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The Veterinary Book for Dairy Farmers: 4th Edition

The Veterinary Book for Dairy Farmers: 4th Edition

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The Veterinary Book for Dairy Farmers: 4th Edition

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Oct 12, 2016


The ever-changing world of cattle farming requires farmers to be up-to-date with best-practice procedures and the latest advances in husbandry techniques. Now in its 4th edition, Roger Blowey's updated version of the acclaimed A Veterinary Book for Dairy Farmers deals with newly emerging problems in cattle farming, as well as covering the necessary knowledge required for maintenance and prosperity. In this practical guide to animal health and husbandry, Blowey highlights developments in established conditions, including lameness, Johnes, BVD, and mastitis. Other updates include the prevention and treatment of emerging diseases, such as Schmallenberg and Blue Tongue, and current issues in farming, such as developments in calf rearing and the increasing incidences of botulism and antimicrobial resistance. This book is a comprehensive and practical text for dairy farmers, stockmen, veterinary academics, and students to navigate this changing field. [Subject: Veterinary Medicine]
Lançado em:
Oct 12, 2016

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The Veterinary Book for Dairy Farmers - Roger W. Blowey


Preface to the Fourth Edition

It is now over 30 years ago that the first edition of this book was published in 1985, and 17 years since the third edition in 1999. Perhaps what is particularly interesting about this fourth edition is that the major increases in our knowledge have occurred in the basic subjects of calf feeding, mastitis and lameness and hence it is in these chapters where many of the fourth edition changes have occurred. Comparing this text with the Preface to the Third Edition, I think we can now say that improvements in our knowledge have led to a decrease in disease.

The big changes have been in farming itself. Large modern units with far more space, better ventilation, better feed access and a well-balanced diet have all contributed to decreased disease. The biggest contributor, however, has probably been the increased knowledge and skill base of those working on farms. With larger units, farms have been able to justify considerably greater expenditure on training, and as a consequence animal health has benefited. I certainly do not agree with the concept that large units are ‘factory farming’ and therefore constitute poor animal welfare. My own opinion would be the reverse, namely that well-run large units with highly trained professional staff have the capability to provide excellent conditions for livestock and there is now published data to support this opinion. Training is key, however, and I hope that this book goes some way to assisting with that challenge.

I have again found it difficult to know where to condense material, providing sufficient information to make this book useful but at the same time not so large that it becomes economically unviable. For those requiring more detail my other books have also been updated, namely Cattle Lameness and Hoofcare, Mastitis Control in Dairy Herds and A Color Atlas of Diseases and Disorders of Cattle, and as before I have included a list of suggested further reading.

In my Preface to the Third Edition I wrote, ‘There will be no further new edition until we are well into the 21st century. By that stage BSE will be history.’ That was one prediction that I did get right. What has been disappointing, however, has been the rise of bovine TB in the UK. Who could have predicted the massive increase in incidence and geographical spread from the West Country starting in 1998? At the time of writing there is an ongoing cull of the wildlife reservoir in three small areas of the country, although this has resulted in active and occasionally violent protests from a small part of the community. Considering that it is accepted by all parties that badgers are significant carriers of bTB infection, I find this both surprising and disappointing. However, assuming that the fifth edition of this book will be written after 2025, my prediction is that a targeted removal of bTB-infected wildlife, combined with cattle control measures, will result in control of the disease.

As with previous editions, one of my greatest pleasures is to see an obviously well-worn copy of this book lying open at the relevant page when I arrive on farm. Improvements in animal health must surely be founded upon a thorough understanding of the nature of disease, and this should be the goal for all of us.

Roger Blowey




Further Reading

AHDB Dairy, production statistics and other information http://dairy.ahdb.org.uk/

A.H. Andrews, R.W. Blowey, H. Boyd & R.G. Eddy (eds) (2004) Bovine Medicine 2nd Edition. Published by Blackwells Scientific Publications, Oxford

ARC (1980) The Nutrient Requirements of Farm Livestock, Commonwealth Agricultural Bureau, Slough

R. Blowey (1992) Footcare in Cattle [video]. Written and presented by R.W. Blowey. Released by Farming Press/5M Publishing

R. Blowey (2015) Cattle Lameness and Hoofcare 3rd Edition. Published by 5m Publishing

R.W. Blowey & P. Edmondson (2010) Mastitis Control in Dairy Herds. Published by CABI

