rumen degradable and undegradable protein for
Holstein and Jersey cows for yields consistent with modern intensive systems (i.e.
Holsteins 25 and 45 kg/day. In the USA, energy requirements are defined in terms
of net energy for lactation NEl, where NEl = 0.7ME, on the assumption that the net
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Table 5.1 Nutrient allowances for dairy cows (based on UK recommendations).
Jersey Guernsey Friesian Holstein
Body weight (kg) 350 450 600 700
Daily allowance for maintenance

Metabolizable energy (ME) 40 49 61 68
Metabolizable protein (g) 188 227 282 317
Calcium (g) 12 16 21 23
Phosphorus (g) 15 23 28 30
Magnesium (g) 5 7 9 10
Milk composition (g/kg)
Protein 37 37 33 33
Fat 49 49 37 37
Total solids 140 135 124 124
Allowances for milk production (/kg)

Metabolizable energy (ME) 6.0 5.7 5.0 5.0
Metabolizable protein (g) 60 56 53 53
Calcium (g) 3.2 3.2 2.8 2.8
Phosphorus (g) 1.7 1.7 1.7 1.7
Magnesium (g) 0.6 0.6 0.6 0.6
efficiency of utilisation of ME for maintenance and lactation is 0.7, as explained in

Chapter 2.
Table 5.2 includes recommended minimum values for neutral‐detergent fibre (NDF)
and maximum values for non‐fibre carbohydrates (NFC, i.e. starches and sugars) consist-
ent with diets designed to promote stable fermentation in the rumen. The range given for
these values are worryingly broad (25–33% for NDF, 36–44% for NFC). I would certainly
be concerned about the risk of rumen acidosis from diets formulated to the extremes of
25NDF/44NFC.
Tables 5.1 and 5.2 are intended only to illustrate the terms of reference used by
computer‐wielding nutritionists in the creation of models for the formulation of
rations for dairy cattle. In the previous edition I described in some detail the calcu-
lations used to create these models. This time I have left them out. They are pretty
heavy stuff and not essential to the producer, agriculture or veterinary student. All
you need to know is enough of the principles to be able to understand the specialist
nutritionist, and to be aware of the links between specific nutrients, production and
health and formulate intelligent ‘what if’ questions for the computers.
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Table 5.2 Nutrient requirement of Holstein and Jersey cows in mid lactation based
on USA recommendations (NRC 2001). Holstein = 680 kg body weight, milk fat 3.5%,
Jersey = 450 kg body weight, milk fat 4.2% (from NRC 2001). NDF = neutral detergent
fibre, NFC = non-fibre carbohydrate.
Holstein Jersey
Milk yield (kg/day) 25 45 25 35

DM intake (kg/day ) 20.3 26.9 18.0 21.7
Net energy, lactation 27.9(117) 41.8(176) 27.7(116) 35.6(150)
(Mcal(MJ) per day
Metabolizable protein 1862 2954 1991 2639
(g/day)
Diet %MP 9.2 11.0 11.1 12.2
Rumen degradable 1937 2636 1747 2125
protein (g/day)
Diet %RDP 9.5 9.8 9.7 9.8
Rumen undegradable 933 1677 1151 1632
protein (g/day)
Diet %RUP 4.6 6.2 6.4 7.5
NDF, min% 25–33 25–33 25–33 25–33
NFC, max% 36–44 36–44 36–44 36–44
Mineral Requirements
There are several ways of thinking about minerals. The nutritionist seeks to deter-
mine the specific elements involved in body form and function and determine the
exact amount of each that needs to be provided in the diet. The farmer and veteri-
nary surgeon only become concerned if requirement is likely to exceed that provided
by the major constituents of the diet. The manufacturer of compound feeds can
afford to err on the side of generosity unless the mineral is particularly expensive or
could prove toxic if fed to excess. UK recommendations for the major minerals are
given in Table 5.1. Table 5.3, based on data from NRC (2001) gives recommended
dietary concentrations for major minerals and trace elements, and compares them
with mineral concentrations in a typical forage (alfalfa grass) and concentrate (bar-
ley). Some of these values (e.g. iron and manganese) are significantly lower than in
NRC (1978) as reproduced in the previous edition of this book. Table 5.3 illustrates,
for example, that while cattle have substantial requirements for potassium and iron
it is most unlikely that they will in practice ever be short of either. For copper and
cobalt, on the other hand, supply from these basic feeds only just meets average
Mineral Requirement 89
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Table 5.3 Recommended mineral concentrations in total rations and in two feeds
for dairy cattle.
Concentrations
Concentrations in rations in feeds
Lactating
Dry cows cows Alfalfa Barley
Major minerals (g/kg DM)

Calcium 8.7 6.7 17.2 0.5
Phosphorus 2.6 3.5 3.1 3.6
Magnesium 1.6 2.8 2.7 1.4
Potassium 2.3 2.3 20.3 4.5
Sodium 1.0 2.2 1.5 0.3
Trace elements (mg/kg DM)

Iron 17 300 90
Copper 11 10 9
Cobalt 0.1 0.1 0.1
Manganese 13 50 20
Zinc 52 20 20
Iodine 0.4
Selenium 0.3
requirement, which means, inevitably that some of these feeds will fail to meet the
requirements of some of the animals.
Calcium is required in largest quantity to mineralise bone: at least 98% is contained
within the skeleton. The remaining 2% is essential to the initiation and maintenance of
nerve and muscle function. Thus, acute calcium deficiency is associated with neuro-
muscular failure (‘milk fever’, Chapter 7). Chronic calcium deficiency is associated with
bone weakness or osteoporosis. Grasses are good sources of calcium: alfalfa (lucerne)
and brassicae (kale and rape) are particularly rich; cereals and roots tend to be poor. The
physiological regulation of the absorption and secretion of calcium was discussed in
Chapter 2. There are several nutritional factors that affect calcium availability:
1) High calcium: phosphorus ratios in diets such as alfalfa predispose to the forma-
tion of insoluble (therefore not absorbed) tricalcium phosphate, (Ca3(PO4)2. While
this is unlikely to create a primary calcium deficiency, it could predispose to a
phosphorus deficiency.
2) High fat diets, e.g. protected fats for high‐yielding cows, can reduce calcium
availability by forming insoluble soaps.
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3) High dietary intake of vitamin D3 can assist the physiological mechanisms

involved in calcium uptake.
4) High concentrations of organic ions, especially phytates in cereals can form
complexes that reduce the true availability of calcium in simple‐stomached ani-
mals like pigs and humans, and hind‐gut fermenters like the horse. This is not,
however, a problem for ruminants since the rumen organisms contain phytases
that break down phytates before entry to the small intestine.
Clinical problems associated with deficiencies of calcium, other minerals and
trace elements will be considered in Chapter 7.
Phosphorus is also primarily required to mineralise the skeleton and about 75% is
contained in bone. It is also the essential element of adenosine triphosphate (ATP),
the energy currency of the body. Protein‐rich feeds such as soya and groundnut are
relatively rich in phosphorus. Cereal grains and cereal offals (e.g. wheat bran) con-
tain phosphorus mostly in the form of phytates that are of very low availability
unless degraded by rumen microorganisms. Grasses and forages are low in phos-
phorus and get lower as they mature. The animals most prone to phosphorus defi-
ciency are those that get nearly all their nutrients from grass, e.g. growing heifers
and some low‐input, low‐output lactating cows in pasture‐based systems.
Magnesium is in reasonably plentiful supply in most cattle feeds. Magnesium
levels may be low in young spring grass and availability can be reduced by two
factors relating to the practice of applying fertilisers early in the growing season
to promote high crop yields. High levels of protein in spring grass or NPN from
fertiliser lead to rapid production of ammonia in the rumen and the formation of
insoluble magnesium‐ammonium phosphate (MgNH4PO4.6H2O). Magnesium
availability can also be reduced by the application of potassium‐rich fertilisers. It
is important for dairy farmers to delay the application of potash fertilisers until
after the high‐risk period for magnesium deficiency (‘grass staggers’) is over.
Potassium is plentiful in all green feeds.
Sodium is relatively deficient in most cattle feeds. It is essential for maintenance
of the volume of blood and extra‐cellular fluid. Moreover, cattle like the taste of salt
(NaCl) and it is included in compound feeds partly to increase palatability. Where
dietary sodium concentrations are especially low, typically a long way from the sea,
cattle will travel many miles to salt licks. On a dairy farm, they are cheap and easy
to provide – and very attractive to the cows.
The nutritional importance of the vitamins and trace elements, especially copper,
cobalt and selenium, will be considered in Chapter 7. Iron, manganese and zinc are
essential elements for metabolism, but deficiencies are seldom likely to occur in
practice. Iodine deficiencies can occur, usually, as with sodium, far from the sea.
Nutritive Value of Feeds
Having formulated the quantity of specific nutrients required to meet the needs
of the dairy cow for maintenance, pregnancy and lactation, it is necessary to
define the nutritive value of the available feeds using the same currency.
Nutritive Value of Feed 91
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Publications from the various agricultural services provide comprehensive tables

of nutritive value. Table 5.4 lists nutritive values of some of the more common con-
stituents of dry feeds used in dairy cow rations, expressed in terms most used in
modern ration formulations in the UK: ME and FME, CP, ERDP and DUP, calcium
and phosphorus. It also includes values for concentration of neutral‐detergent fibre
(NDF), to aid formulation of rations that contain at least the minimum concentra-
tion of NDF to minimise the risk of rumen acidosis (>300 g/kg). Cereals are high in
energy, and low in protein and NDF. The oil seed cakes and meals are fed primarily
as protein supplements. The miscellaneous by‐products include sugar beet pulp,
maize gluten feed, brewers’ and distillers’ grains, all good sources of energy, protein
Table 5.4 Nutritive values of some common constituents of dry feeds for dairy cattle.
All are assumed to have a DM concentration of 900 g/kg.
ME FME CP ERDP† DUP† Ca P

(MJ) (MJ) (g) (g) (g) (g) (g) NDF
Cereals
Wheat 13.6 12.9 115 95 8 0.3 0.4 140
Barley 12.8 12.3 114 89 14 0.4 0.4 210
Oats 12.1 10.7 105 82 5 1.0 3.0 300
Oil cakes and meals

Cottonseed meal 12.5 11.2 486 301 133 1.9 12.4 310
(dec)
Groundnut meal 13.7 11.3 570 386 131 1.6 6.3 210
(dec)
Soyabean meal 13.3 12.7 497 315 145 4.5 7.6 150
Rapeseed meal 12.0 10.8 400 288 57 4.2 8.3 180
Linseed cake 13.4 10.4 334 177 118 4.0 8.0 360
Miscellaneous
by‐products
Brewers’ grains 11.7 9.0 249 91 120 3.3 4.1 470
Maize distillers; 14.7 10.9 317 159 50 3.0 3.8 390
grains
Maize gluten feed 12.7 11.5 207 141 31 0.4 3.4 360
Maize gluten meal 17.5 16.4 666 244 358 1.6 5.0 110
Sugar beet pulp 12.5 12.3 103 49 38 10.0 3.0 460
(mol)
Dairy concentrate* 13.0 12.1 180 108 50 8.0 6.0 350
*
An arbitrary but common value included for use in ration formulation exercises.
†
ERDP and DUP are calculated at a rumen outflow rate of 0.05/hour.
NDF = neutral‐detergent fibre; dec= decorticated; mol = molassed.
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and a healthy amount of NDF. Maize gluten meal, which is expensive, is used in
small amounts as a protein source. The biological value of the protein in maize glu-
ten for simple‐stomached animals is very low due to deficiencies of the major
essential amino acids. However, this is of less importance for ruminants because
about 40% is as ERDP and the poor quality of the DUP is offset by the excellent
amino acid balance of microbial protein.
Table 5.5 gives approximate values for common bulk feeds. Two values are given for
fresh grass, spring grass with an apparent digestibility (D value) of 75–80% and summer
grass with D value 60–65%. The values for maize silage, excellent and moderate grass
silage refer to that stored in clamps. Big‐bale grass silage, harvested when more mature
has a lower ME value. Note that the ME values of maize silage and excellent grass silage
are greater than that for fresh summer grass. From the discussion of rumen fermentation
and N degradation in Chapter 2, one can approximately calculate the optimal ratio of
ERDP to FME in the diet as 9–11 g ERDP/MJ FME. The values in Table 5.5 give
ERDP:FME ratios of 15.3 for excellent grass silage and 13.7 for fresh grass. This imbal-
ance in grass silage is exacerbated by the fact that much of the CP is in the form of NPN,
thus QDN, and this is clearly acknowledged when formulating TMRs. It is less well rec-
ognised that spring grass, especially when heavily fertilised to grow in abundance, is also
an unbalanced feed, not perhaps enough to create digestive problems or a fall in appetite,
but certainly enough to cause a significant increase in N excretion, thereby contributing
to potential problems of pollution.
Table 5.5 Typical nutritive values per kilogram of dry matter (DM) of some common
bulk feeds for cattle.
DM ME FME CP ERDP† DUP† Ca P

(g kg–1) (MJ) (MJ) (g) (g) (g) (g) (g)
Fresh grass, 75–80 D 200 12.3 11.4 156 116 22 6.5 3.0
60–65 D 200 9.8 9.1 98 59 26 6.0 2.5
Grass silage, excellent 280 11.4 8.9 175 115 20 6.5 3.0
moderate 240 10.4 7.9 160 05 18 6.0 2.5
Big bale silage 280 9.9 7.9 109 71 20 5.5 2.0
Maize silage 240 11.2 9.0 86 55 5 4.0 3.0
Grass hay 850 8.5 7.3 85 45 20 4.0 2.0
Alfalfa hay 850 0.5 8.3 190 112 25 17.0 3.0
Barley straw, spring 860 7.0 6.5 36 21 0 3.5 1.0
Kale, marrowstem 140 11.0 10.2 160 118 22 21.4 1.0
Swedish turnip 110 13.0 12.4 110 81 10 2.0 1.5
Fodder beet 180 12.6 11.9 60 45 5 1.5 1.5
†
ERDP and DUP are calculated at a rumen outflow rate of 0.05/hour.
Ration Formulatio 93
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Ration Formulation
Prediction of Food Intake

The first step in the formulation of rations for dairy cows is to predict the energy
density (ME in DM, or M/D) necessary to meet requirement within the limits of
food intake. The calculation is based on an estimate of DM intake. This presents a
problem since published estimates of DM intake vary widely and are, in my view,
extremely unreliable. The estimate I gave in the previous edition (1993) was based
on that proposed then within UK namely,
DMI kg / day = 0.025W kg + 0.1milk yield kg .
The more recent (2001) equation from NRC (USA), simplified slightly, is
DMI kg / day = 0.1W 0.75 kg + 0.38FCM kg

where FCM = fat corrected milk. Note that these two equations differ widely in
their estimate of the effect of increasing milk yield on appetite. Using the estimates
in Table 5.1 of ME requirements for maintenance and production, we get the
following.
Jersey, 350kg, 25L milk/day Holstein, 700kg, 50L milk/day
ME requirement (MJ) 190 318

DMI (kg/day), UK 14.0 22.5
DMI (kg/day), USA 18.5 32.5
M/D requirement, UK 13.5 14.1
M/D requirement, USA 10.2 9.8
The old UK value is certainly out of date and was never very realistic. By basing
maintenance requirement on body weight, rather than metabolic body weight
(W0.75), it failed to take account of the cattle ranging in body weight from the 350 kg
Jersey to the 700 kg Holstein. Moreover, the predicted increase in DMI with increas-
ing milk yield was only 0.1 kg. In consequence, the UK equation calls for a ration
with an M/D of 13.5 for the Jersey and 14.1 for the Holstein. Inspection of Table 5.4
shows that this could barely be achieved with a ration formulated exclusively from
concentrates; i.e. it clearly underestimates what happens in real life. The NRC equa-
tion is better. It calculates maintenance requirement according to W0.75 and esti-
mates that DMI increases at 0.38 kg/kg fat‐corrected milk. This gives estimates more
in line with what happens at the feed face although, in my opinion, probably goes too
far in the other direction. It predicts that the Holstein cow could sustain a yield of
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50 kg/day on a ration in which M/D = 9.8. Table 5.5 indicates that this could be
achieved by a diet consisting entirely of moderate grass silage. This is clearly ridiculous.
All this raises the question as to whether it is, in practice, necessary to attempt to esti-
mate DMI. It is, at best, only an estimate of the average intake of the animals in the
group. Cows that sustain higher yields than predicted from DMI and M/D must be
eating more than predicted since all the nutrients must come from somewhere.
When feeding high genetic merit Holstein (or Jersey) cows in barns and at peak
yield, the aim will normally be to present a TMR formulated to sustain the highest
possible intakes of ME and MP. The critical word here is ‘sustain’. Sustained maxi-
mum intake of ME is achieved by formulating a ration with the highest possible
M/D consistent with sustained high appetite and healthy digestion. This is why the
NRC recommendations for minimal NDF and maximum NFC (Table 5.2) are so
important. It is possible to formulate rations with M/D > 11 MJ/kg DM and NDF
>30% for example, through the incorporation of by‐products such as maize gluten
feed or sugar beet pulp that are high in NDF (Table 5.4).
Assessment of an Existing Ration
Whether the diet is fed in the form of a TMR or based on more traditional feeding
practices involving a mixture of fresh or conserved pasture, supplemented by con-
centrate mixtures, it will be necessary to evaluate the ration to see whether current
milk yield, rate of decline in milk yield and other indices of performance, e.g. body
condition and fertility, are in line with expectations. To give a traditional example:
consider a group of Friesian cows, weighing approximately 600 kg and giving an
average yield of 27 kg/day. They are receiving moderate silage ad libitum plus 3.0
kg/day hay. A dairy cake is fed in parlour at 0.4 kg/kg milk in excess of 10 kg milk/
day (i.e. 6.8 kg). Using values from Tables 5.4 and 5.5 plus (uncertain) estimates of
DMI we can set down the supply of nutrients as follows.
Nutrients per day (MJ or g)
DM intake (kg/day) ME FME ERDP DUP MP Ca P
Dairy cake 6.1 79.3 73.8 659 305 726 49 37

Hay 2.6 22.1 19.0 117 52 126 10 5
Silage (9.3) 96.7 73.5 976 167 791 56 23
Total (18.0) 198 166 1752 524 1643 115 65
Requirement 196 1713 97 74
Balance +2 68 +18 9
In this calculation, MP from ERDP is assumed to be 0.64. This ration closely

matches requirements for ME, which is hardly surprising since that is what it was
Feeding Plans for Dairy Cow 95
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formulated to do. MP supply is slightly but probably not significantly below

requirement. However, this is only the beginning. Three questions arise at once.
‘Are the cows able to sustain milk yield on this ration?’
‘Could they do better?’
‘Could I feed them more cheaply?’
The answer to the first question may well be yes. However, if the cows are failing
to sustain yield, the problem lies almost certainly with the grass silage. Either the
nutritive value has been overestimated, or intake is below expectations, or probably
both, since silage that is poorer than expected tends to be less palatable.
‘Could they do better?’ The first limitation to milk yield in the short term is usually
metabolizable protein. When MP is in plentiful supply, cows may ‘milk off their
backs’, draw on body energy reserves to supplement a shortage of ME and lose body
weight. If this continues then condition may deteriorate to the state where milk yield
cannot be sustained and fertility falls. In this example MP supply is marginal so there
is a case for increasing supply, most simply by increasing the protein concentration
in the dairy cake. If this does achieve a significant increase in yield that justifies the
additional feed costs, it then becomes necessary to monitor the cows closely for signs
of a relative deficiency of ME, i.e. loss of body condition and reduced fertility.
Could I feed them more cheaply? In this new edition of ‘Understanding the Dairy Cow’
I hesitate to give costed examples of alternative feeding strategies because the econom-
ics of dairying are so variable and uncertain, across both time and space. However, the
indicators of economic returns, such as ‘margin over concentrates’ and ‘margin over all
feeds’ are robust (or as robust as the data used to generate them). It is normal to include
these estimates in any feed plan. The people who sell the dairy cake will, in their own
interests, have prepared their compound feed according to a least‐cost ration formula-
tion. The most effective use of this information at farm level comes at the strategic plan-
ning stage; the prime question being ‘to what extent can I achieve my output target at
least cost throughout the year through best use (and choice) of home‐grown feeds?’
Feeding Plans for Dairy Cows
The main items of information necessary for a farmer and nutrition advisor or feed
supplier to draw up a feeding plan are as follows.
Inputs
Average cow weight.
Predicted weight change in early, mid and late lactation.
Average milk yields and composition.
Adjustments to standard predictions of appetite to account for feeding practice, e.g.
TMR, ‘out of parlour’ feeding, apparent low palatability of grass silage.
Availability of home‐grown feeds, their nutritive value and estimated cost of
production.
Milk price (pence per litre).
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Outputs
‘Best buys’ within available range of bought‐in concentrate feeds: cereals and
by‐products.
Raw materials needed to produce ‘best buy’ compound feed. For obvious reasons
this information is normally restricted to the supplier.
Recommended rations for groups of cows (or individuals) according to milk yield
and stage of lactation.
Calculated nutrient balance in terms of ME, ERDP and DUP.
Economic analysis of costs and margins using recommended ration.
Economic value of alternative feeds.
Table 5.6 presents an example of some of the most important information that
can be obtained from a computer print‐out in a form that can be given to, discussed
with, and understood by a dairy farmer. While the numbers here have been created
by me, the programme closely follows the protocol used by the Kingshay Dairy
Manager Scheme as applied to the dairy herd owned by my immediate neighbour
Clive Snell in the South West of England. I acknowledge my gratitude to both.
Table 5.6 summarises values for milk production, feed use and profit margins over
purchased feeds (MOPF) per cow and per litre. The three columns show figures for
June, a summer month with the cows at pasture, January, when the cows are
housed, and the rolling values for annual performance (production over the preced-
ing 12 months). The values for MOPF are, of course, critical to the producer, but of
less importance to our general understanding of the principles of good nutrition,
since they are so susceptible to volatility in the price of milk and purchased feeds.
The critical points to be derived from Table 5.6 relate to the evaluation of the extent
to which the dairy farmer can produce milk from the resources available on farm.
The ‘annual’ column in Table 5.6 reports that the average annual yield per cow in
milk was 8250 L. Approximately half (49%) was obtained from home‐grown forage,
of which 55% was grazed and 45% conserved. Total concentrate use for the year
was 2215 kg/cow or 0.27 kg/L. In this example I have assumed that the only concen-
trate fed during the summer months was dairy cake; in the winter the cows
were given 2 kg/day maize gluten feed as a lower‐cost source of ME and MP. In the
summer month, with the cows at grass 56% of yield came from grazed pasture and
concentrate use was 0.20 kg/L. In the winter, 35% yield came from home‐grown
feeds, in this case a mixture of grass silage, maize silage and fodder beet (not a for-
age but a home‐grown feed nevertheless). This example addresses issues that are
most important for a traditional, pasture‐based, dairy farm. Other issues which the
farmer and nutritionist could consider are the extent to which the cost of purchased
feed could be reduced by greater use of ‘straights’ (e.g. beet pulp, brewers’ grains)
relative to compounded dairy cake. The most important aim, of course, must be to
maximise the margin of income from milk sales over all feeds, purchased and home
grown (MOAF). This requires accurate estimates of the true costs of producing
feeds on farm, (e.g. fertiliser, fuel, labour and amortisation on farm machinery).
These are outside the scope of this chapter, or indeed my competence.
Allowances for Growing Heifer 97
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Table 5.6 An example of performance statistics for milk production, feed supply
and profit margins (income from milk over purchased feeds) for a pasture-based dairy
farm milking Holstein-Friesian cows.
June January Annual
MILK PRODUCTION
Yield/cow in milk 28.4 L/day 25.7 L/day 8250 L
Yield from all forage 16 L/day 9 L/day 4070 L
Yield from grazed forage 16 L/day 0 L/day 2250 L
% total yield from forage 56 35 49
Milk price (pence per litre) 27.5 33.0 30.2
FEED
Total concentrate use 5.6 kg/cow Day 9.2 kg/cow Day 2215 kg
Total concentrate use (kg/L) 0.20 0.36 0.27
Dairy cake price (pounds per 240 240 240
tonne)
Other purchased feed cost 0 8.2 4.5
(pounds per cow)
All purchased feed cost (pence 5.68 7.93 6.46
per litre)
MARGINS
MOPF per cow £195/month £183/month £1940/year
MOPF per litre (p) 22.1 23.7 23.2
In intensive systems where relatively little feed is likely to be produced on

farm, cows are housed and fed TMRs for most or all of the period of lactation, the
inputs will differ but the aim will be the same, to achieve the best profit margin
over all feeds. In this case ration formulation will be based on detailed analysis
to include not only nutrient supply from all available sources measured in terms
of ME, ERDP, DUP and major minerals, but also diet quality, in particular, limit
values for minimum concentration of dietary fibre (NDF) and maximum con-
centration of quickly fermented non‐fibre carbohydrates (NFC, Table 5.2).
Allowances for Growing Heifers
In areas where heifers are raised mostly at pasture, and even when they are
reared indoors, there is little call for complex ration formulation. However, it is
important to ensure that feeding is controlled to ensure that heifers conceive and
calve down at the desired time. Table 5.7 lists targets for daily weight gain and
end‐weights for Holstein‐Friesian calves either autumn‐born and reared to calve
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Table 5.7 Target weights and daily gains for rearing dairy heifers and concentrate
allowances for growing calves.
Targets Concentrate ration
Daily gain (kg) End weight (kg) (kg/day)
Autumn‐born heifers to calve at 2 years

3–6 months 0.55 140 1
6–12 months 0.71 270 zero
12–18 months 0.55 370 1–2
18–24 months 0.77 510 zero
Weight at service 330
Spring‐born calves to calve at 2.5 years

3–6 months 0.55 140 1
6–12 months 0.38 210 1
12–18 months 0.66 330 zero
18–24 months 0.33 390 0.5–1
24–30 months 0.77 530 zero
Weight at service 360
at 2 years of age or spring‐born and reared to calve in autumn at 2.5 years of age.
The aim is to feed as little expensive concentrate as possible. The table includes
the approximate amounts of concentrate that may be necessary to supplement
forage provided ad lib to heifer calves while housed over winter. For the first six
months the concentrate ration should contain 180 g/kg crude protein and be
generously supplemented with minerals. Calves over 200 kg require about 14%
crude protein (CP) in their concentrate feed if the forage is hay. If they are given
grass silage, the CP concentration should not exceed 120 g/kg, which makes it
possible to feed straight cereals such as rolled barley. The quantity of concentrate
feed necessary to achieve targets weight gains is best determined from observa-
tion of body composition and (ideally) records of weight gain. It should, for
example, be possible to achieve 0.33 kg/day weight gain in 18 month old heifers
from silage alone if the quality is good.
One note of caution. The more reliance that is placed on home‐grown forage and
straight cereals the greater the risk of mineral deficiencies. This can be avoided by
sprinkling 50 g/day of a mineral supplement over the forage. Specific problems of
trace element and vitamin deficiencies will be considered in Chapter 7.
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Feeds and Feeding Strategies
The most precious attribute of the dairy cow is her ability to produce food of the
highest nutritional value for us from pasture that we cannot eat ourselves. Grazing
land constitutes more than 50% of total land available to agriculture so it is ecologi-
cally unrealistic to conceive any scenario for feeding the world that, by removing
the food animals from the equation, removed half the land as well. In Chapter 1,
I discussed the ethics and sustainability of animal‐based farming systems and will
return to the subject in more detail in Chapter 13. At this stage I shall simply recall
the fact that the dairy cow can produce significantly more food energy and protein
for humans than she consumes in the form of food directly available for human
consumption (see Table 1.4.)
Traditional dairy farming has been inextricably linked to areas where pasture (typ-
ically grasses and clovers) has been the most productive, sustainable and therefore
ecologically sensible crop for most of the land, most of the time. Here, the aim is to
maximise the contribution of pasture to milk production and minimise the depend-
ence on bought‐in feeds, typically concentrate mixtures (dairy cakes). Even in the
most intensive systems, where cows are housed throughout lactation, the bulk of the
ration is likely to be based on forage crops such as grass, lucerne (alfalfa) and whole
crop maize (corn). Thus, in nearly all systems, metabolisable energy (ME) will be
provided from a mixture of fresh and conserved forages, sources of slowly digestible
fibre (cellulose and hemicellulose) supplemented with quickly fermented starches
from cereals and sugars from root crops.
When the price of milk is high relative to the cost of concentrate feeds then it
may appear economic for the producer to provide as much as 70% of ME require-
ment in the form of high starch, high energy feeds, the limit being defined only by
the need to ensure that fibre (NDF) levels are not too low, nor non‐fibre carbohy-
drates too high (Table 5.2). In pastoral systems like New Zealand, where the price
of milk sold on the world market is relatively low, then the optimal contribution of
concentrate feeds will be much lower (Figure 5.1). At the time of writing the sec-
ond edition of Understanding Dairy Cows, milk quotas were in operation through-
out the European Community and the general aim was to devise rations to meet a

100 Feeds and Feeding Strategies
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fixed output at least cost. These quotas are no more. However, the basic aim within
all systems remains the same: to achieve the maximum profit from the sale of milk
relative to all costs (net profit margin). Since a large proportion of total costs is
unrelated to the cost of feed (e.g. labour, amortisation on buildings, etc.) it follows
that the more expensive feed that produces more milk may be the preferred option,
especially in intensive systems where the expenditure on housing, feed and manure
handling is high.
This chapter is not, however, directly concerned with profit margins. The biologi-
cal issue is how to provide nutrient requirements within the constraints of appetite
(DMI). The primary question is not therefore ‘how much concentrate should I feed
in addition to the basic forage ration?’ but ‘to what extent should I substitute a con-
centrate ration for pasture or forage to meet nutrient requirements?’. This chapter
considers the many feeds available to dairy cattle and discusses how they may be
used in practical feeding strategies to maximise the biological and economic effi-
ciency of nutrient use.
Pasture
Fresh young pasture, for example a five‐year lea of perennial ryegrass and clover,
would appear at first sight to be the ideal feed for dairy cows. It is rich and reason-
ably well balanced in energy and protein, healthy, highly palatable and keeps on
growing, so in the right climate and over a good growing season can yield more ME
per hectare than any other crop. It does, however, have its limitations. Few, if any,
high genetic merit dairy cows can sustain their metabolic capacity for milk produc-
tion simply from grazing even the best of grasses. There are not enough hours in the
day for them to take in enough food to meet their energy requirements for mainte-
nance and production. High genetic merit American Holsteins kept in barns
throughout lactation can consume much more ME when it is brought to them at
the feed face: time at pasture is seen as time wasted.
Another problem with pasture grasses is that, with increasing maturity, yield
increases but nutritive value falls. Figure 6.1 illustrates the effect of season on yield
and nutritive value of two grass species, perennial ryegrass, a high‐yielding, early
maturing grass, and meadow fescue, a lower yielding, later maturing cultivar.
Given reasonable growing conditions in the UK, perennial ryegrass outperforms
other grass species, yielding about 12 t dry matter (DM) per hectare by mid‐June;
in UK normally the time for the hay harvest. During the period of growth to this
point the proportion of fibre has increased and this has reduced digestibility, con-
ventionally defined by D value, which describes the in vitro digestibility of organic
matter in the dry matter (DOMD). In Figure 6.1 ryegrass cut for hay in mid‐June
yields 11 t DM at a D value of 60%, giving 0.6 t of digestible organic matter (DOM)
with a CP concentration of 80 g/kg. Grazed, or cut for silage on 20 May, it yields 5
t DOM at a D value of 67% and a crude protein concentration of 130 g/kg. Meadow
fescue is later maturing as assessed by the time taken for the emergence of the
Pastur 101
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Yield (tonnes/ha)
10
12
2
8
20
Perennial ryegrass
April
30
D
10
0.5 E
May
DM
20
CP
DOM
30
June
9
19 20
Meadow fescue
April
30
D
10
May
20
30
DM
DOM
CP
0.5 E
June
9
19
50
100
150
200
250
55
60
65
70
75
Crude protein (g/kg) D value (%)
Figure 6.1 The effect of season on yield and nutritive value of two grass species,
perennial ryegrass, a high-yielding, early maturing grass, and meadow fescue, a lower
yielding, later maturing cultivar.
‘ears’ or seed heads. It has a higher CP concentration than perennial ryegrass but a
much lower yield. Moreover, the D value declines with the advance of the season
in a similar fashion to ryegrass. Fescues and other grass species such as cocksfoot
and timothy can usefully be incorporated into grazing pastures to provide a more
even supply of ME and CP well into the summer months but Figure 6.1 makes it
easy to understand why perennial ryegrass is a preferred species for grass crops
conserved as hay and especially silage. Re‐inspection of Table 5.5 shows that first
cut ryegrass silage is richer in ME and CP than ryegrass grazed in mid‐summer.
The ‘best’ grasses tend to contain an excess of CP (more specifically RDN) with
respect to fermentable energy. This imbalance is greater when the grass is conserved
as silage since this involves almost total loss of QFE (Figure 2.8). This leads to
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increased concentration of urea in blood, urine and milk. An elevated concentration

of urea in a milk sample may be associated with reduced appetite. It is also an indica-
tor that too much dietary N is being wasted and potentially contributing to environ-
mental pollution. Recent years have seen the development (especially at Aberystwyth)
of new cultivars of ‘high sugar’ grasses, better balanced with respect to QFE and
ERDP. A strong case can be made for growing these grasses as the source of top qual-
ity silage. Their potential for incorporation into grazed pastures is more equivocal.
Much of the sugar is in the stem rather than the leaf and may not be taken up by the
grazing action of the cow. This may partially explain why the performance of cows
on these high‐sugar pastures can be lower than on more conventional leys.
Grazing Strategies
The production of milk from cows let out to free‐range verdant pastures would
appear to be the most natural and, at first sight, the most economic thing in the
world. Would that it were so simple. Left to their own devices, cows use pastures
indiscriminately as a source of food, a bed, a footpath and a latrine. The aim of good
pasture management is to maximise the number of nutrients (principally ME) that
cows can derive from pasture, grazed and conserved, throughout the growing sea-
son. This is determined by the nutritive value of the pasture and the amount that the
cow can eat in the time available. Young, rapidly growing spring grass should have
an ME concentration (M/D) of 12 MJ/kg DM and a CP concentration of 160–180 g/
kg DM. In terms of these major nutrients this should provide enough to sustain
maintenance plus 30 kg milk/day for a large Holstein cow. Intake of nutrients is
greatest when sward length is between 10 and 15 cm.
Grazing strategies are, in practice, a compromise between the need to get the
most out of grass and the exigencies of time and expense.
Strip grazing is the method whereby each day, or between each milking, cows are
given access to a new strip of fresh grass, the access being controlled by moving an
electric fence down the line of the field. This method is particularly effective for the
first growth of high‐quality spring grass since the cows mostly lie and defaecate on
areas of the field that have previously been grazed down. Later in the summer, when
the quality of the pasture will be poorer, strip grazing may not be worth the effort.
Rotational grazing describes the practice of moving the herd from pasture to pas-
ture to give the grass time to recover (and to control parasitic roundworms). Cows
are turned out into a paddock for, say, two weeks or, more precisely, until the avail-
ability of grass is reduced to the point below which intake will decline (average
sward height <8–10 cm) and then moved on. Pastures may be rested for 4–8 weeks
according to the rate of regrowth.
Set stocking involves stocking the pasture with the right number of cows to ensure
a good match between consumption and regrowth. When rainfall is adequate, the
stocking rate in summer will be about 60% of that during the period of maximum
growth in spring. However, these pastures become increasingly covered by faecal
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pats, which encourage patchy growth of green, rich‐looking grass but which the
cows are reluctant to eat. A pasture that was continuously set‐stocked all summer is
likely to become a complete mess.
In practice many farmers operate a grazing strategy that owes something to each
of these measures, for example strip grazing the young spring grass then adopting a
mixture of rotational grazing and set stocking during the summer months. In the UK
it is also common practice to bring sheep on to cattle pastures in the autumn to tidy
things up.
On/off grazing. This, in theory, is probably the most efficient way of maximising
the contribution of grazed pasture to meeting the nutrient requirements of high‐
performance, intensively managed dairy cows. It has been shown under experi-
mental conditions, and when sward height is optimal (10–15 cm), that cows milked
twice daily will consume as much grass in two three‐hour periods as when at pas-
ture throughout the entire period that they are not in for milking and feeding in
parlour. In other words, to the producer aiming for maximum possible yields, time
spent at pasture not eating (e.g. resting, socialising and generally seeing the world)
when they could be in the yard and at the feed face is time wasted. The ME require-
ment of high genetic merit Holstein cows at peak lactation may be twice that which
they could meet from the best of pastures and is unlikely to be met by pasture plus
concentrates fed only in parlour, so this makes commercial sense when assessed
strictly in nutritional terms. However, the ancillary costs of manure handling and
moving the cows around suggest that it may not be worth the effort. There is an
excellent case, on nutritional grounds, for incorporation of fresh grass in the total
mixed ration of high yielding, intensively housed cows. However, in these circum-
stances, it probably makes more commercial sense to use machinery to cut and
carry the grass to them.
Table 6.1 Calculation of utilised metabolizable energy (UME, GJ/year) from pasture.
Average production figures

Cow weight = 600 kg. Yield 5500 kg milk plus one 50 kg calf
Concentrate intake = 1 t. Grassland = 0.5 ha per cow
Annual ME requirement GJ
Maintenance + pregnancy 26.2
Lactation (5000 kg at 5 MJ/kg) 27.5
Total 53.7
Annual ME supply
Concentrate (900 kg at 13.2 MJ/kg DM 11.9
ME from pasture (grazed and conserved) per cow 41.8
Utilised ME per hectare 83.6
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The contribution of pasture to milk production can be calculated in terms of

utilised metabolizable energy (UME) per cow or per hectare per year. The units of
UME are usually expressed in gigajoules (103 MJ). Table 6.1 presents an example
of the calculation of UME from grazed and conserved grass for a herd aiming for
relatively modest yields (by modern standards) but wishing to maximise the con-
tribution of home‐grown feeds. The first step is to calculate annual requirement
for ME per cow, then subtract ME intake from dairy cake and other purchased
feeds to estimate UME from pasture. In this example the average cow is getting
41.8 GJ ME from pasture, or 78% of requirement. If the cows had eaten 2 t of pur-
chased feed only 56% of requirement would have been met from pasture. It is, of
course, possible to subdivide ME from pasture into that from obtained from graz-
ing and that eaten as conserved forage. Suppose the cows in Table 6.1 consumed
2.2 t of silage DM having an M/D from October to April, this would amount to 22.9
GJ ME from silage and 18.9 from summer grazing.
The attraction of the UME calculation is that the farmers can assess the perfor-
mance of their cows from year to year against the performance of other farms in the
area, and also evaluate the consequences of any changes in feeding strategy.
Legumes
Alfalfa or lucerne (Medicago sativa), a high‐yielding, nutritious legume, is the most

important green food for cattle in dry, tropical and sub‐tropical environments. Fresh
alfalfa can be grazed but is more commonly conserved or cut, carted and fed fresh
to cattle while the crop is at the optimal stage of growth. At best, it contains about
9.5 MJ ME and 190 g CP per kg DM. Lucerne is also rich in calcium and magne-
sium. Most of the nutrients are contained in the leaf. The stem is fibrous and indi-
gestible, which means that the D value falls sharply as the plant matures. Moreover,
lucerne hay, fed in racks, tends to shatter: the nutritious leaves fall out and tend to
get lost and the cattle are left with the highly fibrous stems. The high CP concentra-
tion in lucerne hay makes it particularly susceptible to fungal contamination.
The most common legumes in temperate pastures are the red and white clovers
(Trifolium sp.). The bacteria in their root nodules enable them to fix nitrogen and
they are drought resistant. In pure swards they have a slightly higher nutritive value
than ryegrass but if eaten in large amounts can cause bloat (Chapter 7). The most
successful short‐term leas for cows in temperate climates are likely to be ryegrass/
clover mixtures.
Grass Silage
This is, in essence, pickled grass. When weather permits, the crop is cut and har-
vested at a stage of maturity that achieves the best balance between yield and nutri-
tive value, then packed, consolidated and sealed into a silo to exclude as much air as
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possible. This is conventionally described as clamp silage. In these anaerobic condi-

tions fermentation of sugars in the grass by naturally occurring microorganisms
attached to the grass forms organic acids that reduce pH to the stage where the crop
is preserved against further microbial attack. In ideal circumstances of warm, dry
weather when the grass is rich in sugars and the predominant microorganisms are
lactobacilli, pH falls to about 4.0–4.2, bacterial growth ceases and the crop becomes
stable after minimal loss of original nutrients. If this rapid fermentation does not
occur due to lack of sugars in the grass, lack of suitable microorganisms, or expo-
sure to air then secondary fermentation by other organisms (e.g. clostridia) can
occur. The greater the degree of secondary fermentation, the greater the loss of
organic matter, the poorer the quality of the organic matter that remains and the
closer the silage gets to becoming compost.
An alternative way to conserve pasture is to make big‐bale silage. Here the grass
is cut at a later stage of maturity, compressed into big round bales and packed into
plastic bags. This gives a greater yield but lower nutritive value (Table 5.5). Big bale
silage is an excellent source of forage for dry cows and heifers with relatively mod-
est metabolic demands. However, it is seldom likely to be nutritious enough to
make a significant contribution to the diet of high yielding cows.
The nutritive value of silage is a highly variable commodity, determined by the
species of grass/clover mix, stage of maturity at harvest, the weather and chemical
changes that take place during harvest and storage. The aim, of course, is to mini-
mise these changes so that the chemical composition of the silage is as close as pos-
sible to the grass from which it was made. However, even the best made silage is less
well balanced than the pasture from which it came since some of the protein will
have been degraded to QDN and the fermentable sugars (QFE) to organic acids
(lactic acid and the VFAs, acetate, propionate and butyrate), which can be used as
an energy source by the tissues of the cow but not by the anaerobic microorganisms
in the rumen. Conservation of grass as silage therefore inevitably reduces both the
rate and extent of fermentation of organic matter, unbalances the supply of fer-
mentable energy and degradable protein and so reduces the yield of microbial pro-
tein to the abomasum.
Dry Matter
The true feeding value of any forage is determined not only by its nutritive density
(ME and CP) but also by its palatability. What might appear ideal to a nutrition
chemist will be less than ideal for the cows if they are reluctant to eat it. The dry
matter (DM) concentration in spring grass at the time of first cut is unlikely to
exceed 20%. The optimal DM concentration in clamp silage, assessed in terms of
peak ME consumption, is about 25%. Some wilting of the crop is necessary; the
amount being determined by the DM of the grass and the weather at the time of
harvesting. Very wet silages (<20% DM) are difficult to preserve without the use of
additives and generate large quantities of effluent. Very dry silages (>40% DM) are
likely to be palatable but relatively low in ME, tend to have a high pH (>5.0) and
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may suffer from spoilage, especially if a large area at the front of the silage clamp
is exposed to the air. DM concentration can be assessed on farm simply by squeez-
ing the silage. If moisture cannot be squeezed out, DM concentration is greater
than 25%. If a tight squeeze leaves a little moisture in your hands, it is between 20
and 25%. If it runs through your fingers it is less than 20%.
Effluent loss from silage is negligible when DM is >25%, rising to about 50 L/t
conserved grass at 20% and 200 L/t at 15%. Wet silage is not inherently unpalatable
since the ingested water is rapidly absorbed so does not contribute to gut fill.
However wet silage made without additives is usually bad silage both in terms of
palatability and nutritive value through deterioration of organic matter. Finally, the
wetter the silage, the wetter the faeces. The foot problems of cows confined over
winter in cubicle houses can be attributed in part to standing for long periods in
wet, corrosive slurry (Chapter 8). Conservation of grass as silage rather than hay
has undoubtedly improved the amount of nutrition that can be obtained from for-
age. It has, however, created new problems, particularly those of effluent and slurry.
Metabolisable Energy
Because the quality of grass silage is so variable it is necessary to carry out an analy-
sis of each clamp to obtain a reliable estimate of ME concentration. The most accu-
rate approach to silage analysis is to measure the digestibility of organic matter in
vitro using a two‐stage fermentation process involving fermentation with rumen
microorganisms followed by digestion in acid and pepsin. However, this is time‐
consuming and therefore expensive. An alternative approach has been to use a
modified acid‐detergent method (MADF) to measure the fibre concentration. The
current method of choice in commercial laboratories is based on near infra‐red
(NIR) spectroscopy. Bombardment of the sample with NIR radiation generates a
complex wave form that reflects both its physical and chemical composition. Using
complex computer analysis, variations in (say) six of these peaks can be correlated
with direct measurements of digestibility measured in vivo or in vitro. This approach
is not only cheaper but more accurate than methods based on a single measurement
(e.g. MAD fibre). It is however empirical and can only be used to predict M/D (or
other criteria of nutritive value) by reference to known values for specific classes of
feeds, i.e. a prediction equation based on NIR values for ryegrass silages could not
be extrapolated to maize silage.
Protein
Even in the best silage about 60% of the crude protein in the grass crop is degraded
into peptides and individual amino acids. In wet, or poorly consolidated silages,
secondary fermentation by clostridia and other microorganisms leads to further
breakdown of CP into ammonia and, in some cases, accumulation of potentially
toxic nitrogenous compounds such as histamine. Laboratory analyses describe the
proportion of total N present as ammonia as an indicator of fermentation quality.
As a rule of thumb:
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NH3–N as percentage total of N Type of fermentation
Less than 5 Excellent