J.S. Brickell and D. C. Wathes (2011) A descriptive study of the survival of Holstein-Friesian heifers through to third calving on English dairy farms. Journal of Dairy Science, 94: 1831–8

L.A. Brunton, D. Duncan, N.G. Coldham, C. Snow & J.R. Jones (2012) A survey of antimicrobial usage on dairy farms and waste milk feeding practices in England and Wales. Veterinary Record, 171:296. doi:10.1136/vr.100924

T. Chamberlain & M. Wilkinson (1996) Feeding the Dairy Cow. Published by Chalcombe Publications, Welton, Lincs

P. Edmondson (2014) How to Control Somatic Cell Counts. Published by Context Products Ltd, Ashby de la Douche

Esslemont et al. ‘The Incidence and Costs of Disease in Dairy Herds’, Dairy Information System, Dept Agriculture, University of Reading, UK

J. Griffiths (2015) The acidification of waste milk as a method to control Johne’s disease in dairy replacement heifers. Reading University School of Agriculture dissertation

T.J. Parkinson, J.J. Vermunt & J. Malmo (2010) Diseases of Cattle in Australasia. Published by VetLearn

J. Webster (1993) Understanding the Dairy Cow. Published by Blackwells Scientific Publications, Oxford

About the Author

Roger Blowey trained at Bristol University where he gained honours degrees in veterinary science and biochemistry. After a period at the Central Veterinary Laboratory, Weybridge, studying metabolic profiles, he returned to the Wood Veterinary Group Gloucester where he spent 45 years in farm animal practice.

His special interests are preventive medicine and the interaction of nutrition, disease and environment on the productivity of livestock units.

He has lectured extensively on these subjects in Britain and overseas, featured in educational programmes on radio and television and has written numerous original research papers and books on a wide range of topics. He is an RCVS Specialist in Cattle Health and Production, and has been awarded a Fellowship of the Royal College of Veterinary Surgeons for meritorious contributions to learning, the RW Hall Award and the RASE Bledisloe Veterinary Award for outstanding achievements in the veterinary field, and the BVA Dalrymple-Champneys medal for work of outstanding merit in the advancement of veterinary science. He has regularly lectured at Cambridge and Bristol University Veterinary Schools, and is an Honorary Research Fellow of the University of Liverpool.

The skeleton and internal organs of the cow as seen from the left side.

Chapter 1

A Concept of Disease, Immunity and Treatment

For some diseases there is a simple relationship between the infection, the animal and the treatment needed. Examples include foul-of-the-foot, caused by a bacterial infection and treated with antibiotics, or ringworm, a mycotic infection that can be treated with antifungal drugs. However, many of the more common conditions seen on farms today are due to an interaction between the animal, its environment and a wide range of infectious organisms. Probably the best example is calf pneumonia and this will be referred to again later in the chapter. Another example of the complexity of disease is milk fever. At calving, the cow’s requirements for calcium may exceed her capabilities to mobilise the mineral, although she has ample reserves in her skeleton. The clinical symptoms are due to a deficiency of calcium in the blood. Milk fever is known as a metabolic disorder or a production disease.

Both the farmer and his veterinary surgeon must thoroughly understand the mechanisms of disease if we are to reduce some of the enormous losses that are incurred, and I would urge the reader to spend a short while studying this first chapter before embarking on the main text. This chapter describes the nature of disease; some of the ways in which the animal protects itself; how infection, environment and immunity interact in a clinical situation; and finally it describes an approach to the treatment of an individual sick animal.

Causes of Disease

Although we often think of infectious agents as the cause of disease, in fact many of the ailments we see in farm livestock are nothing to do with infection. Lameness is a good example, where simple trauma to the foot plays a major role in the aetiology of hoof problems. Poisoning, or, at the other extreme, trace element deficiency, can also lead to major health problems. The major factors leading to poor health in farm livestock may be listed as follows:

Infectious agents

Nutritional imbalance, deficiency and excess

Metabolic disorders


Physical injury

Congenital disorders

Neoplasia (‘cancer’)

Infectious agents

A wide range of infectious agents can cause disease. Some exist as normal organisms on the animal or in its environment and only cause disease when in an unusual site or when the immunity of the animal is compromised (i.e. reduced). A good example of this is the bacterium Escherichia coli, most commonly known as E. coli. It is present in the intestine of all cattle, where it usually causes no problems. However, if it gains access to the udder it can cause quite severe disease, especially in the early lactation animal, whose udder defences against infection are poor.

For other infections, for example foot-and-mouth virus, disease occurs whenever the infection is present.

Infectious agents may be subdivided into the following categories:



Mycoplasma, ureaplasma, rickettsia and chlamydia


Fungi, yeasts and moulds


Ectoparasites (mange, lice, etc.)


These are single-celled organisms which contain all the components needed for a separate existence. A typical bacterium is shown in Figure 1.1. It is a single cell, and consists of a thick outer polysaccharide structure, the cell wall, inside of which there is a protein membrane enclosing the cytoplasm and the nuclear material. The nuclear material contains the genetic components, the DNA (deoxyribonucleic acid), which is arranged as a double-stranded helix. Each strand consists of a sequence of the four nucleic acids, adenine, cytidine, guanine and thymine, A, C, G and T. It is the sequence of these nucleic acids that determines our genetic structure. For example A-C-T-G would be a different gene to C-T-G-A. DNA ‘instructs’ cell function by transcription of a second material, RNA (ribonucleic acid, sometimes referred to as mRNA, messenger RNA), which in turn determines which proteins and enzymes the cell produces.

DNA therefore functions as the regulator for all cell processes, determining the size and shape of the cell and the activities that take place within its cytoplasm. These ‘activities’ are the processes of reproduction and growth. The whole bacterium may be enclosed by a gelatinous capsule, a thick membrane which renders the bacterium more resistant to phagocytosis (i.e. being engulfed by white blood cells). Bacteria are therefore individual discrete units of life.

Figure 1.1 A typical bacterial cell. Even the largest bacteria (e.g. anthrax) are only 0.005 mm long. They multiply by dividing into two, and under favourable conditions this may occur every 30 minutes, so that one bacterium could produce 17 million offspring in 12 hours!

Given ideal conditions of warmth, nutrients and moisture most of them can also multiply outside the animal’s body. For example E. coli is said to double in numbers every 20 minutes. Under adverse conditions some bacteria produce a very resistant spore form, which can survive for many years. The classic example is that of anthrax, whose spores can persist in the soil for up to 40 years. Bacteria absorb nutrients for their growth from their immediate surroundings (e.g. blood, milk or body tissue) and excrete waste products, especially when they die. It is often these waste products that cause disease. The ‘waste’ is known as a toxin and the animal is said to be suffering from a toxaemia. Typical examples of toxaemia are acute E. coli mastitis and severe uterine infections.

Bacteria are the major cause of mastitis and foot infections, they are commonly involved in respiratory disease and they comprise the clostridial group of diseases such as blackleg, tetanus and anthrax. Bacteria commonly form pus and are also responsible for conditions such as navel ill, calf diphtheria and abscesses. Bacteria are killed by antibiotics, with different antibiotics being needed to kill the different species of bacteria. This is explained in more detail in the treatment section.


Viruses are much smaller than bacteria and may even infect and cause disease in bacteria. They cannot be seen with a normal light microscope; electron microscopy is required. They consist simply of central nuclear material, which may be DNA or RNA (ribonucleic acid), and this is surrounded by a capsule of fat and protein (Figure 1.2).

Because viruses have no cytoplasm or proper nucleus, they cannot carry out their own metabolic functions of growth and reproduction and they are therefore unable to multiply outside the animal’s living cells. For their survival away from the animal, and hence their transfer from one animal to another, viruses must be protected, for example in sputum (pneumonia viruses), milk (foot-and-mouth virus) or blood (EBL virus).

Once within the animal, viruses inject their own RNA or DNA into the animal cell and then use the metabolic processes within the cytoplasm of that cell for their own purposes of multiplication and growth. When a cell is packed full of viruses, it bursts and virus particles are released to penetrate and infect adjacent animal cells. It is the bursting of these cells that generally causes the detrimental effects on the animal and hence the signs of disease, although some viruses (e.g. those causing teat warts or EBL) induce a proliferation or excessive multiplication of animal cells to produce a tumour.

Figure 1.2 A virus particle. A virus is very much smaller than a bacterium. It uses the processes of metabolism within the animal cell for its own multiplication and growth, and as such it cannot live a separate existence away from the animal. This is very different from bacteria.