5–10 Very good
10–15 Satisfactory
15–20 Poor (slightly
butyric)
20 plus Bad (butyric).
When fermentation is excellent, there is a rapid fall in pH and lactobacilli pre-

dominate: the silage has a clean, if somewhat clinging, acid smell. Poorly fermented
silages, where clostridia and aerobic organisms have become established, generate
large amounts of ammonia and butyric acid that has a characteristic sickly smell.
Such silages are poor in nutritive value and very unpalatable.
Silage Additives
Silage additives are used, initially, to encourage a rapid fall in pH and thereafter to
minimise losses due to aerobic microbial degradation at the exposed feed face. The
traditional approach was to hasten fermentation by incorporation of sources of
QFE such as molasses. Cereals and beet pulp have also been used but this is sel-
dom realistic since they are not harvested at the right time. Today it is easier and
cheaper to use fermentation stimulants, inoculants mostly based on lactobacilli, to
accelerate fermentation rate or fermentation inhibitors, organic acids that directly
lower pH to stable levels. Current wisdom would have it that inoculants are best
suited to harvests likely to make ‘good’ silages (i.e. 25–28% DM). Fermentation
inhibitors are the additive of choice for wet silages (<20% DM) that will not benefit
from inoculants since they contain so little QFE. They are also recommended for
high DM crops (>30% DM) that are susceptible to aerobic degradation at the
exposed feed face during the winter‐feeding period. The manufacturers of silage
inoculants claim that the benefits justify the costs even for crops harvested under
ideal conditions. They may well be right.
Hay
Because hay must be stored dry under aerobic conditions it needs to be harvested
when the grass is relatively mature and fibrous so inevitably has a poorer nutritive
value than grass silage. Typical values are M/D = 8.5 MJ, CP 85 g/kg DM (Table 5.5).
Green grass conserved as silage retains most its carotene (a precursor of vitamin A)
but this is lost during sun‐drying of hay. However, the concentration of vitamin D is
increased. The high yielding cow requires a diet with about 11.5 M/D, which cannot
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be achieved if hay is the major forage source without inclusion of an unhealthy (and
expensive) proportion of cereals and protein supplements. However, well‐made hay
is highly palatable and likely to be the forage of choice for cows that are sick or expe-
riencing discomfort from sub‐clinical rumen acidosis. It is common to see a fall in
the butterfat concentration of milk when cows are turned out onto spring pasture. In
these circumstances hay can provide an excellent supplementary source of digestible
fibre, which the cows are usually glad to eat – a good example of the extent to which
appetite in the cow is dictated by the need to ensure healthy, comfortable digestion.
Badly made, mouldy hay is not only nutritionally destitute but unpalatable and
potentially dangerous to both cows and humans.
Straw
Untreated straws have no significant role to play in the feeding of dairy cattle.
However, it is possible to treat straws with chemicals that disrupt the lignified
structure of the cell walls and so render more of the cellulose available for fermen-
tation. Application of sodium hydroxide (NaOH) in liquid or solid form can
increase M/D to 8.5, making it comparable in energy terms to moderate hay. An
alternative, more difficult and expensive method is to create an airtight seal around
a straw stack and admit gaseous ammonium hydroxide (NH4OH). This method not
only improves M/D but also NPN concentration to the point where it is approxi-
mately balanced with respect to fermentable energy and degradable protein. It also
contains a large amount of sodium in the form of sodium carbonate and bicarbo-
nate, which are, of course, excellent buffers. However, I believe that it is rarely
likely to prove economical. Nutritionally improved straw (NIS) produced using
NaOH can make a useful contribution to ruminant nutrition in areas where straw
is plentiful and grass at a premium. In more traditional, pasture‐based systems,
NIS may be a cost‐effective alternative to hay in years when the hay crop has been
ruined by bad weather.
Ensiled Whole-crop Cereals
Whole‐crop maize (corn) silage is an excellent forage for dairy cows wherever it can be
grown and harvested reliably and well. It is high yielding and as good as, or better than,
the best of grass silages as a source of ME (Table 5.5). Considerable starch is retained so
it is well balanced between QFE and SFE. It lacks ERDP but this can be provided at low
cost by non‐protein nitrogen sources such as urea. Normally, it ferments rapidly to a low
pH (<4.0). This may be a little too acid both in terms of palatability and optimal rumen
fermentation. Maize silage stings if it comes into contact with a cut finger. Cows per-
form extremely well when fed a 50:50 mixture of grass and maize silage, which is to be
expected since this achieves an excellent balance between the supply of fermentable
energy and degradable nitrogen.
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There has been some interest in the production of forages for dairy cattle based on
whole‐crop wheat or barley, treated with urea that hydrolyses to ammonia and pre-
serves the crop at high pH (ca 8.5). However, there can be problems with aerobic
degradation and the high ammonia concentration (300 g/kg total N) makes it rather
pungent. Current wisdom would suggest that these crops are best fed in combina-
tion with grass silage. I cannot think of a good reason why anyone would plan to
grow barley or wheat for forage on a farm that is able to grow maize. A crop that
proved unsuitable for conventional harvesting, e.g. after a period of especially bad
weather, could be ensiled but would then best be fed to followers.
Other Green Feeds
Other than grasses, the most popular green feeds for cattle are the brassicae,
such as kale, rape and the tops of root crops such as turnips and swedes. The
leaves and stems of kale and rape are rich in the major nutrients, containing
about 11 MJ ME and 160 g CP per kg dry matter. They are rather unbalanced
with respect to Ca and P (Table 5.5) and contain toxic substances that can, if fed
in excess, cause thyroid deficiency and/or haemolytic anaemia. Both these
problems can be avoided by restricting the intake of kale or rape to a maximum
of 30% DM intake. Swede and turnip tops are probably as safe as kale but man-
golds, sugar or fodder‐beet tops can provoke diarrhoea unless wilted before
feeding.
Root Crops
Root crops fed whole or chopped to cattle include turnips, mangolds and fodder
beet. They differ in water content from about 82% for fodder beet to 90% for tur-
nips. The nutritive value of their dry matter is similar (M/D 12.6, CP 60–100 g/kg,
Table 5.5). Over 50% of DM is in the form of sugars that are highly palatable and
provide an excellent source of QFE. This makes them particularly suitable for
feeding along with grass silage that contains a relative excess of QDN. In coun-
tries such as Denmark cows may be fed as much as 40 kg fodder beet per day. In
these circumstances it is necessary to ensure that the roots are as free as possible
from soil contamination and it may be necessary to hose them down before
feeding.
Cereals
The nutritive values of the major dry cereals, wheat, barley, oats and maize were
given in Table 5.4. They are all rich in starch, which is an excellent, safe source of ME
for cows provided that it is properly incorporated into a balanced diet containing
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sufficient digestible fibre (>300 g/kg NDF, <400 g/kg NFC). It is important to roll or
otherwise crush the husk of cereals fed to cattle (but not sheep) since a proportion of
whole grains pass rapidly through the reticulo‐omasal orifice and appear unchanged
in the faeces.
Oats are traditionally considered to be the safest of all cereals when fed ‘straight’.
They contain the highest ratio of SFE to QFE and are least likely to provoke over‐
rapid fermentation leading to ruminal acidosis and bloat. Rolled barley and wheat,
having less fibre and more starch, are fermented more rapidly and more likely to
cause problems if eaten to excess. Most cereal starches are almost totally fermented
to VFAs with a relatively high proportion of propionate to acetate. The protein is
about 80% degraded in the rumen so acts primarily as a source of microbial protein.
The ratio of degradable protein to ME in barley is 6.8, which means that it needs to
be supplemented with a source of RDP to achieve an optimal balance for microbial
protein synthesis.
Uncooked maize starch is not fermented completely in the rumen. Most of the
maize starch that escapes fermentation is reduced to monosaccharides by acid
digestion and the rest is likely to be fermented in the hind gut. Flaked maize is pro-
duced by cooking the grain in steam and passing it through rollers. This increases
digestibility in both the rumen and abomasum, which makes it particularly suitable
for young calves.
Incorporation of starchy cereals is of major importance in the feeding of dairy
cattle since they are needed to ensure that the M/D in the mixed ration is high
enough to meet ME requirement within the constraints of DM intake. The feed
compounder is not concerned whether barley (say) is or is not better than wheat, he
considers both simply as sources of starch energy in a mixed ration. If, at any time,
wheat provides ME at a lower cost than barley, then wheat will appear in the ration
formulation.
Cows that consume starchy feeds to excess can suffer bloat, and ruminal and met-
abolic acidosis, which may, in severe cases, lead to death or chronic crippling dis-
eases such as laminitis. If cereals are to be offered as separate feeds, rather than
incorporated into a TMR, they need to be fed with caution. Consumption of a sub-
stantial quantity of cereals in a single meal (e.g. >5kg while in the milking parlour)
will cause a significant fall in rumen pH, some destruction of cellulolytic (grass‐fer-
menting) bacteria and a relative increase in the production of propionate relative to
acetate. This is likely to reduce the butterfat concentration in the milk. A reduction
in the population of cellulolytic bacteria will reduce the rate of digestion of forage,
thereby reducing retention time in the rumen and so reducing appetite. Overfeeding
starchy concentrates (purchased, e.g. in concentrate feed mixtures) will reduce the
capacity of the cow to derive nutrients from home‐grown forages. As a general rule,
it is recommended that the feeding of starchy concentrates at a single feed (e.g.
while in the milking parlour) should be restricted to 4 kg. This may require out‐of‐
parlour feeding. It is better to mix them with more fibrous, slowly digested material
and incorporate them into a mixed ration.
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By-products
In Chapter 1, I illustrated the extent to which dairy cows can be fed on by‐products
of industrial processes primarily, or partly designed to extract food for man from a
wide variety of plant materials. Cattle feeders and feed compounders have worked
on the premise that almost any organic matter containing carbohydrate and protein
is worth a try and no by‐product is too bizarre to escape the attention of the nutri-
tionist, e.g. coffee grounds, kapok cake, guar meal, chicken feathers. In some coun-
tries feeds for beef cattle have included chicken litter, rumen contents and even
recycled cattle faeces as a source of NPN. Of course, no product can be assessed
simply on the basis of its potential yield of digestible nutrients; it must also be
shown to be safe (for animals and humans). This issue was highlighted by the out-
break of bovine spongiform encephalopathy (BSE) in UK cattle first identified in
1986 and shown to be caused by the inclusion of bovine material in feeds for dairy
cattle and (I firmly believe) their early‐weaned calves. The subsequent confirmation
of a direct link between BSE and fatal new‐strain Creutzfeldt–Jacob disease (nCJD)
in humans led to a total ban on the feeding of products of animal origin to cattle and
a temporary ban, now rescinded, on the sale of specified bovine material (essen-
tially anything that might contain nervous tissue) for human consumption. The
BSE/nCJD outbreak will be discussed further in Chapter 10. Within the European
Union, the ban on feeding products of animal origin extends to fishmeal, through
application of the precautionary principle rather than as the result of direct evi-
dence, which is a pity since fishmeal contains an excellent balance of amino acids
(Table 6.2). Many countries permit the feeding of fishmeal and we have no evidence
that this is contributing to disease problems of any sort.
Oilseed Cakes and Meals

The oilseed cakes and meals made from the residue after extraction of the plant oils
make an excellent complement to cereals in concentrate diets for cattle because they
are relatively rich in protein, while also high in ME. The oil is extracted from the seeds
either by heat and pressure or by chemical means using an organic solvent such as
hexane. Linseed cake, for example, is produced by the ‘expellar’ process, which
employs heat and pressure and leaves a residual oil content in excess of 50 g/kg. Soya
bean meal is solvent extracted and contains less than 20 g/kg oil. The major regions of
oilseed production are the tropics and sub‐tropics. Here the main crops are soya bean,
groundnut, cottonseed, palm seed and linseed. In recent years the development of
improved rapeseed cultivars suited to growth in temperate climates has led to a great
increase in the use of rapeseed meal, especially in Europe, where it has been encour-
aged by generous subsidies designed to encourage less dependence on imports.
Soya bean meal is the most popular protein‐rich, vegetable‐based by‐product in
animal feeding. It is rich in CP (>500 g/kg) and the protein is of high biological
value, having an excellent balance of amino acids. Table 6.2 lists the composition of
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Table 6.2 Amino acid composition of some livestock feeds g/kg DM.
Limiting amino acids
First Second Third
Crude Methionine plus

protein Lysine Threonine Histidine cystine
Milk, dried skimmed 340 24 14.o 11.0 9.6

Soya bean meal 520 30.7 19.5 10.6 16.2
Groundnut meal (dec) 450 14.4 12.2 10.9 11.6
Maize gluten 250 6.0 9.4 6.6 11.0
Linseed meal (exp) 340 12.3 12.9 6.1 8.5
Rapeseed meal 396 19.1 17.8 10.5 8.2
Field bean meal 284 18.0 12.2 7.2 5.7
†
Fish meal 657 45.0 26.0 12.0 24.6
Amino acid proportions (g/kg CP) relative to skimmed milk
Soya bean meal 0.87 0.95 0.66 1.16

Groundnut meal (dec) 0.45 0.66 0.75 0.91
Maize gluten 0.34 0.91 0.82 1.56
Linseed meal (exp) 1.51 0.92 0.55 0.91
Rapeseed meal 0.68 1.10 0.81 0.71
Field bean meal 0.96 1.04 0.79 0.71
†
Fish meal 0.97 0.94 0.56 1.33
†
Currently prohibited for use as a cattle feed within the European Community.
a range of feeds for livestock in terms of CP and the most important of the essential
amino acids. Lysine is defined as the first limiting amino acid. In other words, when
protein supply is restricted, lysine becomes the first amino acid to fall short of tissue
requirement. The first feed listed in Table 6.2 is dried skimmed milk, whose major
protein is casein, considered (unsurprisingly) to be the ideal protein as defined by
its amino acid composition in relation to requirements for growth and lactation.
Table 6.2 shows that although the balance of amino acids (g/kg CP) in soya bean
meal is not quite as good as casein, it is reasonably well balanced for lysine, threo-
nine, methionine and cystine, and slightly deficient in histidine, although not to a
degree likely to be of commercial significance in diets for dairy cows.
One potential problem with conventional soya bean meal is that the protein is highly
degradable in the rumen so not particularly suitable for rations requiring substantial
Miscellaneous By-product 113
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amounts of undegradable protein (UDP). It is however possible to purchase ‘protected

soya’ that has been exposed to formaldehyde or similar process to reduce degradability.
There are a number of toxic, allergenic and antinutrient substances in soya, as there
are in nearly all the other high protein vegetable feeds. Most of these are inactivated by
rumen microorganisms. However, it is necessary to destroy them, usually by heat treat-
ment, when soya bean meal is fed to simple‐stomached animals (which includes
young calves) or when it is treated to reduce degradability and so convert it into a
high‐quality source of UDP.
In the 25 years since publication of the previous edition of this book, there has
been a ten‐fold increase in the use of rapeseed meal as a protein supplement in
animal feeds. This has arisen from the breeding of improved (low glycosinolate)
cultivars that grow well in temperate climates and has been aided by generous sub-
sidies intended to reduce dependence on imported soya. At high levels of inclusion
there is a risk of toxicity or, at least, reduced appetite. In consequence, most models
for ration formulation set a limit to inclusion rates.
Miscellaneous By-products
Sugar Beet Pulp

Dried sugar beet pulp (Table 5.4) is an excellent, highly palatable source of ME. It
contains only a small amount of residual sugar and the main source of energy is
digestible fibre (SFE), which aids in the maintenance of a stable rumen pH, optimal
digestion of forage to give a high acetate:propionate ratio and encourages the syn-
thesis of butterfat. It is similar to cereals in CP but relatively rich in calcium. Its
palatability and stable fermentation make it a particularly suitable third ‘lunchtime’
feed for dairy cows, providing an element of novelty and helping to maximise DM
intake. Magnesium‐enriched sugar beet pulp is particularly effective as an ‘in‐par-
lour’ feed for dairy cows newly turned out on to spring grass. Not only does it reduce
the seasonal risk of ‘grass staggers’ (acute magnesium deficiency, Chapter 7), it also
balances the supply of digestible fibre, magnesium and metabolizable protein.
Maize Gluten
Maize gluten is a by‐product of starch extraction from maize and is available in large
quantities. Maize gluten feed is normally sold at 20% CP and is an excellent source of
ME (M/D =12.7, Table 5.4) principally in the form of digestible fibre. It has, however,
been rather oversold as a source of protein. Prolonged exposure of maize to heat dur-
ing the process of starch extraction creates Maillard reaction products, complexes of
carbohydrate and organic N in which the original amino acid structure has been
destroyed. These Maillard reaction products appear as increased ADIN (acid‐deter-
gent insoluble nitrogen, see Chapter 2), some of which may be degradable in the
rumen but none of which can contribute to amino acid supply from DUP. As a rule,
the darker the sample of maize gluten and the more ‘Marmitey’ its taste, the poorer
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its protein value. The major feed companies are aware of these differences in protein
value and select the best. In consequence, some of the darker samples that are avail-
able to farmers as ‘straights’ are those that have been rejected by the compounders. I
repeat, maize gluten is an excellent source of ME but cannot be considered a suffi-
cient and satisfactory source of MP.
Maize gluten meal is sold at 60% crude protein and most of this is in the form of
undamaged true protein. It tends to be relatively deficient in lysine (Table 6.2) but
provided this need can be met from elsewhere (principally microbial protein) maize
gluten meal is an excellent source of DUP. However, because it is good, it is
expensive.
Brewers’ and Distillers’ Grains

These are the residues after extraction of starch by malting and fermentation from
barley. They can be fed wet or dry. In both cases they are excellent sources of digestible
fibre. However, they are likely to contain about 10% fat and this may interfere with
rumen fermentation and thereby restrict appetite if they form too large a part of the
overall diet. Their protein value is extremely variable depending on the extent to which
they have been exposed to heat and moisture. Wet brewers’ grains have a low ADIN
concentration, which suggests that the protein is largely undamaged. In some dark
distillers’ grains over 50% of CP has been converted to ADIN and will be unavailable.
Wheat Bran
Wheat bran is relatively rich in CP although a substantial proportion may be in the
form of ADIN. It is too low in ME to be a serious contender with other by‐products
in feeds for dairy cows, not least because it has acquired a cash value out of all pro-
portion to its nutritive value for ruminants because of its appeal to humans seeking
a natural laxative.
Balancing Forages and Concentrates
I repeat: the first limit to the physiological capacity of the modern, high genetic
merit dairy cow to produce milk is her ability to take in enough nutrients to
meet the demands of maintenance and lactation. The aim of ration formulation
is to provide the maximum possible balanced yield of available nutrients and
this depends on ensuring a healthy, sustainable high food intake. So far, all cal-
culations have estimated DM intake as a simple function of cow size, milk yield
and state of lactation. This is an obvious oversimplification. The constraint on
appetite imposed by gut fill is far greater for slowly fermented material with
large particle size (e.g. big‐bale grass silage) than for a milled mixture of rapidly
fermentable starchy concentrates. At the other end of the spectrum, a ration
containing too high a proportion of starchy concentrates will destabilise rumen
Balancing Forages and Concentrate 115
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pH and destroy rumen microorganisms. This will also reduce DMI. Rations for
dairy cows are therefore formulated to contain a mixture of forages and cereals.
The optimal mixture will be determined by the relative nutritive and cash value
of the two. When and where high‐quality pasture is available it may be more
profitable (and healthy) to minimise concentrate feeding and accept lower milk
production. When cows are confined and all food is delivered from a mixer
wagon, then the aim will be to maximise milk yield, not least to offset the large
fixed costs of buildings and equipment.
Figure 6.2 illustrates the effect of increasing concentrate intake on total DMI when
fed with high quality (M/D = 11.0, CP = 170 g/kg) and low‐quality (M/D = 9.5,
CP = 140 g/kg) grass silage. DMI for the high‐quality silage fed alone is 14 kg/day
The addition of 4 kg DM from concentrates increases total DMI to 16.5 kg/day,
40
250
Total ME intake (MJ/day)
Milk yield (L/day)

30
200
20
150
10
100
18
16
Total DM intake (kg/day)
14
Concentrate
12
10
8
Forage
0 2 4 6 8 10 12
Concentrate intake (kg Dm/day)
Figure 6.2 The effect of increasing concentrate intake on total DMI when fed with
high quality (M/D = 11.0, CP = 170 g/kg) and low-quality (M/D = 9.5, CP = 140 g/kg)
grass silage.
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a net gain of 2.5 kg DM. A further increase in concentrate intake from 8 to 12 kg/day
only increases total DMI from 17.6 to 18 kg/day. At this level of concentrate feeding
concentrate is almost entirely substituting for, rather than supplementing forage.
When poor quality silage (M/D = 9.5) is fed alone DMI is only 11.4 kg/day and
increasing concentrate has a substantial effect on total DMI up to about 8 kg d−1.
Figure 6.2 also expresses the effect on total ME intake in relation to ME allowance
for milk yields from 10 to 40 L/day of feeding increasing amounts of a concentrate
(M/D = 13.2, CP = 160 g/kg). With the high‐quality silage, an intake of 6 kg concen-
trate will sustain a milk yield of 30 kg/day. Increasing concentrate intake to 12 kg/day
increases total ME intake by only 22 MJ/day, enough to sustain only an extra 4 L of
milk. When the only silage on offer is of poor quality 10 kg/day concentrate is
required to achieve a milk yield of 30 L/day. The higher the ME value of the forage,
the lower the incremental gain in ME intake achieved through feeding increasing
amounts of concentrate.
When the ME value of the forage is high (e.g. from a 50:50 mixture of grass
and maize silage), the most important role for the concentrate is to provide pro-
tein. Figure 6.3 illustrates the effect on the supply of metabolizable protein
(MP) in relation to allowances for milk yield of feeding concentrates with a CP
concentration of 160 or 280 g/kg. In this example 6 kg of high protein concentrate
supplies more MP than 12 kg/day of a conventional, cereal based concentrate at
160 g/kg CP. Figure 6.2 showed that (in this example) there is little to be gained
from feeding more than 6 kg/day concentrate when the quality of the forage is
40
2.5
280 P
30
Milk yield (l/day)
2.0
MP intake (kg/day)
160 P
1.5 20
1.0
10
0.5
0 2 4 6 8 10 12
Concentrate intake (kg DM/day)
Figure 6.3 The effect on the supply of metabolizable protein (MP) in relation to
allowances for milk yield of feeding concentrates with a CP concentration of 160 or
280 g/kg.
Feeding Strategie 117
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very good. Thus 6 kg/day of a concentrate containing 280 g/kg high quality
protein meets requirement for both ME and MP. When the quality of forage is
poor, and twice as much concentrate is required to meet ME requirement, then
the concentrate will be formulated to a different specification – less CP, more
digestible fibre.
Feeding Strategies
On traditional dairy farms, where cows go out to graze in the summer and are
housed over winter, feeding programmes are influenced by several factors not
directly linked to nutrition, such as the quality of forage available, the labour and
equipment for handling it, facilities for feeding concentrates in and out of par-
lour, etc. Here I shall examine feeding strategies old and new strictly within the
context of nutrient requirements for lactation. Implications of these strategies
for production diseases will be considered in the next chapter.
Feeding to Yield
The traditional practice of the British dairy famer has been to estimate the amount
of production to be obtained from basic, home grown sources of grazed pasture and
forage eaten in the barn, e.g. maintenance plus 10l milk/day, then feed concentrate
in the form of dairy cake in the milking parlour at a rate of (e.g.) 0.4 kg/L (formerly
4 lbs/gal) for every extra litre. This is, by definition, feeding to yield, although a rather
crude way of doing it. The modern dairy farmer with access to a computer‐based
rationing system seeks to meet stated allowances for ME and MP from the best pos-
sible combination of home grown and purchased feed. This too, is feeding to yield,
although, as we shall see, the concept of ‘feeding to yield’ embraces a very broad
church, from the ‘forage in the barn, cake in the parlour for each individual cow’ to
the feeding of cows en masse with a total mixed ration entirely at the feed face.
Feeding concentrates in parlour has been a particularly British practice. It is
quite unusual to see it elsewhere in the world. Moreover, it has several drawbacks.
The amount of concentrate that a cow might be expected to eat during two visits to
the parlour is unlikely to exceed 8 kg/day. Many in‐parlour dispensers will usually
only dispense feed in the form of highly concentrated (and expensive) dairy pel-
lets. Large amounts of concentrate eaten quickly are likely to destabilise rumen
fermentation. In‐parlour feeding is, by definition, incompatible with the practice
of feeding a total mixed ration and not, therefore, compatible with modern con-
cepts of good, healthy nutrition for high‐yielding dairy cows. There is however one
practice for which it is essential, namely robot milking, since dairy cows will not
enter the robot unless they are rewarded by a feed. I shall discuss this further in
Chapter 9. When moderately high‐performance dairy cows, like British Friesians,
can get a high proportion of their nutrient requirements from grazing high quality
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pasture, then it can be both practical and nutritionally sound to feed all the con-
centrate ration in parlour. When the nutrient requirements for lactation call for
substantial amounts of concentrate in addition to the farmer’s basic forage ration,
then it becomes necessary to provide some of these out‐of‐parlour, typically as a
‘lunchtime’ feed. In the example illustrated by Table 5.7, the winter feeding of
dairy cake in parlour was supplemented by a lunchtime feed of (relatively cheaper)
maize gluten. How the concentrate ration is split between in‐ and out‐of‐parlour
feeding will depend on the special circumstances of the farm but I would recom-
mend that the aim should be to keep in‐parlour feeding for Holstein Friesians
below 8 kg/day; smaller amounts obviously for the smaller breeds.
The strategy of feeding to yield is inherently efficient but should not be interpreted
too rigidly because of inherent uncertainties attached to estimates of nutritive value
and, especially, individual variations in food intake. Moreover, in its most rigid form,
the strategy assumes that each cow is producing milk exactly to its genetic potential
and would not, for example, produce a little more milk if fed more concentrate, espe-
cially during early lactation when yield is rising to a peak. This argument produced
the strategy of lead feeding, which involves giving cows in early lactation an amount
of concentrate corresponding to a milk yield (say) 5 L/day greater than current yield.
This strategy has largely gone out of fashion. Feeding increased quantities of concen-
trates to cows in early lactation tended not to increase gross profit margins for milk
sales over the cost of purchased feed. Moreover, it can increase the risk of inducing
disorders of digestion and metabolism. In other words, I believe that lead feeding is,
in most circumstances, pointless and potentially dangerous.
At the time of publication of the previous (second) edition, dairy farmers in
Europe were operating within a quota system designed to make it unprofitable to
produce milk in excess of the amount specified for each farm. This gave rise to a
strategy known as brinkmanship. It starts with the assumption that the cows in the
herd are performing satisfactorily to their genetic potential, which then poses the
following questions:
1) Could they perform as well given less cake, either because the quality of the
forage, or their appetite for the forage is better than predicted? The two things
are, of course, linked.
2) Can I therefore reduce the cake ration by (say) 2 kg/day without incurring a fall
in milk yield and thereby increase my gross profit margin (GPM) over purchased
feed?
The removal of milk quotas has reduced the attraction of this strategy since the aim
of most farmers is to maximise income from milk sales, even at a reduced gross profit
margin per litre, in order to offset fixed costs. Nevertheless, given the inherent uncer-
tainties attached to estimates of nutritive value and food intake, it will always be worth-
while exploring possibilities for reducing feed costs without reducing production,
whether the feeding strategy involves the traditional practice of feeding forage ad lib
plus controlled amounts of concentrate according to yield, or the newer practice of
flat‐rate feeding total mixed rations.
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Total Mixed Rations and Flat Rate Feeding

Perhaps the most important message to be taken from the previous chapters on nutri-
tion, digestion and metabolism is that the healthiest way to feed high‐yielding cows
large amount of rich food is to ensure that the diet provides at all times a balanced
mixture of quickly and slowly fermentable energy, degradable and undegradable
(bypass) protein. This involves the feeding of a ‘total mixed ration’. All the ingredients
are combined in a mixer wagon and laid out before the cows at the feed face. In effect,
the ration is provided ad libitum. It is however necessary to clear the residues on a
daily basis in order to keep the feed fresh. This practice is now just about universal in
large industrial dairy enterprises where cows are housed throughout lactation. In
these circumstances it is normal to provide the entire ration at the feed face unless, of
course, the system includes robot milkers, in which case it will be necessary to pro-
vide some feed within the milking stall to encourage the cows to enter.
Feeding a total mixed ration entirely, or almost entirely, out‐of‐parlour means that
cows must be fed in groups, rather than according to their perceived individual needs.
In practice, it is customary to divide the milking herd into (say) three groups according
to yield and state of lactation. Table 6.3 illustrates how rations may be formulated to
meet the requirements for high, medium and low yielders. It takes as a starting point the
average milk yield for each group, those in early, mid and late lactation taken as 40, 28
and 14 L/day. It then calculates nutrient requirements for these yields. Values for ME,
CP, NDF and NFC only are given here but, of course, the computer‐based formulation
will be comprehensive, taking into account ERDP, DUP, MP, minerals and vitamins.
Table 6.3 An example of formulation of total mixed rations for flat rate feeding
to three groups of Holstein–Friesian cows.
Milk yield
High Medium Low
Average milk yield (L/day) 40 28 14

Composition of DM
ME (MJ/kg) 11.5 10.9 10.2
Crude protein (g/kg) 160 150 140
ND fibre (g/kg) 340 380 420
NFC (g/kg) 320 280 230
Estimated intake
Dry matter (kg) 25 22 18
ME (MJ) 288 240 184
Crude protein (kg) 4.0 3.3 2.5
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If the cows calve down in blocks then they can stay in the same house and feeding
area throughout lactation, the ration for the group being changed from high to
medium to low as dictated by the trend in their milk yield. Alternatively, the alloca-
tion of cows to groups can be based on their individual yields. In this case individ-
ual cows are demoted as yield declines. This strategy can create behavioural
problems as demoted cows are forced to adapt to a new social group, leading to a
further fall in milk yield that has nothing to do with the quality of the ration. For
the sake of the cows, as much as for the sake of convenience, it pays to move several
animals at the same time.
Flat rate feeding of total mixed rations has undoubtedly been a major contributor
to the spectacular increase in lactation yields that has occurred in herds of high
genetic merit housed throughout lactation. Continuous access to a diet containing
a correct balance of quickly and slowly fermented energy encourages stable rumen
fermentation, so that the digestive health of cows in these systems is generally good
even at very high levels of food intake. The capital necessary to invest in specialist
housing and feeder wagons is high, so the economics of the system calls for a large
herd size, perhaps 1000 cows. The traditional, smaller scale farmer whose system is
based on maximum nutrient supply from pasture and other home‐grown feeds, has
little incentive to invest in such a system. Whether these traditional farmers can
continue to compete with the industrial giants will be determined by issues of
socio‐economics and government policies that are quite outside the scope of this
chapter.
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Feeding Problems and Metabolic Diseases
The modern dairy cow is, by far, the hardest worked of all the farm animals.
Table 7.1 compares the daily food energy requirements (expressed as intake of
metabolizable energy, IME) energy expenditure as work (heat production, H) and
energy output in food for human consumption (meat, milk or eggs). For compara-
tive purpose the sedentary human (e.g. the office worker) as taken as a baseline of
1.0 for both IME and H. All other values are expressed as multiples of this baseline.
Relative to an adult sedentary male, a lactating mother will eat 38% more food
energy and work 13% harder; 25% of the food energy she consumes will be carried
into her milk. Growth in farm animals is not particularly energy demanding. Even
in rapidly growing broiler fowls, H is less than 20% above maintenance. The egg‐
laying hen is faced by considerable metabolic demands, particularly in respect to
calcium metabolism. However, the energy cost of egg laying is not particularly
severe, only about 30% above maintenance and this is unlikely to change until ruth-
less scientists discover a way to persuade the hen to lay more than one egg per day.
All these costs pale into insignificance when set against the cost to a dairy cow of
sustaining a milk yield of 50 L/day. She must consume an amount of food energy
nearly six times that of maintenance and her work load (H) is more than twice that
of maintenance. Synthesis of so much milk not only presents the cow with an enor-
mous metabolic load, the need to consume enough feed to meet this metabolic
demand can drive the digestive system to its absolute limits. Moreover, the motiva-
tion to keep eating to sustain this demand can seriously compromise her needs to rest
and sleep. The metabolic demands of lactation for a sow with 14 piglets are also high,
although less than that of the high yielding dairy cow but the sow is almost never
expected to lactate for more than eight weeks (usually much less than that). The dairy
cow is expected to produce large quantities of milk for over 80% of her adult working
life. Given this sustained, exceedingly high level of demand, it comes as no surprise
that feeding problems and metabolic disorders present such high risks.
Some of the challenges to the digestive and metabolic capacity of the dairy cow in
early lactation are outlined in Figure 7.1. The cow does her best to meet this large
increase in demand for nutrients (energy, protein and minerals, especially calcium)

122 Feeding Problems and Metabolic Diseases
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Table 7.1 ‘How hard do animals work?’. A comparison of the daily food energy
requirements (IME), energy expenditure as work (H), and energy conserved as food
(meat, milk or eggs) in domestic animals. The sedentary human is taken as a baseline
of 1.00 and all values are expressed as multiples of this (from Webster 2017).
Energy exchange
Species Activity ME intake Work/heat ‘Food’
Human Sedentary 1.0 1.0

Lactating 1.53 1.28 0.25
Pig Grower 2.10 1.30 0.80
Lactating 3.20 1.73 1.47
Poultry Broiler 2.10 1.18 0.92
Laying hen 1.73 1.30 0.43
Beef cow Suckling 2.22 1.32 0.90
Dairy cow Lactating 50 L/day 5.68 2.14 3.53
Energy Protein Minerals

Demand
>DMI >Nutrient density >Tissue mobilisation

Supply
rumen overload ketosis
Risks rumen acidosis hypocalcaemia
Consequences < appetite

common
<milk yield
<body condition
Consequences
severe INFERTILITY toxaemia
laminitis DEATH
Figure 7.1 Challenges, risks and consequences of the large increase in nutrient
demand to support the onset and maintenance of lactation in high-yielding dairy cows.
Feeding Problem 123
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by increasing food (DM) so far as she can within the constraints of rumen fill and
digestive comfort (Chapter 2). The farmer does what he can to increase the concen-
tration of nutrients with the ration within the constraints of the recommended lim-
its; minimal for fibre and maximum for starchy cereals (NDF and NFC respectively,
Table 5.2). However, it is inevitable that the high yielding cow in early lactation will
‘milk off her back’, i.e. mobilise energy, protein and minerals from her body reserves.
If all goes well these physiological and behavioural responses to the demands of
early lactation can be accomplished without compromise to her health and welfare
so that by about the tenth week of lactation she should have achieved a stable
balance between demand and supply.
The first weeks of lactation are the period of greatest risk to the dairy cow.
Increasing DMI increases the risk of rumen overload, leading to subsequent loss of
appetite and fall in milk yield. Increasing the ratio of starch to fibre in the diet
increases the risk of rumen acidosis, whose effects, depending on the severity of
the acidosis can range from loss of production to toxaemia, laminitis and, in
extreme cases, death. Excessive mobilisation of body fats can lead to ketosis. The
sudden rapid increase in demand for calcium at the onset of lactation can lead to
peracute hypocalcaemia (‘milk fever’) that, if untreated, is likely to be fatal. All
these conditions are considered in more detail below.
F
eeding Problems
Rumen Acidosis
The nature of carbohydrate fermentation in the rumen was described in
Chapter 2. The rumen microorganisms ferment carbohydrates in cell walls
(digestible fibre) and cell contents (starches and sugars) to yield volatile fatty
acids (VFA). In a stable environment the rate of acid production is countered by
absorption of VFA across the rumen wall and the buffering effects of sodium
bicarbonate and other salts in saliva so that rumen pH is mildly acidic, pH = 6.0,
which is consistent with the maintenance of a large, stable population of rumen
microorganisms. However, if the rate of production of VFA exceeds the rate at
which they can be absorbed, buffered and washed out of the rumen, then the
acidity will rise (pH will fall). With only a slight fall to about pH 5.5 there will be
destruction or, at least, inhibition of certain cellulolytic species of microorgan-
isms (Figure 7.2). This will reduce the rate of fibre digestion, increase rumen
retention time and so decrease appetite. There may also, at this stage, be a
decrease in the acetate:propionate ratio, leading to a fall in milk fat concentra-
tion. In most texts, particularly those from North America, this condition is
described as subacute rumen acidosis, (SARA) when rumen pH is within the
range 5.2–5.8.
In acute rumen acidosis (pH < 5.2), there is major disruption of the normal
microbiota. Lactobacilli predominate, producing a mixture of L‐ and D‐lactic acid.
The latter is less rapidly metabolized by the cow, and the acidosis that was, at first,
localised within the rumen, now becomes systemic. There is damage to the rumen
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Absorption of VFA,
water, saliva, fibre, buffers
6 normal
5 First microbes killed, appetite,

acetate, milk fat
fermentation 4 Lactobacilli predominate, anorexia,
production of diarrhoa, panting, laminitis
VFA Shock, toxaemia, death
3
Figure 7.2 Rumen acidosis and its consequences. The tendency for fermentation to
increase rumen acidity (lower pH) is opposed by buffers and other physiological
regulators to maintain a normal pH of about 6.0.
wall, and release of endotoxins. This degree of acidosis is a high risk for beef cattle
given high starch ‘finishing’ rations on feedlot and commonly leads to laminitis,
rumen parakeratosis and liver abscesses. Acute acidosis is fortunately rare in dairy
cattle except in extreme circumstances, e.g. cows breaking into a grain store and
gorging themselves on cereals. At the time of writing the second edition (1993)
laminitis consequent on rumen acidosis was thought to be a major cause of lame-
ness in dairy cows but subsequent evidence has shown that this is not the case (see
Chapter 8).
The prevalence of subacute rumen acidosis is high (SARA), especially in high‐
yielding North American cows fed high energy North American rations where esti-
mates of prevalence range from 20% to 40%. The incidence of SARA is highest in the
first weeks of lactation, especially in cows that have a high condition score (too
much fat) at the time of calving. The mechanics of this are straightforward. In the
final weeks of pregnancy, the expanding uterus reduces the space available for the
rumen, especially if the abdomen also contains a large quantity of fat (dairy breeds
have been selected to have a higher proportion of intra‐abdominal to subcutaneous
fat than beef breeds so can have quite high fat reserves while looking quite thin).
Because the metabolic demands of pregnancy are much less than those of lactation,
their appetite is relatively low, especially when they have generous reserves of body
fat. At the onset of lactation, the cows are likely to be presented with unlimited
access to a ration containing a much higher ratio of starch to fibre than they were
getting in the final weeks before calving. This presents a considerable challenge to
the digestive processes in the rumen, especially in cows for which DMI prior to
calving has been low. In these animals DMI intake in the first weeks of lactation is
likely to be irregular: high DMI one day causing a degree of acidosis, leading to
Feeding Problem 125
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discomfort and reduced appetite until things get back to normal. During periods of
reduced appetite, especially in overfat cows, the metabolic demands of lactation
will call for increased mobilisation of body fats and the risk of ketosis (q.v.), which
will exacerbate the severity of any systemic acidosis. The aim of transition feeding
during the final weeks of pregnancy is to ensure that the rumen is as large and
active as possible at the time of parturition by, first, ensuring that the cows are not
too fat, then feeding a high fibre, low ME diet to encourage the cows to consume as
much DM as possible to satisfy their (relatively low) metabolic hunger. The art of
transition management will be discussed further in Chapter 12.
Cows with SARA may not appear sick. However, their irregular DMI (which must
reflect discomfort) and unstable patterns of rumen fermentation mean that their
milk production will fail to achieve their potential. Irregular food intake also
increases the risk of displaced abomasum. SARA is recognised as a major threat to
production and profit, especially in the USA, where high starch diets are the norm.
The problem has inevitably attracted the attention of the manufacturers of feed
supplements. The most common of these are simple buffers and yeast products,
promoted as ‘aids to increased production’. This is, of course, a con. In reality, they
are indigestion remedies whose purpose is to restore normal milk production in
cows in which the normal processes of rumen digestion have been impaired by
improper feeding.
Abomasal Disorders
In a cow subsisting largely on grass or conserved forage, the organic material
flowing out of the rumen into the abomasum consists mostly of microbes and the
undigested cell walls of plants. The main role of the abomasum is to achieve acid‐
digestion of microbial protein. However, if carbohydrate fermentation in the
rumen is incomplete, the abomasum may become overloaded with partially fer-
mented starches (etc.). In these circumstances abomasal pH is too high to permit
rapid acid digestion of the microbiota. Fermentation continues, generating gas
that distends the abomasum and inhibits its ability to contract and propel food
into the duodenum. The abomasum is said to become atonic. This condition, like
SARA, is most likely to occur in early lactation while the cow is attempting to
adapt to more food in general and more starch in particular. It is also more com-
mon when the starch is from corn (maize) since this is more likely to escape fer-
mentation in the rumen than starch from barley, oats or wheat. Extensive
distension of the abomasum can lead to extreme discomfort, abomasal ulcers and
sudden death from gastric haemorrhage. This is however a rare occurrence in
dairy cows, more commonly seen in veal calves drinking large quantities of a
liquid, milk‐replacer diet.
As I have described already, in late pregnancy the gravid uterus occupies a large
amount of space in the abdomen, restricting the space available for the rumen.
After calving, and before the lactating cow achieves peak appetite, there is effec-
tively ‘room to spare’ in the abdomen. If the abomasum becomes distended or
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atonic at this time, there is a risk that it can become displaced from its normal posi-
tion on the right of the rumen and part of it may become trapped, typically between
the rumen and the left side of the abdominal wall. This can sometimes resolve itself
naturally or respond to rolling the cow but is more likely to require surgical inter-
vention. The main predisposing factors to left‐side abomasal displacement (LDA)
are SARA and irregularities in rumen volume. LDA occurs almost exclusively
within the first three weeks of lactation, most commonly in large bodied, mature
cows fed high energy diets, lacking in digestible fibre. The overall occurrence of
LDA in North American dairy herds has been estimated at 3.5%; interestingly, 2.5%
and 4.8% in herds of more and less than 500 cows respectively, suggesting that in
this regard, the large herds are being managed better. It is however, impossible to
escape the conclusion that LDA is a production disease, consequent upon ‘unnatu-
ral’ feeding practice and therefore our fault.
Bloat
Bloat occurs when the normal process of eructation (belching) is interrupted and
fails to expel the gases produced by fermentation. The rumen rapidly swells, the
cow experiences severe pain and may, in extreme cases, die within minutes of
showing clinical signs. A distinction can be made between gassy and frothy bloat.
In gassy bloat, the gas above the rumen contents cannot escape either because the
cow has lost the ability to belch or, uncommonly, because of a mechanical obstruc-
tion to the oesophagus, caused perhaps by the cow choking on a large piece of
root crop or external pressure from an abscess in the throat. The more common
cause of gassy bloat, simply failure to belch, is still not completely understood. In
the early phase, belching is not completely inhibited but becomes less and less
effective as the rumen distends with gas. This condition is typically seen in calves
after weaning and in intensively reared beef cattle receiving a high proportion of
their feed as concentrates, where the rate of gas production is relatively rapid and
rumen movements relatively slow due to the lack of long fibre in the diet. In these
circumstances some individuals may become chronic bloaters, whose condition
may only be kept at bay by passing a stomach tube to release the gas or puncturing
the rumen wall through the upper left flank with a trochar and cannula. This
form of gassy bloat associated with high concentrate feeding is uncommon in
dairy cows unless, for example, they get into a grain store and gorge themselves.
Normally they eat enough forage to ensure normal rumen movement.
Frothy bloat occurs when the bubbles of gas produced within the rumen contents
fail to burst when they reach the top so combine to create a mass of foam or froth
that fills the entire gas space. The surface tension of the liquid holding the gas bub-
bles together makes belching impossible. The foam cannot be cleared by passing a
stomach tube. Puncturing the rumen wall with a trochar and cannula usually, but
not always provides, relief. Frothy bloat typically occurs in cows at pasture, most
commonly when they have access to large amounts of clovers or alfalfa (lucerne).
Metabolic Disorder 127
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However sometimes several cows may suddenly develop frothy bloat for no apparent
reason on a previously blameless pasture. In this case there is little option but to
move the cows to another pasture and hope that the problem will resolve itself
with time.
When a dairy cow bloats at pasture, it is reasonable to assume there has been
frothing of rumen contents and administer an anti‐frothing agent by drench or
direct injection into the rumen. If no suitable veterinary preparation is to hand,
then 500 ml of linseed oil or liquid paraffin can be used for first aid. With luck, the
cow will start to belch at once. In all cases of moderate bloat, it is useful to encour-
age the cow to keep walking so as to swill the rumen contents around and stimulate
belching.
The very rapid progress from onset of clinical signs to death in some cases of bloat
has led some scientists to suggest that the cows may have been poisoned by toxins
released from the rumen. This may sometimes occur but it is more probable that
deaths arise from heart failure as a consequence of intense abdominal pain and
massive pressure on the great blood vessels in the thorax and abdomen obstructing
the flow of blood to and from the heart.
Metabolic Disorders
Ketosis
Ketosis, or acetonaemia, is a common disorder of potentially high‐yielding dairy
cows due to a failure to balance the metabolic demands of early lactation. Figure 7.3
illustrates the final pathways of the main substrates for energy metabolism in the
ruminant. The metabolism of organic compounds to make energy available as ATP
first involves the splitting up of the large molecules into fragments containing two
or three carbon (C) atoms. Fatty acids from body fat reserves break down into 2C
fragments. Fermentation in the rumen yields the volatile fatty acids: acetate and
butyrate are 2C fragments. Propionate is a 3C fragment. Glucose, which is essential
for life, is made up of two 3C fragments. The nature of ruminant fermentation and
digestion is such that little, if any, glucose is absorbed from the gut so that the cow
must synthesise its own glucose from 3C fragments arising from propionate or cer-
tain amino acids, such as glutamate, which are described as glucogenic.
The final common pathway for oxidation involves the combination of 2C and 3C
fragments as acetyl coenzyme A and oxaloacetate to form citrate. This is then
metabolised through a series of intermediates to generate nearly all the energy cur-
rency (fuel) for the body in the form of ATP. This is a cyclic process (usually called
the Krebs cycle, after its discoverer, Sir Hans Krebs) that is completed by the regen-
eration of oxaloacetate, able to link with more acetyl CoA and so continue the cycle.
At the onset of lactation, the specific demand for glucose is greatly increased to
meet the demands of the mammary tissue to synthesise lactose. At the same time
the metabolic demands for synthesis of milk fat and protein stimulate the cow to
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FAT DEPOTS
RUMEN
fatty acids
(C2) – amino acids

acetate
(C2)
(butyrate) (C2)
ketones
acetyl CoA
propionate (C3)
citrate (C3) - amino acids
pyruvate
oxaloacetate
(C3)
KREBS (C3)
CYCLE
oxygen
respiratory chain
lactose glucose (C6) oxidation
carbon
dioxide
ENERGY
Figure 7.3 Pathways of energy metabolism in the ruminant. C2 and C3 define

two‐ and three‐carbon compounds.
mobilise energy from her reserves of body fat. This comes in 2C fragments
(Figure 7.3). In early lactation therefore, 3C fragments are being driven towards the
production of lactose, via glucose, fatty acids are being broken down at an increased
rate to acetyl CoA. When the rate of production of acetyl CoA from acetate, butyrate,
fatty acids from body reserves and 2C (ketogenic) amino acids is high, and when a
substantial amount of oxaloacetate is used for glucose synthesis, the rate of acetyl
CoA production exceeds the rate at which it can be incorporated into the Krebs
cycle, so is diverted into the production of ketones (acetone and beta‐hydroxybu-
tyrate). Small quantities of ketone bodies can be metabolised or excreted. High con-
centrations are toxic.
The cow with ketosis becomes progressively dull and lethargic. She loses her
appetite, usually refusing concentrates before she refuses forage. This is a paradox
because starchy concentrates generate more 3C as propionate than forage and this
should improve matters by generating more oxaloacetate. Milk yield declines pro-
gressively. In severe cases the cow loses weight rapidly and becomes dehydrated.
Some cows may show nervous signs such as blindness and delirium, bellowing,
pressing their head against the wall and walking in circles. Milder cases of ketosis
in dairy cows are self‐limiting as milk production declines to the level at which the
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supply of oxaloacetate and acetyl CoA are back in balance. This condition is meta-
bolically similar to pregnancy ketosis or ‘twin‐lamb disease’ in sheep caused by a
high demand for glucose from the foetal lambs at a time when the food intake of the
ewe is depressed by the space occupied by the gravid uterus. In pregnant sheep the
condition can be fatal since the ewe cannot reduce glucose demand other than by
aborting her lambs. Ketosis seldom kills dairy cows but it can ruin their
productivity.
Almost every cow that gets ketosis will suffer to some degree from the condition
known as ‘fatty liver’. Ketone bodies are synthesised in the liver although oxidised
elsewhere. The liver also synthesises lipoproteins that are used to transport fat
through the body. When the liver becomes overloaded with ketones and fatty acids
from mobilisation of body reserves, some liver cells are damaged or destroyed and
others lose their functional capacity as they fill up with fat. This liver malfunction
is the main cause of depression and inappetence in the ketotic cow.
Prevention and Treatment