Both bacteria and viruses may be very specific in the site they choose to infect. For example, certain groups will grow only in the respiratory tract – and these cause the clinical signs of a cold, influenza or pneumonia. Others can live only in the intestine and they will cause scouring. It is by this mechanism that we associate particular strains of bacteria or viruses with specific diseases. Different strains of bacteria and viruses vary considerably in shape and size, in the same way that the different species of animal or bird are so variable.

Viruses cause a wide range of disorders including foot-and-mouth and diseases of the teat skin, and they are often the primary cause of calf pneumonia. Whereas antibiotics will kill bacteria, there is no specific drug to kill viruses. This is one reason why many virus diseases are controlled by vaccination. Mycoplasma, ureaplasmas and rickettsia are organisms that have some characteristics of bacteria and some of viruses.

Mycoplasma, ureaplasma, rickettsia and chlamydia

Mycoplasmas (and related ureaplasmas) are similar to bacteria except they have no cell wall. As such they are resistant to those antibiotics (especially the penicillins) that act by damaging the cell wall. Mycoplasmas can cause pneumonia and occasionally mastitis, joint, ear and brain infections.

Chlamydia and related rickettsia have nucleic acid and no cell wall. They cause enzootic abortion in sheep, psittacosis and Q fever.


Protozoa are also single-celled organisms, although they are larger and more complex than bacteria and may have a free-living existence. Examples include Babesia and Trypanosoma, which live in the blood of cattle and cause redwater, and coccidia and Cryptosporidia, both of which live in the intestine and cause scouring. Other protozoal diseases of cattle include Neospora, a cause of abortion, Theileria, which causes East Coast fever in southern Africa, and Besnoitia, which causes skin disease and abortion.

The treatment of protozoal infections requires specific therapy. For example, there is one drug specifically used against Babesia (imidocarb) and others against coccidiosis (e.g. toltrazuril; amprolium) and Cryptosporidia (halofuginone).

Fungi, yeasts and moulds

Fungi are very simple members of the plant kingdom. They are commonly found in the environment and primarily cause disease when they enter an unusual site, e.g. the udder, where they can cause a chronic mastitis. They do not respond to antibiotics and they need special therapy, e.g. natamycin (see Chapter 7) for therapy. There are some specific fungal diseases of cattle, e.g. ringworm, and another group of diseases where a common environmental fungus invades an unusual site. A good example of this is abortion caused by the fungus Aspergillus. Aspergillus may be seen as a blue-grey mould growing on silage (Plate 1.1), and if eaten by a pregnant cow it can lead to abortion.

Worms (helminth parasites)

Cattle can be affected by a wide range of helminth or endoparasitic worms. In low numbers worms cause no problems, although if allowed to multiply they can cause serious disease. As with bacteria and viruses, different worms live in different parts of the body. Examples include nematodes such as the lungworm (Dictyocaulus viviparus), the stomach worm Ostertagia ostertagi and the intestinal worms Nematodirus and Oesophago stomum. There is even a worm (Thelazia) that lives in the eye! Tapeworms (cestodes) are found in the intestine. Flukes (trematodes) are parasites of the liver and rumen.

Plate 1.1 Aspergillus mould growing on silage. This led to five abortions when fed to dry cows.

Most worms have a direct life cycle; that is, eggs laid by adult worms are passed in cattle faeces, develop into mature larvae on the ground and are then ingested by grazing animals. Other helminth parasites may have an indirect life cycle, for example the liver fluke spends part of its life in the host animal and part in a snail.

An anthelmintic is the general name given to drugs that are used to treat worms (i.e. wormers). The same drug will often treat all species of lungworm and gutworm, although different products are usually required to treat liver fluke. Anthelmintics are often subdivided into white drenches and clear drenches. The white drenches are the benzimidazole group of compounds, examples of these being oxfendazole and fenbendazole. Clear drenches include levamisole and the avermectin range of products, e.g. ivermectin, doramectin and moxidectin. Each drug has a slightly different spectrum of action and length of activity, so make sure that you have read the manufacturer’s instructions before use.


An ectoparasite is the name given to an organism which lives on the body surface of an animal (intestinal worms are known as endoparasites). The range of different ectoparasites on cattle includes lice, mange, flies, maggots and ticks. Some have a direct life cycle (lice and mange) where all stages of the life cycle can be found on the same animal. Others, such as ticks, are more complex and part of their life cycle is spent off the animal.