To prevent ketosis and the fatty liver syndrome it is necessary to avoid the accumu-
lation of 2C fragments in early lactation. One way to achieve this is to ensure that
cows are not too fat at the time of calving. The amount of fat and muscle cover on a
cow is conventionally assessed according to a ‘condition score’ from 1 to 5, where 1
is emaciated and 5 is obese (for an illustration and fuller description see Figure
12.3). Current wisdom dictates that condition score at calving should not be above
3.0. This, of course, implies that the average will be less than this. This may appear
a little harsh but remember that in cows selected for extreme dairy type such as the
modern Holstein a high proportion of fat is deposited intra‐abdominally (where it
can’t be seen) rather than subcutaneously. This is a secondary consequence of
selecting for high milk production, since abdominal fat can be mobilised more rap-
idly than subcutaneous fat in times of high energy demand, such as early lactation.
As I have indicated already, the thinner cow with less abdominal fat is also likely to
have a greater appetite both before and after parturition. Some vintage research
from Sweden also demonstrated that the incidence of ketosis was significantly
greater in cows permanently tethered over winter in tie barns relative to those get-
ting moderate exercise in free stall units. This suggests that for cows, like us, some
healthy exercise can both stimulate appetite and reduce the risk of obesity.
A traditional method for the treatment of ketosis has been to drench the cow with
a solution of propylene glycol for 3–5 days. A more recent, effective method for
control of ketosis is by administration of the ionophore antibiotic, monensin, which
selectively alters the population of rumen organisms so as to increase the produc-
tion of 3C propionate relative to 2C acetate. This is now licensed for use in the UK
in the form of an intraruminal bolus available under veterinary prescription. It can
be very effective in herds with a previous high incidence of ketosis and there are no
restrictions on sale of milk from treated cows. Long term administration of
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onensin, even where it is legal, is contraindicated, since by its mode of action,

m
selective inhibition of rumen microorganisms, it will restrict appetite.
There is a proven association between ketosis and other disease conditions in
early lactation including retained placenta and metritis (inflammation of the
uterus), infertility, mastitis and cystic ovaries. This has led to the hypothesis
that the ketosis/fatty liver complex may be a predisposing factor for these condi-
tions. It is difficult to construct a hypothesis to support the claim that ketosis
may be a predisposing factor for (e.g.) cystic ovaries. It makes more sense to
assume that primary stresses in early lactation, such as metritis and mastitis,
would increase the risk of ketosis. However, one should always be cautious
when drawing inferences from associations as to cause and effect. The incidence
of conditions such as retained placenta and cystic ovaries appears to be greater
in cows that are too fat at the time of calving. We may conclude that, for what-
ever reasons, the cow that is fit but not fat at the time of calving and well pre-
pared for the diet she will receive in early lactation is less likely to suffer not
only from ketosis but from a lot of other conditions too.
Parturient Hypocalcaemia (‘Milk Fever’)

The condition known to every dairy farmer as ‘milk fever’ is described in veteri-
nary textbooks as parturient hypocalcaemia or parturient paresis. These scientific
titles are ponderous but correct; the popular expression ‘milk fever’ is memorable
but wrong (there is no fever). The condition arises from a severe, sudden drop in
the concentration of calcium in the blood and extracellular fluid (ECF). Calcium
is essential for normal function of all types of muscle: striated muscle in the mus-
culo‐skeletal system, smooth muscle in heart and gut. Its concentration in the
ECF is regulated by parathyroid hormone (PTH) and vitamin D (cholecalciferol).
These control both net movement between the ECF and gut and the mobilisation
of calcium from the skeleton. At the time of parturition and the onset of lactation
the cow suddenly increases her demand for calcium from the ECF at a rate that,
if not replenished, could exhaust her reserve of freely available calcium within
10 hours (recap Figure 2.10b). It is inevitable therefore that blood calcium con-
centration will fall to some extent during parturition and the onset of lactation. If
the fall becomes too severe, the muscles of the cow become progressively weaker
(paresis) and she is unable to stand. In some cases this is preceded by a period of
hyperexcitability with muscle tremors. When she ‘goes down’, she initially, at
least, adopts a reasonably normal posture, lying on her brisket but with a charac-
teristic S‐shaped bend in her neck. Later her head may fall against her chest. Her
anal region becomes swollen with faeces that her gut is too weak to expel. Unless
treated, her condition will rapidly deteriorate; she shows signs of shock, her ears,
muzzle and limbs become cold to the touch. Finally, she falls onto her side,
becomes progressively bloated and dies, probably of respiratory or cardiac
failure.
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An incidence of milk fever of 5–8% in dairy herds may be considered normal,

which is a somewhat alarming definition of normality. Parturient hypocalcaemia is
almost exclusively a problem of dairy cows, being rarely seen in suckler beef cows
at pasture. Beef cows secrete less milk. Moreover, their calves are unlikely to drink
more than about 6 L/day during the first days of life. Thus, in truly normal circum-
stances the build‐up of demand on the mechanisms for supplying more calcium to
the ECF are much more gradual.
Some cows are more prone to milk fever than others, which suggests a genetic
predisposition. The condition is particularly common in Jersey cows. The incidence
also increase with age since older cows are less able to mobilise calcium from the
skeleton. Milk fever can be induced experimentally by feeding pregnant cows diets
with a high calcium:phosphorus ratio (Ca:P). The function of parathyroid hormone
(PTH) is to increase net uptake of calcium into and excretion of phosphorus from
the ECF. High Ca:P diets downregulate the secretion of PTH so that it fails to mobi-
lise sufficient calcium at the onset of lactation. In practice, the incidence of milk
fever tends to be higher when cows graze large quantities of lush spring or autumn
grass with a high Ca:P ratio. Spring grass that has a high concentration of nitrogen
and a low concentration of magnesium may impair calcium uptake from the gut.

A condition that may affect 10% of the dairy herd and can kill a cow within a few
hours of the onset of clinical signs would be catastrophic were it not for the fact
that diagnosis and treatment are usually simple. Most cows respond to the injec-
tion of 100–200g calcium borogluconate in a 25% solution (i.e. 400–800 ml of solu-
tion). This is best delivered by slow intravenous injection since this produces a
rapid response and no tissue damage. Subcutaneous injections may be adminis-
tered by the farmer as preventative measure for cows that have suffered milk fever
at a previous parturition or to prevent relapses following a previous intravenous
injection. The cow that fails to rise following treatment with calcium borogluco-
nate is not suffering from simple parturient hypocalcaemia and requires the
skilled attention of a veterinary surgeon. She may respond to an injection of
a mixed solution of calcium, magnesium and phosphorus. If not, she may be
suffering from a different post‐calving problem. The problem of the ‘downer cow’
is discussed below.
There is, as yet, no ideal strategy for the prevention of milk fever, which is why
the incidence can remain high even in the best managed herds. It is, in theory, pos-
sible to feed cows in late pregnancy on diets that are relatively low in calcium and
have a Ca:P ratio of 1.0, (ca. 30 g/day of each) to ensure sufficient secretion of PTH.
In practice, cows at pasture are likely to be consuming at least 100 g calcium/day.
Moreover, the best transition diets for housed cows are likely to be based on forages
with a Ca:P ratio well in excess of 1.0. While it may be impractical to reduce calcium
intake, there is a case for increasing consumption of magnesium and phosphorus in
late pregnancy. These minerals may be added to the drinking water, mixed into the
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total mixed ration or offered in a mineral block. The last of these three options is not
ideal because cows lick mineral blocks in an erratic fashion and cannot be relied on
to consume minerals according to requirement.
Other approaches to the prevention of milk fever include oral drenching with a
calcium solution at the time of calving, the injection of a large dose of vitamin D
about 8–10 days pre‐calving and (more recently) the feeding of rations designed
to induce systemic acidosis. None of these has proved to be especially successful.
Injection with vitamin D appears to be effective if the calving date has been esti-
mated correctly. If not, it may be counter‐productive. The technique for inducing
acidosis is based on the principle of the dietary cation‐anion difference (DCAD),
defined by the dietary balance of cations (Na +K) to anions (mostly Cl +S). When
the balance is strongly positive (as on grass‐based diets, the cows have a (manage-
able) tendency to systemic alkalosis and this is associated with an increased pre-
disposition to milk fever. This has led to the DCAD approach to milk fever control,
which involves the feeding of diets including salts such as CaCl2, NH4Cl and
MgSO4 to create a negative cation:anion balance and a degree of systemic acido-
sis. The cow with acidosis will seek to restore a normal pH in the ECF principally
by mobilising calcium phosphate from bone reserves. This upregulates the excre-
tion of PTH so primes the cow for the challenge of the onset of lactation. It is, by
definition, an approach that relies on the disruption of homeostatic mechanisms
and needs to be fine‐tuned, e.g. by monitoring the state of systemic acidosis
through measurements of pH in urine. Moreover, these diets rend to be unpalat-
able. On balance, I am not convinced that this is a clever approach.
The Downer Cow

The downer cow is one who goes off her feet, usually at or shortly after calving, and
cannot get up. The condition is often, but by no means always, precipitated by milk
fever. Other causes include:
1) Generalised weakness following a difficult calving, possibly with excessive blood
loss.
2) Nerve damage during calving, especially the obdurator nerve. Affected cows lose
control of the inner muscles of the thigh and ‘do the splits’ when forced to rise.
3) Fractures to the pelvis or hind limbs, possibly incurred because of muscle weak-
ness brought on by hyopocalcaemia.
4) Severe pain and illness from acute infections such as mastitis
If the downer cow lies in one position for too long matters deteriorate. Anyone
whose arm or leg has ‘gone to sleep’ after an hour or so of sitting or lying in the
same position should appreciate the problem for the nerves and muscles in the
limbs between 600 kg of recumbent cow and the hard ground. Unless she is moved,
severe destruction of nerve and muscle tissue will begin within 3–4 hours. The aim
must be to get her onto a soft bed, such as deep straw and in such a position that she
can be assisted to lie alternately on the left and right side, ideally about six times
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every 24 hours. This is easier said than done. If she is bright and otherwise healthy,
she should be helped into a standing position for short periods. There are various
ways to achieve this, none of them ideal. Probably the most effective approach is to
support her on a sling supported from a beam. A more traditional method is to use
the Bagshaw hoist, a method that hauls the cow to her feet via a clamp attached to
the ileac wings of the pelvis. This is undoubtedly less comfortable than the sling and
may be considered excessively harsh. The problem is that some cows make no effort
to support themselves within a sling and just hang there. The Bagshaw hoist gives
them more incentive to try. If cows do make the attempt to stand, with or without
support, it can help to put hobbles on the back legs to prevent them from ‘doing the
splits’ if there has been obdurator nerve damage.
Recovery can take anything from a few hours to over ten days. Some cows will never
get up. It is difficult for the vet to forecast which cows will and will not recover and so
advise the farmer whether to persevere with nursing or whether to arrange for emer-
gency slaughter. What is certain is that if she is not nursed she will never get up.
Hypomagnesaemic Tetany (Grass Staggers)

Magnesium has a controlling, inhibitory effect on nerve and muscle activity. In
acute magnesium deficiency this inhibition is removed and the cow simply goes
mad. The condition is usually sudden in onset and, unless treated, proceeds rapidly
to death. An affected cow first appears reckless and hyperexcitable. She may bellow
or gallop around the field for no reason. Wild‐eyed and frothing at the mouth, she
becomes increasingly uncoordinated, staggers and falls to the ground where she
may lie rigid in total muscle spasm or, more commonly, thrash out with her legs in
convulsive movements. Having exhausted herself she may then lie quietly but the
whole mad process may be triggered off again by a mild stimulus such as the arrival
of the farmer or vet. Death may occur within an hour of the onset of clinical signs
and cows with hypomagnesaemic tetany are commonly found dead. The condition
can usually be distinguished from other causes of common death (like lightning
strike) by the amount of grass and earth stirred up by the cow in her convulsions.
While hypomagnesaemia usually takes this peracute form, cows that are marginally
deficient in magnesium can show intermittent signs of nervousness, tremor and
irrational behaviour, especially when disturbed. Appetite and milk yield are also
reduced. If these signs are accompanied by evidence of low magnesium concentra-
tions in blood (<1.8 mg/L) the herd should be treated before things get worse.
The movement of magnesium (Mg) through the body compartments of a cow
yielding 30 L milk/day is illustrated in Figure 7.4. Mg intake is 30 g/day. Faecal
excretion is 24 g/day, thus apparent absorption is only 20%. The cow appears to
have no effective mechanisms for regulating net uptake of Mg from the gut or
mobilisation of Mg from the skeleton. Moreover, as with calcium (see Figure
2.10) the amount of freely available Mg in the ECF is very small (3 g) relative to
the daily movement of Mg across the gut wall and into milk and urine. Thus, the
cow can run out of Mg quickly.
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young grass (low Mg)

wet weather
wet grass
N,K fertilisers low fibre
food faeces
30 24
chilling
ECF
3g
urine 3 3 milk
Figure 7.4 Exchanges of magnesium in a cow yielding 30 L milk/day. K = potassium,

N = nitrogen, Mg = magnesium. The extracellular fluid (ECF) contains 3 g Mg.
Exchanges are in g Mg/day.
The absence of a physiological mechanism for regulating the concentration of Mg

in the ECF suggests that Mg deficiency did (and does) not present a problem of
survival to wild ruminants, which implies that hypomagneaemic tetany is an
acquired problem of domestication and intensification. Mixed, unimproved pas-
tures nearly all contain sufficient Mg to support maintenance and ‘normal’ levels of
milk production (i.e. enough to feed a calf). The Mg concentration in grass is lowest
in the spring when the grass is young and leafy, especially if heavily fertilised with
nitrogen and potash (K), both of which reduce Mg concentration in the rapidly
growing plants. Grasses rich in N and K form insoluble complexes with Mg in the
rumen thus inhibiting net Mg absorption (Figure 7.4). Moreover, young, lush, wet
grass lacking long fibre leads to large amounts of wet faeces thereby further increas-
ing Mg loss.
In the cool, temperate grasslands of northern Europe hypomagnesaemic tetany is
typically seen in dairy cows shortly after turnout onto high‐quality spring grass.
Beef cows and other less productive animals kept out on poorer land throughout
the year, may show signs of chronic hypomagnesaemia (with the occasional pera-
cute episode) in autumn and winter. In both circumstances, individual cases of
peracute hypomagnesaemic tetany are often precipitated by a period of foul weather,
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especially driving rain or snow. Cold stress will elevate metabolic rate and therefore
Mg demand. Moreover, in conditions of driving rain or snow cows typically stop
grazing and stand motionless with their backs to the wind and their heads bowed.
This is a very effective way of reducing water penetration of the coat in the same
way that humans caught out in the rain in mackintosh or oilskins stand still to pre-
vent the water running down the back of their neck. While this is undoubtedly a
less uncomfortable option for the cow than continuing to graze during the storm,
she cannot afford to interrupt the supply of dietary Mg to the ECF for more than a
few hours. The dairy cow turned out in the spring to grass that is low in Mg but high
in N and K may become marginally deficient in Mg. If, if this high‐risk condition,
she elects not to graze for 10 hours during a stormy night, this may be enough to tip
the balance.

Acute hypomagnesaemic tetany may, if caught in time, be treated by infusing mag-
nesium salts. Intravenous infusion is risky and should not normally be attempted
by the farmer since a sudden increase in Mg concentration can stop the heart.
However, the progress of the condition is so rapid that by the time the vet arrives it
may be too late! Farmers should have an emergency supply of a 25% solution of
magnesium sulphate and administer 400 ml subcutaneously at the first onset of
clinical signs. This may be followed by oral administration (drenching) of 60–90 g
calcined magnesite (MgO) in solution.
In this disease above all others, prevention is the most cost‐effective solution,
even if it only saves one good cow a year. Several approaches have been recom-
mended, some more realistic than others.
1) Magnesium salts (MgCO3 or MgO) can be spread onto pastures or the strips to be
grazed next when strip grazing. This is expensive, time consuming and tractors
can really mess up a wet spring pasture.
2) Magnesium licks may be effective especially for beef cows at risk from chronic
hypomagnesaemia. This may be offered in the form of Mg ‘lollipops’ since Mg
salts are unpalatable. However, as with most minerals offered free choice, intake
is erratic and unlikely to be proportional to demand.
3) Cows may be dosed with Mg ‘bullets’ that lodge in the reticulo‐rumen. This
method can be very effective in nearly all cases but some individuals may lose
their bullets and one dead cow is too many.
4) If cows normally drink from a trough, magnesium may be added to the drink-
ing water. Commercial Mg dispensers work well but, like all gadgets, need to
be checked daily.
5) Most lactating cows at pasture are likely to be fed some concentrate feed during
milking. Compound feed manufacturers produce high Mg, high fibre ‘spring
grazing nuts’ and these provide an excellent way of ensuring controlled, gener-
ous Mg uptake during the high‐risk period.
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In general, I believe that hypomagnesaemic tetany is severe enough to justify a

‘belt and braces’ approach: e.g. Mg supplemented drinking water for all cows and
heifers, Mg‐rich cake for cows in milk and possibly Mg bullets for heifers and dry
cows getting no cake.
Other Mineral Deficiencies
Much has been written about mineral deficiencies in grazing animals, especially in
regard to phosphorus and the trace elements, copper, cobalt and selenium.
Deficiencies of these elements can cause disease and serious loss of production in
cattle that are expected to obtain most, or all of their nutrients from grass, which is
seldom, if ever, perfectly balanced with respect to minerals and many pastures are
known to be deficient in specific elements like copper. Moreover, the increased
application of inorganic fertilisers (N, P and K) to increase yields has tended to
reduce the concentration of other elements such as copper. In dairy herds, the ani-
mals most likely to suffer from mineral deficiencies are the in‐calf heifers since it is
these animals that will be eating most or all of their food in the form of fresh or
conserved grass. Lactating cows will either be fed a balanced total mixed ration or a
concentrate supplement formulated to balance nutrient supply from forage, includ-
ing supply of essential minerals. Lactating cows are therefore unlikely to experience
problems associated with deficiencies of phosphorus or the trace elements unless
fed ‘straights’ without mineral supplements. For this reason, I shall deal with these
problems only briefly.
Phosphorus
The main mineral constituent of bone is calcium phosphate and about 75% of body
phosphorus is contained in the skeleton. Most of the remainder is intimately linked
to the processes of energy metabolism, principally as adenosine triphosphate (ATP),
the energy currency (fuel) for the body. The first signs of phosphorus deficiency are
a non‐specific slowing down of metabolism, marked by reduced performance (body
condition, growth rate or milk yield) and reduced appetite. Many authors have
linked infertility in beef cattle on open range to phosphorus deficiency. There may
be a direct link but I think it more likely that infertility is a secondary consequence
of loss of body condition in phosphorus‐deficient animals. I know of no evidence
foe a link between phosphorus deficiency and infertility in high‐yielding dairy
cows. Osteoporosis (bone demineralisation and weakness) can result from phos-
phorus deficiency but, once again, this is a feature of unproductive cattle in poor
body condition getting little food of any sort. It is not likely to affect cows fed for
high yields.
Grasses, on the whole, tend to be marginal or slightly deficient in phosphorus
(<3 g/kg DM) and the concentration falls as the grass matures. Deficiencies are
Other Mineral Deficiencie 137
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most likely during the winter in the higher latitudes and during the dry season in
the tropics. Whole cereals are usually adequate and products such as soyabean meal
and wheat bran are rich in phosphorus. Most compound feeds and feed blocks
include inorganic phosphates.
It is difficult to make a specific diagnosis of phosphorus deficiency. Blood concen-
trations below 40 mg/L would be grounds for suspicion. There is circumstantial
evidence that cows with phosphorus deficiency exhibit ‘pica’, an ‘abnormal’ appe-
tite for bones and soil. This suggests that cows may have a specific ability to seek out
and consume dietary sources of phosphorus and experience some physiological
reward thereby, but I know of no sound experimental evidence to confirm this
hypothesis. I have seen cases of ill‐thrift and infertility in heifers who have been at
pasture almost all the year round in the gentle climate of south west England and
who have responded to high phosphorus mineral supplements. The animals con-
sumed these supplements avidly – although whether that was because they specifi-
cally associated feeling better with eating these high‐phosphorus diets I cannot say.
Copper and Molybdenum

Pastures are considered to be copper deficient if they contain less than 10 mg cop-
per per kg DM. The metabolic roles of copper are listed in Table 7.2. As with most
mineral deficiencies, the initial symptoms are non‐specific: ill‐thrift and inappe-
tence. Diagnostic signs like depigmentation of hair, especially around the eyes
(‘grey spectacles’), tend to appear some time after the animals have begun to lose
condition. This also applies to swelling and (occasionally) fractures of the distal
metacarpal and metatarsal bones just above the fetlocks. Blood copper concentra-
tions are not particularly helpful in reaching a diagnosis. However, copper is stored
in the liver and, in rare cases, liver biopsies on a small selection of animals may be
justified.
A secondary copper deficiency can be induced if cattle graze pastures rich in
molybdenum (>10 mg/kg DM) and sulphur. In the anaerobic conditions of the
rumen these combine to form insoluble copper thiomolybdate. The problem of
such ‘teart’ pastures has been recognised for over a thousand years in my home
county of Somerset. Affected animals display the typical ill‐thrift and specific
symptoms of copper deficiency but this is complicated by a chronic profuse grey
Table 7.2 Metabolic roles of copper and signs of deficiency in cattle.
Synthesis of red blood cells Anaemia

Synthesis of melanin Depigmentation, ‘spectacles’
Bone growth Bone swelling and fractures, especially above fetlocks
Tissue respiration Ill‐thrift, inappetence
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diarrhoea (‘teart scour’). This appears to be due to a toxic effect of molybdenum

within the gut. More recently it has been suggested that low levels of dietary molyb-
denum, insufficient to cause teart scours, may contribute to infertility in dairy
cattle.
Copper supplements need to be administered with care, since excessive copper
intake can be toxic. When copper‐rich mineral licks are offered free choice, indi-
vidual consumption is erratic and bears no relation to copper requirement. High
copper licks must be kept away from sheep who are particularly susceptible to cop-
per poisoning, which can lead to sudden deaths. Acute copper poisoning is unlikely
to occur in cattle. However dietary concentrations in excess of 40 mg/kg DM (unless
inhibited by high dietary concentrations of molybdenum and sulphur) will inhibit
rumen microorganisms and so reduce appetite. There are many commercial prepa-
rations for oral administration that are designed to lodge in the reticulo‐rumen or
abomasum and provide a slow release of copper (probably in combination with
cobalt and selenium). These work very well so long as they stay where they are
intended, which is not always. Since copper is stored in the liver, the most reliable
way to ensure an adequate controlled supply is by injection at appropriate intervals
(perhaps 2–3 times per year). In the case of teart scours (secondary copper defi-
ciency associated with excess molybdenum and sulphur) or possible molybdenum‐
induced infertility it makes sense to provide a copper bolus for the rumen (to bind
the molybdenum as thiomolybdate) plus a secondary source of copper downstream
(e.g. by injection) to prevent the symptoms of primary copper deficiency.
Cobalt
Cobalt is the essential mineral constituent of cyanocobalamin in vitamin B12. The
rumen microbes synthesise vitamin B12, which is then absorbed by the cow. A vita-
min B12 deficiency causes anaemia in all species. Ruminants have an additional
requirement for vitamin B12 to support glucose synthesis from propionate
(Figure 7.3). Cobalt (and thus B12) deficiency jams a large spoke in the wheel of
intermediary metabolism. Affected animals suffer a severe loss of appetite and rap-
idly lose condition (‘pine’). The cobalt‐deficient pastures of the world are well
known. Cobalt supplementation must be by mouth since the element is required
not by the cow but by the rumen microbiota. Long‐acting cobalt bullets or glass
boluses are the carrier of choice for cattle at pasture with no access to concentrate
supplements.
Selenium
Selenium is incorporated in the enzyme glutathione peroxidase whose metabolic
role, in association with vitamin E, is to regulate oxidation and prevent the accumu-
lation of harmful organic peroxides in, especially, muscle membranes. The dietary
requirement for selenium is extremely small (about 0.1 mg/kg DM) but it appears
Vitamin Deficiencie 139
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that an increasing number of ‘improved’ pastures are, or are becoming, deficient.

However, selenium is also extremely toxic in excess and the safe zone between defi-
ciency (<0.1 mg/kg) and toxicity (>5 mg/kg) is narrow. It is therefore an element
that needs to be treated with caution. A deficiency of selenium and vitamin E,
known as ‘white muscle disease’ can occur in young calves at grass. This presents as
ill‐thrift, stiffness and, classically, extreme weakness of the shoulder muscles so
that the shoulder blades stick up above the line of the spine.
There is good evidence that dairy cows with low concentrations of blood sele-
nium or glutathione peroxidase may be at higher risk of retained placentas after
calving. There are less well proven suggestions of links between selenium defi-
ciency and other problems around calving such as abortions and weak calves.
It may be worth while giving injections of selenium and vitamin E to cows
shortly before calving in herds with a worrying incidence of these problems for
which no other cause can be found.
Vitamin Deficiencies
Vitamins are organic compounds needed in small quantities for metabolism that
cannot be synthesised in the body so must be provided in the diet. Vitamin require-
ments of animals are species‐specific. The water‐soluble compounds such as thia-
mine, riboflavin, biotin, cyanocobalamin classified as B vitamins for humans and
other simple‐stomached animals, are not true vitamins for ruminants since they are
synthesised in adequate amounts by the rumen microbiota. Vitamin C (ascorbic
acid) is not required by ruminants either. Some manufacturers produce vitamin B
supplements for cattle. The only circumstance in which they might have any benefit
would be when a cow has not eaten properly for several days and the rumen popula-
tion is severely diminished.
Vitamin B12 (cyanocobalamin) is a special case. While there is no justification for
including it as a regular supplement to the diet of healthy cattle, it does appear to
stimulate appetite in cows with ketosis or other non‐specific cause of inappetence.
This can be explained in part by its direct effect on gluconeogenesis but it may have
other unknown tonic effects. In any event, anything that encourages a ketotic cow
to eat will help her on the road to recovery.
The fat‐soluble vitamins, A, D and E are all essential for cattle. However, the
vegan cow does not normally consume the vitamins themselves, since they are most
commonly found in animal tissues, but the precursors (or provitamins) that are
converted to the active vitamin after absorption into the tissue of the body.
Vitamin A
Vitamin A, retinol, is present only in animal tissues. Cattle obtain their vitamin A
mainly from the pro‐vitamin beta‐carotene in grass and other green foods. Cereals
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(except yellow maize), hay and straw are deficient in beta‐carotene. Severe defi-
ciency of vitamin A can cause blindness. Marginally deficient animals are at
increased risk of infections of the mucous membranes of the gut and respiratory
tract because vitamin A is essential for their maintenance and repair.
Vitamin A is stored in the liver and a cow that has been at grass for six months
will probably store enough to meet her demand over winter. Moreover, compound
rations for dairy cows are normally supplemented with vitamin A to be on the safe
side. However, the vitamin A status of cows does tend to fall over winter. This may
do her no harm but can be a problem for calves born in late winter and spring since
colostrum at this time may contain insufficient vitamin A to protect the calves
against enteritis and pneumonia.
Other than young calves, the only classes of cattle likely to suffer vitamin A defi-
ciency are growing stock overwintered on some combination of hay, straw, cereals
or roots. Silage is not as rich a source of beta‐carotene as grass but is good enough.
Vitamin D
Vitamin D is the generic name for a range of compounds called calciferols which, as
described earlier, regulate the absorption of calcium from the gut and the concentra-
tion of calcium in the extracellular fluid (see Figure 2.10). The main source of vita-
min D for cattle is the provitamin ergosterol in green plants, which is converted by
ultraviolet light into ergocalciferol (D2). Sun‐cured hay can be rich in vitamin D2.
Moreover, cattle, like ourselves, synthesise D vitamins from provitamins when out-
doors during daylight.
Most of the time the vitamin D requirement of cattle is small because their diet is
rich in calcium. Young stock, overwintered in sunless hovels on poor quality silage
or cereals and straw may benefit from supplementation, probably by injection, with
vitamins D and A. The onset of lactation dramatically alters calcium metabolism
(Figure 2.10). As indicated earlier, injection of large amounts of vitamin D, or the
inclusion of vitamin D in high phosphorus supplements fed to cows prior to calving
may reduce the risk of milk fever.
Vitamin E
Vitamin E is the generic name for compounds called tocopherols which, together
with selenium, regulate oxidative processes, especially in nerve and muscle mem-
branes. Grass and other green foods are rich in tocopherols. These are reasonably
well preserved in silages but almost entirely lost during hay‐making. The cereal
germ and by‐products containing the germ are also rich in vitamin E. Deficiency
conditions such as white muscle disease were considered under selenium. Vitamin
E is stored in the body and suspected deficiency states can be controlled by an
injection usually containing both tocopherol and a slow‐release source of
selenium.
Last Words on Minerals and Vitamin 141
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Last Words on Minerals and Vitamins
Minerals and vitamins are essential elements of any diet. Moreover, specific defi-
ciency of a mineral such as selenium, required only in minute amounts, may be
sufficient to impair the performance of a ruminant since metabolism can only pro-
gress at the rate of its slowest performer. In practice, however, minerals and vita-
mins only assume importance in circumstances where the basic diet for the cow is
deficient. This should always be considered as a possibility when cattle are getting
all, or nearly all, their nutrition from fresh or conserved pasture. When dairy cows
are fed substantial amounts of concentrates or a well‐balance total mixed ration to
promote high yields, mineral and vitamin deficiencies are rare. Metabolic disorders
leading to loss of production are far more likely to be due to shortages (or excesses)
of the major elements of the diet fed to meet energy and protein requirements. It is
dangerously easy to grasp at a symptom that has been linked to deficiency of a spe-
cific mineral or vitamin and so prescribe a simple (and relatively cheap) solution
that may or may not improve matters. Generous supplementation of diets with
minerals and vitamins is likely to be relatively harmless and not too expensive.
However, it should not be allowed to divert the mind from more realistic sources of
the problem.
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143
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Part III
Housing Health and Management

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145
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Healthy and Humane Housing and Handling
The owner of arguably the most well‐known dairy enterprise in the south west
of England was asked for the secret of their success. Standing among his beauti-
ful looking Friesians, he gave his answer: ‘we look after our workers’. The most
successful dairy enterprises are those that best meet the need to achieve eco-
nomically sound, sustainable production within systems of housing and man-
agement that best meet the need to provide for the physiological and
psychological needs of their workers, the dairy cows. These were discussed in
Chapter 4. To recapitulate briefly, these are:
1) Optimal productivity.
2) Comfort and security.
3) Health and hygiene.
4) Behavioural satisfaction and freedom of choice.
These principles apply to all accommodation and management practices whether
on the farm, in transport, in lairage or, finally, at the point of slaughter. This chapter
considers systems of housing and management primarily from the point of view of
the dairy cow. Links to detailed descriptions of the structure of buildings, fixtures
and fittings are given in the suggestions for further reading listed at the end of the
book.
A
ccommodation
In the UK most dairy cows are housed for about seven months per year and spend
five months at pasture. This system of management is only appropriate to cool tem-
perate maritime climates where cows can get easy access to high‐quality pasture
during the grazing season close enough to the milking parlour to permit twice‐daily
milking. Realistically, the need to move the herd between good pasture and the
milking parlour also puts an upper limit on herd size. When viewed in an interna-
tional context, this system, which I grew up to think of as normal, must now be
ranked as a minority pursuit. These days, most of the world’s biggest dairy producers

146 Healthy and Humane Housing and Handling
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operate in areas that are too hot, cold and/or too dry to be pasture‐based so operate
on the principle of housing cows throughout lactation close to the milking unit and
bringing the feed to them, probably in the form of a total mixed ration. These sys-
tems have evolved in parallel with increases in milk yield through developments in
breeding and nutrition to the point where the daily nutrient demand of the high‐
yielding cow far exceeds that which can be provided from fresh or conserved pas-
ture. Having accepted the principle of continuous housing throughout lactation
and the substantial capital outlay required for this system, the economics of scale
dictate that the larger the unit, the greater the potential for profit. In the 25 years
since the publication of the second edition of ‘Understanding the Dairy Cow’ there
has been a huge increase in the quantity of milk coming from herds of one thou-
sand cows or more. There are, of course, conspicuous exceptions to this trend, rang-
ing from high‐yielding dairy herds in pastoral New Zealand to low‐yielding but
successful dairy cooperatives in India. Nevertheless, huge, intensive cow ‘factories’
are here to stay. Inevitably they have been criticised or condemned on more‐or‐less
valid welfare and environmental grounds. I shall consider in more detail the social
and environmental issues arising from the extreme intensification of dairy produc-
tion in the final chapter. At this stage, as through most of the book, I try to view
systems of housing and management through the eyes of the cow and, in this light,
I suggest that herd size is irrelevant, provided that adequate provision is made for
provision of those elements of the ‘five freedoms’ achieved through housing and
management, namely comfort and security, health and hygiene, behavioural satis-
faction and freedom of choice. Each cow within the herd should have access to a
clean and comfortable bed, reasonable shelter from the worst of the weather, unim-
peded access to a sufficient quantity of clean, wholesome food and water, sufficient
space to move around without difficulty or interference from other cows and to
express natural patterns of social behaviour including, of course, oestrous behav-
iour (‘bulling’). Provision should also be made to direct cows without difficulty to
specialist areas such as the milking parlour, calving boxes, and restraining stalls for
procedures such as artificial insemination, veterinary inspection, foot trimming
and treatment for lameness.
The Cow House

We should never forget that the main reason we house cows is to serve our needs,
not theirs. As explained in Chapter 4, cows can achieve thermal comfort in a wide
range of climates. On pasture‐based farms in the cool, wet regions they will appreci-
ate protection from wind, rain and snow but the main reason we bring them indoors
in the winter it to prevent them ruining (‘poaching’) the pastures. In all but the
most extreme of the hot, dry zones, it can be enough to provide simple shelters for
dairy cows where they may rest in comfort under cover and out of the rays of the
sun (see Figure 4.1). Within this shelter there should be enough space for all cows
to lie down on a suitably comfortable bed, which could be of straw or deep sand
Accommodatio 147
(q.v.). The values given in Table 8.1 of 3.2–5.8 m2 in loose housing for cows ranging
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from 350 to 700 kg body weight should be taken as minimum standards. When sun-
shades can be erected cheaply from local materials the covered area could be dou-
bled to allow each cow to stretch out on a hot day at a reasonable distance from her
neighbours so as to dissipate as much body heat as possible. When the climate is dry
for most of the year the feed fence and loafing area of the dry lot need neither be
covered nor surfaced with concrete. This obviously saves money and permits one to
be generous with space, which can be very valuable when the rains come.
In pasture‐based systems within the cool, temperate maritime regions where
cows are normally confined only during the winter months, the main problem is
rain, not so much for its direct chilling effect on the cows but because any uncov-
ered area of bare ground will rapidly deteriorate into a sea of mud. In these circum-
stances it is essential for the cows to have a covered bedding area and for the
passageways between bed, feed face and milking parlour to be made of an impervi-
ous material that drains freely and can be scraped clean (this usually implies
Table 8.1 Dimensions and space requirements for cows and heifers.
Cows Heifers
Friesian
Jersey Friesian (2 year old) Holstein
Body weight (kg) 350 600 450 700

Height to withers (cm) 115 135 125 150
Body length (cm)* 140 162 145 172
Reach of mouth (cm)
At floor level 85 90 84 92
30 cm above floor level 100 105 102 107
Cubicle dimensions (cm)
Length to wall 200 220 240 240
†
Length behind trough 140 160 160 180
Width between partitions 110 115 115 120
Height of neck rail 100 105 105 110
Feeding face width (cm) 55 70 70
2
Loose housing (m )
Bedded area/cow 3.2 5.0 4.0 5.8
Feeding, loafing etc. 1.3 1.8 1.5 2.0
* Tailhead to shoulders; † where present.
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c oncrete). Since roofing material and concrete floors are both expensive the amount
of space allotted to each cow is reduced to a minimum and loafing space tends to
disappear altogether. There is a further constraint on the amount of concrete‐based
loafing space outside the roofed area, namely the problem of disposal of the large
amount of dirty water resulting from rain on slurry.
There are three ways of accommodating dairy cows under cover:
●● The cow house or byre in which cows may remain tethered in individual stalls all
winter and fed and milked where they stand
●● The loose‐housed cattle court, usually divided into a bedded area (e.g. straw or
sand) and an unbedded feeding/loafing area, usually of concrete.
●● The free stall or cubicle house in which cows are unconstrained and can enter a
cubicle of their choice to lie and rest.
The traditional cow byre in which cows are tied up all winter is much less common
than it was, but still common in Nordic countries and in Alpine regions where the
cows spend the winter having grazed idyllic mountain pastures during the summer.
The tie stall has come under considerable criticism from animal welfare organisa-
tions, mainly on the grounds that it denies freedom of movement and social behav-
iour. Cows that are tied up all winter are also likely suffer from swollen knees and
hocks, especially if the bedding is inadequate. They are however at lower risk of foot
lameness than cattle in many free stall/cubicle systems (q.v.). The system is likely to
occupy a lower and lower proportion of the international dairy herd, mainly because
it is only realistic for herds that are very small by modern‐day standards.
Housing for the great majority of dairy herds is based either on free stalls/cubicles
or a loose‐housed cattle court (Figure 8.1). Although the recommended bedded
area for a Friesian cow in a straw yard is 5.0 m2 compared with 2.5 m2 for a single
cubicle (Table 8.1) the amount of space allocated to passageways and the feeding
area is the same. The costs of construction for a cubicle house are estimated as
about 20% greater than that of a loose‐housing unit. However, the costs of providing
adequate bedding with straw will be at least four times as great with loose housing.
The cattle court in which cows can luxuriate in a deep dry straw bed is ideal but
only likely to be an economic proposition on farms which grow enough cereals to
provide one tonne of straw for every cow/winter. The dairy cow lying on a thin, wet,
dirty bed would be better off in a cubicle.
The problems of winter‐housing dairy cows have been exacerbated by the switch
from hay to silage as the main source of winter fodder. Silage is indisputably more
nutritious than hay but it is very much wetter so cows eating silage excrete far
greater quantities of water in faeces and urine. This makes it more difficult to avoid
wet bedding in a cattle court or large amounts of slurry in the passageways of a
cubicle house. Both increase the risk of foot damage. Large amounts of slurry or
foul water lying around the cow house ensure that the bedding is seldom, if ever,
dry and this encourages the growth of bacteria such as Escherichia coli that can
cause environmental mastitis.
Accommodatio 149
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2600
600
CROSS SECTION
SIDE ELEVATION
3000 2100 2400 2100
C U B I C L E S
SLATTED PASS
C U B I C L E S
w
w
225
FEED STANCE
4200
23 850
FEED PASS
2100 3000
FEED STANCE
225
C U B I C L E S
w
w
2100 2400
SLATTED PASS
C U B I C L E S
30 000
PLAN
Figure 8.1 Plan of a cubicle house for 90 cows (from Scottish Farm Buildings
Investigation Unit 1985).
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It is important to minimise the amount of water and slurry lying on the floor. The
cubicle house illustrated in Figure 8.1 has slatted floors in the passageway between
the cubicles. This reduces the accumulation of slurry but slats themselves, espe-
cially when worn, are a risk factor for foot lameness. An effective alternative is to
install a mechanical slurry scraper that ‘cleans’ the passageways several times per
day. If it must be done by tractor it should be done at least twice daily. The problem
is further complicated by the fact that the average Friesian‐Holstein cow evaporates
about 20 L of water per day from the skin and respiratory tract. During a damp
British winter, the relative humidity in cattle houses frequently approaches 100%:
they are very clammy places indeed. The most practical way of removing water
from a cowshed is by natural ventilation. This is best achieved by the use of space
boarding along the side walls to a depth of at least one metre below the eaves and
space boarding from eaves to ridge at each gable end. Space boarding as based on
vertical wooden planks (4 in or 100 mm) with 20 mm (1/4 in) gaps between each
plank. This permits the natural convection of relatively warm, moist air out of the
building but is extremely effective at preventing strong draughts and keeping out
the rain and snow. It also has the merit of letting in a lot of light. If the building has
a central feeding passage then the roof ridge should also be open (Figure 8.1).
Several other important features are also illustrated by Figure 8.1 and Table 8.1.
Since the width of the cubicles plus stanchions is almost twice the space required by
each cow at the feed fence, it follows that there should be two rows of cubicles for
each feed fence. Water troughs are sited at each end of the inner row of cubicles and
there is a passageway at each end of the rank of cubicles. This makes it easier for
each cow to go where she wants to go and avoids a bullied or timid cow from becom-
ing trapped at the dead end of a passage by a real or imagined threat from another
cow. The building is also well equipped with roof lights that, together with the space
boarding, give good visibility even on sunless winter days. This makes inspection
easier and is good for the morale of the herders and (probably) their cows.
An alternative to the cubicle house is cow kennels, which involves a simple cov-
ered shelter with an open ridge wherein the sides of each cubicle form the support
to the roof (Figure 8.2). The relative economics of cubicle house versus cow kennels
(capital cost, labour, slurry disposal) are outside the scope of this book. From the
cows’ perspective they are much the same.
Cubicle Design
The cow cubicle or free stall differs from the tie‐stall in that the cow may enter and
leave at will. She gets her food (and is milked) elsewhere (Figure 8.3). The design
should ensure that:
●● The bed should be comfortable, clean, dry and free from excess contamination
with faeces and urine.
●● The cow should be able to lie down in a normal position and without risk of being
trodden on or kicked by other cows.
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Figure 8.2 Cow kennels.
(a)
manger
lip
bedding
(b)
head rail
mat brisket
board
Figure 8.3 Stalls for dairy cattle: (a) a cow lying in a tethered stall, (b) a cow rising to
her feet in a free stall or cubicle.
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●● The cow should be able to stand with all four feet in the cubicle (not with the hind
feet in the dunging passage).
●● The cow should be able to change position from standing to lying (and vice versa)
in a normal manner and without difficulty.
Considerable attention has been given to addressing these needs through cubicle
design since the first cubicles were installed by Howell Evans on his farm in
Cheshire, UK in 1961.
The cow must stand with her head at the front of the cubicle so that faeces and
urine fall into the dunging passage. She is persuaded to enter head first by providing
a step up of about 250 mm from passage to cubicle. Cows are apparently reluctant
to back into a cubicle up a step of this height. Cows (nearly) always pass faeces and
urine while standing up, so that if the cubicle is the correct length, she should stand
with her back legs just in the cubicle so that she excretes into the passageway. When
she lies down all her body should be on the bed. Her hocks and especially her udder
should not overlap the lip at the back of the cubicle, her legs should not intrude into
the space allocated to her neighbour. There is no reason to assume that cows prefer
to align themselves this way, especially if there is nothing before their eyes but a
blank wall. I did once visit a cubicle house designed for Friesians after the farmer
had decided to switch to (much smaller) Jerseys. The cows entered the cubicles
head‐first but at least half of them turned around and lay down looking out in order
to see what was going on. Needless to say, this called for an expensive design change.
Cows normally lie down front legs first and stand up front legs last. During both
movements, especially standing up, they need to lunge forwards in order to main-
tain their balance (Fig 8.3b). There should be sufficient space at the front of the
cubicle to permit this normal forward lunging motion. Some cattle in cubicles that
are too short learn to change position in reverse order (i.e. get up front legs first) and
may adopt a ‘dog‐sitting’ posture on their rumps with their front legs straight. This
form of adaptation by some cows to an unnatural constraint is no justification for
building smaller cubicles. The need to ensure that cows dung in the passageway,
have enough lying room and enough space to stand up and lie down without diffi-
culty can be achieved by the provision of a head rail or brisket board that prevents
them from lying too far forward but gives them plenty of lunging space. The head
rail only works if it is in exactly the right place and at the right height. Personally, I
prefer the brisket board.
The divisions between cubicles have evolved in response to experience and to
fashion and there is now a bewildering choice of designs. The objectives are to align
cows properly in their own cubicle, to prevent their feet interfering with, or injuring
their neighbours and to minimise the risk to limbs or teats as the cow changes posi-
tion. Many of the early cubicles had solid horizontal rails at an elevation of 300 mm
(one foot) from the ground under which cows could trap, or even break a leg. The
modern trend is to minimise the amount of pipework or other rigid material. One
effective solution is to replace the lower horizontal bar by (for example) polypropylene
rope that is flexible and can, in an emergency, be cut.
Accommodatio 153
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The Cubicle Bed

A clean, dry cubicle bed can be maintained on top of a base of rammed chalk or soil
with a lip at the back of the cubicle, or on a base of concrete or bitumen macadam
with an 80 mm slope from front to back and no lip to impede drainage. Whether the
base is chalk, soil or concrete, the dairy cow can only obtain a reasonable degree of
comfort is she is provided with some form of bedding. Her size and shape are such
that the pressure exerted on skin and bone at sites like the knee and hock, and the
shear forces when she changes position, are far more severe than we would experi-
ence if lying on the same surface. Anyone who doubts the need for bedding should
spend a night lying on concrete! Smaller, non‐lactating beef cows with small udders
can be housed successfully, though not to their satisfaction, on concrete slats in
areas such as the Islands of Orkney where straw is prohibitively expensive. However,
slats are not an acceptable bed for lactating cows whether of dairy or beef type.
Several types of bedding can be used successfully in cubicles. Each has its pros
and cons.
Straw is likely to be the cheapest bedding when produced on farm. Its value is
greatly improved if it is chopped since this makes it bulkier and more absorbent and
should reduce usage by about 25%. The bed should be made to a depth of at least
50 mm if the base is made of concrete. New straw should be provided three times a
week and any straw fouled with urine or faeces should be raked into the dunging
passage twice daily.
Wood shavings make a very comfortable, hygienic and dry bed though they tend
to be expensive. Depth of bedding and frequency of application should be the same
as for straw (50 mm and three times a week). Sawdust is more absorbent and prob-
ably even more comfortable than shavings. However, in damp conditions sawdust
can be a medium for the growth of E. coli and is therefore a risk factor for environ-
mental mastitis.
Sand is both hygienic and extremely comfortable if the bed is deep enough (think
about it sometime when lying on a beach). This requires a depth of at least 50 mm and
80 mm would be better. A thin coating of sand can be as abrasive as sandpaper.
Cubicles bedded with sand need a lip to keep the sand in. The bed should be cleaned
and raked daily but new sand need only be added at intervals of 2–3 weeks. When
managed properly, it is probably the best choice. It can present problems for some
slurry disposal systems but it is, in my opinion, such a good option that slurry han-
dling systems should be installed or modified to accommodate it. In hot, dry, sandy
regions (e.g. Australia, South Africa) the lying area in large loose‐housed units com-
monly consists of a deep bed of sand that is regularly topped up but may only be
cleaned out once a year. My experience of cows housed throughout lactation in these
units is that they not only appear very comfortable, they are also free of the most obvi-
ous signs of uncomfortable bedding, namely scraped and swollen knees and hocks.
Cow mats are a popular choice with dairy farmers, especially those without access
to cheap straw. They are initially expensive but can be kept clean and are less time‐
consuming than straw. Over‐zealous use of the hose should be resisted as wet mats
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can be very slippery and increase the risk of injury to the cow when changing posi-
tion. Within the range currently on sale, the ones with the most ‘give’ are best for
the cows, for obvious reasons. Thin mats are better than just concrete but not much.
A dry, interior‐sprung mattress, whether bought off the shelf or home‐made using
old tyres, and covered with a little clean, chopped straw, is pretty good.
Passageways
The floor surface of passageways needs to be skid‐resistant so that cows may walk
freely without risk or fear of slipping and injuring themselves. However, the surface
should not be so rough as to cause excessive abrasion to the sole of the hoof and
predispose to foot damage. Finally, the surface should be kept as clean and dry as
reasonably possible since a build‐up of slurry can erode the sole and heel and pre-
dispose to lameness. Moreover, if cows enter their cubicles with their feet soaked in
slurry, this will foul the cubicle bed so increase the risk of environmental mastitis.
In Figure 8.1 the floors of the passageways are made from concrete slats, 125 mm
wide with a 35 mm gap between the slats. This is a relatively expensive option but
one that ensures that the passageways stay relatively clean, dry and free from
slimy – and therefore slippery – moulds. Solid concrete floors for passageways
should be scraped at least twice daily to avoid the build‐up of slurry. New, solid
floors are tamped and brushed to roughen the surface slightly. Old concrete floors
that have worn smooth and slippery can be restored by cutting shallow grooves with
a special grooving machine. Newly‐laid concrete floors in cow houses have some-
times been associated with an increase in foot lameness. This is probably not due to
abrasion per se but to a chemical reaction between new concrete and wet slurry that
produces caustic chemicals that erode the sole of the hoof.
It is generally accepted that concrete, however well laid and managed, is less than
an ideal surface for cows, whether walking, standing to eat or just standing idle.
There are several ways to reduce the stress, most of them involving rubber. Rubber
mats can be installed, typically at the feed face, where hungry dairy cows will spend
most of their standing hours. It has been suggested that this might encourage the
cows to eat more. A more comprehensive (though expensive) approach is to surface
the passageways with a rubber/concrete mix. There is good evidence that cows find
this a more attractive surface to walk on and it probably helps to reduce the preva-
lence of foot lameness.
Calving and Isolation Boxes

All dairy units must include accommodation for cows that require individual atten-
tion because they are sick or about to calve – the bovine equivalent of hospital beds.
The number of calving boxes required per 100 cows depends on the calving pattern
(i.e. the period during which most cows calve) and how many cows are likely to
calve while out at grass. A clean pasture is a splendid, hygienic place for a cow to
Accommodatio 155
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have a normal delivery but it can present problems if she requires assistance, and
even bigger problems if she can’t get up afterwards. In circumstances where most or
all the cows calve indoors five boxes per 100 cows are recommended to ensure that
each cow has access to a clean, disinfected box at calving and that any cow that
experiences complications can be nursed in specialist accommodation for as long as
necessary. The specialist requirements for calving and isolation boxes are as
follows.
●● They should, wherever possible, be separate from the main cow house while close
enough to permit a cow that is sick, injured or about to calve to be moved with as
little fuss as possible.
●● Each box should be individually drained. The floors and walls should be rendered
so that they can be power‐washed or steam‐cleaned.
●● The boxes should be large enough for a calving cow to lunge about without risk
to the stock(wo)men, vet or herself. This requires a floor area of at least 4 x 4 m.
There should be at least one tethering ring (preferably more) to restrain the cow’s
head during assisted calving whichever way she has chosen to lie down.
●● There should be good electrical lighting and a protected power socket close to
hand.
●● The boxes and their doors should be sited so that any cow that dies can be con-
veniently be removed by tractor.
It should go without saying (but doesn’t) that the needs of the individual cow for
comfort, security and hygiene become even more paramount when she is sick or
about to calve. Ideally, she needs a spotless box with a generous deep bed that will
need to be mucked out and thoroughly disinfected when she leaves. Unchopped
straw is the bedding of choice.
Where there is a policy for transition management of cows around the time of
calving, especially in large herds, dry cows will be housed in groups, fed and man-
aged according to their calving dates (see Chapter 12). When calving is imminent,
they should ideally be moved into individual pens. Many aren’t, and this seems to
suit the farmers, but it must carry an increased risk of infection.
The most interesting approach to the business of transition management that I
have seen was on a very highly mechanised farm housing about 1000 cows in cubi-
cle units. After drying off, 6–8 weeks before they were due to calve, cows were
moved away from the hurly‐burly of the cubicle house. At first, they were housed in
kennels, then about 2 weeks before calving they were moved into deep‐strawed cat-
tle courts in groups of about twelve. Sufficient individual boxes were provided to
accommodate each cow at the time of calving and these were equipped with closed‐
circuit television so that the herders could observe the cows when they calved, as
expected, during the night. I first saw this unit when it had been in operation for
about three years. All was working splendidly – except for the closed‐circuit televi-
sion, which had been abandoned after about 6 months. Before the creation of the
maternity suite, the cows had been exposed to the noise and distraction of the main
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dairy unit right up to the point of calving. In these circumstances about 80% of the
cows calved between 10.30 pm and 6.00 am. In the peace and quiet of this new unit
this pattern was reversed; nearly all cows calved between the times of the first and
last visits of the day at 6.00 am and 10.30 pm respectively. Needless to say, the cow-
herds, who didn’t care much for television even when it showed pictures of cows,
were delighted.
Heifer Yards
The problems of housing dairy calves during their first winter are mostly concerned
with the business of minimising infectious diseases, principally diarrhoea and pneu-
monia. These are endemic diseases, involving viruses and bacteria that are ever with
us. Strategies for disease control are outside the scope of this book. All that can be
said here is that they should be tailored by the farmer and veterinary surgeon to meet
the specific circumstances of the individual farm. They will probably include a vac-
cination policy but much can be achieved through attention to housing and manage-
ment: e.g. rearing susceptible calves, if possible, at a distance from the main herd,
attention to stocking density and ventilation within the buildings.
During their second winter, heifers should be housed in groups well matched for
size and preferably in accommodation similar to that which they will experience as
lactating cows. If they are destined for a cubicle house, they should gain experience
of the routines before they calve down for the first time and enter the adult world of
cubicles, milking and boss cows with a tetchy sense of who goes where and when.
Dimensions for cubicles for heifers are given in Table 8.1. Heifers can be discour-
aged from defaecating in cubicles by placing the head rail further back. However,
this may deter them from entering the cubicles and they may stand for long periods,
or even worse, lie in the dunging passage. Wise cowherds will allow heifers time to
adapt to cubicles even if this means, in the early days, shovelling a bit more dung
into passageways. Head rails can be adjusted when the heifers are ready.
Handling Facilities
The handling facilities on a dairy unit must include:

1) A race leading to a holding pen or crush in which most or all of the herd can be
restrained for routine procedures such as blood sampling, vaccination, tubercu-
lin testing. The race should incorporate a foot bath. Most milking parlours are
unsuitable for any procedures other than milking.
2) A treatment stall in which individual cows can be restrained for artificial insemi-
nation (AI), pregnancy testing, foot trimming and treatment of lameness. This
can be the same crush and at the end of the same race as that used for the more
general procedures listed in (1) but it may be advisable to have a more expensive,
specialist unit for foot treatment (Figure 8.4).
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Figure 8.4 A restraining crush as used for routine foot treatment.
Marshalling areas should be designed to ensure that cattle are not forced to enter
darkened areas or disturbed by sudden changes in floor surface (gullies, gratings,
etc.). Because their centre of gravity is quite far forward, they are uncertain when
walking downhill. If this is essential it is better to use widely spaced steps than
ramps. Ideally, they should be able to see where they are going but not distracted by
things happening to the left and right of them.
Cattle, like all ruminants have a clearly defined ‘flight zone’. So long as the poten-
tial threat from a predator (animal or human) is perceived to be outside this flight
zone, cattle will go about their business undisturbed. If a human enters this flight
zone slowly and calmly, the cow, equally smoothly and calmly, will move away. If
the human intrudes too far or too fast, or if she can see no way of escape, then she
is liable to panic. Details and designs of facilities for cattle handling are given under
further reading.
Lameness
The dictionary definition of lameness is a disability in movement of the limbs. A

cow may limp and show reluctance to move because of pain in one or more feet or
joints. Her movement may also be impaired by partial paralysis, muscle weakness,
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nerve damage, things that may or may not actually hurt. She may also appear lame
and reluctant to move when affected by a condition unrelated to the locomotor sys-
tem, such as severe mastitis, pleurisy or traumatic reticulitis (Chapter 12). However,
over 90% of all cases of painful lameness in dairy cows are caused by injury and/or
infection to the hoof, heel or skin between the claws of the hoof. Other afflictions of
the limbs include swollen knees and hocks. These do not appear to cause a great
deal of distress unless the skin is broken and there is a deep‐seated infection.
Nevertheless, swollen knees and hocks are an indicator of bad housing, which can
be a major contributor to foot lameness. Occasionally a cow may dislocate her hip
or fracture her pelvis through slipping and falling, especially when weakened by
calving and hypocalcaemia. Some of these cows may struggle on and even milk
quite satisfactorily but they tend to lose condition rapidly and it may prove not only
humane but also economic to send them for slaughter. If they are in too much pain
to move they should be slaughtered on farm.
Most recent surveys of foot lameness in dairy cows reveal that the prevalence of
cows with moderate or severe impairment of movement is over 20%. This places
foot lameness as one of the three big production disorders of dairy cows, the others
being infertility and mastitis. In terms of cow welfare, it has to be the worst of the
three since it is always associated with chronic pain. To understand foot lameness,
it is necessary to understand the structure of the bovine foot. The horny hoof of the
two claws is made up of the wall, which grows down from the coronet, and the sole
(Fig 8.5). The junction between the wall and the sole is called the white line, which
is confusing, since in cattle, the line is not white. It is rather closer to white in the
hoof of the horse, from which the name originates. The hard, insensitive tissues of
the wall and sole (which may be thought of as the cow’s shoes) are joined to the liv-
ing tissues of the foot by the laminated folds of the corium. These are formed by the
Extensor tendon
CORIUM Laminae Deep digital flexor
Connective tissue
Pedal bone
Wall horn
Bulb of heel
Sole papillae Digital cushion

White line
Figure 8.5 Schematic illustration of the bovine foot, indicating the suspensory
apparatus.
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interdigitation of lamellae, modified epithelial tissue pointing inwards from the

horn wall and collagenous connective tissue growing outwards from the perios-
teum of the pedal bone. This laminated structure creates a very large surface area
of contact between the horn and the pedal bone, thus permitting much of the
weight of the cow to be borne by the suspensory apparatus in the corium. The sur-
face area of the laminae in the cow is much less than in the horse but further sup-
port is provided by fatty digital cushions under the pedal bone.
Conditions that Cause Lameness

Over twenty different conditions have been described as causes of foot lameness in
cattle. In my opinion, this degree of discrimination is largely unnecessary and,
indeed, unhelpful since it increases the probability that two different observers
regarding similar lesions will put them into different categories, thereby confound-
ing attempts to assess prevalence of the different conditions in relation to environ-
mental and other risk factors. For practical purposes, I suggest that, in the first
instance, foot lesions can be divided into three categories, those due to injury, infec-
tion and injury complicated by infection. A separate subdivision can be made
between the high prevalence, endemic sources of injury (sole lesions) and infec-
tions (digital dermatitis), which must be considered as production diseases (i.e.
largely our fault) and sporadic (rarer) conditions such as ‘foul in the foot’, which
arise by accident: although likely to be in an environment that predisposes to
accidents.
Sole Haemorrhage and Sole Ulcers

Most routine foot inspections of dairy
cows in the first 12 weeks of lactation
reveal evidence of haemorrhage to the
sole of one or more feet in over 50% of
animals. These range from slight bruis-
ing to a sole ulcer, where there has been
complete destruction of the sole with, in
most cases, infection at the site of the
open wound. Slight to moderate bruising
of the sole may not be associated with
lameness, as seen by limping, arching of
the back and reluctance to move. Sole
ulcers, unsurprisingly, are very painful
indeed. By far the most haemorrhages
and sole ulcers arise towards the heel on
the lateral claw of the hind feet (Fig.8.6).
For many years it was thought that these Figure 8.6 A sole ulcer.
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lesions were caused by external damage, e.g. a stone getting caught in the hoof.
That, of course, could not explain why stones should have a predeliction for this
particular site. It was later recognised that the damage came from within, pressure
of the pedal bone on the sole, resulting, in some part, from external pressures on the
sole when walking on hard surfaces such as concrete, but also from loss of integrity
in the suspensory apparatus provided by the laminated tissues in the corium. This
condition, common to dairy cows, was for many years (and in many references still
is) described as subclinical laminitis, because it appeared to be a less severe form of
laminitis seen especially in beef cattle being finished on high cereal diets (Chapter 7).
This diagnosis failed to explain why laminitis in beef cattle (or horses) typically
presents as an extremely painful affliction of all four feet, while ‘subclinical lamini-
tis’ in dairy cows typically affects the outer claws of the hind feet only. More recent
histological evidence has shown that most cases of sole haemorrhage in dairy cows
do not involve inflammation of the laminated papillae of the epithelium but show
signs of damage to the collagenous connective tissue that attaches the laminated
papillae to the pedal bone (Figure 8.5). The effect of this is to weaken the suspen-
sory apparatus, allowing the pedal bone to sink and apply increased pressure on the
sole. The typical site of the sole ulcer (Figure 8.6) is at the point where the base of
the pedal bone presses most strongly on the sole.
The first signs of sole haemorrhage typically appear about 4–6 weeks after calving.
However, as anyone who has hit their thumb with a hammer will recognise, the
black bit of the nail, evidence of haemorrhage, does not reach the tip of the nail
until several weeks after the original injury. So too with cows. The first pressure
damage to the inside of the sole occurs some time before the haemorrhage becomes
visible on the outside, i.e. before calving. It is well known that, prior to calving, the
connective tissue in the ligaments of the pelvic birth canal relax in the days before
calving to ease the passage of the calf. The mechanism for this appears to be linked
to the increased secretion of the hormone relaxin and there is good evidence from
other species, including humans, that the effect of relaxin is not specific to the pel-
vic ligaments but has a more widespread relaxing effect on connective tissue. This
hypothesis implies that the feet of cows in the periparturient period are more sensi-
tive to stresses on their feet around the time of calving and therefore in need of
special care. The management of lameness in cows resulting from sole lesions is not
a simple business and will be discussed in detail later. One very effective way to
reduce the incidence of sole lameness is to house newly‐calved cows (and especially
heifers) in deep straw bedding from 4 weeks before to 8 weeks after calving rather
than introduce them immediately to cubicles and concrete floors.
The control of sole lesions and other causes of lameness through attention to
housing and management is discussed later. At this stage, it can be said that treat-
ment and relief of pain for a cow with a sole ulcer involves pairing the foot to allow
drainage from the centre of inflammation, bandaging the foot to prevent further
infection and fixing a block (or shoe) on the unaffected claw so that she does not
have to bear weight on the claw that hurts. A long‐acting painkiller, such as
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etoprofen will also provide relief. However, the effect of the block alone can be
k
dramatic. A cow in extreme pain on entering the treatment crush will often move
quite freely as soon as she leaves.
White Line Disease

The white line is the junction between the horn of the wall and the sole (Figure 8.5).
Separation of this junction exposes the living tissue to infection that may track up
the laminae of the wall or across the sole causing inflammation with the formation
of pus. The pus can break the surface either at the coronet or, having completely
underrun the sole, through the softer skin at the bulb of the heel. While the pus is
trapped within the hoof, the pain is intense. The actual separation of the white line
is probably cause by external shear forces on the foot. The factors that weaken the
white line and predispose it to damage are not well understood, although damage
and sinking of the pedal bone associated with sole haemorrhage are likely to be
contributing factors. Supplementation of the diet with biotin appears to offer some
protection against white line disease, although not sole haemorrhage, which is dif-
ficult to understand.
Digital Dermatitis
Digital dermatitis is an infection of the skin of the foot. It was first recognised quite
recently (1973) in Italy but has spread rapidly to become a major problem on dairy
units worldwide. It is caused by spirochaete organisms, Treponema sp., which are
anaerobic – they thrive in oxygen‐free environments like deep slurry. However, they
can survive in encysted form while exposed to air so can be transmitted from farm
to farm, for example on claw trimming equipment. One way or another, the organ-
isms are very persistent. Once digital dermatitis is on the farm it is almost impossi-
ble to get rid of, so must be managed as an endemic disease.
The condition typically appears first on the bulb of the heel, or in the interdigital
space as a wet, warty lesion. If allowed to develop, there will be erosion of the skin,
expanding the area of damage and penetrating the underlying tissues. Digital der-
matitis (DD) is extremely painful. The nature and symptoms of the pain are quite
distinct from those associated with sole ulcers. A cow with a sole ulcer will wince as
the affected foot makes contact with the ground during locomotion but will stand
quietly so long as she can keep the weight off the affected claw. Cows with DD (pos-
sibly in all four feet) are very uncomfortable while standing still. They are said to
‘paddle’, constantly lifting one foot after another off the ground. This must be
because the lesions of DD sting all the time and most severely when the cow’s feet
are covered in slurry.
Since DD usually presents as a herd problem, treatment is usually carried out on
a herd basis. The approach involves the use of locally applied antibiotics or skin
disinfectants such as copper sulphate. These can be sprayed on to affected feet at the
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time of milking. However, it is more common to put them into a foot bath through
which all cows are made to walk, ideally on a daily basis, while the disease is
prevalent.
Interdigital Necrobacillosis ‘Foul’

Interdigital necrobacillosis or ‘Foul in the foot’ is a sporadic condition, i.e. not trans-
missible between cows. It is caused by bacterial infection (most commonly
Fusobacterium necrophorum) of broken skin, typically incurred when damaged by
a stone or other sharp object when walking through a muddy gateway. Individual
treatment involves cleaning up the affected area followed by antibiotics. Prevention,
obviously, involves steps to remove the risks of cows injuring their feet, especially
when coming in from pasture.
Aseptic Laminitis, ‘Founder’

True laminitis is an excruciatingly painful condition leading to damage and destruc-
tion of the laminated corium, usually affecting all four feet. The skin above the
hooves is hot to the touch, although the hooves themselves may feel cold. While the
condition is not fully understood, it is known to be associated with the release of
vasoactive toxins into the blood that cause capillary damage especially in the foot,
leading to secondary destruction of the suspensory laminae. The main factor pre-
disposing to this toxin release is the disruption of the normal population of the
rumen microbiota during periods of severe acidosis associated with excessive feed-
ing of starchy concentrates, which is why the condition is most prevalent in beef
cattle being finished on feedlots (Chapter 6). Most competent dairy farmers avoid
feeding such unbalanced rations, so the incidence of true laminitis in dairy cows is
very low. However, as I described earlier, the high prevalence of sole lesions was for
many years attributed to subclinical laminitis (and still is by many). This misdiagno-
sis is not just a matter of semantics. It implies that a prime risk factor for sole lesions
in dairy cows is improper feeding. This is not the case.
Risk Factors for Lameness

Over 100 potential risk factors for dairy cow lameness have been identified from
on‐farm inspection and review of management. Any of these factors that I describe
as ‘tangible’, may be important but they are rather too many to work with for epide-
miological purposes. They can however be categorised under three main headings
into eight ‘proximate’ risks, i.e. factors that impose directly onto the integrity of the
foot. These proximate risks, and a few examples from the long list of tangible risks
included within each category are summarised in Table 8.2.
The first category, environmental risks, includes prolonged standing on hard
surfaces such as concrete, claw trauma caused by stepping or slipping on stones,
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Table 8.2 Proximate and tangible risk factors for cow lameness.
Proximate risk ‘Tangible risk’
Environmental
Prolonged standing on Poor cubicle design, overstocking
concrete
Claw trauma Rough concrete and walkways, large kerbs to cubicles
Standing in slurry Inadequate or infrequent scraping
Managemental
Prophylactic foot care No routine, preventative foot trimming, foot bathing
Diagnosis and treatment No routine locomotion scoring
No early inspection and treatment of cows with slight
lameness
Animal
Dietary disorders Suboptimal lactation ration or transition diet
Body condition Suboptimal foot conformation, body condition
broken concrete or the lip at the rear of cubicles, and weakening, erosion and infec-
tion of the sole and skin associated with prolonged standing in wet slurry. The
second category of proximate risk is that associated with failures of management.
One example is inadequate attention to prophylactic foot care for cows and heifers,
including proper foot trimming and routine foot bathing. The more serious omis-
sion is failure to diagnose and treat lameness at an early stage through regular loco-
motion scoring and inspection of any cow showing slight to moderate abnormality
of movement. The third category of proximate risk includes factors relating to the
anatomy and physiological state of the cow herself. These include poor conforma-
tion of the hoof and dietary disorders, probably resulting from improper feeding.
It is too soon to present any definitive conclusions as to the relative importance
of these proximate risk factors. However, the evidence so far strongly suggests
(unsurprisingly) that prolonged standing on concrete, especially in early lactation,
is a major risk factor for sole haemorrhage and prolonged standing in slurry is a
major risk factor for DD. In UK herds, dietary disorders associated with improper
feeding, do not appear to present a major problem, which is consistent with the
contention that sole damage is not caused by subclinical laminitis. Suboptimal
claw condition at the time of calving, unless corrected by prophylactic foot trim-
ming, is a major risk factor for sole horn disorders. However, the major, confirmed
risk factor for severe lameness is failure to diagnose and treat cows as soon as pos-
sible when they first show signs of impaired mobility. There is good evidence now
that effective early treatment can reduce the prevalence of moderate to severe
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lameness in dairy herds from >20% to <5%. This, of course, calls for the expendi-
ture of a lot of time and effort from farmers, aided and abetted by professional hoof
trimmers. However, it carries the reassuring message that most farmers can resolve
a major lameness problem without the expense of redesigning and rebuilding the
entire cow house.
Transport and Slaughter
Cows need to be transported safely from farm to farm, through lairage in markets
and, at the end of their lives, treated with care and respect to ensure that their death
is without pain and, so far as possible, without fear. We must recognise that they are
timid creatures, alarmed, at least initially, by any novelty that may appear to present
a threat. They are reassured by the normal sights, sounds and smells of their home
farm and the presence of other, familiar members of their herd. We should try to
ensure that the physical and social environment of a cow in transit and lairage is as
close as possible to that to which she is accustomed. It would, however, be anthro-
pomorphic to presume that a cow was under stress simply because she was in a
lorry that was ‘taking her away from home’ or that, in a well‐run abattoir, her
passage down the race to the stunning pen was inherently more stressful than her
passage down a race to a tuberculin test. Each procedure needs to be considered
simply in terms of potential direct effects of the immediate environment and the
handling procedures on the cow.
Loading and Unloading

Walking up a ramp is a potentially alarming experience for a cow that is unused to
it. Cattle that have been transported frequently tend to enter lorries with much less
fuss, which suggests that they do not remember transport to be a particularly
aversive experience. This is a good example of the capacity of a fundamentally neo-
phobic animal to adapt to experiences that have, in the past, done it no lasting harm.
The main problems of loading and unloading, as perceived by the cow, are:
●● Fear and risk of injury when walking up, and especially down, steep slopes
●● Fear of entering an unknown, dark area
●● Alarm created by sudden noise and movement especially close to, or within their
flight zone.
To avoid these stresses, slopes on loading ramps should not exceed 20o and the
sides should be protected, preferably with solid partitions. Widely placed steps with
a depth of 100 mm are better than sloping ramps. If ramps are used, the floor should
be designed so that a cow’s foot cannot slip far in any direction. Bars running hori-
zontally across the ramp will not stop a foot from slipping sideways. The entire
surface of the ramp should be non‐skid.
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Aluminium has largely replaced wood in cattle lorries since it is longer lasting
and easier to clean and maintain. However aluminium, or any other metal ramp is
very noisy compared with wood and should be covered by non‐slip matting or a
generous amount of straw. The inside of the vehicle should be well lit so that the
cow can see where she is going. She should not be hurried but allowed to proceed at
her own pace. After leaving school I worked on a dairy farm where lived a Shorthorn
cow named Bluebell, whose milk yield was meagre but whose disposition was
phlegmatic. Whenever any adult cattle were to be transported Bluebell was kept in
with them. She was haltered and led into the lorry first to encourage the others.
When all were aboard, she was led out again. Fortunately for my peace of mind, I
left the farm before she did.
Unloading from a lorry is potentially less stressful because cows are moving from
darkness into light. It is, however, particularly difficult for cattle to descend a steep
slope. The offloading area at markets, lairages and, wherever possible, on farms
should be designed to ensure that cattle can leave the lorry via the backboard/ramp
down as gentle a slope as possible.
The Journey
The potential stresses incurred during the journey itself may be assessed using the
protocol of the ‘five freedoms’ (Chapter 1). These are:
1) Hunger, and more especially thirst due to deprivation of food and water.
2) Heat or cold stress and physical discomfort; if prolonged, leading to physical
exhaustion.
3) Injury from fittings within the vehicle or other cattle: disease resulting from
cross‐infection incurred during transit, especially when animals from different
farms are transported together.
4) Fear and pain resulting from aggressive encounters with other cattle.
The European Committee for the Protection of Animals states that adult cattle
shall not be left (in vehicles) for more than 24 hours without being fed and watered.
This period may be extended if the journey can be completed in reasonable time. In
other words, if the journey can be completed in (say) 26 hours it would be an
absurdity to submit cattle to the stress of unloading and reloading to offer them
food and water when only 2 hours short of their destination. Lactating cows should
be milked twice daily. Dry cows in good condition can tolerate 24 hours without
food and water with little, if any distress, because the amount of undigested food
(and water) within the rumen will continue to supply a sufficient flow of nutrients
for at least this time. In fact, it may pay to restrict the food intake of cull cows to hay
only prior to transport to reduce the flow of wet faeces, so improve both comfort
and hygiene within the vehicle.
The thermal environment within cattle transporters is usually controlled (to some
degree) by natural ventilation through spaces in the walls. When adult cattle are to
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be transported it should be possible to adjust the wall openings to provide between

20% to 40% open space according to the outside conditions. The lower value should
only be used in very cold conditions and/or when the vehicle is nearly empty. When
a vehicle full of cattle is kept stationary for any length of time, as many ventilators
as possible should be open. This implies that drivers should have a good enough
understanding of cows to recognise hot or cold ones when they see them. When the
driver proceeds smoothly on good roads and the vehicle is not overstocked, cattle
will usually stand, but some may lie down after 1–2 hours. The rougher the drive,
the more likely the cattle are to remain standing.
Although it is common for cattle from several farms to travel on the same lorry,
they should be kept apart by partitions to prevent aggression, or the threat of aggres-
sion, that inevitably accompanies the meeting of strangers. Horned cattle should
not travel with those without horns. Herd bulls travel best in the company of two or
three familiar cows, not in oestrus.
A Gentle Death
The decision to end the life of a cow from the milking herd may be because she has
become unproductive, infertile or because she is suffering from a disease or injury
from which she is unlikely to recover, or which would be too expensive to treat.
Cows destined for travel to an abattoir to be slaughtered for human consumption
should be first examined for fitness to travel without pain or distress. They must be
re‐examined on arrival. Any cow that is injured or incapable of walking without
undue pain should be killed on the vehicle. The physical environment in lairage
should be at least as good as that on farm. Cows should be able, without difficulty,
to stand up, lie down and move without impedance to sources of food and water.
The passage to the stunning pen should be quiet, calm and unhurried, ideally via a
curved, solid sided race sufficiently narrow to prevent a cow from turning around
but able to admit an attendant in the event of an emergency. The curve in the nar-
row race enables them to ‘follow my leader’ but not see what is happening at the
end of the line.
The purpose of stunning is to render an animal ‘instantaneously’ unconscious
prior to sticking and bleeding out. When used properly, the procedures most com-
monly used for stunning cattle, the captive bolt (which penetrates the skull) and the
percussion stunner (which doesn’t) are probably the best methods to rendering an
animal unconscious as near to instantaneously as possible. The most important
welfare issue is to ensure that all animals are bled to the point of death before they
start to recover any degree of consciousness. There has been a belief in the meat
trade, based mostly on myth, legend and the Old Testament, that it is necessary for
the heart to beat during bleeding out to remove ‘all’ blood from the meat. Recent
research has shown this belief to be false, which means there can be no reasonable
objection to a stunning process that also kills the animal.
I shall not consider in any depth the process of religious slaughter since it is not
open to reasoned argument. Suffice it to say that the contention that the conscious
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animal ‘feels no pain’ when its throat is slit cannot be used in defence of religious
slaughter. Many things in a cow’s life are likely to cause it more pain and for longer
periods. What the advocates of religious slaughter fail to address is the fear experi-
enced by a sentient animal conscious of choking to death in its own blood. However,
many practitioners of Halal slaughter now permit pre‐slaughter stunning. The
practice of Shekita is still stuck with Leviticus.
For most dairy farmers the greatest welfare concern relates to casualty and emer-
gency slaughter. Casualty animals (in England) are those that are not in severe pain
but deemed to be suffering from sickness or injury sufficient to require slaughter as
soon as possible. It is both economic and expedient to transport these animals a
reasonably short distance to a local abattoir. However, it is unrealistic to expect
these abattoirs to remain open for business 24/7 and, as abattoirs get bigger and
bigger, they get fewer and further between.
Emergency cases are those where an animal has experienced severe injury or
paralysis so that it cannot be moved without incurring severe pain and distress.
Such animals should be killed on the spot. If all or any of the carcass is passed for
human consumption it must be accompanied by a veterinary certificate indicating
that the carcase is ‘unlikely to have been rendered unfit for human consumption’.
Animals deemed unfit for human consumption will have to be taken away by the
knacker man.
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Milking and Mastitis
A beef cow, feeding a single calf, may produce 10–15 litres of milk per day, which
will be consumed by the calf in about 6–7 separate meals. The calf will suck from
one teat at a time, may or may not drink from all the teats and certainly will leave
some milk within the cisterns of the mammary gland. A modern Holstein cow,
entering the milking parlour 2–3 times a day may yield more than 20 L in a single
milking session. All four quarters are milked simultaneously until the flow of milk
has practically ceased. This enormous difference in daily yield is, of course, primar-
ily due to genetic selection and feeding for increased yield per cow but it is also a
consequence of the milking practice itself. Beef cows produce more milk if stimu-
lated to do so by suckling two calves. Experiments where dairy cows have been
deliberately milked to only 75% of capacity for 20 days have shown that this chroni-
cally reduces subsequent milk secretion.
The let‐down of milk is induced by the natural stimulus from the calf, or the
stimulus conditioned by entry to the milking parlour, feeding and udder washing.
This causes a release of oxytocin that contracts the myoepithelial cells around the
alveoli and ejects milk into the mammary cistern within each quarter (Figure 3.5).
The rate at which milk is released from the udder is determined largely by the diam-
eter of the streak canal. The effect of the oxytocin‐mediated milk ejection reflex
lasts only a few minutes so that if the period between the stimulus to let‐down and
the onset of milking is delayed, or if the process of milking is prolonged, more milk
will be left in the udder. It follows that a single calf, or a milkmaid (having only two
hands) will never fully realise the productive capacity of a dairy cow, whatever her
genetics. Moreover, a cow who is a slow milker by virtue of narrow streak canals is
likely to produce less milk overall.
Figure 9.1 illustrates the changes that occur in udder pressure (kPa) and milk
secretion rate from the alveoli (kg/h) over a period of 40 hours after milking. At
first, pressure within the milk cisterns (or sinuses) is atmospheric and milk secre-
tion from the alveoli is maximal. After a rapid but small initial phase, sinus pressure
rises slowly for 8–10 hours and alveolar secretion rate remains constant. After about
10 hours, when the cisterns fill up, sinus pressure starts to rise more steeply and

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1.5
8
Udder pressure (kPa)
Milk secretion (kg/h)

6 1.0
4 secretion
pressure
0.5
2
0 10 20 30 40
Hours since last milking
Figure 9.1 Changes in intramammary pressure and milk secretion rate with time
after milking (from Theil and Dodd, 1977).
milk secretion rate falls to the point where (in this example) milk secretion ceased
after 35 hours. This implies that when intervals between milkings are extended
beyond 12 hours, this is likely to have an inhibitory effect on overall yield. The cor-
ollary to this is, of course, that three‐times daily milking should increase overall
yield – and it does. However, three‐times daily milking of cows, especially in large
herds, can be an exhausting practice for both milkers and cows, especially if they
have to wait on each occasion for perhaps 90 minutes in collecting yards. This
erodes the time available for eating and resting and can wipe out the advantage of
more frequent milking unless queuing time can be reduced to a minimum.
The exact shape and timing of the graphs shown in Figure 9.1 should be inter-
preted with caution. The rate of pressure build‐up in the cisterns will depend on the
size of the cisterns relative to the secretion rate of the alveoli. As high‐yielding cows
age, their cisterns enlarge (in some cases, grossly enlarge to the point where the
udder is practically touching the ground). I have assumed, with some justification,
that this is uncomfortable for the dairy cow. However, in a trial carried out by one
of my former graduate students, Neville Prescott, to investigate the motivation of
cows to enter a robot milking station (q.v.) he had no option but to work with mature
cows who had both adapted to conventional milking practices and developed quite
large cisterns. Unless food was provided at the milking unit, many cows were reluc-
tant to enter more than once daily. Some made little or no effort to enter the milking
unit under their own volition and had to be driven in. This surprising result sug-
gests that old cows with large cisterns may not experience significant discomfort
simply from the accumulation of milk (although dragging these large udders
around must be a chore). However, I am sure that heifers, particularly in the early
days of their first lactation, do experience discomfort from the pressure of milk
build‐up in the udder.
In the second edition (1993) I wrote ‘The use of computer‐directed robotics has
revolutionised manufacturing industries like the motor trade. There is no reason in
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principle why it should not be possible to design a computer‐controlled milking

parlour that a cow could enter whenever she felt hungry or in need of milking, then
be fed an appropriate amount of concentrate and milked by a computer‐controlled
robot. The machine should be able to recognise signs of mastitis and, if in doubt, call
for help from the herdsman’. Robotic milking is now well established at the more
affluent end of the dairy industry. In strictly mechanical terms, the only significant
advance on the more conventional milking parlour has been the robotic placing of
the milking clusters. However, by taking this single task out of the hands of the milk-
ers they radically alter all the routines of dairy farming.
The whole principle of robot milking, based on the concept that the cow enters the
robot to be milked of her own volition is, at first (and even second) glance, highly
attractive. The people who milk are spared from an endless, mindless, repetitive task.
More important from the perspective of the five freedoms, the cow is (in theory) given
freedom of choice to be milked whenever she wants. More frequent milking, unac-
companied by long queuing, should both increase milk yield and improve cow wel-
fare by permitting more time for rest and recreation. So far, so good. The first, obvious
disadvantage is that the system reduces the contact between cows and cowherds,
most importantly at the time of milking, and thereby increases the risk of failing to
achieve early recognition of disease, especially mastitis. Modern robotic milking sys-
tems may include monitors to recognise signs of mastitis, e.g. from changes in the
ionic composition of milk, and other disorders such as ketosis. However, a member of
the milking team should always be at hand and ready to act if the machine identifies
a problem – or breaks down. Mainly for this reason, most robot milking units are shut
down over night (e.g. between 2200 and 0600 h).
Robot milking systems that operate on the basis that cows enter the unit at their
own volition are also faced by the problem that what motivates the farmer is not
necessarily what motivates the cows. We have already seen that the motivation to be
milked per se is unlikely to be a strong enough attraction. This, plus perhaps fear of
the system, means that some cows do not take to robot milking at all and have to be
culled. The sure‐fire way to get cows to enter the units is to offer them food. This has
two drawbacks. Any system that relies on providing a significant amount of the
daily ration in the form of concentrates (dairy cake) is incompatible with the prin-
ciple of feeding total mixed rations (TMR) and may thereby reduce daily ME intake,
milk yield and increase the risk of rumen acidosis. The system must also be able to
deal with the problem of the greedy cow who keeps coming back again and again
for more cake. Robot milking units deal with this problem by diverting these cows
round the milking/feeding units – but they can still clutter up the approaches and
get in the way of other cows.
The fact that cows need a stronger incentive than milking per se to enter the robot
units means that, in practice, they are only appropriate for systems where the cows
are housed throughout lactation. Attempts to apply them to pasture‐based systems
are faced by the problem that cows grazing and resting in comfort on fresh green
pastures are not much inclined to go indoors in search of cake especially if this
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involves a long walk. Some have used the motivation to drink as an incentive by
providing access to water only at the milking unit, i.e. denying them access to water
in the fields. This is not only an insult to welfare; it will almost certainly reduce milk
yield. In other words, it makes little sense.
The Milking Machine
Among the first attempts to introduce a mechanical substitute for hand‐milking was
one that involved the insertion of metal tubes through the teat canal to allow milk to
escape by force of gravity and intramammary pressure. Given the rudimentary
understanding of hygiene in the early part of the 19th century this must have been
fraught with risks of injury and infection and it is hardly surprising that it did not
catch on. The first effective machines to apply a vacuum to the teat and remove the
milk by suction were developed in the 1850s. The modern milking machine, which
uses a pulsator to create an intermittent vacuum at the teat and so mimic the sucking
action of the calf was patented by Dr Shiels of Glasgow in 1895. The vacuum applied
to the teat pulsated rhythmically between 50 and 15 kPa. While there have been
many developments to the mechanics of milking machines since then, the pulsation
and applied vacuum remain essentially the same as those used by Dr Shiels.
Figures 9.2 and 9.3 illustrate the workings of the milking machine in just enough
detail to explain its effect on the cow. Details of the plumbing, operations and cleans-
ing can be found elsewhere. In brief, a constant vacuum of 40–50 kPa (300–380 mm
mercury) is applied to the inside of the teat cup liner. The pulsator transmits an
intermittent pulsator vacuum (PV in Figure 9.3) to the space between the rim of the
teat cup and the liner. When the pulsator vacuum is equal to the vacuum inside the
liner and thus in the milk line (45 kPa in Figure 9.3) the vacuum within the liner
sucks milk from the teat. When the pulsator vacuum is removed and pressure
between the teat cup and the liner returns to atmospheric, the constant vacuum in
the milk liner causes the liner to contract round the teat and interrupt the flow of
milk. The greater the vacuum applied to the milk line the more rapid the flow of
milk, so the less time taken to milk each cow. On the other hand, the less the vacuum
the gentler the action of the teat cups and the lower the risk of injury and subsequent
mastitis. The optimal vacuum as assessed by the vacuum gauge is affected by the sit-
ing of the gauge and the arrangement of the plumbing and needs to be set and con-
stantly checked by an expert.
The change in PV cannot be instantaneous but should be as quick as possible, i.e.
the periods a and c in Figure 9.3 should be as brief as possible. The overall pulsation
ratio (%) is given by 100(a + b)/(a + b + c + d) and should normally be close to 60%.
The flow of air and milk in bucket machines and pipeline machines in cowsheds
and parlours is illustrated in Figure 9.2. Typical values for pulsation frequency of
55/min and pulsation ratio of 65%, which corresponds to an open ratio of 58%, are
shown in Figure 9.3, which also illustrates the effects of the milking machine on the
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(a) Vacuum gauge

Regulator Vacuum tap
Interceptor
Vacuum tube
Pulsator Teatcups
Claw
Bucket
Vacuum pump
(b)
Air pipeline
Pulsator
Milking pipeline
Long Long
milk pulse
Receiver tube tube
Sanitary
trap
Teatcups
Milk pump
Air Claw
(c) Air pipeline(pulsators)

Air pipeline (milking vacuum)
Transfer pipeline
Pulsator
Teatcups
Claw
Recorder
jar
Air Milk Air and milk
Figure 9.2 Flow of air and milk in milking systems. (a) Bucket machine, (b) milking
pipeline machine, (c) recorder machine (from Theil and Dodd, 1977).
teat during the period of maximum milk flow and during the last phase of milking,
or ‘machine stripping’ when the rate of milk flow has decreased to about 10% of
peak. During the period of peak milk flow the potential vacuum of 45 kPa applied
to the teat extracts milk at about 20 ml/s into the short milk line to the recorder jar.
While the milk flow is this rapid the actual vacuum applied to the teat within the
mouthpiece chamber (MPC) of the teat liner is quite small (5 kPa in Figure 9.3).
However, during the final stripping phase, the lower milk flow will have a lesser
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NON MILKING
PEAK FLOW STRIPPING
PHASE
MPC
PV 45kPa 0 45
45kPa 45 45
PEAK FLOW STRIPPING
30
MPC (kPa)
20
10
open
58% 58%
Liner
1/2
closed
40
Pulsatror vacuum
30
(kPa)
20
10
a b c d a b c d
0 0.5 1.0 0 0.5 1.0

Time (sec)
Figure 9.3 Function of the teat cup. PV = pulsator vacuum, MPC = mouthpiece
chamber. For further explanation see text.
effect on vacuum within the milk line and MPC may increase to 30 kPa or more.
The effect of this increase in suction is to draw the teat deeper into the liner or,
observed from the outside, to allow the liner to ‘crawl’ up the teat. When milk flow
ceases the vacuum increases further. This explains why overmilking predisposes to
prolapses of the teat sphincter or ‘black spot’, a granulating sore at the teat end. Teat
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damage and teat‐end impacts caused by fluctuations in vacuum pressure in the

short milk lines can occur when clusters are being put on another cow or when one
cow kicks its clusters off. Milking systems that incorporate automatic cluster
removal should minimise this risk.
Another problem that was quite common when I wrote the second edition
was teat‐end impact. In most of the machines at that time, milk drawn from
each of the four quarters was mixed within the central claw of the cluster that
joins the short milk lines from each teat cup to the long line to the recorder jar.
When the pulsator vacuum is reapplied, the first effect is to draw some milk
back into the teat cups from the claw. This effect will be greater during the strip-
ping out period. This increases the risk of transmission of infection within the
udder from a single quarter with mastitis. This problem has now been largely
resolved by the use of moulded teat cup liners with a shield at the bottom to
prevent milk flowing backwards within the claw from striking the teat sphincter
directly. An alternative approach is to incorporate a gravity‐operated ball valve
within the claw to prevent any return of milk to the short milk tube.
The Milking Parlour
Most developments in milking parlour design have been directed towards increased
efficiency of operation, especially through reducing the time and labour involved in
milking. These developments have hugely increased the number of cows that can
be milked in one parlour by one person and so have been a major contributor to
increases in herd size. So far as the cows are concerned the design of the milking
parlour is immaterial so long as:
●● They can enter and leave with minimal fuss, without slipping or having to make
excessively sharp turns in narrow passages and without interference from other cows.
●● They can stay in the parlour long enough to consume their concentrate ration
(when in‐parlour feeding makes a significant contribution to their ration). Most
Friesian–Holstein cows should be able to consume 4 kg within 8 min.
●● Proper hygienic procedures are practised (see next section).
●● The clusters are not left on too long. Most cows milk out within 4–5 min and it is
obvious when they have finished. Parlours that incorporate automatic cluster
removal should achieve this aim. Where they are not present there is a consider-
able risk that a milker operating under pressure will fail to remove all clusters in
a timely fashion so increase the risk of teat injuries and infections
Hygiene in the Milking Parlour
A comprehensive description of milk hygiene is beyond the scope of this book.