Nutritional deficiency and excess

Deficiency disorders are the result of an inadequate supply of minerals, vitamins or trace elements. Typical examples would be copper deficiency or vitamin A deficiency. Deficiencies may be either primary, when there is a specific lack of nutrient in the diet, such as vitamin A, or secondary, when some factor interferes with the uptake of a nutrient. Examples of the latter include molybdenum, sulphur or iron interfering with copper absorption to produce an induced copper deficiency. In most cases treatment simply involves providing an adequate supply of the nutrient.

Disease can also occur as a result of ingestion of an excess of some feedingstuffs. The most common example would be overeating syndrome, where cattle gain access to a compound feed store and develop acidosis, which is an excessive fermentation of starch in the rumen.

Metabolic disorders

Homeostasis is the process whereby the body maintains a constant temperature, heart and respiratory rate and also ensures that the levels of various chemicals in the blood remain within a constant range. For example, when there is a sudden increase in demand for calcium (e.g. immediately after calving), the cow may not be able to draw calcium from her ‘stores’ (mainly bone and intestinal contents) rapidly enough to satisfy her requirements. Blood calcium levels then fall, muscle function is lost and the cow sinks to the ground with milk fever and is unable to rise.

It is not that there is insufficient calcium in the diet, or even insufficient stored in the body. It is simply that the cow is unable to cope with the sudden increase in demand for calcium sufficiently rapidly to avoid the short-term drop in blood calcium which follows. Calcium homeostasis fails and the resulting disorder is known as a metabolic disease. Other metabolic diseases include hypomagnesaemia, ketosis and fatty liver.


When we think of poisoning we usually refer to the animal eating some ‘foreign’ substance, for example lead (often old paint on doors) or plants such as yew trees. The clinical signs seen will depend on the poison eaten. Ingestion of lead produces nervous signs, whereas eating yew leads to sudden death due to heart failure. Poisoning can also occur from eating an excess of some substance which in small quantities is essential for growth. Copper is a good example of this, being essential for growth, but in excess causing liver and kidney degeneration.

Treatment of poisoning is difficult. Sometimes there are specific antidotes, but more often all that we can do is treat the symptoms (e.g. scouring) and hope that the cow can overcome and excrete the toxin herself.

Physical injury

Many of the cattle ailments we have to deal with are the result of physical trauma. The best example is lameness. Hoof and limb disorders are frequently associated with either trauma to the foot, for example prolonged standing on a hard surface producing sole ulcers, or damage to the leg, for example resulting in dislocation of the joint or even fracture of a bone.

Examples of other physical injuries include:

Teat damage

Haematomas (blood blisters under the skin)

Skin cuts

Foreign bodies, e.g. barley awn or grass seed in the eye

Burns, either caused by fire or sunburn

Chemical injury, e.g. tank cleaner mistakenly used for teat dip

Abscesses (following penetration of the skin by thorns, nails, fragments of metal, etc.)

Congenital disorders

Congenital diseases are abnormalities that are present at birth. They may be caused by i) genetic factors, i.e. inherited, or ii) by ingestion of teratogens (= chemicals which lead to foetal abnormalities) during pregnancy.

Genetic defects

The incidence of inherited genetic defects in cattle is said to be quite high (one in 500 births), but as at least half of the calves are stillborn, they do not represent a major problem to the cattle industry. Typical examples include cleft palate (Plate 1.2), harelip (Plate 1.3), spina bifida (Plate 1.4), a very small tail or no tail at all (hypoplastic tail, Plate 1.5), atresia ani (no anal opening), contracted tendons (Plate 1.6), hydrocephalus, brachygnathia (parrot mouth, Plate 1.7) and umbilical hernias (Chapter Two). Some inherited defects have a secondary effect; for example cows with CVM, congenital vertebral malformation (Plate 1.8) have an obvious underdeveloped and kinked tail, and commonly have reduced fertility. If it is found that a particular bull is throwing a high incidence of calves with genetic defects, he should be culled. Sometimes the defect is only seen when a bull mates with a particular cow. In this case the defect is said to be caused by a recessive gene, in that the defect will only appear if both the sire and dam are carrying the gene for that defect.