Reference to directions from the UK Food Standards Agency is given in the section
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on Further Reading. Here, I consider only good practice relating specifically to the
milking process itself.
●● The hands and clothing of the milker should be spotlessly clean. Disposable
gloves are recommended (though not always used).
●● The udder should be clean and dry before the clusters are attached. Obvious dirt
should be removed by hosing down. Even udders that appear clean should be
hosed lightly with warm water then dried with individual disposable paper tow-
els. Do not use a common udder cloth. Some units dip the teats in an approved
disinfectant before milking. Others seem to manage successfully without includ-
ing this step.
●● A sample of milk should be drawn by hand from each quarter onto the shiny
black plate of a strip cup and examined for abnormalities such as clots, watery
discolouration or streaks of blood Some contend that this should be done before
washing and drying the teats because these signs are more visible before ‘let‐
down’. However, this does carry a slightly increased risk of cross‐infection via the
hands of the milker.
●● After the milking process is over, the teats should always be dipped in an approved
disinfectant and, ideally, the cows should be kept standing for 30 min before
returning to their cubicles to lie down. The purpose of this is to allow the teat
sphincters to close before they are exposed to pathogens in the cow house, espe-
cially E. coli and so reduce the risk of environmental mastitis.
There is no doubt that improvements to milking machine design and hygienic prac-
tices in the milking parlour have reduced the incidence of contagious mastitis
incurred during the milking process. However, as we shall see, environmental mas-
titis, acquired during time spent in the cow house, remains a major problem
The purpose of milk hygiene is, of course, not just the control of mastitis in the
cows, but to guarantee that the milk sent for sale is fit for human consumption. This
requires attention to hygiene at all stages of the milking process and storage in bulk
tanks. The standard measure of the milk hygiene is the total bacteria count (TBC).
This is measured routinely by the dairies collecting milk off farm. Within the EU,
herd counts of >100 000 bacteria per millilitre are penalised to the extent that action
is called for; counts >50 000 may incur a reduction in the milk price. A marker of
good practice would be counts that were consistently <15 000/ml.
Mastitis
Mastitis, infection and inflammation of one or more quarters of the mammary

gland, is one of the big three production diseases of dairy cows (the other two
being infertility and lameness) The economic cost of mastitis is generally esti-
mated to be well in excess of £100 per case, when all is taken into account: veteri-
nary bills, lost milk sales and the probability that some cows will have to be culled.
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The microorganisms causing the most common forms of mastitis may be consid-
ered within two groups:
●● Contagious pathogens (e.g. Staphylococcus aureus, Streptococcus agalactiae).
These organisms can survive and grow within the mammary gland so that trans-
mission of infection from infected to uninfected quarters and from cow to cow is
most likely to occur during milking.
●● Environmental pathogens (e.g. E. coli, Klebsiella) thrive in the environment of the
cow house so most likely to be caused by entry of infection through the teat canal
from dirty bedding or slurry.
Clinical mastitis manifests as an inflammatory response to infection. In mild
cases the only clinical signs may be abnormalities in the foremilk (first‐milk strip-
pings), such as a watery appearance, clots and perhaps streaks of blood. In more
severe cases there will be classical signs of inflammation in the infected quarter:
swelling, heat and pain. In the most severe cases (10–15%) the infection will become
systemic, producing symptoms of fever, shock and possibly death.
Subclinical mastitis describes the situation where infection is present without clin-
ical signs of local inflammation or systemic involvement. This condition may only be
recognised from evidence of an elevated somatic cell count (SCC). In some cows it
may persist throughout lactation without presenting clinical signs, in others give rise
to repeated episodes of (probably mild) clinical symptoms. In these circumstances,
cows would be defined as cases of chronic mastitis. Whether subject to repeat clini-
cal episodes or not, cows with chronic mastitis (especially with S. aureus) continue
to shed organisms so present a risk of cross‐infection at the time of milking.
Indicators of Mastitis
The most common method for monitoring the prevalence of mastitis is the somatic
cell count (SCC). The number of somatic cells (primarily macrophages and leuco-
cytes) per millilitre of milk is a measure of the immune response, which is itself an
indicator of the presence of infection. SCC counts may be taken from the bulk milk
tank to give an indicator of the prevalence of subclinical mastitis in the herd, from
individual cows or, to give the most precise diagnosis, from single quarters.
Regulatory standards and penalties for high SCC counts in bulk milk samples differ
between countries from <400 000/ml in the EU to <750 000/ml in the USA. In 1975
the average SCC for the UK dairy herd was 586 000/ml. By 2006 this figure had
fallen below 200 000/ml, convincing evidence of success in the management and
control of contagious mastitis through better practice in the milking parlour and
improved recognition and treatment of subclinical carriers of infection. The current
target set by the AHDB is to keep bulk milk SCC below 150 000/ml.
Several other markers have been identified as indicators of inflammation due to
mastitis. The two most practical approaches are rapid ‘cow‐side’ monitoring of fore-
milk samples involving (e.g.) antibody‐based techniques and ‘in‐line’ techniques for
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monitoring (e.g.) abnormalities in the ionic composition of milk during the milking
process itself. This latter approach is well suited to highly automated systems, such
as robot milking, although, at present, it carries a greater degree of uncertainty
(false positives and false negatives) than the antibody‐based techniques.
Contagious Mastitis
Sixty years ago, when penicillin was first coming into veterinary practice, the most
common cause of contagious mastitis was Strep. agalactiae. This organism can only
thrive and multiply within the udder so the only source of the disease was cross‐
infection from a carrier cow transmitted during the milking process. Infection in a
previously clean quarter causes acute inflammation with pain, heat and swelling.
The foremilk usually contains large clots. The cow may have a slightly elevated
temperature and be off food for a couple of days. The organism is sensitive to peni-
cillin and treated cows return to normal within a few days. However, the infection
may persist in sub‐clinical form. Persistent low‐grade infection may continue to
destroy alveolar cells, which are replaced by scar tissue, thereby reducing the capac-
ity of the quarter to produce milk. Such quarters are less productive and, of course,
a constant source of infection to other quarters and other cows. However, because
Strep. agalactiae only lives within the mammary gland and has remained sensitive
to penicillin, it has been relatively easy to control and is now a minor contributor to
the problem of contagious mastitis.
The most important organism now responsible for contagious mastitis is S. aureus.
This is a natural inhabitant of the skin of cows and humans, where it does no harm
unless the cow’s teat or the milker’s hand is cracked, when it can cause the wound to
turn septic. If the organism is able to penetrate the teat in sufficient numbers the dis-
ease takes one of two forms. Peracute staphylococcal mastitis can occur rarely, but
especially in early lactation when the immune defences of the cow are depressed. The
cow becomes very ill with a high fever, depression, inappetence and may become
comatose and die within 24 hours of the onset of symptoms. The infected quarter is
grossly swollen and extremely painful, which makes the cow very reluctant to move.
The secretion from the infected quarter is usually a blood‐stained, serous fluid. If the
cow survives, blue gangrenous patches may appear on the quarter and proceed to
blackened, oozing sores. Although the cow with peracute S. aureus. infection can be
saved by an effective antibiotic, if caught in time, the quarter is almost invariably lost.
It is fortunate that this condition is rare as its consequences are catastrophic.
The more common form of S. Aureus infection is less severe but chronic. The
affected cow may not appear ill and the affected quarter may not be painful. The
foremilk may or may not show abnormalities. However, as with Strep. agalactiae,
chronically infected quarters are sources of cross infection and become progres-
sively less productive as scar tissue replaces secretory tissue. Treatment of S. aureus
infection is complicated by the fact that there are many strains and more and more
of them are becoming resistant to more and more of the antibiotics within the
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v eterinary armoury. It is highly probable that despite treatment with a nominally

effective antibiotic, some degree of infection will persist throughout lactation. The
most effective approach to the management of S. aureus infections is by dry cow
therapy, which I shall address later.
A third class of microorganism, Mycoplasma sp., can cause contagious mastitis.
This should be suspected if the condition does not respond to antibiotics. The dis-
ease typically presents as chronic mastitis; periods in which cows are without symp-
toms interspersed by recurrent clinical episodes. There is no effective treatment for
Mycoplasma mastitis. The disease can be controlled by taking and culturing milk
samples to identify infected animals. If numbers are small, it is probably best to cull
them. If numbers make this unrealistic, they should be milked last, or separately. I
recognise that this is pretty impractical too. At present the condition is quite rare
and most likely to arrive as a result of buying in infected animals. This risk can be
avoided by quarantining and sampling arrivals before entry to the main milking
herd.
In summary, contagious mastitis, these days most commonly caused by S. aureus,
can be, and has been, effectively controlled by attention to hygiene and manage-
ment of chronically infected animals. To recapitulate, these involve:
●● Good hygiene in the milking parlour before, during and after milking.
●● Regular checks on the milking machinery: correct vacuum and pulsation, clean,
soft liners that have retained their original shape.
●● Use of teat shields or claw with ball valves to reduce or eliminate teat‐end impacts.
●● Early diagnosis and treatment of clinical cases.
●● Monitoring of SCCs in bulk milk and from individual quarters of cows suspected
to be carriers.
●● Bacteriological examination of milk from clinical cases to identify the organisms
responsible for infection and determine their antibiotic sensitivity.
●● Dry cow therapy for all cows.
●● Culling of cows that experience repeated attacks of clinical contagious mastitis
within a single lactation.
●● Maintenance of a closed herd (whenever possible); quarantine and testing of
bought‐in cows.
Environmental Mastitis
As indicated earlier, this complex disease is caused by organisms that thrive in the
environment (especially where cows’ faeces are involved). The most important is E.
coli, a class of bacteria with multiple strains of varying pathogenicity for animals
and humans. Others include Klebsiella, and Strep. uberis, a natural inhabitant of
cow’s skin. The principles for control of all infections are essentially the same so I
shall concentrate on environmental mastitis caused by the coliforms since these are
the most common, serious and most likely to be resistant to antibiotics.
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The effect produced by entry of a coliform into a quarter varies greatly according
to the immune defences of the cow, in particular, her ability to recruit neutrophils
to repel the invasion. In mid to late lactation and during the dry period any coli
that enter are likely to be overwhelmed by neutrophils. In late lactation there may
be evidence of mastitis in the foremilk but a milk sample may prove sterile because
the neutrophils have already destroyed the invader. In early lactation, especially
the first few days after calving, the cow’s ability to mount a neutrophil defence is
greatly reduced. In these circumstances, signs of inflammation in the udder may
be relatively minor (since inflammation is an expression of the body’s defence to
infection) but the coliforms are able to multiply and liberate endotoxin that makes
the cow feel very ill indeed. She runs a high temperature, goes entirely off food and
usually develops severe diarrhoea, so rapidly becomes dehydrated with a tight
skin, a ‘hidebound’ appearance and sunken eyes. The mortality rate in such cases
is high.
Severe systemic toxaemia with little local inflammation in early lactation and the
complete localisation and rapid elimination of infection that occur in the dry cow are
opposite extremes of the contest between coli and cow. Most infections fall some-
where in between. There is local infection in the udder, the foremilk becomes a straw‐
coloured liquid with few, if any, clots. The cow may show some signs of toxaemia,
being slightly fevered and reluctant to eat. The clinical signs of this form of coli mas-
titis are difficult to distinguish from contagious mastitis caused by S. aureus without
taking a milk sample for bacteriological examination (which takes time) so a vet can-
not guarantee to prescribe the most effective antibiotic at the first visit. Non‐steroidal
anti‐inflammatory drugs (NSAIDS) may be given at the first signs of mastitis and, in
some cases, will remove the symptoms without recourse to antibiotics.
To control environmental mastitis, everything possible must be done to keep fae-
ces and bedding contaminated with faeces away from the teat sphincter, especially
during the first 30 minutes after milking before the teat canal has fully closed.
Hygiene in the court or cubicle house was discussed in the previous chapter: dry,
clean bedding, scraped passageways or slats, control of relative humidity. There is
now good evidence that deep, dry sand is the least likely to carry environmental
pathogens. I wrote then and emphasise even more strongly now how important it is
to keep calving boxes spotlessly clean. Entry of E. coli into the udder during calving
is likely to cause the most severe form of E. coli mastitis with systemic toxaemia and
a high risk of death. Farmers who operate a tight calving pattern, i.e. calve most of
their cows over a short period, run an increased risk of coli mastitis being con-
tracted in the calving box since even steam‐cleaning cannot guarantee total elimi-
nation of the organisms. They should, if possible, after cleaning, be rested for at
least one week and longer if possible.
Good hygiene in the milking parlour is also essential to eliminate the risk of fae-
cal contamination when the clusters go on. This is a major reason why teats should
be dried with individual paper towels after the initial wash since one drop of water
contaminated with faeces can contain enough coli to cause mastitis.
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The increased incidence of environmental mastitis in recent years can mostly be

a ttributed to a deteriorating environment in damp, dirty cubicle houses wherein
cows are consuming large quantities of wet silage. Another reason for the increased
incidence of environmental mastitis is that it is more common in cows that give the
most milk. Selection for high yielders, who are also fast milkers will select for cows
with wider bore teat sphincters that are more susceptible to the entry of coliforms.
There has been some debate arising from the observation that the incidence of envi-
ronmental mastitis has been going up while SCCs have been going down. Some have
suggested that a reduction in SCCs (mostly macrophages and leucocytes) may have
reduced the cow’s capacity to mount and immune response to E. coli infection. I
know of no good scientific evidence to support this rumour. The relative increase in
the number of cases of environmental mastitis reflects our success in the control of
contagious mastitis. I repeat: good hygienic practice in the milking parlour will
reduce the incidence of both conditions.
Summer Mastitis
This condition affects cows and heifers at pasture during the summer months. It is
most commonly seen in dry cows. Several different organisms, probably acting in
synergy can be the causative agents; the most common being Arcanobacterium pyo-
genes (formerly known as Corynebacterium pyogenes – a title that has, apparently
been determined arcane). The disease manifests as an extreme inflammation (usu-
ally of a single quarter) with swelling, heat and severe pain. Strippings drawn from
the infected quarter are thick, yellow and smell putrid. The cow will display signs of
toxaemia, fever, depression, weakness and inappetence. Many untreated cows die
during the early acute phase and others abort. Large abscesses develop within the
infected quarter, which is likely to end up entirely non‐functional. Summer mastitis
can take a milder form, which may escape notice in a dry cow at pasture but which
can cause sufficient scarring in the udder and teat canal to block the secretion of
milk when the cow or heifer calves.
The main source of infection appears to be transmission by the head fly Hydrotea
irritans. These flies land on all parts of the cow but are particularly attracted to
secretions: blood, tears and sweat. A slight cut or sore on the end of the teat will
attract flies and allow bacteria to enter the udder.
Control of summer mastitis is based on the following steps:
●● Dry cow therapy based on the use of teat sealants and/or long‐acting antibiotics
(q.v.).
●● Fly control. This can involve insecticide sprays around the abdomen and udder
and the use of insecticide‐impregnated ear tags. The cow can spread the insec-
ticide as she grooms herself, although she is unlikely to make much, if any,
direct contact with her own teats. Spraying is probably more effective if done
regularly but insecticidal ear tags are welfare‐friendly since they reduce irrita-
tion about the cows’ heads.
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●● Dry cows should, if possible, be grazed away from woods or standing water during
the months of July to September (in the UK) since these are the areas that will
have a high concentration of flies.
●● Meticulous shepherding of dry cows at pastures to ensure that any affected animal
is treated without delay.
Dry Cow Therapy

The aim of dry cow therapy (DCT) is to reduce the risk of cows getting mastitis in
their next lactation. Cows are particularly susceptible to new intramammary infec-
tion during the early dry period. The most severe form, summer mastitis caused by
Arcanobacterium pyogenes is fortunately rare. Much more common is infection
with E. coli or other gram‐negative bacteria that can infect the udder of the dry cow
without giving rise to symptoms, but precipitate a severe case of mastitis at the
onset of her next lactation when her immune state is depressed. Dry cow therapy is
also used to clear up chronic, subclinical cases of infection with the gram‐positive
organisms, especially S. aureus. When first practised, the protocol for DCT was to
insert antibiotic through the teat canal into every quarter of every cow. While this
blanket approach was undoubtedly effective it did contribute to global concern
about the agricultural use of antimicrobial drugs and increase the local risk of the
development of immune resistance in the causative organisms for mastitis. The
practice of DCT has been advanced by the development of teat sealants, material
introduced through the teat canal to create a barrier to entry of organisms such as
coliforms. While teat sealants have radically reduced the risk of new infection dur-
ing the dry period they can, of course, have no effect on residual infection with
gram‐positive organisms associated with chronic, subclinical mastitis in the lacta-
tion that has just finished. Today, the most common approach is to use selective dry
cow therapy (SDCT). Measurements are made of somatic cell count for individual
cows (or individual quarters). Any cow (or quarter) with SCC > 200 000 will receive
an intramammary antibiotic plus teat sealant. Cows (or quarters) with SCC < 200
000 will get the teat sealant only. Field studies indicate that DCT has, on average,
halved the incidence of clinical mastitis, which, when combined with the practice
of good hygiene in the cow house and milking parlour, should make it possible to
meet a target of less than 10% infected cows per year. Whether SDCT is as effective
as blanket DCT in meeting this target is, as yet, unproven.
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10
Miscellaneous Maladies
An animal (any animal) suffers a malady when all or part of the body is physically
damaged, destroyed or poisoned by:
●● Physical injury
●● Pathogenic microorganisms (parasites, bacteria, or their toxins)
●● Poisonous plants and chemicals
●● Deficiencies or excesses of normal dietary constituents or products of their diges-
tion and metabolism.
The common infectious disorders of calves, enteritis and pneumonia, are caused by
pathogenic microorganisms (viruses and bacteria) that are endemic (always pre-
sent). By the time that heifers calve for the first time they should have become
immune to most of the endemic organisms that enter the body through the gut or
respiratory tract. Thus, scours and pneumonia, the major hazards for young calves,
are seldom seen in adult dairy cows living on the farm where they were born. The
four main disease complexes seen in the dairy cow are production diseases (i.e., I
repeat, largely our fault) because they arise directly from the special stresses and
challenges faced by the breeding, lactating female. They are:
●● Infections of the mammary gland, i.e. mastitis
●● Disorders of the reproductive system, e.g. infertility, metritis
●● Physical ‘wear and tear’, sometimes compounded by infection, e.g. lameness
●● Metabolic disorders, e.g. ketosis.
Three of these have been considered already within the context of the systems of
feeding, housing and management from which they emerge. Afflictions of the
reproductive tract will be considered in Chapter 12. The great majority of health
problems in adult cows fall into one these four categories. There remains a miscel-
lany of maladies that occur sporadically and where systems of husbandry and man-
agement are not the main culprit. Some infections may be brought onto the farm by
infected cattle, or vectors such as birds, flying insects, or human intervention via
(e.g.) infected foot‐trimming equipment or the tyres of vehicles passing from farm

Signs of Diseas 183
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to farm. Others may reasonably be put down to bad luck. This category ranges from
infections with an exotic virus such as foot and mouth or blue tongue to a cow being
struck by lightning. This chapter will present some general points concerning the
recognition and treatment of disease in cattle then briefly describe the most impor-
tant of these sporadic conditions as they occur and as they are controlled in the UK.
Reference to more comprehensive descriptions of diseases of cattle, their diagnosis
and control, are given under ‘Further Reading’.
Signs of Disease
The best way to learn how to recognise signs of ill‐health in a cow is to stand and
stare at healthy cows ‘long and long’, since nearly all signs of ill‐health appear
first as departures from normality in posture, movement, alertness, appetite, etc.,
and these first signs may be quite subtle. Thus good, observant cowherds are
likely to spot the onset of ill‐health in their own cows before the vet. They will be
aware that something is wrong, even if they do not know exactly what, nor what
to do. The following section is intended to help students, farmers, and herders to
interpret the early signs of ill‐health. In Tables 10.1–10.4 common causes of death
and disease have been tabulated in relation to their first and secondary symptoms.
These generate a list of primary suspects and determine an appropriate first
course of action. The list of suspects that appear in these tables are by no means
comprehensive, nor I am identifying a clear diagnosis; merely the first steps in
that direction.
Sudden Death
One (or more) cows can be found dead, most commonly at pasture. Although death
may appear sudden to the cowherd, it may not have been so for the cow – an hour
Table 10.1 Possible causes of sudden death in adult cattle.
First symptom Secondary symptom Suspect
Sudden death Struggling Hypomagnesaemia

Frothy nasal discharge
Extreme bloat Primary bloat
Bleeding from orifices Anthrax
None Plant poisons (e.g. yew)
Perforated ulcer
Peracute mastitis
Burns Lightning strike
184 Miscellaneous Maladies
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Table 10.2 Possible causes of drooling in adult cattle.
First symptom Second symptom Suspect
Choking Physical obstruction

Drooling – one cow Swollen, painful tongue Wooden tongue
Swollen jaw Tooth abscess
Lumpy jaw
Diarrhoea, mouth ulcers Bovine viral diarrhoea
Drooling – several cows Nervous signs Poisons (e.g. rhododendron)
Organophosphorus
compounds
Lameness, mouth ulcers Foot and mouth disease
Table 10.3 Diseases possibly associated with abdominal symptoms.
First symptom Secondary symptoms Suspect
Bloat, severe None Primary, acute bloat

Bloat, mild Drooling, choking Physical obstruction
Pain, grunting Traumatic reticulitis
Diarrhoea, acute Fever, inflamed udder Toxaemic mastitis
Fever, abortion Salmonellosis
Diarrhoea, chronic Weight loss Parasitism, teart
Johne’s disease
Mouth ulcers (abortion) BVD
Straining Constipation Intestinal obstruction
Nervous signs Ragwort poisoning
Vaginal discharge Calving, abortion
Urogenital infection
can be quite a long time when one is dying. Other things to look for include signs of
struggling before death, the extent of bloat, blood at the mouth and anus, and any
evidence of burns, especially around the nose and feet. Table 10.1 relates these signs
to the primary suspects. A bloated carcass does not necessarily mean that bloat was
the cause of death, since all carcasses bloat after death. Other factors that may help
to determine that bloat was the primary cause of death include grazing history,
composition and state of the pasture and evidence of bloat in other cows.
Signs of Diseas 185
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Table 10.4 Diseases associated with nervous symptoms in adult cattle.
General symptom Specific symptoms Suspect
Excitement, frenzy Bellowing Hypomagnesaemia

Muscle spasms Several poisons
Convulsions BSE
Disorientation/ Head pressing Listeriosis
delirium
Circling, incoordination Ketosis
Blindness Lead poisoning
Vitamin A deficiency
BSE
Depression No other symptoms Sub‐acute ketosis/fatty liver
Early hypocalcaemia
Botulism
With fever and other Most systemic diseases
symptoms
A cow found dead at pasture after a wet and windy night shortly after turn‐out
in spring, with much froth about the mouth and nose, and the ground around her
torn up by her convulsions has almost certainly died of hypomagnesaemia. In this
unusually straightforward case, the preliminary diagnosis has been made on the
basis of information available at the scene. Factors predisposing cows to acute
hypomagnesaemia were discussed in Chapter 7. Most cases are far more difficult.
A small amount of blood loss from the nose, mouth and anus is not uncommon in
cows that have been killed by primary bloat but it can also be a symptom of
anthrax, a notifiable disease communicable to man. Anthrax is now extremely
rare. Other cause of sudden death listed in Table 10.1 such as lightning strike or
poisoning by (e.g.) yew or laburnum are also very uncommon. Nevertheless,
unless the cause of death is obviously bloat or hypomagnesaemia, a vet should be
called to take a blood sample to test for the possibility of anthrax before the car-
cass is collected by the knacker.
Drooling
Drooling, usually accompanied by other signs of discomfort around the mouth,
can signify a range of maladies (Table 10.2). If only one cow is affected, she may
have choked on a piece of root crop or wood. If her tongue is swollen and pain-
ful, particularly at the back of the throat, she is probably suffering from ‘wooden
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tongue’, an infection caused by Actinobacillus lignieresii. If the jaw is swollen,

the primary cause may be a tooth abscess or the specific infection ’Lumpy Jaw’
caused by Actinomyces bovis. In the unlikely event that one or more cows are
found to have ulcers on the tongue or mucous membranes inside the cheeks,
then suspect bovine virus diarrhoea (BVD) or foot and mouth disease. All cases
of drooling that cannot be directly linked to a choking episode, and especially
when they involve more than one cow, require veterinary attention without
delay.
Abdominal Symptoms
Whereas severe bloat usually indicates a primary disorder of rumen fermentation
or complete obstruction of the oesophagus, some degree of bloat can accompany
abomasal displacement (Chapter 7) or traumatic reticulitis (‘hardware disease’ or
‘wire’). It is not uncommon for cows to consume sharp pieces of wire, nails or other
pieces of hardware. These typically settle in the reticulum, where they may do no
harm. However, sometimes a piece of hardware may penetrate the reticulum wall,
puncture the diaphragm, enter the chest and, at worst, puncture the heart. A cow
that stands with her back arched, grunts with pain at the slightest movement, has a
slightly elevated temperature and may be slightly bloated should be suspected of
having traumatic reticulitis and needing the services of the vet. As a first aid meas-
ure, the cow should be tethered in such a way that she stands with her front feet
higher than her hind feet thereby relieving the pressure of the reticulum and the
penetrating foreign body on the diaphragm. Surgical intervention to remove the
culprit and any other hardware lying around in the reticulum is usually
successful.
Although the faeces of cows eating large amounts of grass or silage are very
wet, this is not true diarrhoea, which is a clinical sign of malabsorption from the
small and large intestine. Acute diarrhoea in a large proportion of the milking
herd can often be attributed to a primary nutritional disorder associated, for
example, with a change of concentrate ration. Acute diarrhoea in a single cow,
associated with a high fever may be caused by salmonellosis or E. coli mastitis
(Table 10.3). Chronic diarrhoea accompanied by weight loss in a high proportion
of the cows could be caused by gastrointestinal parasites. If so, it really is inex-
cusable. Scouring and weight loss in heifers at pasture could be due to teart
(Chapter 7). Chronic diarrhoea in a few individuals could be caused by BVD or
Johne’s disease.
Abdominal straining is more likely to be a symptom of infection of the urinary or
reproductive tract than problems in the gut. Intestinal obstruction is very rare.
Ragwort poisoning is a possibility but dairy farmers (surely!) recognise ragwort as a
poisonous plant and ensure that it does not get into hay or silage cut in late summer.
Cows normally avoid ragwort in the field but may fail to recognise it or be unable to
avoid it in conserved forage.
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Nervous Symptoms
The first symptom of many diseases is a change in the cow’s state of mind. She may,
often quite suddenly, become hyperexcitable: wide‐eyed, bellow aimlessly and over-
react to the slightest stimulus. This is most often an early indication of hypomagne-
saemia. Other possible causes are tetanus or one of several poisons. At the time of
writing the previous edition, bovine spongiform encephalopathy (BSE or ‘mad cow
disease’) was an alarming possibility but we may now (I trust) take it that that prob-
lem has been resolved.
Other diseases may cause a cow to appear disorientated to a degree that varies
from mildly bemused to a state of delirium. Specific signs include head shaking,
walking in circles, partial or complete blindness and pressing the head against a
wall or post. This last symptom has been variously interpreted but I think it signifies
a severe headache. These signs can be caused by a wide range of conditions: over-
eating of concentrates, some cases of ketosis, or listeriosis, an infectious encephali-
tis, probably acquired by eating contaminated, poorly fermented grass silage. More
on this later.
Any cow suffering from a systemic infectious disease is likely to appear
depressed but in this case there are likely to be other, more specific symptoms.
Sometimes however, a cow will appear depressed, probably with some loss of
appetite but no other obvious symptoms. In these cases, it can be difficult to
know what is wrong. She could be suffering from fatty degeneration of the liver,
so feeling ‘liverish’. She could also be in the early stages of a variety of conditions
raging from hypocalcaemia to botulism. However, many of these conditions are
rare. It is the common conditions that occur commonly1. Readers scanning the
tables of symptoms in this chapter should resist the temptation to develop a
sense of hypochondria by proxy in regard to their cows, akin to that of the neu-
rotic who rushes to Google at the slightest twinge and self‐diagnoses a multiplic-
ity of conditions, many of them lethal.
Fever
Fever is an elevation of body temperature induced by chemical substances called
pyrogens that may be produced by invading bacteria but, more often, from damaged
tissues and/or the cells of the body’s immune system (neutrophils, macrophages,
etc.). These pyrogens reset the cow’s thermostat in the hypothalamus. When we
take rectal temperature with a thermometer we may classify fever, somewhat arbi-
trarily, as normal 38.2 °C, moderate fever 38.6–39.5 °C, severe fever >39.5 °C. In the
early stages of fever, the cow (like any other homeotherm) increases body tempera-
ture both by elevating heat production and reducing heat loss. She shivers and
reduces blood flow to the extremities so that her ears and feet may feel cold even
though her deep body temperature is elevated. After body temperature has stabilised
1 Thank you Roger.

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at the new level her metabolic rate will remain elevated. Her extremities (ears and
feet) may now feel hot but she may continue to shiver. She is dull, off her food and
may pass excessive amounts of urine. The combination of high metabolic rate,
inappetence and high fluid loss can cause her to lose condition very rapidly.
Since fever is a natural manifestation of the body’s defences to infection or tissue
damage it is, presumably, not in itself, a bad thing, although I have yet to read a con-
vincing argument in its favour. Since most fevers in cattle are caused by infections,
treatment is usually based on antibiotics that destroy or inhibit the causative organ-
isms and allow the natural processes of healing to take their course. We should,
however, acknowledge that when we ourselves have a fever, it is likely to be of viral
origin so not susceptible to antibiotics. Moreover, we find that the most effective
action is to treat the symptoms, with (e.g.) paracetamol and anti‐inflammatory drugs.
We should always consider symptomatic treatment for our sick animals. If a cow has
so severe a fever that it constitutes a risk to life, she may be hosed down with cold
water. The need for this is rare. What is far more common is the cow with a moder-
ate, persistent fever who lies shivering in a cold box in order to maintain a deep body
temperature of, say, 39.5 °C. This cow will benefit from a rug, straw bedding or any
other means of reducing heat loss. We should, without recourse to anthropomor-
phism, assume that the fevered cow is feeling rotten and nurse her accordingly.
In recent years we have become increasingly concerned about the problem of bacterial
resistance to antibiotics. In a veterinary context, this concerns relates not only to the
development of resistant strains to the infection suffered by the animals in our care, but
also the extent to which the use of antibiotics to treat and, more seriously, to manage
endemic infections in farm livestock can contribute to the emergence of antibiotic‐resist-
ant strains of bacteria that infect humans. However, whereas the blanket, long‐term
administration of antibiotics to hold the line against infectious disease has been wide-
spread in the intensive pig and poultry industries, this has never been the case for the
dairy industry for the sound reason that antibiotics inhibit essential rumen bacteria and
so impair productivity. Looked at another way, the rumen microbiota may be thought of
as the ultimate probiotic, greatly reducing the risk from enteric pathogens. The one case
where antibiotics may be used in a prophylactic capacity is for dry cow therapy to reduce
the risk of mastitis, but here, as discussed in Chapter 9, policy is now (or should be) based
on the most parsimonious use of antibiotics combined with teat sealants.
Inappetence and Anorexia

To be pedantic for a moment, inappetence describes reduced food intake, anorexia
means that food intake has stopped altogether. In Chapter 2 I considered what
motivates a healthy cow to start and stop eating. Inappetence and anorexia in a sick
cow are governed by the same signals that control hunger and appetite. A cow may
refuse food if:
●● It hurts to eat.
●● The rumen or abomasum is already distended by undigested material or gas.
Notifiable Disease 189
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●● The chemicals circulating in the blood stream (normal metabolites, pathogens or

pyrogens) indicate satiety rather than hunger to the appetite centre in the
hypothalamus.
Eating can be a painful process in diseases such as wooden tongue, lumpy jaw or
traumatic reticulitis. Also, although less obviously, a cow with sore feet may prefer
not to eat if it means walking to the feed face where she must stand and compete
with other cows. One can sustain food intake, and thus milk yield, in very lame
cows by allowing them to lie, between milkings, in deep straw in a calving pen and
bringing the food to them.
An excess of undigested food will reduce food intake in cases of rumen or abo-
masal impaction, obstruction of the small intestine, or neuromuscular damage
leading to a reduction in the rate of propulsion of fluid through the gut.
When an animal is fevered, or poisoned by toxins arising from viruses, bacteria
or cell damage, there is a rise in concentration of certain chemicals circulating in
the blood, in particular, certain amino acids known to be associated with satiety.
Stress shifts the balance of the endocrine system from anabolic hormones such as
insulin and growth hormone that potentiate the uptake and incorporation of VFAs
and amino acids, to the release of catabolic hormones from the adrenal cortex that
stimulate the release of glucose and amino acids from body reserves into the circu-
lation. These factors combine to inform the hypothalamus that no more food is
required until these substances already in circulation have been processed. The
animal with liver damage may become anorexic because it cannot process the
products of its own tissue metabolism, let alone the end‐products of digestion.
Prolonged inappetence presents the ruminant with two special problems. First,
the loss of fermentable carbohydrate from the rumen means a loss of rumen
microbes and consequently a reduced ability to digest food when the cow begins to
recover her appetite. Secondly, any dairy cow that is lactating or in late pregnancy
(i.e. nearly all of them) and goes off food is likely to develop ketosis. Ketones, para-
doxically, inhibit appetite (a phenomenon that appeals to human slimmers) and
even more paradoxically, appetite for concentrate feeds that are high energy, rap-
idly digested and absorbed. Once a cow has gone off her food, it can be difficult to
rekindle her appetite. Most vets will dispense stimulant drenches that may or may
not work for reasons that I don’t understand. Cyanocobalamin (vitamin B12) can
work sometimes. The caring cowherd can also titillate the cow’s appetite with tasty
bites of fresh green feed, succulents, or a warm mash that may contain sugar beet
pulp, a cereal/bran mixture, molasses or even stout!
Notifiable Diseases
The UK Animal Health Act (1981, with subsequent amendments) empowers the
Department for the Environment and Rural Affairs (DEFRA) through the State
Veterinary Service and Local Veterinary Inspectors to record and control the movement
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of livestock both within the country and overseas. All calves must be fitted with tags on
both ears within 20 days of birth and be issued with a passport. The act requires owners
of cattle to inform DEFRA or the police if they suspect an animal may be suffering
from a notifiable disease. ‘Notifiable’ diseases are animal diseases that farmers are
legally obliged to report to the UK Animal and Plant Health Agency (APHA), even if
they only suspect that an animal may be affected. Notifiable diseases can be:
●● Endemic – already present in the UK, such as bovine TB
●● Exotic – not normally present in the UK, such as foot and mouth disease.
Some endemic and exotic diseases are zoonotic, which means they can pass between
animals and humans, such as bovine tuberculosis. Notifiable diseases for which
cattle in Great Britain are at risk are listed in Table 10.5. The most serious endemic
disease of cattle is bovine tuberculosis, which is transmissible to humans and
endemic in some livestock, e.g. badgers and deer. Anthrax is also zoonotic.
Technically it is endemic because the anthrax spores can survive in the soil for
many years. Many years ago, when I was a student and young vet in Northampton,
traditional home of the leather industry, the risk of anthrax in cattle grazing pastures
downstream of the tanning factories was significant but, in the UK, it is now very
rare indeed.
Of the exotic diseases, foot and mouth disease presents the greatest threat to cattle
in the UK. Blue tongue, a viral infection of cattle and sheep, presents a risk because
it is present in Europe and is transmitted by midges that can spread to the UK when
the wind is right. Diseases that APHA pronounce as ‘eradicated’ include brucello-
sis, enzootic bovine leucosis and warble fly. The term ‘eradicated’ needs to be inter-
preted carefully. Brucellosis used to be a major problem because of the risk of
Table 10.5 Notifiable diseases for cattle in Great Britain.
Category Disease Other important hosts Latest outbreak
Endemic Bovine tuberculosis Humans, dogs, cats

Wildlife
Anthrax Humans (etc.)
Exotic Foot and mouth Sheep, pigs 2007
Blue tongue Sheep, ruminants 2007
‘Eradicated’ Brucellosis Humans 2004
Bovine spongiform Humans
encephalopathy 1996
Enzootic bovine
leucosis
Warble fly
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transmission of a most unpleasant ‘undulant fever’ in humans. Indeed, all three

partners in the vet practice where I first worked were chronic sufferers. According
to APHA the last case recorded case of brucellosis in England was in 2004. However,
a few more recent cases have been diagnosed in Northern Ireland. Warble fly was a
most unpleasant affliction of cattle when I was young but proved easy to eliminate.
I have included bovine spongiform encephalopathy (BSE) in the eradicated list.
Although there have been isolated cases the epidemic appears to be over.
The APHA list of notifiable diseases includes several exotic infections such as
rinderpest and contagious bovine pleuropneumonia that have not affected UK cat-
tle in living memory and, barring extreme consequences of climate change, are
unlikely to do so, thus need not concern us here.
Bovine Tuberculosis
Bovine tuberculosis is caused by the microorganism Mycobacterium bovis. Cattle
become infected by eating contaminated material or inhaling infected droplets.
Initially the disease infects one or more lymph nodes near the point of entry,
where it forms a slowly developing ‘cold’ abscess, or tubercle. In many otherwise
healthy cows (or humans) the disease may not progress beyond this stage but the
animal is sensitised to the antigens in the bacteria. If the disease is allowed to
progress, infection will spread to the udder, enter the milk and become a source
of infection to humans. Before the initiation of a control policy for bovine TB,
which includes pasteurisation of milk, miliary, or generalised tuberculosis in
humans, especially children, was primarily due to drinking infected milk.
Tuberculosis of the lung, or ‘consumption’ was more often transmitted by drop-
let infection between humans.
The policy for control of bovine tuberculosis (bTB) in the UK has been based
on routine testing of cattle for sensitisation to M. bovis using a tuberculin skin
test. Reactors are removed for slaughter and post‐mortem examination and a
movement restriction is placed on the entire herd until proven bTB‐free at a sub-
sequent test. In the previous edition (1993) I wrote ‘the eradication scheme for
bovine tuberculosis (bTB) has been a triumph of public health’. Since then things
have gone sadly awry. According to DEFRA the incidence of bTB in 1979 was
0.01% (1 case in 10,000). In 2013, the herd incidence was 9% and in SW England,
the worst affected area, one quarter of all herds were held under movement
restriction.
There are many reasons for this breakdown of control. The first of these is the
presence of bTB in wildlife, especially badgers but also deer and feral cats. Without
necessarily ascribing cause and effect, the increased prevalence of bTB in South
West England correlates with the increased population density of badgers. The sec-
ond major factor, easier to control, is the movement of infected cattle from farm to
farm. The third, and most exasperating explanation for the failure of the control
policy arises from the inadequacy of the current test, based on the skin reaction
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indicating sensitivity to antigens in M. bovis. The test is not entirely accurate, i.e.
there are some false positives and false negatives. Moreover, what it actually meas-
ures is the immune resistance following exposure to the disease, not the disease
itself. In theory, the best policy for control of bTB in cattle would be through the
development of an effective vaccine. Indeed, the BCG vaccine used to immunise
humans against tuberculosis is based on M. bovis. However, at the time of writing,
we have failed to produce a vaccine that can be distinguished from natural infection
using current tests. Current vaccines are being used to vaccinate badgers and, epi-
demiologically, this makes sense since it would not be necessary to immunise every
animal: if 60% of the population were immune, this should in time lead to virtual
eradication of bTB in the badger population. However, immunisation of 60% of the
badger population is easier said than done, although trials are in progress. The per-
fect solution must lie in the development of an effective new vaccine for cattle
linked to an improved test procedure that is more accurate and does not confuse
post‐vaccination immunity with exposure to natural infection.
Foot and Mouth Disease

Foot and mouth disease (F&M) is established in most areas of the world with the
exception of North America, Australia, Eire and the UK. The disease, which
affects cloven‐hooved animals, e.g. cattle, sheep and pigs, is highly infectious.
The virus may be transmitted by direct contact, by vectors such as birds and
insects, in feedstuffs (such as pig swill) or by inhalation of infected aerosols that
may, according to wind speed and direction, transmit the infection up to 100 km,
e.g. across the English Channel. In cattle it causes an initial acute phase of
extreme sickness with almost complete loss of appetite and milk production.
Ulcers appear in the mouth and just above and between the hooves. If permitted,
most cattle will recover but convalescence is prolonged and the equivalent of one
lactation is lost. Morbidity is close to 100%, i.e. nearly all cattle exposed to infec-
tion will fall sick.
The policy for control of F&M in the event of an outbreak in the UK has always
been to eradicate the disease and retain disease‐free status as quickly as possible. To
date, this has involved the killing of all animals on infected premises and those
close enough to the site of infection to be considered ‘dangerous contacts’. This
approach is augmented by extreme biosecurity measures including control of ani-
mal movements outside the affected area. There are vaccines against F&M. However,
vaccination of all cattle, or animals at risk, has not been recognised as an effective
or complementary control strategy. This is partly because the immunity conferred
by vaccination is short‐lived and animals may have to be revaccinated at intervals as
short as four months, which would be expensive. However, the main justification
for the no‐vaccination policy has been that it would acknowledge that the disease is
established in the country and so destroy the export trade of live cattle to countries
that are F&M‐free.
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Through repeated outbreaks of F&M in my lifetime this policy, though draco-

nian, has achieved its primary objective, namely the rapid eradication of the epi-
demic. However, in 2001 there was a massive, widespread epidemic, arising from
pigs and disseminated largely by sheep movements that resulted in the slaughter
of 6.5 million cattle at a cost to the nation of £5 billion, (which dwarfed the
potential loss of income from the export trade). Some time after this outbreak
(2011) DEFRA published a revised policy in the event of a new outbreak of F&M
that would retain the essentials, culling and control of movement, but ‘consider
from the outset the use of vaccination as an extra control measure’. This change
of policy was taken for reasons of economics and animal welfare (less slaughter
of healthy animals) and reflects a welcome insertion of humanity and common
sense.
Other Infectious Diseases
This section deals very briefly with some of the more common infectious and para-
sitic diseases that can affect cow and heifers. There are no detailed descriptions of
the clinical signs and pathology of these diseases. In each case I concentrate only on
features that affect the transmission of these diseases and control on the farm.
Bovine Viral Diarrhoea (BVD)

Bovine viral diarrhoea (BVD) was previously called bovine virus diarrhoea. The
name change arose, I guess, from the tautology implicit in referring to the causative
organism as bovine virus diarrhoea virus (BVDV). This is a complex disease pre-
senting problems for individual animals that range from the mild to the lethal. The
number of herds in the UK where BVD is endemic has been over 30%. The aim of
the industry is to eradicate it altogether and we now know enough about the disease
to make this a realistic prospect.
Typically, a herd of cattle may be infected for the first time when a carrier is
purchased into the herd, especially during the winter months when the cows
are housed. On this first occasion most of the cows may experience diarrhoea
and a sharp drop in milk yield for a few days, then recover. Some may abort.
Most of those that recover will become immune and show no chronic symp-
toms. However, the disease becomes endemic in the herd and will continue to
infect heifers and bought‐in animals. The most serious problems arise when
cows become infected with BVDV in the first trimester of pregnancy (<120
days). In these circumstances some cows will abort. Others will carry their
calves to full term. However, in the first trimester of pregnancy the immune
system of the calf Is too immature to recognise the virus as ‘non‐self’ and so
manufacture antibodies to it. After birth, these calves may survive to maturity,
although they are likely to be stunted and more susceptible to other infections.
Some of these calves may be subsequently exposed to a virulent strain of BVDV
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and develop mucosal disease, a very severe disease involving anorexia, mouth
ulcers, profuse bloody diarrhoea and usually proceeding to death in 2–3 days.
This is bad enough. Even more serious, in a herd context, is the calf that does
not develop mucosal disease but remains in the herd as a persistently infected
individual that can and will transmit the infection to all the other cows in the
herd. There has been a train of thought that says the presence of a persistently
infected individual can render the rest of the herd immune after an initial mild
infection. There is, however, good evidence that herds in which BVD is endemic
suffer the financial and welfare consequences of low‐grade infection so that
eradication has to be the better policy.
The policy for eradication of BVD, herd by herd to the point where the nation is
BVD‐free, involves three steps, biosecurity, biocontainment and vaccination.
Biosecurity involves maintaining, so far as possible, a closed herd, buying in cattle
only from herds that are proven free from BVD and avoiding contact with adjacent
herds, e.g. by double fencing. Biocontainment begins with screening tests to iden-
tify those cows with antibodies to BVD, immediate culling of any persistently
infected carriers and vaccination of all cows and heifers. The vaccines are effective
but repeat vaccination is necessary until the herd is demonstrably free of infected
carriers of disease.
Johne’s Disease
The main clinical feature of Johne’s disease is a profuse, persistent watery diar-
rhoea. Initially the cow is bright and has a good appetite but the severe loss of water
and electrolytes causes a rapid loss of body condition and progressive weakness.
The disease is caused by Mycobacterium paratuberculosis, which causes a progres-
sive thickening of the lower small intestine and colon, thereby progressively reduc-
ing the capacity to absorb water, nutrients and electrolytes from the gut. Affected
cows should be culled as soon as possible. Although it is mature cows that experi-
ence the disease they are, in fact, resistant to infection, which can only become
established in calves infected before six months of age. The onset of clinical disease
only appears in later years, typically provoked by the stress of calving. Control, in
theory, is based on the principle of keeping calves away from infection before six
months of age. This is easier said than done. Infection may occur in utero but is
more likely to arise from drinking contaminated milk or colostrum. Vaccination (in
the UK) is not a realistic option since vaccinated calves react positively to the tuber-
culin test.
Salmonellosis
The two species of salmonella most often responsible for salmonellosis in cattle are
S. typhimurium and S. dublin. The former can affect most animals including
humans, the latter is almost entirely specific to cattle. The organism is almost
impossible to eliminate from infected farms since it can survive for long periods
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both outside and inside animals unless their resistance is upset by a stress such as
calving, transport or a dietary disturbance. The problem of salmonellosis, especially
that due to S. typhimurium, is greatest in young calves who may be infected by their
mothers or in transit from their farm of origin to a rearing unit. S. dublin can cause
outbreaks of diarrhoea in well‐grown heifers and is one cause of abortion in adult
cows (Chapter 12).
Leptospirosis
Leptospirosis is a highly contagious infectious disease of cattle and other species, most
critically in this context, rats, sheep and humans. Transmission between animals (and
to humans) is by direct or indirect contact with body fluids, most commonly urine but
also aborted materials and semen. In herds where the disease is endemic, infection
may first arise in calves, who become acutely ill but usually recover after antibiotic
treatment. Adult cows infected for the first time with the most common pathogen
Leptospira hardjo, may not appear clinically ill but show a marked drop in milk pro-
duction and may abort some 3–12 weeks after initial infection. After apparent recov-
ery, infection is likely to persist in the kidney, bacteria are shed in the urine and the
affected animals become persistent carriers. Once established, the infection will
become widespread through the herd. It will not present as a lot of sick animals but
compromise performance through reduced milk yield, an increased incidence of early
foetal death, abortion and retained placenta (see Chapter 12). It also presents a con-
stant risk of transmission to humans working with cattle, typically when cattle urine
comes into contact with a cut finger. Leptospira excreted in the urine will survive for
some time in the environment. Cows can become infected by consuming grass that has
been contaminated by urine from other cattle or sheep. It follows that a high propor-
tion of animals become infected during the grazing season.
Although there are many dairy herds content to live with leptospirosis, it is
undoubtedly better on grounds of welfare, productivity and risk to human health to
eliminate infection from the herd and protect it from reinfection by strict attention
to biosecurity. Carriers can be treated with antibiotics. Vaccination is very effective,
although while the disease remains it is necessary to revaccinate annually. Strict
biosecurity is also essential. This includes maintenance, so far as possible, of a
closed herd. Any bought‐in animals should come from a guaranteed lepto‐free herd
or tested before purchase. Any farmer using natural service for any cows or heifers
should see evidence that the bull is lepto‐free. Cross‐infection from other infected
animals, neighbouring cows, sheep or rats, should be avoided through control of
fencing at borders and strict attention to pest control.
Parasitic Diseases
The most important parasitic diseases of adult cattle in the UK are husk (or hoose)
caused by the lungworm Dictyocaulus viviparous that is acquired by cattle consum-
ing the larval stages from pasture, and liver fluke, Fasciola hepatica, which requires
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a second host Lymnaea truncatula, a snail whose natural habitat is around poorly
drained, chronically muddy areas around ponds, streams and water holes.
The parasite D. viviparous can cause severe pneumonia in young cattle at pasture.
The mature lungworms live in the bronchioles, interfere with the normal move-
ment of air during respiration and cause moderate to severe damage to the lungs. In
a few cases, affected animals develop severe respiratory distress accompanied by a
high temperature and may die within a few days. In the more common, chronic
form of the disease, the cattle cough repeatedly and lose condition. In the UK the
risk of lungworm in young cattle at pasture is extremely high and on most farms
some form of prevention is essential for calves in their first summer. Eggs from
mature lungworms are coughed up, swallowed into the gut where they mature into
larvae that are shed in the faeces. They can survive the winter, mature further on
the pasture to the point where they are able to re‐infect cattle the following spring.
Prevention can involve immunisation of calves before turn‐out with two doses of a
vaccine such as Dictol, made by irradiating larvae to the point where they are una-
ble to mature to adults but still induce immunity. Natural exposure to lungworm in
the first and subsequent seasons at pasture is sufficient to sustain immunity so vac-
cination does no need to be repeated. A less elegant but probably cheaper form of
control is to give young cattle one or more preventive doses with a broad‐spectrum
anti‐parasite drug, which carries the added benefit of killing other internal and
external parasites.
The liver fluke, F. hepatica, spends its adult life in the liver and bile ducts where
it sucks blood. Severely infected animals become anaemic and emaciated. Eggs are
shed in the faeces, hatch in the warm, wet weather of early summer and are taken
up by the snail Lymnaea truncatula living in the muddy water. The snails do not
thrive in highly acidic peat bogs but can survive if the land is limed to improve its
potential as a cattle pasture. The intermediate stages of the parasite mature and
multiply inside the snails, are then cast onto the pasture to reinfect cattle in the
autumn. It then takes about three weeks for the mature flukes to develop so the
clinical disease is usually a problem of mid‐winter. To control the fluke, wet areas of
pasture should be drained or fenced off. If this is not possible then cattle can be
given a preventive dose of a fluke‐killing drug in early winter when the flukes are
inside the cows but before they begin to do any damage.
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Part IV
Breeding and Fertility

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11
Breeding
The traits that define the appearance, physiology, behaviour and commercial perfor-
mance of any animal are governed by its phenotype. The extent to which each trait is
determined by the genes it inherited from its parents is its genotype. The phenotypic
value of any trait is defined by the interaction between the genotype and the environ-
ment to which it is exposed. For a qualitative trait such as colour or the absence of
horns, genotype and phenotype are usually synonymous. Conformation (or ‘type’) is
largely determined by genotype but influenced to a degree by environment. The phe-
notypic expression of important quantitative traits such as milk yield are greatly
influenced by environment. To a geneticist, ‘environment’ refers to everything else,
most notably in this case, nutrition. To give an extreme example: the daughter of a
high yielding Holstein cow and the highest ranked Holstein bull in the USA will not
produce very much milk if shipped to Africa and fed on very fibrous hay. The envi-
ronment prevents her from expressing her genetic potential. Indeed, for a variety of
reasons (poor nutrition, heat stress, resistance to internal and external parasites) she
may produce less milk than an African cow of humbler parentage1.
A farmer who wishes to use breeding methods to improve the performance of his/
her herd according to a specific trait (e.g. total lactation yield) has three options.
●● Buy in proven cows from a breed known to produce more milk (e.g. Holstein
versus Ayrshire)
●● Select superior animals within the breed (especially proven sires)
●● Crossbreed animals between two selected lines.
The direct consequences of buying in cows known to produce more milk are obvi-
ous, although for many reasons this is unlikely to be the favoured choice. The effec-
tiveness of selective breeding of ‘superior’ animals according to a defined trait will
depend on the heritability of that trait, where heritability is a statistic that defines
the degree of variation in a phenotypic trait within a population that is due to the
genetic variation in that population. Heritability values for the more important
1 This casts serious doubt on the charitable notion: ‘Send a cow to Africa’.

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Table 11.1 Heritability of production and fitness traits and emphasis

on traits used in £LPI selection index (from Better Breeding, AHDB, 2015).
Selection
Traits Heritability emphasis (%)
Production
Milk yield 0.55 32.2
Milk composition 0.68
Linear type
Stature and body depth 0.34 9.6
Udder characteristics 0.2–0.3 7.0
Management
Somatic cell count 0.11 9.1
Locomotion 0.10 5.5
Lifespan 0.06 14.4
Fertility 0.03 20.3
Calving ease 0.05 1.9
traits in the context of dairy farming are listed in Table 11.1. At this stage, simply
note that traits relating to milk production and body type are relatively high, those
relating to fitness, fertility and lifespan are very low. The heritability of maternal
traits such as the number of piglets reared by sows per year, itself a complex func-
tion of prolificacy and mothering ability, is close to zero, which implies that any
observed phenotypic variation will be of environmental origin. In practice, mater-
nal traits in cattle, sheep and pigs are enhanced by crossbreeding between two
genetically different inbred lines to induce heterosis or ‘hybrid vigour’. Cross‐breed-
ing is not really an option within a dairy enterprise where income is dominated by
the sale of milk, although the Hereford–Friesian crossbred cow makes an excellent
suckler cow for beef production.
It is important at this stage to consider the difference between natural selection
within a wild population operating according to the Darwinian principle of survival
of the fittest and artificial selection within a domesticated population designed to
promote the economic needs (or indeed the whims) of their owners. Before domes-
tication, natural selection within a species, together with random mutations, oper-
ated to promote ‘fitness’ (survival and reproduction) of species, combinations of
species and individuals within species best adapted to a particular environmental
niche. After a prolonged period of natural selection, the phenotypic variation
between individuals within a species becomes less and less for traits essential to fit-
ness like survival, fertility and food conversion efficiency. Thus, a population of
wild rabbits within a wood will tend to reproduce at similar rates and grow to a
similar size. Their coats will be of a similar colour since the wild rabbit needs cam-
ouflage, so coat colour is critical to survival. In general, natural selection within a
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species tends to reduce phenotypic variation for traits that are important to fitness
within that environment.
Domestication of farm and pet animals (in the ‘care’ of humans) has largely freed
them from the problems of seeking sufficient food, competing for a sexual partner
and avoiding the ravages of predators. At the same time, it has allowed humans to
engage our fancies for manipulating the phenotype of our animals by selecting for
traits that are unrelated to (or may directly conflict with) the principle of survival of
the fittest. There is, in nature, no example of phenotypic variation within a species
comparable to that which we have inflicted on dogs. Consider the Great Dane and
the French bulldog; both unnaturally selected for traits so far removed from fitness
as to create unhealthy freaks. Cattle selection has been more hard headed but still
produced extreme phenotypic variation between (e.g.) the Hereford, a medium
sized, deep‐chested, heavy‐bodied animal designed to produce meat from grass and
the modern Holstein, a massive udder on stilts, designed to produce a very large
quantity of milk while confined in a barn and lavished with rich food.
While the animal with a lower genetic potential for milk production may well
outperform the genetically ‘superior’ animal in very challenging environments
there is good evidence that the ‘superior’ cow, defined strictly in terms of poten-
tial milk yield, will outperform unselected cows across a broad range of nutrition
regimes from high cereal to high fibre.
Table 11.2 presents the results of a trial carried out at the Langhill estate of the
(then) Scottish Agriculture College, designed to examine the effect of selection for
performance on high energy diets, when transposed to a system more dependent on
forage. The high‐performance cows were selected on the basis of their cow genetic
index (CGI), a largely outdated approach that predicts the weight of fat plus protein
that an individual cow will transmit to her progeny relative to a herd standard of 500.
In Table 11.1 the CGI of the high genetic merit group was 700, the unselected group
500. Lactation yield of the CGI700 cows was 14% higher than that of the CGI500 cows
on the high energy ration, 13% higher on the low energy (forage) ration. There was a
Table 11.2 Performance of Friesian–Holstein cows with high (700) and average
(500) genetic indices on high (0.45) and low (0.20) concentrate rations (Oldham
et al., 1992).
High concentrate Low concentrate
Predicted CGI 700 500 700/500 700 500 700/500
Lactation yield (kg) 7032 6164 1.14 6030 5309 1.13

Fat (g/kg) 42.5 44.7 0.94 46.2 45.1 1.02
Protein (g/kg) 30.4 31.5 0.96 30.4 31.3 0.97
Fat plus protein (kg) 512 466 1.10 463 406 1.14
Dry matter intake (kg) 4645 4408 1.05 4065 4010 1.01
Efficiency (MJmilk/MJME) 0.39 0.37 1.06 0.41 0.37 1.12
Profit margin over food costs (£) 759 643 1.18 732 599 1.22
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suggestion that the increased milk yield of the CGI700 cows was associated with a
reduction in milk fat concentration on the high energy ration only (possible explana-
tions for this should emerge from Chapters 5 and 7). Of particular interest, (and some
surprise) is the observation that the overall superiority of the CGI700 cows, whether
measured in terms of food conversion efficiency (MJ milk/MJ ME intake) or profit
margin over feed costs, tended to be slightly greater on the lower‐energy, forage ration.
Table 11.3 describes lactation trends for four breeds of dairy cows in UK during
the period 2000–2014. The greatest absolute and relative increase in yield has
occurred in the Holstein breed; 7637 to 9239, an increase of 21%. By contrast the
increase in the British Friesian breed has been only 7%. What this shows is that
there has been more selection pressure for increased milk yield for Holsteins than
for Friesians. This reflects the first great truth of genetics: when the trait is heritable
you get what you select for. The second great truth is that there are correlated
responses to selection that may yield responses that you did not anticipate and some
of which you would rather avoid. Table 11.3 shows that there has been a far greater
increase in lactation yield in the Holstein breed than in British Friesians. However,
somatic cell counts, an indicator of mastitis prevalence have increased in the
Holsteins and not the Friesians. Calving intervals, a marker for fertility, have
increased in both breeds. There is much more to the business of breed improvement
than simple selection for improved milk yield.
S
election Criteria
The aims of a breeding policy should be to achieve steady improvement in traits

associated with the quantity and quality of the product for sale, the health and wel-
fare of the cows and the profitability of the enterprise. Let us begin by considering
what traits that it might be worth attempting to improve through breeding, ignoring
for the moment how easy or difficult each might be to achieve.
Table 11.3 Lactation trends in UK dairy cow breeds 2002–2014 (from CDI breed
performance statistics, 2015).
Milk (kg) Protein (kg) Fat (kg) SCC CI
Holstein 2000 7637 248 275 148 402

2014 9239 293 361 186 418
Friesian 2000 6501 216 258 151 392
2014 6966 233 284 163 396
Jersey 2000 5048 197 275 184 392
2014 6024 230 329 186 406
Ayrshire 2000 6201 207 219 191 406
2014 7037 233 288 204 416
SCC = somatic cell count (000 cells/ml), CI = calving interval (days).
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1) Total yield of milk solids, especially protein and butterfat.

2) Milk composition, especially protein and fat concentrations.
3) Conformation of the cow
–– To reduce the incidence of mastitis, lameness, trampled teats, etc.
–– To improve the value of her male calves for beef production.
4) Reproductive efficiency.
5) Food conversion efficiency: increased milk yield per tonne of purchased concen-
trate food, or per MJ of utilized metabolizable energy.
6) Disease resistance: reduced incidence of mastitis, lameness, etc.
7) Longevity: prolonged active life through improvements in 3, 4 and 6.
8) Profitability: through improvements in all the above.
At the time I wrote the previous edition (1993) selection pressure was dominated by
the wish to increase production of milk solids as fast as possible, especially in the
North American Holstein breed. This was based on measurements of the perfor-
mance of the progeny of selected bulls in their first lactation and, in terms of this
primary aim, it has been conspicuously successful. However, the single‐minded drive
to higher milk yields generated increasing opposition, not only from animal welfare
groups but also within the industry itself because of an increasing body of evidence to
indicate that this policy was leading to a reduction in fitness as measured by reduced
fertility and, especially, increased culling of worn‐out cows, so that in many high‐
yielding herds the average working life of cows had fallen below three lactations. This
was not only a serious welfare problem but also bad for business. In order to maximise
the lifetime profit to be derived from a dairy cow it is necessary for her to achieve at
least four lactations to offset the costs of rearing her as a heifer to the time of first calv-
ing and to exploit the fact that, if she remains healthy, lactation yield will increase
from the first to the second and third lactations. There is now international recogni-
tion of the need to breed more ‘robust’ cows with a longer working life through the
implementation of a selection index that gives greater attention to traits relating to
fitness. The full benefits of this policy will take time to emerge but there is already
evidence of an increase in longevity in Holstein cows. The average for recorded herds
currently stands at 3.5 lactations, which is far from ideal, but it’s a promising start.
Before describing how the aims of breeding more productive, more robust cows may
be achieved in practice, it is necessary to state, in simple terms, some fundamental
principles that are governed by the strict mathematical roles of population genetics.
1) The more traits chosen for inclusion in a selection programme, the slower will be
the rate of change for any single trait.
2) Selection for a single trait invariably produces correlated responses; changes in
other traits that may or may not be desirable.
3) An animal gets half its genes from each parent, one quarter from each grandpar-
ent and one‐eighth from each grandparent.
The first practical recommendation that may be drawn from the third of these
principles is that the quickest way to promote genetic improvement is by select-
ing semen from superior bulls. The bull is (obviously) responsible for half the
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genetic make‐up (genotype) of his daughters. What may be less obvious perhaps,
is that after two generations 75% of the genotype comes from the bulls, rising to
94% after four generations. The other side of this coin is that pedigree records
going back more than two generations may be historically interesting but, for
quantitative traits like milk production, practically worthless. The message to be
taken from the second conclusion is that while it is clearly undesirable to select
for a single production trait such as production of milk solids because it carries
the risk of harm to traits linked to fitness, it is also unrealistic to try to improve
everything at once.
The selection index currently adopted by the independent Dairy Cow Breeding
Company in the UK is based on a Test Day Model that records performance and fit-
ness traits for the progeny of selected bulls up to and including the fifth lactation.
The emphasis given to the selected traits is shown in Table 11.1. The importance
attached to production traits, milk production and composition, is 32%. Body and
udder conformation are valued at 9.6% and 7.0% respectively. Somatic cell counts
and locomotion, markers for mastitis and lameness, are given values of 9.1% and
5.5%. Traits directly linked to profitable lifetime index, lifespan and fertility, are
given values of 14.4% and 20.3%. The good news coming from this selection index is
that now nearly 70% of selection is based on traits relating to fitness, longevity and
good welfare. However, a note of caution: it is necessary to look at the values for
selection emphasis in Table 11.1 alongside those for heritability. Where heritability
is relatively high, e.g. milk composition, body conformation and udder characteris-
tics, an individual farmer should expect a favourable response to selection for supe-
riority in one of these traits when selecting semen from a specified bull. Of the traits
listed under fitness one should hope for a slow and modest response to selection for
traits relating to mastitis and lameness (heritabilities ca 0.10) but little response to
selecting for fertility.
Selected bulls are progeny tested for their predicted transmitting ability (PTA) for
traits related to production, type and fitness. This does not predict actual perfor-
mance: obviously this depends greatly on nutrition and management. What it does
predict is the amount of a trait that the offspring will, on average, receive from its
parents compared with average parents, whose PTA is set at zero. The impact of
selection for all the measured traits is integrated in the form of the profitable lifetime
index (£PLI). This describes the additional profit a high £LPI bull is expected to
generate from his daughter relative to an average bull, defined as £LPI zero.
Table 11.4 compares PTA values for two progeny tested Holstein bulls. The crite-
ria selected for inclusion in this table, which is not comprehensive, are set out in
three categories, performance, linear traits and fitness. Performance is defined by
predicted increase in milk yield, fat and protein composition. Linear traits that
impact on lifetime performance include features of general body conformation,
here classified as type merit, udder conformation and the set of legs and feet. Traits
that define resilience to production disorders associated with management include
SCC (for mastitis prevalence), locomotion (for lameness) and body condition.
Selection Criteri 205
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Table 11.4 A comparison of the predicted transmitting ability of two

(imaginary) Holstein bulls for production, linear and fitness traits.
Taurus
Trait Windsor Milkomax Robuster
Performance
Milk (kg) +752 +535
Fat (%) –0.06 +0.20
Protein (%) –0.10 +0.07
Linear traits
Type merit (‐3 to +3) +0.6 +1.65
Mammary (‐3 to +3) +0.5 +1.4
Legs and Feet (‐3 to +3) +0.2 +1.2
Fitness
SCC (%) –6 –20
Fertility index (£‐30 to +30) +2.4 +16.2
Locomotion (‐3 to +3) +0.04 +0.5
Body condition (‐3 to +3) –0.28 –0.01
Lifespan (‐1 to +1) +0.1 +0.3
Productive life index (£) +658 +580
The fertility index (£) is a prediction of the financial gain to result from reduction in
infertility as assessed from a reduction in calving intervals and returns to first
insemination. Lifespan is an overall indicator of sustained fitness. The predicted
financial impact of bull selection is estimated by the £PLI.
The two bulls described in Table 11.4 are fictitious but representative of top‐rated
proven Holstein bulls within the UK. The first bull, Windsor Milkomax, carries a
very high PTA for total milk yield, with a slight reduction in fat and protein concen-
tration. A modest improvement is predicted in linear traits, body shape, and indica-
tors of fitness, with the exception of body condition. The second bull, Taurus
Robuster predicts a more modest increase in milk yield but an increase in fat con-
centration, which would appeal to producers supplying cheese manufacturers. This
bull (as my imagined name implies) is superior in terms of his PTAs for linear traits,
SCC, fertility index and lifespan. In consequence his £PLI is only 12% less than
Windsor Milkomax, despite a 29% lower PTA for milk yield.
As I have written already, it would be counter‐productive to select for everything
at once. Moreover, £PLI, the overall estimate of superiority derived from all indica-
tors should not be taken to apply for all cows and in all circumstances. The broad
list of PTAs for performance and fitness traits enables the farmer to be selective
when choosing bulls according to the special circumstances of the farm (what crops
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grow best) and the individual strengths and weaknesses of individual cows. For
example, my neighbour Clive Snell has a herd average yield of about 7500 L for his
Holstein–Friesian cows, which may appear modest in comparison with fully housed
Holsteins in the USA, but approximately 70% of their ration is grown on farm (fresh
and conserved grass, maize silage, roots and cereals). Moreover, most years, they
are at pasture from late March to early November. Clive gives high emphasis to
PTAs for linear traits, which makes good sense, because they not only contribute to
overall fitness but are also realistically heritable. The low heritability for fertility
suggests to me that while it is given high emphasis (20.3%) in the current selection
index (Table 11.1), choice of bull based on fertility index score is unlikely to have
much direct impact. The potential influence of the bull on ease of calving is included
on its record. The heritability of this trait is very low so not likely to be transmitted
to his offspring. However, it does make sense to avoid using a bull with a poor record
for calving ease on heifers or cows that have previously experience problems of
dystocia. Poor performance consequent on fertility problems such as delayed return
to oestrus and failure to conceive are much more likely to respond to improvements
in nutrition and management. I would make one exception to this general rule.
Cows in poor body condition are less fertile. I would therefore only be inclined to
select a bull such as Windsor Milkomax (PTA for body condition ‐0.28) for individ-
ual cows with a modest milk yield and a tendency to get fat in late lactation.
G
enomic Selection
Modern techniques for genetic profiling based on DNA analysis have made it pos-
sible to establish strong correlations between genotype and performance that will
more accurately predict the performance of offspring than those derived simply
from the average performance of parents. The reliability of this prediction is how-
ever significantly lower than that obtained from progeny testing (75% versus 95%).
The potential advantage is that the PTA of a bull can be assessed from its genome as
soon as it is born. This approach carries the potential to speed up the rate of genetic
improvement but with a reduced reliability of success. It may be compared with a
high potential gain/high risk investment.
S
exed Semen
The biggest constraint to the genetic improvement of dairy cows using conven-
tional inseminations from proven superior bulls is, of course, the fact that only
half the calves will be females that can be reared as heifers and carry their genetic
superiority into the next generation. Moreover, extreme selection pressure for
dairy type, especially within the Holstein breed has produced male calves that
have a conformation unsuited to most systems of rearing calves for beef. They can
be reared very rapidly for white (or pink) veal on a predominantly liquid (milk
replacer) diet and slaughtered at about 16 weeks of age, or reared slightly less
Cow Selectio 207
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r apidly on a barley‐based diet to be sold as baby beef at about 10 months of age.

Both systems present considerable problems of health and welfare (which are out-
side the scope of this book) and neither is likely to generate much profit. In many
extreme dairy systems, it may be policy to consider a high proportion of Holstein
male calves not worth rearing, so they are killed in the first days of life. The same
policy is likely to apply for the Channel Island breeds, especially extreme dairy
type Jerseys. Today, however, sexed semen from proven dairy bulls is widely avail-
able and at a reasonable price. Ideally, unless the farmer plans to increase herd
size, every cow only needs to be inseminated once with sexed semen from a proven
sire to produce one heifer calf to succeed her in the herd. However, in herds when
average life expectancy of the cows has been less than three lactations, many farm-
ers who did not have access to, or chose not to use, sexed semen, have used Holstein
(or dairy type) semen for all cows and heifers at all times. In pastoral systems, the
maiden heifers may be turned out at grass with a relatively small beef‐type bull
(e.g. Hereford or Aberdeen Angus) to produce cross‐bred calves with good confor-
mation for beef production and a reduced risk of obstetric problems.
The trend towards the increased use of sexed semen, together with the breeding
of the more robust cow with a longer lifespan, opens the door to a breeding strategy
based on one successful insemination of each cow with sexed semen from a suitable
proven dairy bull and all other inseminations from a beef‐type bull to produce valu-
able crossbred calves having a conformation suitable for beef production within
systems where the animals spend one or two summers at pasture. This offers a
high‐tech approach to improved cattle welfare. It should (almost) eliminate the
need to slaughter ‘bobby’ calves at, or shortly after, birth. It avoids the health and
welfare problems of rearing calves intensively for veal or baby beef. It also, on the
right farm, makes good economic sense.
At present, the overall probability of conception to sexed semen appears to be
less than for conventional semen. The difference is least (or non‐existent) for
heifer inseminations, which suggests that the lower conception rate for older,
multiparous cows may be attributed more to the poor condition of the cows than
to a significant deficiency in the semen. In any event, many farmers use sexed
semen from proven dairy bulls for heifers only. This carries an increased risk of
obstetric problems but potentially speeds up the rate of genetic progress.
C
ow Selection
Unless dairy farmers are in the business of breeding cows and potential mothers of
premium bulls, the selection decisions available with respect to cows in their own
herd are rather limited. They can:
1) Choose to cull individual cows on grounds of inadequate performance or
poor conformation.
2) Select the bull most appropriate to the individual cow on the basis of perfor-
mance, conformation and ease of calving.
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If the farmer is in the happy position of having so few casualties due to infertility,
mastitis and lameness that he can selectively cull on the basis of performance, then
a sound approach would be to set an independent culling level for fat plus protein
yield over 2–3 lactations. Any cow that is within (say) the bottom 20% is culled. It
would also be nice to cull cows on the basis of conformation, especially in regard to
legs and udder, to reduce the risk that these traits are passed on to her daughters.
However, in practice, this is likely to be an unrealistic luxury. If her conformation
flaws are serious enough to precipitate problems such as mastitis and lameness, she
is likely to be culled sooner or later anyway.
The genetic merit of individual cows is conventionally assessed from the PTAs of
their sires and maternal grandsires. This is not a particularly useful statistic for
conventional herds because of the relatively low potential of individual cows to
transmit their superiority relative to the semen contributed through artificial
insemination from superior bulls. Twenty years ago, when bull selection was
dominated by the milk yield of their progeny, there was good evidence that cows
of higher genetic merit with regard to milk production were more prone to prob-
lems related to loss of fitness, especially infertility. Now bull selection indices are
more heavily weighted towards fitness traits, this should be less of a problem.
In most commercial situations therefore, the process of genetic improvement
has been achieved almost entirely through artificial insemination to distribute
the genes of superior bulls. It is now possible to increase the contribution of the
cow to genetic progress using the technique of multiple ovulation and embryo
transfer (MOET). With this technique, a single female may contribute (say) 16
heifer calves for progeny testing either after selection on the basis of her first
lactation (adult MOET) or on the basis of her pedigree, reinforced by genomic
selection, when she first begins to ovulate (juvenile MOET). The rate of improve-
ment in milk yield to be expected from bull selection only is estimated to be 1.5–
2.0% per year. In theory, the successful application of a juvenile MOET programme
designed to select for milk yield could increase the rate of progress to 3.5–4.5%
per year. An even greater rate of progress could be achieved, again in theory, by
cloning identical copies of superior animals using the technique of embryo split-
ting. This will however greatly increase the risk of problems associated with
inbreeding. Radical reduction of genetic variation (e.g. within a single herd)
could prove to be a disaster if near‐identical animals proved to be particularly
susceptible to an infectious agent or metabolic disease.
Advice from the best geneticists indicates that the adult MOET scheme is likely to
achieve the best compromise between gains from accelerated genetic progress and
losses from inbreeding. However, the theoretical net gains from this scheme are not
significantly greater than those based on wise selection from progeny‐tested bulls.
This raises serious questions as to the cost‐benefit of the procedures involved in
MOET, especially when the welfare implications of these procedures are taken into
account. My personal view of MOET and cloning schemes is that they fail to pro-
vide a satisfactory answer to the question ‘gee whiz but so what?’, i.e. they are scien-
tific advances that offer a clever answer when there is no real question.
Beef Bull 209
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B
eef Bulls
The choice of a beef‐type bull for dairy cows is a relatively simple matter. The spe-
cialist dairy farmer wants a live calf that can be sold on to a beef rearing farm at a
good price following an uncomplicated calving that does not compromise the cow’s
lactation or her ability to return to service. The most suitable bull for cows in the
dairy herd is not the same as the best bull for suckler beef cows whose role in life is
to produce and rear one calf a year. To maximise efficiency of beef production from
suckler cows on range it is necessary to produce the largest possible calf with the
best possible conformation from small, thrifty cows so as to get the maximum pos-
sible income from the slaughter generation relative to the cost of maintaining the
breeding generation (recap Table 1.4). Thus large, heavily muscled continental
breeds of bull like the Charolais and Limousin have become favoured sires for this
system, despite the fact that the use of these large bulls carries an increased obstet-
ric risk for the cows.
In a dairy enterprise, the production of beefy calves with a high cash value at
birth can make a significant contribution to farm income. However, this has to
be offset against any increase in the direct effects of obstetric problems and the
long‐term consequences of these problems on subsequent fertility and perfor-
mance over the whole lactation. Table 11.5 shows the effects of bull breed on
gestation length, calf size (on a scale of 1, very small, to 5, very large) and the
incidence of dystocia in cows and heifers born to Friesian cows. In this study,
Charolais bulls, unsurprisingly, gave rise to the biggest calves, and the highest
incidence of dystocia, especially in heifers. Limousin bulls increased gestation
length to about 287 days. However, this increase in gestation length did not
appear to be associated with an increased risk of dystocia. Table 11.5 clearly
demonstrates the reduced obstetric risk in heifers from Hereford and Friesian
bulls. There is no value for obstetric risk in adult cows mated to Aberdeen Angus
bulls because it rarely occurs.
In recent years there has been a great increase in the use of ‘double‐muscled’
Belgian Blue bulls to inseminate dairy cows. The gene that is responsible for this
Table 11.5 Effects of bull breed on gestation length, calf size and obstetric
problems in Friesian cows.
Gestation Calf size Dystocia (%)

(days) (score*) Cows Heifers
Holstein/Friesian 281 3 2.7 5.7

Aberdeen Angus 279 1 n.a. 1.4
Hereford 282 2 1.2 2.7
Charolais 284 5 3.4 6.7
Limousin 287 3 2.4 3.2
* Calf weight is ranked on a five‐point scale from 1 = very small to 5 = very large.
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condition, which appears in most heavy beef breeds, does not, in fact, alter the
number of muscles but predisposes to abnormally overdeveloped muscles, espe-
cially in the expensive cuts around the hind quarters. The attraction of such ani-
mals to the butcher is obvious. However, this excessive muscular development of
the hindquarters is associated with a relative reduction in the circumference of
the pelvic canal to the extent where normal calving becomes extremely difficult or
impossible. In many purebred lines of Belgian Blue cattle it is standard practice to
deliver all calves by premeditated Caesarean section performed under local anaes-
thesia. In the view of the UK Farm Animal Welfare Council this premeditated,
repeated imposition of major surgery to accommodate a deliberate and painful
distortion of normal shape constitutes an unacceptable insult to welfare. I must
stress however that the obstetric problem is more a consequence of the distorted
shape and pelvic dimensions of the double‐muscled cow than the size of her calf.
The incidence of obstetric problems in Holstein/Friesian cows inseminated by
Belgian Blue bulls is no worse than for other large breeds such as the Charolais.
This does not, of course, exempt the dairy farmer from the ethical responsibility
to select bulls that have been bred without cruelty. There are Belgian Blue lines
that involve natural breeding. Farmers could select from these.
Whether the sire is of beef or dairy type, the pelvic anatomy and body condition
of the cow are major factors affecting obstetric risk. In suckler beef herds, it is rec-
ommended that the cows should not be overfat (body condition score 3 or less, see
Chapter 12) at the time of mating with large bulls. Overfat dairy cows are rare birds!
Pelvic dimensions are important, especially individual and breed differences in the
length of the pubic bone. This accounts for the acceptably low incidence of obstetric
problems in small Jersey cows mated, for example, with large Limousin bulls. The
big message here is that cows within any dairy herd are likely to vary considerably
in their susceptibility to obstetric problems, and this variability can be transmitted
(admittedly with a low heritability) to their daughters. When selecting bulls for
individual cows it is therefore vital to take the calving history of the cow and her
mother into account.
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12
Fertility
The traditional aim for dairy farming has been for each cow to deliver one calf per
year. Since gestation length is approximately nine months, she will be expected to
conceive three months (±90 days) after calving. Cows would be dried off after
approximately 300 days when seven months pregnant, to give them two months
rest prior to next calving. Milk yield at this time may have been 10 L/day or less, so
that drying off caused little stress to the cow and had little impact on milk sales. In
traditional pastoral systems this annual cycle was arranged so that calving and the
onset of lactation coincided with the flush of spring grass, thereby maximising milk
production from grazed pasture. In areas like Ireland and New Zealand, this is
largely still the case. In the UK many herds adopted an autumn‐calving policy to
take advantage of higher payments for winter milk. This policy was also consistent
with maximising milk production from pasture and home‐grown crops, since corn
silage and the best grass silage can have a higher nutritive value than late summer
and autumn pastures. However, the seasonal variation in the farm gate milk price is
itself an uncertain factor. In UK it currently stands at four pence per litre (14%).
The development of large intensive dairy units, in which very high yielding cows
are confined throughout lactation and all the food is brought to them, removes the
need to link calving patterns to the seasons. Moreover, a high genetic merit cow fed a
high energy ration and in good condition may still be producing 20–30 L milk/day
when 300 days into lactation. In this case she is still earning her keep. However, if she
conceived at 90 days post‐calving she will need to be dried off to give her a sufficiently
long period to prepare for her next calf and ensure that she can sustain performance
in the next lactation. Since, in these circumstances, there is no need to link calving
time to the seasons, a 400‐day calving interval may be as good as, or better than, a rigid
policy to adhere as closely as possible to a conventional 365‐day strategy. In Chapter 3
I briefly considered the idea of extending lactations for high yielding cows, perhaps to
18 months. There are many potential attractions to this strategy, not least the fact that
most problems for the dairy cow, e.g. ketosis, mastitis, lameness, occur in early lacta-
tion. If cows could be kept in good condition to achieve the same lifetime production
(£LPI) by way of fewer, longer lactations, this could lead to less stress and better

212 Fertility
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elfare for both cows and cowherds. To date, however, this approach has been
w
disappointing, largely because fertility following artificial insemination (AI) 7–9
months into lactation has been paradoxically lower than at three months.
Calving interval is recognised as a critical measure of the impact of fertility on
herd performance and profit. In traditional herds producing moderate amounts of
milk on pastoral systems, an extended calving interval is a measure of infertility: too
many cows failing to conceive within three months of calving, thereby prolonging
the period when they are relatively or entirely unproductive (i.e. low yields in late
lactation followed by an extended dry period). In a high‐yielding, fully housed herd,
an average calving interval of over 420 days could describe a herd with an average
yield of 24 L/day over a 365‐day lactation followed by a dry period of only 60 days.
It should be clear from this that optimal economic performance, quantified by the
PLI, is based on maximising the ratio of the productive period (high yields in early
and mid‐lactation) to the unproductive period (late, low yield lactation and dry
period), and the optimal calving interval will differ in different circumstances.
F
ertility Management
Whatever the overall strategy, it is necessary to ensure, so far as possible, that all
phases of the reproductive cycle progress normally and without interruption.
●● After calving, the uterus must be free from infection and regress rapidly to the
non‐pregnant state.
●● The ovaries must recommence the oestrus cycle of follicular development, ovula-
tion and formation of a corpus luteum.
●● The cow must display sexual behaviour that is recognised and acted upon (rarely)
by a fertile bull, or (commonly) by the cowherd who then arranges for the cow to
be inseminated.
●● The single artificial insemination must lead to a successful fertilisation.
●● The fertilised ovum must implant in the endometrium of the uterus and avoid the
range of hazards that can lead to early foetal death or abortion in late pregnancy.
●● Mother and calf must emerge unharmed from the ordeal of parturition.
All this is a lot to ask.
Behaviour at Oestrus
The behaviour of cows in oestrus is bisexual and indiscriminate. When a small
group of feral cows runs with one or more bulls at a ratio of about 10 cows per bull,
the bull identifies the cow about two days before the onset of oestrus or standing
heat and attempts to isolate her from other females. Bull and cow may favour each
other’s company for 2–3 days. However, the period of oestrus when the cow will
stand to be mated is only about 16 hours (range 8–24 h). The number of copula-
tions, as distinct from unsuccessful mounts may be two to four.
When cows are at pasture in the absence of a bull, or when the ratio of cows to
bulls is large (>40:1), the cow that proceeds through pro‐oestrus into oestrus
Fertility Managemen 213
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isplays a number of characteristic signs of increasing sexual arousal and further-

d
more becomes increasingly sexually attractive to other cows in the herd. She is said
to be on heat or ‘bulling’. During pro‐oestrus she becomes progressively restless.
She may approach other cows in oestrus, sniff and lick around the area of the vulva
and attempt to mount them. More significantly, she becomes increasingly sexually
attractive to other cows and increasingly tolerant of their attentions. In pro‐oestrus
she will tolerate licking and sniffing but move away if another cow attempts to
mount. In oestrus she will stand to be mounted from the rear (Figure 12.1), hence
the expression ‘standing heat’. This is the most reliable single behavioural indica-
tion of a cow in oestrus.
Cows are more likely to make sexual advances – sniffing, licking and mount-
ing – when in oestrus or pro‐oestrus but may perform these actions at any stage of
the oestrus cycle or when pregnant. It follows that the cow making the approach is
probably not in oestrus. There is one exception to this. Occasionally one cow will
mount another cow head to head (Figure 12.1). In this case, the cow doing the
mounting is probably, but not certainly, in oestrus. The one responding to this head‐
first advance is definitely not. Other indications of oestrus include restlessness,
signs of rubbing round the tailhead, a temporary loss of appetite and drop in milk
yield. Whether at pasture or confined, she is likely to spend a lot of time calling for
a bull. This bulling call is quite distinctive and certainly differs from the bawling of
a cow in pain.
Table 12.1 presents some very approximate figures to describe oestrus behaviour
in cows. The intensity and duration of oestrus behaviour at summer pasture are
both considerably greater than in housed cows during the winter. This is due, in
part, to a lower secretion of oestrogen during the dark winter months but is also a
consequence of the separation imposed by cubicles and the reluctance of cows to
mount one another on slippery floors. For this reason, oestrus detection during the
winter is easier when cows are housed in strawed cattle courts.
The number of times a cow allows herself to be mounted, or mounts another
while on heat, is very large, 40–120 episodes. In summer it is most unlikely that a
herder would fail to notice a cow ‘bulling’ while bringing her in from pasture to the
milking parlour. However, in winter, when the cows are housed, the number of
episodes is less and may occur outside of normal working hours when the cows are
otherwise undisturbed Here, the chances of making a confident diagnosis of oes-
trus during a 15 min period of observation is probably less than 50%. The recom-
mended strategy is to observe the cows for at least 20 min over three periods at, say
0600, 1400 and 2200 hours. This should achieve a detection rate of over 80%. The
final night time round (2200 hours) is particularly effective for housed cows.
Aids to Oestrus Detection

The two first essentials for accurate heat detection are to know which cows to look
out for and to recognise oestrus in these individuals when you see them. The follow-
ing information should be available and constantly updated on a wall calendar and/
or computer record.
(a)
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(b)
No
(c)
No
(d)
Figure 12.1 Signs possibly associated with oestrus behaviour in cows. Only the cows
marked in black are in oestrus. (a) Cow in oestrus stands to be mounted. (b) Cow not in
oestrus rejects attempts at mounting. (c) Cow in oestrus mounts head-to-head. (d)
Mutual grooming: one of the two cows may be in pro-oestrus.
Table 12.1 Oestrus behaviour of cows in groups, housed over winter and at pasture
in summer.
Winter, housed Summer, at pasture
Duration of pro‐oestrus and oestrus (h) 12–24 24–36

Duration of oestrus (standing heat, h) 8–16 16–28
Number of mounts 40–80 80–120
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●● Cows due to come into oestrus for the first time: i.e. cows that have calved more
than 15 days previously but not yet displayed oestrus.
●● Cows due for service: i.e. calved more than 45 days ago but not yet served.
●● Cows that showed oestrus 18–23 days ago and were or were not served.
●● Cows that have already been served more than once, or served but diagnosed as
non‐pregnant.
With this information to hand it should be possible within a traditional, relatively
small dairy herd (<150 cows) for experienced cowherds to recognise oestrus from
the behavioural signs described above reinforced by clearly visible signs such as
reddening, the presence of mucus and possibility of blood streaks at the vulva. A
problem with this observation is that these signs tend to appear quite late in oestrus
so that by the time they are noticed it may be too late to book an insemination.
As herd sizes increase, it becomes more and more unrealistic to rely on these tra-
ditional skills. Within a herd of more than 1000 cows, housed throughout lactation
and probably milked by contracted staff with little or no knowledge of the individ-
ual animals, traditional methods for oestrus detection may not be a realistic option.
Table 12.2. lists current aids to oestrus detection within three groups. The first and
most widely used approach uses markers applied to the tailhead of the cow to indi-
cate when she has been mounted by other cows. Application of paint (or chalk) to
the tail head of cows within the group that records indicate should be coming on
heat can be very effective. Simple application of paint has the limitation that it can
be disturbed by chin rubbing, rather than actual mounting. Proprietary heat detec-
tors stuck onto the tailhead, that break and release paint when the cow is mounted,
are also very effective, although they can sometimes be knocked off, perhaps during
mounting, perhaps not.
The most reliable of the physiological indicators is milk progesterone. As
described in Chapter 3, progesterone secreted by the corpus luteum stops at the end
of dioestrus. Small quantities of progesterone in blood pass into the milk and can be
used as an indicator of the state of the oestrus cycle and of subsequent pregnancy.
Table 12.2 Comparison of aids to oestrus detection in lactating cows.
Method Reliability Limitations
Visual
Tail paint/chalk *** False positives from chin rubbing
Paint‐based heat detectors *** Can be knocked off
Physiological
Milk progesterone **** Only practical in fully automated parlours
Vaginal mucus *** Skilled procedure, inflammation risk
Body temperature ** Requires continuous monitoring, expensive
Activity ** Requires continuous monitoring, expensive
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Milk progesterone levels in non‐pregnant cows fall sharply 19 days after previous
oestrus and remain low for about 4 days through pro‐oestrus. Analysis of milk pro-
gesterone levels on days 7, 19 and 21 after previous oestrus can be a very effective
predictor of oestrus, provided, of course, that the previous oestrus has been cor-
rectly spotted. This does not identify the first oestrus after calving (there being no
corpus luteum to degenerate) but this is no problem because it would be most unu-
sual to attempt to fertilise cows at this time. Milk progesterone testing can be done
by trained staff but the process is probably too time‐consuming for modern large
dairy enterprises. The most promising application of this approach will be through
incorporation of on‐line milk progesterone testing within a high‐tech, automated
milking and milk recording unit. Taking swabs of vaginal mucus can be a more reli-
able predictor of oestrus than simple observation of the vulva. However, it is a
skilled procedure and carries the risk of causing inflammation through damage to
the vagina.
Gadgets marketed as aids to oestrus detection include body temperature moni-
tors, installed as a bolus into the reticulum, and activity monitors (pedometers).
The reliability of these, which is no better than quite good, depends on continuous
monitoring of changes in temperature or activity associated with the onset of pro‐
oestrus. The package, including sensors and recording equipment, is rather high. In
a very large herd, with good records but very limited scope for regular observation
of individual cows, the best strategy for oestrus detection is likely to involve a range
of techniques: comprehensive records, tailhead heat detectors, possibly activity
recorders reinforced by careful inspection of the primary suspects by skilled
operators.
Synchronisation of Oestrus
One way to get around the problem of failure to recognise oestrus is to control the
time at which it occurs. The strategy of oestrus synchronisation can be particularly
useful for the breeding of dairy heifers by artificial insemination, which may be
desirable for farmers who wish to accelerate genetic progress by mating maiden
heifers with superior dairy sires or, of course, if the farmer does not have a bull.
Oestrus synchronisation is also becoming the method of choice for rebreeding cows
in very large herds where, for reasons outlined above, conventional strategies have
failed to achieve adequate detection of ‘normally occurring’ oestrus or the staff have
simply given up trying.
Several methods for synchronisation of oestrus have developed over the years.
The exact details need not concern us here but all are based on controlling the
time of regression of the corpus luteum and the onset of pro‐oestrus. For many
years in UK the most popular method was to prolong dioestrus and inhibit the
development of a new follicle by inserting a progesterone‐releasing intravaginal
device (PRID). This is withdrawn after 12 days, the inhibitory effect of proges-
terone on the release of follicle‐stimulating hormone is removed and the cow
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should come into oestrus within 2–3 days. The mix of oestrogen and progester-
one in a PRID is also usually effective in stimulating follicular development and
ovulation in cows previously in anoestrus with inactive ovaries.
The alternative to the use of PRIDs is to break down the corpus luteum and
thereby end dioestrus through injection of Prostaglandin (PGF2α.). A single
injection of PGF2α is only effective during the last 10–12 days of dioestrus when
the corpus luteum is actively secreting progesterone. For this approach to work,
you need some idea of the time of previous oestrus, which rather limits its appli-
cation. Today, this method of synchronisation usually involves an injection of
gonadotropin releasing hormone (GnRH) followed, after 7 days, by prostaglan-
din, then 2 days later, a second injection of GnRH. This is claimed to stimulate
oestrus and ovulation 2–3 days after the second injection, so remove any need to
look out for signs of oestrus. Most reports indicate that the success rate for
inseminations using this method of synchronisation unsupported by visual
inspection for signs of oestrus is rather lower than that based on traditional
methods for oestrus detection.
Time of Insemination
Cows normally ovulate about 12 hours after the end of standing heat. The optimal
time for insemination is 12–18 hours before ovulation, i.e. during the last 6 h of
oestrus. Thereafter the probability of fertilisation declines sharply (Figure 12.2).
Assume a cow is seen bulling for the first time prior to morning milking at 0600 and
this happens to be the first time that she has stood to be mounted. The observer
then rings the AI service who respond at once and inseminates the cow at 1000.
Assume further that she has a long oestrus period of 24 h. In this extreme case she
has been inseminated about 32 h before the time of ovulation. Fertility may be sub‐
optimal, about 60% but no worse than if insemination were delayed until the fol-
lowing day (Figure 12.2). If she had a short heat of 8 h, insemination on the
following day would carry a low probability of fertility (<40%). It follows that cows
seen bulling in the morning should be inseminated on the same day, especially in
the winter months when the duration of standing heat tends to be short.
Insemination on the following day is generally satisfactory for cows seen bulling in
the afternoon or at the time of the evening inspection. Farmers who practise ‘do‐it‐
yourself’ AI can, of course, manage the time of insemination with greater precision
and may, with good technique, achieve conception rates greater than 60%.
Pregnancy Diagnosis
The veterinary student spends many hours with his or her hand in a cow’s rectum
learning to recognise the structure of the ovaries and uterus by palpation and to
diagnose the existence and state of pregnancy. This is an art best learnt by experi-
ence and is outside the scope of this book. Briefly, pregnancy diagnosis may be
based on one or more of the following:
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0.8
long oestrus
0.6
ovulation
0.4
oestrus
0.2
Probability of fertilisation
12 24 36 48
0.8
short oestrus
0.6
ovulation
0.4
oestrus
0.2
12 24 36 48
Hours from onset of oestrus to insemination
Figure 12.2 Effect of time on insemination on fertility in cows with a long and short
period of standing heat.
●● Non‐return to oestrus 21 days after insemination.

●● Palpation of the developing foetus and foetal membranes per rectum at least 35
days after insemination.
●● Ultrasound scanning per rectum at least 42 days after insemination
●● High progesterone concentrations in milk >24 days after insemination.
Non‐return to oestrus, on its own, is an inadequate indicator of pregnancy for sev-
eral reasons. A cow may have been incorrectly diagnosed as bulling, inseminated at
the wrong time of the cycle or while in anoestrus. In either case she would not be
seen on heat 21 days later. The milk progesterone assay at 24 days is a good way of
identifying a cow that is not pregnant but false positives can occur if fertilisation has
not occurred but the life of the corpus luteum is unusually prolonged, if there is an
early death of the embryo prior to implantation or if there is a failure of
implantation.
Diagnosis of pregnancy by rectal palpation is impractical until the 35th day of preg-
nancy. Thereafter it gets progressively easier as pregnancy progresses. One reason why
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it should not be attempted earlier is that it is possible to abort a cow when performing
a rectal examination during the critical stage of implantation. The diagnosis of preg-
nancy in cattle by manual palpation has now been largely replaced by the use of ultra-
sound, which is highly accurate but still requires the protocol of a rectal examination.
Pregnancy diagnosis is a vital tool in fertility management, by identifying cows
that are thought to be pregnant but aren’t through failure to conceive to a first or
second insemination, failure of implantation or early foetal death. I repeat, infertil-
ity, conventionally described by an extended calving interval (e.g. >400 days) or,
more usefully, defined by a high ratio of days dry to days in milk, is a major con-
tributor to inefficiency and thereby loss of profit in dairy herds. The most common
reason for poor fertility and an extended calving interval in dairy herds is human
failure to diagnose oestrus and thereby ensure that AI is carried out at the correct
time. It follows therefore that the poorer the heat detection, the greater the need for
routine pregnancy diagnosis. This should also identify any disorder of the ovaries or
uterus that will require veterinary treatment.
Rebreeding
If all goes well, the cow that is inseminated will conceive, carry her calf to term and
deliver it without complications or subsequent infection. The next question becomes,
‘how soon should she be rebred?’ A healthy cow will normally recommence follicular
development and ovulate for the first time 15–25 days after calving. In about 50% of
cows this first ovulation is accompanied by a silent heat, i.e. she displays no sexual activ-
ity nor sexual attraction to another cows or bull in the days prior to ovulation. The sec-
ond ovulation at 36–46 days is normally accompanied by a standing heat. The first
standing heat should be recorded but there is little to be gained from attempting insemi-
nation at this time since conception rates are less than 50%, probably because, in many
cows, the uterus has not been restored to a degree when it will permit implantation. It
is recommended that cows should be inseminated at the first oestrus that occurs more
than 50 days after calving. If conception rate (to all inseminations) is 60% then:
Cows served Cows conceiving Mean calving to conception interval
First service 100 60 60

Second service 40 24 81
Third service 16 10 102
and so on, giving an average calving interval of 354 days.
Infertility
It is an inescapable fact that the intensification of dairy production over the last 40
years – more and more milk per cow, larger and larger herds – has been associated
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with a decline in fertility. While poor oestrus detection remains a major cause of
failure to rebreed, I am inclined to conclude that, given all the modern aids to oestrus
detection and synchronisation available to very large, well‐financed dairy units, their
success rate is no worse than on small, traditional farms of 100 cows or less, tended by
one overworked family. Problems associated with calving, possible leading to infec-
tion, such as retained placenta, also contribute to the problem of infertility but, once
again, there is no reason that these problems should have increased as a direct conse-
quence of intensification. The main reason for the decline in fertility is physiological
in nature but nutritional in origin: the hormonal consequences of the negative energy
balance experienced by high yielding cows in early lactation when nutrient intake
(especially ME) fails to keep pace with energy demand. These are most likely to impair
the re‐establishment of normal ovarian function after parturition.
Ovarian Dysfunction
The three main failures of ovarian function are:
1) Anoestrus. The ovary becomes quiescent. There is no follicular development, no
ovulation and cycling stops.
2) Follicular cysts. One or more follicles fail to rupture and enlarge further into a
cyst that secretes excessive amounts of oestrogen.
3) Luteal cysts. A ruptured follicle or (more probably) a mature, unruptured follicu-
lar cyst, luteinises and persistently secretes progesterone.
A few cows and rather more heifers may exhibit true anoestrus with no follicular
development for more than 60 days after calving. Other cows will commence cycles
within the first 30 days after calving but then stop. The most common cause of this
is negative energy balance.
About 4% of cows develop follicular cysts. Reasons for this are unclear but
blame tends to be directed at the usual suspects: negative energy balance, retained
placenta or possibly ketosis. The condition appears to be heritable. In the UK it is
claimed to be a greater problem in Jerseys than in Holstein/Friesians. In Sweden,
the national incidence has been reduced from 10% to <5% by rejecting bulls for AI
if from a family of cows with a history of cystic ovaries. A cow with cystic ovaries
displays erratic and usually excessive sexual behaviour. In most case she comes on
heat at irregular but abnormally short intervals, maybe 8–12 days apart. This heat
may last 3–4 days. Furthermore, the cow may be almost permanently excited by
the presence of other bulling cows in the herd. This condition is accurately
described as nymphomania. Affected cows are infertile and rapidly take on a very
ragged appearance, not only because of the amount of riding that they give and
take but also because the excessive secretion of oestrogen relaxes the ligaments of
their pelvis and alters the shape of the caudal spine, elevating the tailhead. Cows
with persistent follicular cysts become progressively masculinised due to secre-
tion of androgens and display bull‐like behaviour, rearing, pawing the ground and
generally creating a nuisance. A nymphomaniac cow can, in theory, be used as an
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aid to heat detection but, in practice, she is usually too much bother. A few cows
with follicular cysts may show no sexual behaviour at all.
About 70% of ovarian cysts are follicular. The other 30% are luteal cysts that
secrete progesterone. Most of these start life as unruptured follicular cysts. It is not
easy to distinguish between follicular and luteal cysts by simple rectal palpation but
they can be distinguished by ultrasound scanning or a milk progesterone assay.
Treatment of luteal cysts is likely to involve the same procedures as for synchronisa-
tion of oestrus: follicular cysts are treated by an injection of GnRH followed by
prostaglandin (PGF2α.), luteal cysts are resolved by a single injection of PGF2α.
Uterine Disorders
In normal calving, the calf is ejected from the sterile environment of the uterus, the
epithelium of the placenta separates from the uterine tissue at the cotyledons and the
afterbirth is expelled shortly afterwards. The uterus, (muscle and endometrium) at
this time weighs about 8 kg. There follows a rapid loss of uterine tissue such that its
weight falls to about 2.5 kg by day 7 and 1 kg by day 25. Phagocytes invade the tissues
in massive numbers to clear up the cellular debris, some of which is absorbed directly
into the blood and lymph nodes and some of which passes into the body of the uterus
and is expelled through the vagina. Despite the large amount of cell destruction and
the involvement of cells of the immune system, this is normally a sterile process, i.e.
no infectious organisms are involved. However, the natural processes of involution
can be complicated by infection in the following circumstances:
●● Abortion caused by organisms that attack the placenta such as Brucella abortus or
Campylobacter.
●● Introduction of infection through the vagina when calving without assistance but
in an infected environment.
●● Tissue damage and introduction of infection during an assisted calving.
Any of these can cause complications that impede the normal process of uterine
involution and may lead to retained placenta or endometritis (inflammation of the
uterus).
Retained Placenta
Most cows expel the afterbirth within 6 h of calving. A few may wait up to 24 h then
expel the whole afterbirth normally in a single piece. Any cow that has not shed it
normally within 24 h may retain the placenta for several days until the cotyledon
attachments have putrefied. Most cows tolerate the consequences of this increasingly
stinking mess hanging from the vulva without showing signs of ill‐health. In a few
cases, the cow may develop metritis (uterine infection) and can become very sick.
Retained placenta is caused by a failure of the placental epithelium to separate
from the maternal tissues of the uterus at the cotyledons. There are many possible
reasons why this may occur. In the past, a major cause was infectious abortion
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caused by Brucella abortus but, in the UK, this should be no more. Today the major
(putative but uncertain) risk factors include prolonged, assisted calving, probably
involving some damage to the birth canal, abortion, whether spontaneous or
induced by prostaglandin injections, periparturient hypocalcaemia (milk fever) and
possibly nutritional deficiencies of the antioxidants vitamin E and selenium.
When I first graduated as a veterinary surgeon the recommended action in the case of
a retained placenta was to attempt to remove it manually by teasing out the attachments
at the cotyledons, followed by an antibiotic douche. This process risked causing further
damage to the cow and, in the days of brucellosis, infecting the vet with undulant fever.
Two partners in the practice where I first worked were chronic sufferers. Today there is
good evidence that if the cow is showing no signs of fever, it is probably better to do
nothing and wait (‘masterly inactivity’). There is good evidence that the subsequent
fertility of cows with retained placenta is unlikely to be worse if left alone than follow-
ing manual removal. In either event affected cows are nearly always slow to return to
oestrus and even then, conception rates to first service are less than 50%. About 15% of
cows that have had a retained placenta are likely to be culled for infertility.
Endometritis
In practice, endometritis is nearly always associated with infection acquired at the
time of calving and the organisms involved are usually the pus‐forming inhabitants
of dirty cowsheds, Corynebacterium pyogenes and Fusobacterium necrophorum. The
immune mechanisms of the cow are naturally depressed at the time of parturition
and her ability to combat infection may be further compromised by malnutrition or
a metabolic disorder such as ketosis. In severe cases the cow may be very ill indeed,
with high fever, anorexia, shock and a foul‐smelling brown discharge from the vulva.
These animals require immediate veterinary attention and some die before any treat-
ment has time to work. More commonly, endometritis proceeds to a chronic stage in
which the cow is quite well but continuously discharges a mixture of mucus and pus
from the uterus into the vagina. This condition, ‘the whites’, can, if untreated, persist
for many weeks and seriously delay rebreeding. Treatment involves antibiotics and
prostaglandin injections to contract the uterus and help expel the pus. Once again,
the main consequence of endometritis is a prolonged calving‐to‐conception interval
and, once again, the main cause of endometritis is poor hygiene at calving, in par-
ticular the insertion of an unscrubbed hand into the vagina.
Early Foetal Death

The probability of a successful fertilisation following insemination at the right time is
about 90% yet only about 60% of cows are likely to be pregnant when examined after
40 days. About 8% of fertilised ova will fail to develop because of some genetic defect
in, or incompatibility between, sperm and ovum. However, most cases of early foetal
death occur at the time of implantation (25–30 days after insemination). In some cases,
the tiny embryo may be aborted unnoticed. More often, the foetus and its membranes
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are absorbed into the uterine tissues. This can inhibit the secretion of luteolysin (the
natural prostaglandin) and cause the corps luteum to persist so that the cow may not
return to oestrus for many weeks after the death of the embryo. Such cows will typi-
cally show oestrus 60–80 days after an apparently successful insemination. If the cow
does not return to oestrus the condition can be treated with an injection of prostaglan-
din. However, it is first necessary to distinguish between the presence of a live foetus
and a dead, reabsorbing foetus since prostaglandin administered by mistake to a preg-
nant cow will cause it to abort. Both will give high progesterone levels; distinction by
rectal palpation alone can be tricky but an ultrasound sensor should do the job.
Abortion
Abortion means, in common parlance, the abnormal premature expulsion of a foe-
tus either dead or in no fit state to live. In fact, the distinction between abortion and
early foetal death is arbitrary. Some foetuses that die at 25 days are aborted, others
that die at a much later stage are not aborted (or not at once) but retained in the
uterus where they mummify.
Most cases of abortion in late pregnancy are due to infection. Physical trauma,
such as bad handling during transport, can cause abortion but such cases are rare.
In areas of the world where Brucella abortus is endemic, this is the main cause of
infectious abortion. In the UK the incidence of infectious abortion is only about 2%.
Sporadic cases of abortion in the UK may result from salmonellosis or summer
mastitis caused by C. pyogenes. These days most cases of infectious abortion occur
in herds in which leptospirosis or bovine virus diarrhoea are endemic. The control
of these infections was discussed in Chapter 10.
Nutrition and Infertility

Cows in poor condition are harder to get back in calf. This is obvious to any dairy
farmer with high‐yielding cows ‘milking off their backs’ and even more obvious to
a beef farmer whose cows are grossly short of food. Malnourished cows not only
lose fat but also protein in muscle and skin. As fat reserves run out, increased
dependence on protein as a source of energy increases the rate at which the cow
loses condition since muscle protein contains less than 15% energy than fat. As
body condition falls, the endocrine system switches into survival mode and avoids
ovulation as a dangerous luxury.
Figure 12.3 illustrates a standard protocol for condition scoring cows according to
the amount of subcutaneous fat and muscle in the loin area around the lumbar verte-
brae and in the area between the pelvis and the tailhead. The scoring is as follows:
5. Grossly fat: tailhead buried in fatty tissue, pelvis impalpable even with firm
pressure.
4. Fat: folds and patches of soft fat under the skin. Pelvis palpable with firm pres-
sure but transverse processes of lumbar vertebrae impalpable.
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Figure 12.3 Condition scoring of dairy cows from the appearance of the tailhead.
5 = grossly fat, 4 = fat, 3 = good, 2 = moderate, 1 = poor, 0 = very poor. (For further
information see text.)
3. Good: all bones are palpable but well covered with fatty tissue
2. Moderate: all bones easily palpable, muscle concave around tailhead, some fatty
tissue.
1. Poor: muscles around tailhead and lumbar vertebrae shrunken and concave. No
fatty tissue palpable. However, skin is supple and freely moveable.
0. Very poor: emaciated, skin is thin, tight, with no tissue palpable between muscle
and bone.
It is generally agreed that dairy cows should have an average condition score
between 2.5 to 3.5 at the time of calving. Lower scores mean less milk and lower
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fertility. Cows with condition scores above 3 are prone to the ketosis/fatty liver com-
plex that compromises their ability to attain peak yield and may predispose to
retained placenta and cystic ovaries. It is important for cows not to be too fat at the
time of calving. However, the high‐yielding cow is expected to lose 30–60 kg in body
weight during the first 80 days of lactation, which corresponds to a drop of 1.0 to 1.5
in condition score. In heifers, a drop in weight of 15 kg is consistent with a 1.0 fall in
condition score. When the condition score falls below 2.0 fewer cows come into oes-
trus and the conception rate in those that do is likely to be below 50%.
The diagnosis of a problem of poor fertility, presenting as an unacceptably long
calving‐to‐conception interval, must be based on good records. If it can be estab-
lished that the problem is not one of poor heat detection and there is no evidence of
infectious diseases such as BVD or leptospirosis, then the most probably cause of
delayed conception is improper nutrition. Feeding strategies to ensure that cows are
neither too fat at calving or too thin when due for rebreeding were considered in
Chapter 6 and I shall consider broader aspects of transition management in the
next section. Here, I list the questions that need to be addressed in order to assess
the nutritional state of the herd.
Condition Score at Calving?

Is an average condition score satisfactory (2.5–3.5)? If cows are, on average, fatter
than this, is there other evidence that this is causing problems, e.g. ketosis, poor
appetite, or other possible complications such as retained placenta? If not, then this
is probably not the source of the problem. Are the cows too thin at calving? This can
often happen in autumn‐calving herds in the UK after a dry summer with insuffi-
cient grass. If a high‐yielding cow is too thin at the time of calving, she is likely to
be much too thin by rebreeding time.
Condition Score at the Time for Rebreeding?

A comparison of condition scores of cows due to calve, in early, mid and late lacta-
tion will reveal how accurately nutrient supply is meeting demand at each stage of
lactation. Cows, for example, on a two‐stage flat rate feeding strategy could be too
thin 80 days into lactation and too fat at 300 days.
Milk Yields in Early and Mid-lactation?

Infertility, accompanied by disappointing milk yields in early lactation, is a clear
sign that the cows are not getting enough to eat. Cows that are milking well but los-
ing weight fast are likely to be consuming a ration that more than meets their
requirement for metabolizable protein but is deficient in metabolizable energy.
These cows will be hungry but, for one reason or another, unable to consume
enough to meet energy requirement. This is most likely to occur when a significant
proportion of the daily ration is fed in parlour. In these circumstances, the cows can
be given an extra out‐of‐parlour feed of a highly palatable, relatively low protein
feed such as sugar beet pulp. If this is not possible, it may be necessary to reduce the
protein concentration of the concentrate ration and accept a small drop in milk
yield as the price to pay for restoring fertility.
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How Well Does Nutrient Supply Match Requirements?

This question can be addressed by comparing energy and protein supply with require-
ment as described in Chapter 5 and possibly taking blood samples to establish a meta-
bolic profile of the herd. Most of the necessary information can be gathered from a
mini‐profile based on blood concentrations of glucose, ketones and urea. There are
literally thousands of references in scientific journals to problems of infertility associ-
ated with practically every major and minor nutrient, the most popular being the
minerals phosphorus, copper and selenium. There are undoubtedly specific effects of
these minerals on specific aspects of fertility, e.g. the link between vitamin E and
selenium deficiency and the incidence of retained placenta. However, infertility asso-
ciated with mineral and vitamin deficiencies is most likely to occur in beef cattle on
pasture. Most dairy cows are generously provided with mineral and vitamin supple-
ments in their compound rations. The possibility of such deficiencies should not be
overlooked, especially when dairy cows are getting a high proportion of their ration
from pasture. However, I repeat, common things occur commonly and, in the case of
infertility of nutritional origin, the most obvious solution is more often than not the
correct one.
Transition Management
I trust that I have, by now, firmly hammered home the message that the most criti-
cal time in the life of a dairy cow is the period when she must endure the massive
physiological and metabolic changes that occur during her transition from late
pregnancy, through parturition to the time of peak milk yield. It follows that the
management of cows through this transition period is equally critical to her welfare
and that of the entire enterprise. It has been traditional to allow a dry period of
about 60 days. Inevitably those wishing to maximise profits have explored the
potential of reducing the dry period to about three weeks. I am happy to announce
that this does not appear to achieve much: marginal increases in total lactation
yields for some cows may be offset by an increased incidence of mastitis through
failures in dry cow therapy.
In Part II, Feeding the Dairy Cow, I considered how best to reconcile the need to
promote at least a threefold increase in ME intake in the first weeks of lactation to
support the energy demands of lactation with the equally vital need to ensure
healthy digestion; in particular, the need to maintain a stable rumen environment
during this period of radical change to the diet. The appetite of non‐lactating, heav-
ily pregnant cows is likely to be low, given their relatively low energy demand and
the amount of space‐in the abdomen occupied by the calf. They are best served by a
palatable, forage‐based diet with a relatively low ME concentration to maintain
rumen volume and the population of the rumen biome.
Ensuring that cows eat properly during the transition period is not just a matter
of providing the right food. This is a time when the routine of their lives as lactating
cows in the milking herd has been disturbed. They have been moved to a new area,
in a new group, most probably an unstable group with individual cows coming in
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and going out to calve on a regular basis. This inevitably increases the risk that
some cows will get bullied at the feed face and fail to compete for the available food.
Cows in late pregnancy are most in need of a comfortable bed. Loose housing in
deep clean straw is ideal in terms of comfort but, in unstable groups, may increase
the risk of bullying at the feed face. At very large intensive units it is good practice
to manage the population of dry cows in two stable groups, ‘prefresh’ and ‘close‐up’,
the latter commencing about three weeks before calving. It is also considered good
practice to delay the movement of cows into individual calving pens as long as pos-
sible so that they retain the security of the stable group until the time when they
would prefer to be alone. The exact tactics for the management of cows at these
critical periods of their lives will not be the same for the large commercial unit and
the small family farm. However, the principles should be the same: extra‐special
attention to tender, informed, loving care.
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Part V
Cows, People and the Environment

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13
Cows, People and the Living Environment
I begin this final chapter by restating the central aim of the book, which is to develop
our understanding of the dairy cow. This understanding takes two forms:
1) Scientific understanding of a complex and elegant instrument producing highly
nutritious and highly desirable food for us from a wide range of plant matter,
much of which we cannot eat ourselves,
2) Compassionate understanding of a sentient creature to whom we have a duty of
care to promote a good quality of life and a gentle death.
In keeping with this aim, the substance of the book is directed towards how best
simultaneously to promote these two objectives: efficient production of milk and
good welfare, through a proper understanding of the physiology, metabolism, psy-
chology and behavioural needs of the cow. It has been written primarily for those
who are, or will be, directly working with cows and wish to do the best they can.
What I have not yet considered in any detail are the broader societal and environ-
mental issues relating to the farming of dairy cows, whether on the traditional
dairy farm or the modern, highly intensive factory unit. To paraphrase John Donne
(only slightly, in italics) ‘no dairy farm is an island, entire of itself; every farm is a
part of the Continent, a part of the main; if a clod is washed away by the sea, the
planet is the less’. The bell tolls for us all: most obviously for the majority; omni-
vores and lactovegetarians sustained and satisfied by the consumption of milk,
cheese, yoghurt and ice cream but also for the growing community of vegans who
reject all products of animal origin on grounds of personal health, animal welfare
and/or the unsustainable element of waste involved in growing large quantities of
food for animals that we could perfectly well eat ourselves. I accept all these argu-
ments as perfectly valid within their own terms of reference. However, the prob-
lem with these, as with most arguments, is that they are based on limited premises.
They do not, for example, consider how we can best feed ourselves, sustain the
quality of the living environment and the quality of life of those who live on that
half of the land that is unsuited, or less well suited to arable farming, nor how we
can sustain the quality of the soil on arable land without input from farm animals,

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whether directly in the form of manure or through the rotation of crops between
cereals and pasture.
Nevertheless, modern dairy farming, along with all the ways we choose to pro-
duce and consume food from animals, has a lot to answer for. I open the debate by
stating the case for the prosecution.
●● Most of those who can, consume too much meat and milk.
●● Food that we could eat is fed to animals while the poor go hungry.
●● Intensive livestock production is incompatible with animal welfare.
●● Livestock’s long shadow is destroying the planet.
I shall do my best to address each of these concerns without prejudice but I’m
aware that my arguments, like all the others, will fail to tell the whole story.
Nevertheless, my aim here, as throughout, is to set out an evidence-based frame-
work to aid and inform the debate and lead us to a better understanding.
Most of Those who can Consume Too Much Meat and Milk
This accusation is impossible to deny. The big problem with meat and dairy prod-
ucts is that they are both are tasty and highly nutritious. In consequence, most of
those who can afford to eat these things each too much – for our health, for the
health and welfare of the food animals, and for the sustained health of the planet.
Expansion, intensification and competition within systems of animal production
have magnified this problem by making food cheaper and cheaper relative to
average incomes. Chicken, once considered a luxury for feast days, is now as
cheap as cat food. Milk, on supermarket shelves, can cost less per litre than spe-
cialist brands of fizzy water. As more and more people acquire the means to
indulge themselves on foods of animal origin, the demand for land to grow crops
for animals and for fossil fuels to fertilise and harvest these crops has become
unsustainable. It has been calculated that if the Chinese were to eat as much meat
per capita as those in the USA this would require approximately 130% of our cur-
rent global harvest of grain. Our global need to consume less meat and milk is not
just a matter of ethics, it is a matter of survival. Progress towards this end will
involve an untidy combination of good science, good husbandry, political will and
painful economic reality. The complexities and difficulties of the global task will
be enormous. However, each of us can help by adopting the simple strategy: ‘eat
food, not too much, mostly plants’.
The conventional response of agribusiness to the problem of excessive consump-
tion has been to advocate the principle of ‘sustainable intensification’. In the case of
food from animals this is too often interpreted as more food from pigs and poultry
because they convert their feed (grains and beans) into meat and eggs much more
efficiently than cattle and sheep convert their feed into meat and milk. Moreover, all
this can be done in big buildings, out of sight and out of mind; thereby, in theory,
making more land available as countryside for us to enjoy, habitat for wild species
Intensive Livestock Production is Incompatible with Animal Welfar 233
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(animals and plants), and forests and lakes for the sequestration of carbon and
management of water resources. I demonstrated one of the limitations of this argu-
ment in Chapter 1, namely the extent to which ruminants, especially the dairy cow,
can subsist on land unsuitable for arable cropping and provide food for human con-
sumption from plant material (e.g. pasture, forages and by-products) that we can-
not, or choose not to eat ourselves. Table 1.4 illustrates that a moderately high
yielding dairy cow can produce over 40% more energy and protein in milk than she
consumes in the form of food directly available for human consumption. I shall
consider the ecological impact of dairy farming (e.g. pollution, greenhouse gases,
etc.) in more detail later. At this stage, I merely state the obvious: we can only afford
to care for the land if we can derive value from the land. To date, the value of farm
land has too often been linked almost entirely by its capacity to provide food for
human and animal consumption; too little economic value has been given to the
other essentials of a sustainable living environment, soil, water, wildlife, both plant
and animal and, not least, the sustained social cohesion and welfare of those who
derive their living from the land.
ood We Could Eat is Fed to Animals While the Poor

F
Grow Hungry
This is impossible to deny. Vast quantities of land have been cleared and ploughed
for the cultivation of cereals and protein-rich pulses (e.g. soya) to feed to farm ani-
mals: pigs, poultry and ruminants. The obvious reason for this is that, for millions
of people, disposable income has increased while the relative cost of meat, milk and
eggs has declined. This may be good news for the haves, and for now, but the accel-
erating rate of inequality between the haves and have-nots is exacerbating the
impact of poverty on the latter. Moreover, I repeat, this trend simply cannot be sus-
tained. Most public concern is currently directed at the health risks associated with
eating too much food of animal origin (FoAO) and the impact of intensive agricul-
ture on climate change. However, the most inconvenient truth is that it is simply
not possible to raise the FoAO diet of the poor to match the current diet of the rich.
There is simply not enough suitable land, water and energy to go around.
I ntensive Livestock Production is Incompatible

with Animal Welfare
The growth of public concern for the welfare of farm animals can trace its origin to
the 1964 publication of Ruth Harrison’s book ‘Animal Machines’. This was a pas-
sionate, but well researched attack on the factory farming of broiler chickens, bat-
tery hens and veal calves reared in such intense confinement that they were unable,
without difficulty, to ‘stand up, lie down, turn around, groom themselves and
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stretch their limbs’. Subsequently the Brambell Committee recommended that all
farm animals should be given sufficient space to do these things. This recommenda-
tion became known as the five freedoms. When I was first appointed to the UK
Farm Animal Welfare Council I argued that while these things were important,
there was so much more to animal welfare then just space allowance. This led to the
broader concept of the five freedoms as defined in Chapter 1. Nevertheless, there is
still great public concern that intensification of animal production (‘factory farm-
ing’) per se is bad for welfare. In the context of this book, the most challenging
accusation is that at a time when public concern has freed hens from the battery
cage and given them free range, lack of public concern has enabled the dairy indus-
try to take cows out of the fields and confine them on concrete. This is an oversim-
plified image but it is a powerful one that needs to be addressed.
Table 13.1 uses the protocols of the five freedoms to compare the welfare of differ-
ent production systems for ruminants: two intensive systems, dairy production and
the feedlot finishing of beef cattle, two extensive systems, beef cattle and sheep at
pasture. For both dairy cattle and beef calves on feedlot, the biggest threat to welfare
arises from digestive disorders arising from the diets fed to promote maximum rates
of production. While digestive disorders, especially rumen acidosis, are a major
threat to the welfare of dairy cows (and feedlot calves) it is only fair to say that
improvements in understanding of ruminant nutrition and the application of this
new knowledge to the formulation of total mixed rations has done much to reduce
the risks attached to the selection and management of high genetic merit cows to
produce prodigious quantities of milk.
The risk of physical discomfort, pain and injury in dairy cows attributable to poor
housing and inadequate control of lameness is high. However, there is no convinc-
ing evidence to suggest that these problems are worse in large, intensive units where
cows are confined throughout lactation than in small family farms, where cows are
at pasture during the summer. Indeed, the physical environment within large, new,
Table 13.1 Welfare implications of different rearing systems for cattle and sheep
(from Webster (2018). The number of + signs indicates the potential magnitude
of the welfare problem.
Dairy cows Beef on feedlot Beef at pasture Sheep
Nutritional problems +++ +++ +/– +

Physical discomfort ++ + +/– +/–
Pain and injury ++ + n.s. ++
Infectious disease + ++ n.s. +
Fear and stress n.s. + n.s. +
Behavioural restriction + ++ n.s. n.s.
Exhaustion ++ n.s. n.s. n.s.
Livestock’s Long Shadow is Destroying the Plane 235
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highly expensive units can provide more comfortable beds and less injurious walk-
ways than on many an old, undercapitalised dairy farm in urgent need of mainte-
nance and repair.
I have already stressed more than once that the biggest welfare problem for the
high yielding dairy cow is one not properly addressed by the five freedoms, namely
the problem of metabolic (and probably emotional) exhaustion due to the pro-
longed demands of lactation. At the time of writing the second edition (1993) this
problem was undoubtedly getting worse. However, things have started to improve,
partly through improved nutrition, but most notably through improved recognition
of the need to reduce the risk of burn-out by selecting cows and sires on the basis of
lifetime performance (Chapter 11).
Table 13.1 provides an instructive comparison of animal welfare in intensive
dairy units to that of beef cattle and sheep at free range on pasture. Suckler beef
cows with their calves at foot on the green and pleasant pastures of south west
England, where I live, have, in my opinion, a life that is about as good as it gets for
any domestic animal; in the company of their own kind and with almost total
behavioural freedom; freedoms seldom enjoyed by domesticated dogs and horses.
Strictly on grounds of animal welfare, I attach less guilt to eating free-range beef
than cheese. Extensive sheep flocks also experience behavioural freedom but they
are under greater threat from predators, foul weather, undernutrition and neglect.
The preceding paragraphs should not be taken as an attack on farmers. Most
farmers and herders have a great affection for their animals and care for them to the
best of their ability. My message is that different systems present different risks and
require different strategies. Large, intensive systems are likely to restrict behav-
ioural freedom and reduce our ability to identify individual needs and remedy indi-
vidual problems. However, individual dairy cows, unlike, for example, broiler
chickens, carry a high value. It is therefore essential, and not just on grounds of
humanity, that they receive individual care, whatever the size of the enterprise. In
large, modern units this individual attention may depend on high-tech methods
such as robot milking combined with in-parlour automated monitoring of such
things as oestrus and incipient illness (e.g. ketosis and mastitis) but, if these high-
tech solutions work for the cows, then that’s fine by me. The biggest threat from
large, intensive dairy units is environmental; the problem of pollution.
Livestock’s Long Shadow is Destroying the Planet
The Food and Agriculture Organisation Report ‘Livestock’s Long Shadow’ (LLS)
carries the message that food production from animals carries a far higher environ-
mental cost than arable farming for crops. Cattle and sheep come under special
attack on account of the amount of methane they produce as a result of rumen
fermentation, methane having approximately 20 times the global warming poten-
tial of CO2. Once again, this criticism is valid within its own terms of reference but
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it does not tell the whole story. The LLS approach calculates the environmental cost
of production systems in terms of the land required to produce a standard amount
of different foods for humans of plant and animal origin. This is measured in global
hectares but does not adequately account for the differing capacity of different
classes of land to produce crops, e.g. grasses versus cereals. Furthermore, it does not
properly account for such things as differences in the availability and therefore the
value of site-specific resources, most especially, water. Problems of water supply
and disposal are very different for dairy units in Israel and the west of Scotland.
An alternative and, to my mind, more elegant and useful approach to the analysis of
the environmental cost of different systems of food production is that known as
‘emergy analysis’, where emergy (Em) is a measure of the amount of the original, effec-
tively inexhaustible source of solar energy embedded at each stage of the process. This
approach, illustrated by Figure 13.1, has the merit that it identifies and distinguishes
the renewable (R) resources of sun, soil and water embedded in farmland from non-
renewable sources (NR) such as fuel, fertiliser, labour and imported feeds.
According to the LLS approach, the environmental cost (based simply on land
use) of feeding people on beef is 10 times the cost of cereals and 40 times the cost of
soya. The emergy approach yields a diametrically opposite conclusion (Table 13.2).
By this analysis and in this example, corn and soya are the least sustainable because
of their dependence on non-renewable resources of (e.g.) fertiliser and fuel; beef
from cattle grazing the pampas of Argentina are the most sustainable, both in terms
of food emergy yield relative to the consumption of non-renewable resources (F/NR)
and in terms of overall sustainability, defined by the Emergy Sustainable Index,
which measures the relative contribution of renewable emergy and non-renewable
emergy to emergy yield as food. This is a fiercely complex approach to environmen-
tal analysis that uses solar energy as the basic unit of measurement but quantita-
tively incorporates other material inputs such as water, soil and labour. The emergy
SUN
R LAND
Livestock FOOD, F
Land degradation NR
Waste
Imported emergy NR
Figure 13.1 The ‘Emergy’ approach to the evaluation of renewable (R) and non-renewable
(NR) sources of energy and matter to the production of food for human consumption.
Methane Production and Climate Chang 237
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Table 13.2 Contrasting measures of sustainability for crops and livestock production
(from Webster 2018).
Ecological footprint1 Emergy yield ratio2 Emergy sustainable index3
Corn 31.0 1.07 0.06

Soya 8.0 1.74 0.50
Grazing cattle 353 3.73 6.80
1
Global hectares required to feed 100 people (Pereira and Ortega 2013).
2
Emergy yield ration (EYR) = Em,food/Em non-renewable resources (F/NR).
3
Emergy sustainable index = EYR/(NR +F)/R (Rotolo et al. 2007).
model also takes into account the loss of resource arising from land degradation
(Figure 13.1). I concede that the examples illustrated in Table 13.2 have been cho-
sen by me to make a point. Other examples could have told different stories. My
point, however, is a critical one. The key to sustainable farming is to manage the
land in the way that best preserves the value of the location and land as defined by
its own special resources of sun, soil and water. This, indeed, is the essence of hus-
bandry. Nobody, I hope, would consider ploughing up the Argentine pampas;
nobody, at least, who is aware of the disastrous consequences of ploughing up the
North American prairies that led to the dustbowl of the ‘dirty thirties’.
The implications of this argument are broadly the same as those arising from
‘livestock’s long shadow’, although more convincing, both quantitatively and in
detail, because they are based on a more comprehensive ecological model. We can
only sustain the production of food for human consumption from ruminant ani-
mals if we restrict, so far as possible, feed for ruminants from land that is best suited
to grazing and from the by-products of foods grown on arable land primarily for
direct human consumption. This is, of course, entirely consistent with the argu-
ment that we must reduce our consumption of milk and meat.
Methane Production and Climate Change
Current methane production from ruminants is estimated to contribute approxi-

mately 10% to the planetary production of greenhouse gases. Various approaches to
the reduction of methane emissions from rumen fermentation have been consid-
ered in earlier chapters. These will have limited impact in pastoral systems, maxi-
mum impact in intensive units where cows are housed throughout lactation and fed
carefully formulated total mixed rations with additives designed to modify rumen
fermentation so as to reduce methane production. Moreover, the higher the milk
yield of the individual cow, the greater the overall efficiency of utilisation of feed
energy (Figure 2.6), and thereby the greater the yield of milk relative to methane.
Intensification of dairy production, producing higher yields from housed cows is,
by this measure, an effective approach to sustainable intensification.
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While it is undeniable that a large reduction in the net production of greenhouse

gases (GHG) from ruminants would make a significant contribution to our need to
reduce the impact of climate change, the current assault on ruminants is a classic
example of the fallacy of arguing from limited premises. Grazing ruminants have
been around for a long time. The current cattle population of the USA is (very
approximately) 100 million animals, of which about 40 million are adult cows. It has
been estimated that in the 17th century, before the arrival of Europeans bent on
slaughter, the bison population of North America was approximately 60 million.
After adjusting for the fact that grazing animals produce more methane per unit of
digestible energy than cattle fed on high concentrate rations, one can make a rough
estimate that methane production from ruminants in North America is only about
20–25% higher than it was 300 years ago. If, as seems inevitable, we are compelled to
reduce world production and consumption of meat and milk by 20–25%, then levels
of methane production from ruminants should return to pre-industrial levels.
The other major fallacy of the methane argument is that it only measures one side
of the equation. Well-managed grasslands constitute a significant carbon sink, the
extent of carbon sequestration depending on factors such as the intensity of grazing
and the balance between grasses and legumes. The true impact of ruminants on
climate change through the net production of greenhouse gases can only be deter-
mined by life-cycle analysis of the production and sequestration of greenhouse
gases (CO2 and CH4) in different systems. While it is the case that estimates based
on life-cycle analysis show that all current dairy systems make a positive net contri-
bution to greenhouse gas production, it is far less than estimates based on CH4
emissions alone and least of all when the contribution of pasture to the overall diet
is greatest. Extensive systems of beef production from pasture are likely to be GHG
neutral (as would have been the herds of prairie bison).
Silvo-pastoral systems, where cattle graze and browse within a parkland area of
pasture, shrubs and trees act as net carbon sinks, in other words as CO2 scrubbers. In
Brazil, for example, there are highly successful commercial silvo-pastoral systems
(both beef and dairy), that generate income both from the cattle and the sale of bio-
mass. In other parts of the world, e.g. the cork-oak parklands of Portugal, income is
provided from the sale of beef, corks for high-quality wines and tourists wishing to
enjoy the natural environment and beautiful Mertolenga cattle (Figure 13.2). A par-
ticularly attractive feature of these systems is that the cows can select what to graze
and where to lie to their satisfaction (e.g. in sun or shade). In all but the most severe
weather, they are comfortable and, above all, have freedom of choice.
Pollution from Dairy Units
The biggest constraint on the expansion of individual dairy units (more and more
cows) is the problem of disposal of wastes: slurry and dirty water. The principal
culprits are nitrogen and phosphates present to excess in ground and surface water.
Pollution from Dairy Unit 239
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Figure 13.2 Mertolenga cattle grazing cork-oak parkland in Portugal (thanks to

Martha d’Andrade).
As with methane production, so with pollution; the poison lies in the dose. Pollution
is caused by too much fertiliser in the wrong place. An extensive or organic dairy
farm, or a dairy enterprise incorporated into a mixed arable/livestock farm should
have a neutral or even beneficial effect on soil fertility. A highly intensive dairy unit,
perhaps 75% dependent on bought-in rather than home-grown feeds will inevitably
produce more N and P than the land can carry so become a significant source of
pollution. On grounds of sustainability, environmental quality and general good
sense, the obvious solution is to restrict the number of animals to that which the
land will support, both in terms of the supply of renewable resources (home grown
pasture and crops) and the disposal of animal wastes. Strict interpretation of this
principle is, of course, incompatible with the current economics of intensive dairy
production within a free market. The European authorities have imposed legal lim-
its on nitrate and phosphate concentrations in ground and surface water in the
vicinity of dairy units, with fines for those who break the law. This has had a signifi-
cant impact on intensive dairy production in, especially, Denmark and the
Netherlands. Producers have responded by reducing inputs of N and P in both fer-
tiliser and feeds, better management of slurry and dirty water and, where this has
proved insufficient, radical reductions in cow numbers. Most of these approaches
are outside the scope of this book. Some of the nutritional strategies discussed in
Part II can help to reduce pollution. For example, that most conventional of feeds,
spring grass, especially when liberally fertilised, will contain N in excess of ME, and
much of this will be in the form of QDN, which, in these circumstances, will be lost
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to the cows and increase the load on the environment. This problem can be reduced
now by feeding the supplements necessary to bring ME and MP into balance. In
future, we hope to achieve this balance through the successful breeding of better
balanced, high sugar grasses.
Alternative Husbandry Systems
Organic Dairy Farming

Increased public concern as to the impact of intensive farming systems on the envi-
ronment, human health and animal welfare has given impetus to the long-estab-
lished practice of organic farming. The Soil Association has set out standards for
organic dairy production in the UK and these are largely similar to those adopted by
the EU. The most critical clauses within the context of sustainability are:
●● Cows should be at pasture whenever possible. In UK this should average
>200 days/year.
●● A minimum of 60% of the ration should be based on fresh or conserved pasture.
●● No artificial fertilisers should be used. Total application of N from faeces from
grazing cows, spread slurry and manure should not exceed 170 kgN/ha/year.
These regulations should, in normal circumstances, eliminate the risk of pollu-
tion of ground and surface water from organic dairy farms. The philosophy of the
Soil Association is rooted in the principles of good husbandry, which imply proper
concern for the welfare of farm animals and all life on the land. This aim is alto-
gether admirable. However, independent review suggests that, in practice, overall
cow welfare does not differ significantly between organic and conventional dairy
farms. To me, this does not imply that most organic farmers are not doing well
enough but that most conventional farmers are doing a good job too. One large
study did reveal a significantly lower prevalence of lameness on organic farms,
which may reflect the longer time that cows are at pasture.
Current indicators are that yields from organic dairy farms are likely to be
about 20% lower than from similar, pasture-based conventional farms. Input
costs should be lower too, but not enough to achieve similar gross profit margins
when conventional and organic milk fetch the same price. Organic dairy farms
are likely to be eligible for more financial support from the EU through the Rural
Development, Pillar 2 of the Agricultural Support System. As yet, this does not
amount to much, but all this may change. The financial success of a well-run
organic dairy farm depends on the premium it can attract from buyers in bulk or
at the farm gate. Googling as I write, I come up with premiums ranging from 20%
to 35%. At the upper end of this range, organic dairy farming becomes an attrac-
tive proposition. In the UK it takes two years to convert the land and nine months
to convert the cows to organic standards. However, as one farmer who has com-
pleted the conversion process said to me: ‘if it no longer continues to pay, I can
go back to conventional tomorrow’.
Alternative Husbandry System 241
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Traditional and Village Systems

Most of this book deals with cows in modern, high-input, high output systems in
the developed world. I justify this because these are the systems that have derived
the most benefit from the application of science, yet are most in need of a proper,
humane, non-mechanistic understanding of the dairy cow. However, most of the
people in most of the world derive their subsistence from very small scale, low
input, low output practices.
In much of the less developed world, lactating ruminants, cows, buffaloes, yak,
are indispensable contributors to the nutrition, income and welfare of pastoral and
village communities. They produce highly nutritious food in circumstances where
the need is great and choices are few. The indigenous animals are well adapted to
challenging environments but individual yields are low. There is some scope for
improvement through cross-breeding with higher yield animals but this needs to be
done with care and a proper, sympathetic understanding of local circumstances in
order to create a phenotype appropriate to the local climate and availability of feed
resources. The UK charity ‘Send a (Holstein) Cow to Africa’ made a great appeal to
the heart but less sense to the head, both in terms of mismatch between phenotype
and environment and, indeed, cow welfare. Today, I gather, the charity makes the
same appeal but spends the money more wisely.
The most fruitful pathways to the production of better, kinder dairy products
within traditional pastoral and village systems will be through education; science-
based, but sensitive and complementary to the substantial knowledge of the local
people. One of the greatest problems for traditional herders is that they cannot
afford veterinary care. It is in the public interest that these farming systems that
contribute so much to community life should receive public support from govern-
ments or non-governmental organisation to improve both productivity, welfare and
sustainability through policies designed to improve animal health and manage-
ment practices that avoid land degradation.
We must exempt these traditional systems from the blanket criticism that it is
immoral/unsustainable to give food to animals when it should go directly to feed
the poor. India is one of the highest producers of milk in the world, mostly from
very small, near subsistence farms that cannot afford to ‘waste’ food resources by
feeding them to animals. Dairy production in India from holy cows and friendly
buffaloes is seen as consistent with the Hindu philosophy of taking only such sus-
tenance from animals that cannot be provided from plants. I repeat here the words
from Michael Halse, of the National Development Board of India, quoted in the
previous edition. ‘It is meaningless to say that Indian farmers should not divert land
to grass fodder from milk production because that is not what happens. India’s
draught and milch animals are sustained mainly on herbage which would other-
wise be wasted. In a successful dairy project, a farmer gets one or two better ani-
mals. He increases milk production by 50–80 litres and increases his income by as
much as 30–50%. He does not ‘divert land’ from food production. He simply makes
his farm more productive. Modern dairy technology can bring rurally produced
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milk to the cities and suburban consumer: rupees can be directed back to the rural
milk sheds through the dairy cooperatives for investment in improved production.’
Fair Play for Cows, People and the Planet
Increasing affluence in the developed world has brought its problems. Too many of
those who can, consume too much food and other resources for our own good and
for the good of the planet. On the other hand, increasing affluence has also enabled
us to afford what G B Shaw expressed as ‘middle class morality’. It is a good line but
I do not share his cynicism. Middle class morality is a good thing. More and more of
us are becoming informed and concerned about such things as animal welfare, pol-
lution, waste and climate change. One way that we can put this concern into action
is through our shopping habits. We can express our wish to know the provenance of
our food and select products identified as organic or high welfare. Through these
actions we acknowledge that food value is not simply a matter of food price.
Individual dairy producers now seek ways to add value at the farm gate by selling
home-made cheeses, yoghurts and ice cream, usually marketed as ‘high welfare’.
However, the vast majority of milk products are retailed through supermarkets. I
often hear people grumble that ‘the supermarkets have all the power’. This is, of
course, untrue. We, the people, have the power. The supermarkets compete to give
us what they believe we want. While much of the competition between supermar-
kets is based on price, there has been a big increase in the marketing and labelling
of food as of local origin, organic, free-range and/or high welfare. A supermarket
that we come to trust on the basis of our concern for these things becomes the
supermarket where we also buy our baked beans and potato crisps. Trust, however,
cannot be bought through slick advertising and quality assurance. It requires qual-
ity control based on published standards of excellence, proper surveillance to ensure
that these standards are met, rewards for those that conform or exceed these stand-
ards and penalties for those that fail.
Herd Health and Welfare
Good health and good welfare (‘wellbeing’) are the goals of good dairy farmers and
their discerning customers. The route to both of these goals, which, of course,
overlap, is through good practice concentrating on prevention of problems rather
than treatment as they occur. All dairy farmers need a herd health plan, arranged
with their veterinary surgeons to promote good health, minimise the incidence of
endemic and production diseases and the risk of acquiring infections. Dairy farm-
ers and the retailers of dairy products also need to establish and adhere to stand-
ards of animal welfare, both for the benefit of their cows and the reassurance of
their customers.
Herd Health and Welfar 243
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Herd Health Management

The aim of dairy herd health management schemes is to promote good production,
health and welfare through the systematic recording and analysis of relevant data,
together with regular inspection of the animals and the environment to endure that
management decisions are based on sound evidence and carried out in good time.
The success of these schemes depends on good strategic planning of objectives and
a structured monitoring of outcomes. Strategic planning should be carried out
by farmers in collaboration with their veterinary surgeons, reinforced wherever
relevant and necessary by input from consultant services on matters relating to
nutrition, breeding and farm economics. Targets for nutrition, fertility, breeding
and health (production and infectious diseases) have all been considered at some
length and need not be recycled here. Suffice it to say that a good herd health plan
requires the diligence of a good accountant to ensure accurate and comprehensive
records, the eye of the good herder to give early warning of incipient problems and,
for all parties, a proper understanding of the dairy cow.
Animal Welfare: Quality Assurance and Quality Control

Animal welfare quality assurance (WQA) can only be guaranteed by proper quality
control. This section sets out the principles of quality control, the approaches
needed to ensure good welfare on the dairy farm and the actions necessary to
encourage the purchase of high-welfare goods through increasing public awareness
and trust in their added value. The steps in this process are:
1) Set high but realistic standards for husbandry and welfare on farms.
2) Establish robust protocols for monitoring husbandry and welfare on farms.
3) Implement and audit actions necessary to ensure overall welfare standards and
address specific problems.
4) Provide incentives and rewards to farmers for complying with standards.
5) Promote public awareness and demand for food and other farm produce that
demonstrably meets these standards.
Standards in animal welfare may be assessed according to the following criteria.
●● Resources – provision of the facilities necessary to ensure proper feeding, housing
and handling of animals.
●● Management – provision of correct husbandry procedures and competent, sym-
pathetic stockmanship.
●● Records – written evidence of use of medicines, deaths and culls, incidence of
disease and injury (etc.).
●● Welfare state – evidence of physical fitness and mental wellbeing as perceived by
the animals themselves.
The first three elements of this assessment relate to aspects of provision (manage-
ment, resources and records). The outcome of these provisions is the welfare state of
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the animals. This is, of course, what matters most to the consumers and to the ani-
mals themselves. The trend in recent years among those who devise WQA protocols
has been to give as much emphasis as possible to outcome measures. However, this
should not be taken too far. An outcome measure of poor welfare, such as a high
incidence of damaged hocks and lameness, is an indication that things have already
gone wrong; a measure of poor provision, such as inadequate bedding in cubicles,
may help to resolve the problem more quickly.
Many WQA schemes for the welfare of farm animals in general and dairy cows in
particular have emerged in recent years, operating on a national level (e.g. the Red
Tractor scheme in the UK, under the auspices of charities, (e.g. RSPCA Assured,
formerly ‘Freedom Foods’) or operated by different supermarkets to assure their
customers that they are rewarding their farmers for good practice. This is not the
place to discuss the relative merits of these schemes, except to say that a national
scheme such as ‘Red Tractor’ only sets baseline standards, selective schemes such
as RSPCA Assured and the schemes operated by competing supermarkets provide
the incentive of higher milk prices.
I have throughout sought, not always successfully, to present an impartial review
of the evidence, uncorrupted by personal bias. However, in these final few words
on quality control I shall present, without apology, a highly personal view. The
practical aims of any quality assurance scheme for animal should be promote high
welfare standards for the animals on the farm, promote increased public demand
for the products of these farms and reward farmers who make the extra effort. All
current protocols for welfare assessment are similar in that they address the prin-
ciples that determine animal wellbeing, namely good feeding, good housing/envi-
ronment, good health and appropriate behaviour (in essence, the five freedoms).
However, the schemes differ in the way they approach these issues, e.g. the empha-
sis given to appropriate behaviour, the time they take to carry out their inspections,
and what they do with the information once they have collected it. A system such
as Red Tractor that monitors farms to ensure that they comply with national Codes
of Practice, can offer reassurance to the public but offers no financial incentive to
the farmer. A complex and time-consuming protocol such as that proposed by the
pan-European ‘Welfare Quality®’ scheme scores farms according to the four princi-
ples of good feeding, housing, health and appropriate behaviour, and rates them as
non-classified, acceptable, enhanced or excellent, but so long as the rating is at
least acceptable, this does not necessarily lead to effective action.
I have proposed an approach that links an on-farm quality control protocol based
on a continuous process of self-assessment, external monitoring, action and review,
to a similarly continuous process designed to promote awareness and encourage the
sale of produce guaranteed to meet the high welfare standards defined by the
scheme. I call this the Virtuous Bicycle (Figure 13.3). The producer cycle, which
forms the right wheel, begins with a formal, written self-assessment carried out by
the farm owner, with input from staff and veterinarians as appropriate. This self-
assessment will be based on the standards of provisions and outcomes set by the
Herd Health and Welfar 245
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Increase awareness,
Standards set by trust and demand for
WQA Scheme high welfare
Self-assessment
Promote standards Revise by farmer
standards as
necessary
Producer
Retailer cycle
Demonstrate cycle Review and
External
proof of revise action
monitor of
compliance plan
welfare
Proof of standards
Establish
Implement action
compliance
plan
Figure 13.3 The ‘Virtuous Bicycle’: a vehicle designed to improve animal welfare on
farm (from Webster 2009). For further explanation see text.
scheme. The farmer should also outline and specific concerns and priorities for
action to address these concerns. The next stage of the cycle is the visit by the inde-
pendent monitor, trained for and operating to the standards of the WQA scheme.
The visit will include a review of the self-assessment and inspection of the animals
and facilities. The report of the monitor will provide an assessment of compliance,
or otherwise, with the standards of the scheme according to the four principles of
good feeding, housing, heath and behaviour. It will also give strategic advice to the
farmer and identify priorities for action, if necessary, to improve welfare. The final
stage of the cycle is for the farmer to see and provide written comment on the report,
identifying actions to be taken where necessary. After an appropriate period (e.g.
one year) there is a further review of welfare in general and the effectiveness of
specific prioritised actions. The aim is to create a continuous cycle of self-improve-
ment. The benefit of starting with self-assessment is that the farmer can address
elements of husbandry, provisions and records in his/her own time, thereby reduc-
ing the amount of work that has to be done at the time of the visit by the independ-
ent assessor. It also recognises that the farmer also knows most (if not best) about
the provisions and outcomes on the farm and why they have evolved. While the first
visit will need to be comprehensive, subsequent assessments can concentrate on the
issues identified as of major concern, thereby avoiding bureaucratic and time-wast-
ing repetition of all elements of the monitoring protocol at every visit. A scheme
where compliance, or star rating, is based not just on the assessment protocol but
on evidence of actions designed to improve welfare is sympathetic to the farmer
because it reduces the risk of subjective bias in the assessor’s report (and variation
in standards between assessors). It is also more challenging to farmers because it
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does not allow them to file away the report and forget it until next year. They must
provide evidence of effective action where necessary.
The left wheel (the retailer cycle, Figure 13.3) is designed to improve public
awareness of, and demand for, food and other produce from farms operating to
proven high welfare standards. The standards necessary for compliance with the
scheme, or ranking within the scheme, are transparent and available for all to see,
both in outline and in detail. Proof of compliance with the scheme can be used by
the operators of the scheme, e.g. RSPCA Assured or specific retail outlets, to pro-
mote the scheme.
This final chapter has considered threats to the living environment, the welfare
of the cows and the social structure of the farming community arising from the
global expansion and intensification of dairy production. These problems cannot
be resolved by farmers alone, with or without the mixed blessings of legislation.
The whole community has to play its part. Effective management and promotion
of welfare and environmentally based QA schemes, subject to independent sur-
veillance, can make a significant contribution to the development of better farm-
ing systems. The complex elements of these schemes are only relevant to those
directly involved, i.e. farmers and assessors. We should not expect the general pub-
lic to be aware of all the details that underpin these standards. However, everyone
should be free, if they wish, to access the details and examine the evidence. We
cannot possibly hope for everyone to become fully informed about everything. As
fewer and fewer people have any direct knowledge of farming, animal husbandry
and land management, consumers have no option but to take most things on trust.
In an era of false advertising and fake news, this is becoming increasingly difficult.
Producers and retailers have the tools to create trust in improved farming methods
but this trust has to be earned.
247
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Further Reading
Part I How the Cow Works
Blowey, R.W. (2016) A Veterinary Book for Dairy Farmers. 4th edition. 5M Publishing
Boivin, X., Lensink, J., Tallet, C. et al. (2003) Stockmanship and farm animal welfare.
Animal Welfare 12: 479–492.
Brambell, F.W.R (1965) Report of the Technical Committee to Enquire in the Welfare of
Livestock kept under Intensive Conditions. HMSO London
Broom, D.B and Fraser, A.F. (2007) Domestic Animal Behaviour and Welfare.
Wallingford, Oxford: CAB International.
Harrison, Ruth (2013) Animal Machines – reissue with commentary of original 1964
publication. Wallingford, Oxford: CAB International.
Hanks, J. and Kossaibati, M. 2016 Key Performance Indicators for the UK National
Dairy Herd. University of Reading. National Milk Records (UK) www.gov.uk
Hultgren, J. (2017) Key issues in the welfare of dairy cattle in Achieving Sustainable
Production of Milk Vol 3 Dairy Herd Management and Welfare (ed. John Webster)
21–52 Burleigh Dodds Science Publishing.
McDonald, L.E. (1980) Veterinary Endocrinology and Reproduction. Philadelphia: PA:
Lea & Febiger.
McDonald, P., Edwards, R.A., Greenhalgh, J.F.D. et al. (2012) Animal Nutrition
7th edition. vetbooks.ir
Noakes, D.E., Parkinson, T.J. and England, G.C.W (2018) Veterinary Reproduction and
Obstetrics 10th edition. vetbooks.ir
Phillips, C.J.C. (2002) Cattle Behaviour and Welfare. Oxford: Blackwell Scientific.
Webster, John (2013) Animal Husbandry Regained: The Place of Farm Animals in
Sustainable Agriculture. Earthscan Routledge.
Webster, John (2016) Animal production systems: animal welfare and environmental
quality in Routledge Handbook of Food and Nutrition Security (eds Bill Pritchard,
Rodomiro Ortiz and Meera Shekar). 137–152. Earthscan from Routledge

248 Further Reading
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Websites
Agriculture and Horticulture Development Board (AHDB) https://dairy.ahdb.org

Dairy cow behaviour and comfort
Dairy cow numbers
GB Dairy Cattle Welfare Strategy 2018–2020.
Part II Feeding the Dairy Cow
Publications
Agricultural Research Council (1980) The Nutrient Requirements of Ruminant

Livestock. 2nd edition. Slough: Commonwealth Agriculture Bureau.
Enemark, J.M.D. (2008) The monitoring, prevention and treatment of subacute rumen
acidosis (SARA): A review. Veterinary Journal 176: 32–43.
Leaver, J.D. (1984) Milk Production, Science and Practice. Harlow: Longman.
McDonald, P., Edwards, R.A., Greenhalgh, J.F.D. et al. (2012) Animal Nutrition
7th edition. vetbooks.ir
Ministry of Agriculture, Fisheries and Food (1980) Nutrient Allowances and
Composition of Feedstuffs for Ruminants Booklet 2087.
Nadau, E. (2007) Effects of plant species, stage of maturity and additive on the feeding
value of whole‐crop cereal silage. Journal of the Science of Food and Agriculture 87:
789–801
National Research Council (USA, 2001) Nutrient Requirements of Dairy Cattle,
7th edition National Academies Press. http//nap.edu/9825
Nordlund, K. (2017). Management of Dairy Cows in Transition and at Calving in
(ed. John Webster) 353–384. Burleigh Dodds Science Publishing.
Owens, F.N., Secrist, D.S., Hill, W.J. et al. (1998) Acidosis in cattle; a review. Journal of
Animal Science 76 (1): 275–286.
Penner, G.B. (2017) Disorders of digestion and metabolism in dairy cattle; the case of
subacute rumen acidosis in Achieving Sustainable Production of Milk Vol 3 Dairy Herd
Management and Welfare (ed. John Webster) 329–352. Burleigh Dodds Science Publishing.
Roche, J.R. (2017) Nutrition management of grazing dairy cows in temperate
environments. in Achieving Sustainable Production of Milk Vol 3 Dairy Herd Management
and Welfare (ed. John Webster) 251–272. Burleigh Dodds Science Publishing.
Suttle, N.F. (2010) Mineral Nutrition of Livestock. 4th edition. Slough: Commonwealth
Agriculture Bureau,.
Webster, A.J.F. (1992) The metabolizable protein system for ruminants in Recent
Advances in Animal Nutrition (eds. J. Wiseman and D.J.A. Cole) 93‐112. London:
Butterworths.
Further Reading 249
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Webster, John (2017) Beef and dairy: the cattle story in The Meat Crisis: Developing
More Sustainable and Ethical Production and Consumption, 2nd edition.
(Eds. Joyce D’Silva and John Webster) 117–139. Earthscan from Routledge
Websites
Agriculture and Horticulture Development Board https://dairy.ahdb.org

Feeding, Section 7
Planning your feeding
Ration formulation
Feeding arrangements
Silage Additives
Kingshay Dairy Manager Dairy Costings https://kingshay.cow>dairycostings
National Milk Records (UK) The Cattle Information Service: www.gov.uk
Part III Housing, Health and Management
Bell, Nick (2017) Prevention and management of lameness in dairy cows in Achieving
Sustainable Production of Milk Vol 3 Dairy Herd Management and Welfare (ed. John
Webster) 431–456. Burleigh Dodds Science Publishing.
Bell, N.J., Bell, M.J., Knowles, T.G. et al. (2009) The development, implementation and
testing of a lameness control programme based on HACCP principles and designed
for heifers on dairy farms. Veterinary Journal 180: 178–188
British Standards Institution (1981) Design of Buildings and Structures for Agriculture
2.2. BS 5502 (2.2) London: BSI.
Divers, T.J. and Peek, S (2018) Rebuhn’s Diseases of Dairy Cattle 3rd edition. Saunders.
Grandin Temple. The Design and Construction of facilities for Handling Cattle.
https://www.grandin.com>references
Green, M.J., Bradley, M., Medley, G.F. et al. (2007) Cow, farm and management factors
during the dry period that determine the rate of clinical mastitis. Journal of Dairy
Science 90: 3764–3776
Moroni, P., Welcome, F. and Addis, M.F. (2017) Aetiology, Diagnosis and Control of Mastitis
in Dairy Herds in Achieving Sustainable Production of Milk Vol 3 Dairy Herd Management
and Welfare (ed. John Webster) 399–430. Burleigh Dodds Science Publishing.
Radostits, O., Gay, C., Hinchcliffe, K. et al. (2007) Veterinary Medicine 10th edition.
Saunders.
Scottish Farm Buildings Investigation Unit (1985) Annual Farm Buildings Cost Guide.
Aberdeen SFBIU.
Skuse, R.A., Allen, A.R., and McDowell, W.J. (2012) Herd‐level risk factors for bovine
tuberculosis: a review. Veterinary Medicine International Article ID 621210.
250 Further Reading
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Theil, C.C. and Dodd, F.H. (1977) Machine Milking Reading: National Institute for
Research in Dairying.
Thilsing‐Hansen, T., Jorgenson R.J., and Ostergard S. (2002) Acta Veterinaria
Scandinavica 43: 1–19
Thilsing‐Hansen, T., Jorgenson R.J., and Ostergard S. (2002) Milk fever control
principles: a review. Acta Veterinaria Scandinavica 151: 694–698
Websites
Agriculture and Horticulture Development Board (AHDB Dairy) https://dairy.ahdb.or

Biosecurity and diseases
Dairy cow behaviour and comfort
Dairy housing 18. Example building designs and layouts
Housing for Dairy Cows
Lameness
Mastitis
Part IV Breeding and Fertility
Beagley, J.C., Whitman, K.J., Baptiste, K.E. et al. (2010) Physiology and treatment of
retained fetal membranes in cattle. Journal of Veterinary Medicine 24: 261–268.
Fisk, R., Stamer, E., Junge, W. et al. (2002) Automation of oestrus detection in cows: a
review Livestock Production Science 75: 219–252.
MacMillan, K. 2010 Recent advances in the synchronisation of estrus and ovulation in
dairy cows. Journal of Reproduction and Development 56 Suppl. 2010: S42–S47.
Nielsen, H.M., Christensen, L.G., and Green, A.F. (2005) Derivation of sustainable
breeding goals for dairy cattle using selection index theory Journal of Dairy Science
88: 1882–1890
Noakes, D.E., Parkinson, T.J., and England, G.C.W (2018) Veterinary Reproduction and
Obstetrics 10th edition. vetbooks.ir
Nordlund, K. (2017) Management of dairy cows in transition and at calving in
(ed. John Webster) 353–384. Burleigh Dodds Science Publishing.
Oldham, J.D., Simms, G., and Marsden, S. (1992) Nutrition‐genotype interactions in
dairy cattle in Recent Advances in Animal Nutrition (eds J. Wiseman and D.J.A.
Cole). London: Butterworths.
Phillips, C.J.C. (2002) Cattle Behaviour and Welfare. Oxford: Blackwell Scientific.
Willis, M.B. (1991) Dalton’s Introduction to Practical Animal Breeding 3rd edition.
Oxford: Blackwell Science.
Woolliams, J.A. and Wilmut, I. (1989) Embryo manipulation in cattle breeding and
production. Animal Production 48: 3–30
Further Reading 251
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Websites
Agriculture and Horticulture Development Board (AHDB Dairy) https://dairy.ahdb.org

4. Selecting your sires
6. Managing heat detection
8. Valuing modern breeding techniques
Centre for Dairy Information UK Breed Performance Statistics ukcows.com>cdi.webmate
National Bovinee Data Centre nbdc.uk/breed improvement
Part V Cows, People and the Environment
Bernues, A., Ruic, R., Olaizola A. et al. (2011) Sustainability of pasture‐based livestock
farming systems in the European Mediterranean context: Synergies and trade‐offs.
Livestock Science 139: 44–57.
Crotty, R. (1980) Cattle, economics and development. Slough: Commonwealth
Agriculture Bureau.
Food and Agriculture Organisation (FAO, 2006) Livestock’s Long Shadow:
Environmental Issues and Options. Rome: FAO.
Garnett, Tara, Godde, Cécile, Muller, Adrian et al. (2017) Grazed and Confused.
Oxford: Food Climate Research Network.
Halse, M. (1975) Food production and food supply programmes in India. Proceeding of
the Nutrition Society 34: 173–181.
Pereira, L. and Ortega, E. (2013) A modified footprint method: the case study of Brazil.
Ecological Indicators 16: 113–127.
Rotolo, G.C., Rydberg, T., and Lieblein G. (2007) Energy evaluation of grazing cattle in
Argentina’s Pampas. Agriculture, Ecosystems and Environment 119: 385–395.
Statham, J.M.E (2015) Practice‐based dairy herd health plansin Bovine Medicine
3rd edition (ed P. Cockcroft) 465–475. John Wiley.
Webster, A.J.F. (2009) The Virtuous Bicycle: a delivery vehicle for improved farm
animal welfare. Animal Welfare 18: 141–147.
Webster, John (2016) Livestock production systems: Animal welfare and
environmental quality in Routledge Handbook of Food and Nutrition Security.
(eds Bill Pritchard, Rdomiro Ortiz and Meera Shekar) 137‐154. Earthscan from
Routledge.
Webster, John (2018) Green and pleasant farming: cattle, sheep and habitat in
Farming, Food and Nature (eds Joyce d’Silva and Carol McKenna) 101–106.
Earthscan from Routledge.
Welfare Quality(R) (2009) Assessment Protocol for Cattle. NEN.
Whay, H.R., Main, D.C.J., Green L.E. et al. (2003) Assessment of dairy cow welfare
using animal‐based measurements. Veterinary Record 153: 197–202.
252
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Index
a b
abomasal disorders 125 barley 89, 91
abomasum 19, 21 barley straw 92
abortion 223 bedding materials 153
acetate 29–31, 127 beef from dairy cows 209
acetonaemia, see ketosis behaviour 14–17, 65
acidosis 31, 123–125, 124 in cubicles 67, 153
Actinobacillus lignieresi 186 as an indicator of welfare 76
Actinomyces bovis 186 lying and resting 66–68
adenosine triphosphate (ATP) sexual and maternal 75, 212, 214
28–29, 127 social 74
adrenocorticotrophic hormone in transport 164
(ACTH) 53 biosecurity 178
aggression 74, 150 bloat 126, 184
alfalfa (lucerne) 89, 104 botulism 185
alveoli of mammary gland 56, 57 bovine growth hormone 61
amino acids 112 bovine spongiform encephalopathy
ammonia 34, 36, 104 (BSE) 111, 185, 190
amniotic cavity 51 bovine tuberculosis 190, 191
Animal and Plant Agency, UK, bovine viral diarrhoea (BVD) 184, 193, 225
(APHA) 190 breeds and breed differences
anoestrus 220 Ayrshires 4, 199, 202
anorexia 188 Belgian Blues 56, 210
anthrax 183, 190 British Friesians 4, 11, 63, 202
antibiotics 177–181, 188, 195 conformation 4, 199, 204
antibiotic resistance 188 cystic ovaries 220
appetite 9, 37, 41–43, 99 Dairy Shorthorns 4
Arcanobacterium pyogenes 180 Dystocia 210
artificial insemination 156, 217, economic efficiency 205
218 Fulani 70, 71, 72
automatic cluster removal 174 gestation length 209

Index 253
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Guernseys 9 cold stress 72, 74

Hereford 63 colon 19
Holsteins 4, 11, 199–202 comfort 145
Jersey 4, 12, 20, 202, 207 physical 64–68
Mertolenga 239 thermal 64, 68–71, 70
milk composition 11 complete-diet feeding, see Total Mixed
milk yield 11 Rations
sexual behaviour 63 computers in dairy production 94–97
thermal tolerance 73 condition scoring 224, 225
brewers’ grains 91, 114 copper 89, 137
brucellosis 190, 221 corpus luteum 47, 48
buffers 23, 125 Corynebacterium pyogenes 180, 222
building design cotyledons 46, 52, 221
calving and isolation boxes 154–156 cottonseed meal 91
cow cubicles 147, 150–154, 151 crossbreeding 199, 200
cubicle beds 153 cystic ovaries 129, 220
heifer yards 156
passageways 154 d
bull selection 204–206 dairy cake 91, 94
bulls for beef 209 diarrhoea 179, 184, 186
bulling, see oestrous behaviour dictol 196
butyrate 29 Dictyocaulus viviparous 196
by-products as cattle feeds 111–114 digestibility 26, 100
digestibility of organic matter in dry matter
c (DOMD) 100
caecum 19 digestion 27, 26–28
calcium 37, 87, 89 digestive tract 19
exchanges 41, 41–42 digital dermatitis 159, 161
in milk fever 129–132 dioestrus 48
calorimetry 32 disease, clinical signs 183–189
calving 200 distillers’ grains 91, 114
calving interval 212 ‘dog sitting’ 152
Campylobacter 221 ‘double muscling’ 56, 209
carbohydrates 28–31 ‘downer cow’ 132
carotene 139 drooling 184, 185
casein 9 dry cow therapy 178, 181
cellulose 29 dry matter intake (DMI) 86, 93, 100, 114,
cereals 108–110 124, 201
cervix 46 prediction 93
choice 17, 145 dystokia 55, 210
climate and welfare 73
climate change 237 e
cloning 208 early foetal death 222
clover 100 eating 22
cobalt 89, 138 economics 97, 100, 175, 201
254 Index
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endometritis 130, 182, 222 fibre digestion 28–31

endotoxins 124 modified acid detergent fibre (MADF) 106
energy neutral detergent fibre (NDF) 88, 91, 97,
efficiencies of conversion 13, 201 99, 119
energy expenditure 122 field beans 112
fermentable metabolizable energy fishmeal 112
(FME) 91, 94 ‘five freedoms’ 16–17, 164, 234
metabolizable energy (ME) 11, 87, 91, fodder beet 92, 109
94, 101 foetal membranes 51
concentration in dry matter, (M/D) 83, foetus 51
115 follicle stimulating hormone (FSH) 47, 48,
efficiency of utilisation 31–32, 33 61
quickly fermentable energy (QFE) 27, food intake 93
26–30, 102–104 foot and mouth disease 184, 192
slowly fermentable energy (SFE) 27, foot care 160–162
26–30 foot structure 158
utilised metabolizable energy ‘foul-in-the-foot,’ see interdigital
(UME) 103 necrobacillosis
value of milk 12 Freemartin 52
‘emergy’ sustainable index 236, 237 Fusobacterium necrophorum 222
environmental needs 64
enzootic bovine leucosis (EBL) 190 g
eructation 126 genetics
Escherichia coli 175, 176 bull selection 209
exhaustion 17, 234 calving ease 200
conformation 200
f cow genetic merit 208
Fasciola hepatica 196 cow selection 207
fatty liver 129 fertility 200
feeding strategies 117–120 genetic index 201
brinkmanship 118 genomic selection 206
feeding out of parlour 95 genotype/environment interaction 201
feeding plans 95–97 gestation length 209
feeding problems 122 lameness 200
feeding to yield 117 lifespan 200
flat-rate feeding 119 milk composition 201
lead feeding 118 milk yield 202
fermentation 28–31 selection 202–206
fermentable metabolizable energy selection index 203
(FME) 91 genomic selection 206
fermentation of silage 106 genotype-nutrition interaction 201
fertilisation 50 glutathione peroxidase 138
fertility 200 grass, nutritive value 92
management 212 grass silage, nutritive value 92, 104
fever 187 additives 107
fibre 28 big bale 104
Index 255
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concentrate supplementation 114–117, interdigital necrobacillosis, ‘foul’, 162

115, 116 iodine 89
slurry 148 iron 89
grass staggers, see hypomagnesaemia
grazing. 237 j
grazing strategies 102–104 jejunum 19
greenhouse gases 30, 237 Johne’s disease 184, 194
groundnut meal 91, 112
k
h kale 92, 109
habituation 14 ketosis 126–130, 128, 182, 185
handling facilities 156, 157 Klebsiella sp. 176
hay 92, 94, 107 Kreb’s cycle 127
heat increment of feeding 32
heat loss 68–71 l
evaporative 69–71, 72 lactation 56–61, 85
sensible 68, 72 extended lactation 59
heat production 68, 71, 72 hormonal control of lactation 60
heat stress 72, 73 lactobacilli 31, 124
heifer rearing 156 lactose 11, 58
hemicellulose 29 lameness 157–164
herd health plans 242 risk factors 162–164
heritability 199, 200 laminitis 160, 162
heterosis 200 legumes 104
housing leptospirosis 195, 225
calving and isolation boxes 154 ‘let-down’ of milk 56
cow kennels 151 lifespan 200
cowshed design 146–150, 149 Lifetime Production Index 205
cubicle bedding 153 lightning strike 183
cubicle design 150, 151 linseed cake 91, 112
flooring materials 153, 154 lipids
passageways 154 digestion 38–39
husk 196 in milk 58
Hydrotea irritans 180 listeriosis 185
hygiene liver-fluke 196
at calving 154 Livestock’s long shadow 235–237
in milking parlour 174, 178 Lucerne, see alfalfa
hypocalcaemia 129–132 ‘lumpy-jaw’, 184
hypomagnesaemia 134–136, 135, 185 luteinising hormone 47, 48, 61
Lymnea truncatula 196
i
implantation 52, 222 m
inappetence 188 ‘mad cow disease,’ see bovine spongiform
infertility 129, 182, 219–225 encephalopathy (BSE)
nutritional 223–226, 224 magnesium 39. 87
injury 154, 182 hypomagnesaemia 133–136, 134, 185
256 Index
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Maillard reaction 113 n

maintenance requirement 31, 33 natural selection 200
maize gluten 91, 112, 113 nervousness as symptom of disease 187
male reproduction 61–63 net energy for lactation (NEl) 86–88
mammary gland 56, 57 nitrogen (N)
manganese 89 acid-detergent insoluble N 37, 113, 114
mastitis 129 basal endogenous N 34
cell counts 176 digestion and metabolism 34
contagious 177 non-protein N 24, 83, 111
economics 175 quickly degradable N 27, 34, 35, 104
environmental 176, 178–180 slowly degradable N 27, 34, 35
indicators 176 truly absorbed amino N 34, 37
summer 180 undegradable dietary N 27, 34, 37
meadow fescue 101 non-fibre carbohydrate (NFC) 88, 97, 99,
metabolic body size 11, 71 119, 123
metabolic disorders 127–136 non-steroidal anti-inflammatory drugs
methane 10, 30 (NSAIDS) 179
contribution to global warming 237 notifiable diseases 191–193
milk nutrients, allowances 84–88
biological efficiency of production 10, growing heifers 98
10–12 requirement 80–84, 81
composition 7, 12, 58, 87, 201, 299 responses 80–84, 81
fat-corrected milk (FCM) 93 nutritionally improved straw 108
health problems for humans 9 nutritive value of feeds 80
hygiene 174, 178 nymphomania 220
nutritive value for humans 6–9
secretion 169 o
species and breed comparisons 11 oats 91
yield 11, 58, 88, 200 oesophageal groove 19
milk fever, see hypocalcaemia oestrogen 47, 47, 48, 213
milking machines 171–174, 172, 173 oestrus
milking parlour 174 oestrus behaviour 212–216, 214
minerals, requirements 88–90 oestrus cycle 48, 49
absorption and secretion 39–41 oestrous detection 213–216, 214
molybdenum 137 oestrous synchronisation 216
monensin 129 omasum 19, 21
motivation analysis 66 organic farming 240
mucosal disease, see bovine viral osteoporosis 136
diarrhoea (BVD) ovaries 46
multiple ovulation with embryo transfer follicles 46, 47
(MOET) 47, 208 follicular development 45–51,
Mycobacterium bovis 191 47, 48
Mycobacterium paratuberculosis 194 ovarian dysfunction 220
Mycoplasma sp. 178 ovulation 47, 48, 49
myoepithelial cells 56, 57 oxytocin 56, 168
Index 257
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p r
parasitism 186, 195 rapeseed meal 91, 112
parathyroid hormone 131–133 ration formulation 80, 93
parturition 46, 53–55 assessment 94
pasture 100–102, 101 balancing energy and protein 115, 116
digestibility 101 rebreeding 219
pastoral systems 79, 80, 99 regurgitation 23, 24
pedal bone 159, 160 relaxin 160
perennial ryegrass 100, 101 reproductive organs
phosphorus 39, 87, 89, 136, 238 female 46
placenta 51 male 62
placental transfer of nutrients 53 retained placenta 221
retained placenta 130 reticulo-rumen 19, 21
poisoning 118, 182, 184 reticulo-omasal orifice 19, 20
pollution 233, 238 robot milking 170
predicted transmitting ability (bulls) robustness 203–206
204–206 root crops 109
pregnancy 51 rumen 19
pregnancy diagnosis 156, 217 rumen acidosis 123, 124
productive lifetime index, (£LPI) 205, 220 rumen movements 24, 23–25
progeny testing 203–206 rumen papillae 20
progesterone 47, 48, 215, 217, 220 subacute rumen acidosis (SARA) 124
progesterone-releasing intravaginal rumination 25–26
device (PRID) 217
pro-oestrus 48 s
propionate 29–31, 127 salivation 23
propylene glycol. 129 salmonellosis 184, 194
prostaglandin 48, 49, 53, 217 security 65, 74, 145
protein (P) selenium 89, 138
allowances 83, 84 sexed semen 222
biological value 37 silage 92
crude protein 83, 101, 104, 105, 116 big-bale silage 92
digestible undegradable P 91 grass silage 92
digestion and metabolism 34 maize silage 92
effective rumen degradable P 91, 102 nutritive value 104–107
rumen degradable P 88 silage additives 107
metabolizable P 94, 116 slaughter 166
microbial P synthesis 34, 35–37 emergency slaughter 167
undegradable dietary protein (UDP) 88 sodium 40
puberty 49–50 sodium bicarbonate 25, 123
pulsation ratio 171, 173 Soil Association 240
sole haemorrhage 159
q sole ulcer 159
quality assurance and control 245, somatic cell count 176, 180, 200
243–246 somatotropin, see bovine growth hormone
258 Index
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soyabean meal 91, 112 transition management 155, 226

spermatozoa 62 transport 164–166
Staphylococcus aureus 177 traumatic reticulitis 184, 186, 189
starch 28 turnips 92, 109
straw 108 twinning 52
nutritionally improved straw 108
Streptococcus agalactiae 177 u
Streptococcus uberis 178 udder, see mammary gland
stress 14 urea recycling 38
sub-acute rumen acidosis (SARA), see uterine disorders 221
acidosis uterus 46, 50
sudden death 183
suffering 14 v
sugarbeet pulp 91, 113 ‘Virtuous Bicycle’ 244–246, 245
sugars 28 vitamins
supermarkets 242 vitamin A (retinol) 7, 139, 185
sustainable intensification 232 vitamin B12 (cyanocobalamin) 139
sweating 70, 73 vitamin D (calciferols) 7, 140
swollen knees and hocks 158 vitamin E (tocopherols) 140
volatile fatty acids 27, 36, 104, 123
t
teart 138 w
teat cups, function 172 warble fly 190
teat-dipping 175 welfare 15, 14–17, 76, 234, 242–245
teat-end impact 174 wheat 91
teat injuries 173 wheat bran 114
testosterone 61 whey proteins 58
temperature/humidity index 73 ‘white line disease,’ 161
thermal comfort 69–71, 72 whole-crop cereals 108
thermal insulation 69 ‘wooden tongue,’ 184, 185
thermal panting 71
thermoneutral zone 71, 72 y
total bacterial count 175 yeast supplements 125
Total Mixed Rations 82, 94, 119, 170
trace elements 89, 137–139 z
traditional and village dairy systems 241 zinc 89
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Understanding The Dairy Cow

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VetBooks.

Understanding the Dairy Cow

Understanding the Dairy Cow

John Webster, MA, VetMB, PhD, DVM (Hon), MRCVS

or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or

Limit of Liability/Disclaimer of Warranty

Library of Congress Cataloging‐in‐Publication Data

Set in 10/13pt STIXTwoText by SPi Global, Pondicherry, India

Part I How the Cow Works 1

1 Introduction – The Dairy Cow of Today 3

2 Digestion and Metabolism 18

­Absorption and Secretion of Minerals 39

3 Reproduction and Lactation 45

4 Environment, Behaviour and Welfare 64

Part II Feeding the Dairy Cow 77

5 Nutrition: Supply and Demand 79

Prediction of Food Intake 93

6 Feeds and Feeding Strategies 99

7 Feeding Problems and Metabolic Diseases 121

Hypomagnesaemic Tetany (Grass Staggers) 133

Part III Housing Health and Management 143

8 Healthy and Humane Housing and Handling 145

9 Milking and Mastitis 168

Environmental Mastitis 178

10 Miscellaneous Maladies 182

Part IV Breeding and Fertility 197

Early Foetal Death 222

Part V Cows, People and the Environment 229

13 Cows, People and the Living Environment 231

Further Reading 247

I thank the following for permission to reproduce illustrations: Geoffrey Pearson,

Preface to the Third Edition

About the Companion Website

Don’t forget to visit the companion website for this book:

The website contains downloadable figures from the book.

How the Cow Works

Introduction – The Dairy Cow of Today

Understanding the Dairy Cow, Third Edition. John Webster.

r­ easonable practical knowledge of dairy cow management and addresses the

The four essential qualities of a good diet are to:

Four‐year‐old child Adult

Requirement % from milk Requirement % from milk

Energy (kJ) 6400 25 12600 13

Daily requirement: energy (kJ) 12600 6400

this is genetic or environmental (i.e. no milk after weaning). In my youth, I was

Taste and Appetite

­Biological Efficiency of Milk Production

Cereal Forage Soya (etc)

Faeces Digestion & Fermentation Methane

Energy Protein Mins Vits

Maintenance Work Production Reserves

Figure 1.2 Nutrient supply and requirement (from Webster 2013).

Metabolizable energy (MJ) = gross energy of feed – energy in faeces, urine

Milk Production: Species and Breed Comparisons

Table 1.3 Yield and composition of milk from different mammals.

Holstein cow Jersey cow Sow Bitch Woman

Body weight (kg) 700 420 240 26 60

Efficiency of Feed Conversion to Milk, Eggs and Meat: Competitive

Absorption and Secretion of Minerals 39

r easonable practical knowledge of dairy cow management and addresses the

Biological Efficiency of Milk Production

Behaviour and Welfare

Structure of the Digestive Tract

Eating and Rumination

Apparent digestibility of N ( N in feed N in faeces) /(N in feed ).

Absorption and Secretion of Minerals

Appetite and Food Intake

Anatomy of the Female Reproductive Tract

Follicle Development and Ovulation

The Oestrus Cycle

Reproduction in the Male