Plate 1.2 Cleft palate. This calf could not even suckle and was destroyed. Where the defect in the hard palate is smaller, the cow’s teat may cover the hole during suckling and it is only when the calf starts eating solid food, or drinking from a bucket, that a severe nasal discharge indicates that something is wrong.

Teratogenic defects

Teratogenic defects are congenital abnormalities resulting from exposure to toxic agents during pregnancy. The toxic agents can be drugs, plants or infections, especially viruses.The most publicised example of this must be the effect of thalidomide in man, which resulted in the birth of deformed children. In cattle, ingestion of some species of the plant Lupinus can produce crooked calf disease, where calves are born with malpositioned legs, either excessively flexed or excessively extended.

Plate 1.3 Harelip (also called cleft lip or primary cleft palate). This can also make suckling difficult, although this calf was able to drink from a bucket.

Plate 1.4 Spina bifida. The tops of two lumbar vertebrae have not closed, leaving a hole into the lumbar spine, seen here as a red area. This calf was partially paralysed in the hind legs and had to be culled.

Plate 1.5 No anus and minimal tail (anal atresia and coccygeal hypoplasia). Calves with a totally blind anus rapidly develop abdominal distension, severe pain and colic. This calf was lucky and faeces were passed through the vagina. No tail or a shortened tail is commonly seen on its own without anal atresia.

Plate 1.6 Contracted tendons at the fetlock, as in this calf, are common, particularly in larger calves. They will correct in time without treatment.

Plate 1.7 Brachygnathia (parrot mouth or overshot upper jaw) is most commonly seen in stillborn calves.

Plate 1.8 CVM, congenital vertebral malformation; note the underdeveloped and twisted tail. Affected cows often have reduced fertility.

Plate 1.9 BNP, bovine neonatal pancytopaenia. Affected calves bleed from multiple points in the body, including the gums, as they are deficient in blood platelets.

Plate 1.10 Cerebellar hypoplasia. Although this calf appeared normal and healthy at rest, as soon as it tried to feed or stand it fell over and its head went into spasm over its back (opisthotonos). BVD and neospora are possible causes.

Plate 1.11 Cerebellar hypoplasia. The cerebellum (C) is the part of the brain which controls balance.

The oral ringworm treatment griseofulvin has been withdrawn from use because of the risk of producing deformed, full-term calves.

A more recent congenital condition is bovine neonatal pancytopaenia, BNP, which is thought to arise as a result of components of colostrum producing an almost total deletion of platelets, and subsequent death from blood loss. The condition is seen within the first few days of life, and calves will bleed from a range of sites, including injection sites (Plate 1.9). In this calf the bleeding has stopped, leaving raw areas devoid of hair. There were marked haemorrhages on its gums. If a calf develops BNP, subsequent calves from the same cow should be fed stored colostrum from another dam.

Infection of mid pregnant cows with BVD (Chapter 4) and Schmallenberg viruses can lead to birth defects. BVD can result in cerebellar hypoplasia, where part of the brain (the cerebellum) is far too small (Plate 1.11) and the affected calf is unable to stand. The calf in Plate 1.10 is a typical example. At birth it was unable to stand or suckle and when lifted it pushed its head back over its back (opisthotonos). Mid pregnancy infection with Akabane Schmallenberg or BVD viruses can cause arthrogryposis (Plate 1.12), a condition in which the hind limbs become fused or deformed.

Not all congenital abnormalities are immediately apparent at birth. Strabismus is a good example. Plate 1.13 shows a Hereford heifer with bilateral convergent strabismus; that is, both eyes (bilateral) point inwards (convergent) with a squint (strabismus). This condition gets progressively worse as the calf gets older and in some instances results in almost total blindness. In one unfortunate incident I dealt with, a dairy farmer purchased a freshly calved heifer with strabismus. A few weeks after purchase she had a bad fright and ran off. Because she could not see very well she became totally disoriented and finished up by drowning in the slurry pit. Fortunately, relatively few congenital defects have such a dramatic ending!

Other congenital defects causing blindness include cataracts (Plate 1.14) and microphthalmia or anophthalmia (very small or no eyes, Plate 1.15).

Plate 1.12 Arthrogryposis. The hind legs are fixed in this extreme flexion position and cannot be moved. Often the pelvis is also involved (when a caesarean birth is necessary). This calf also had spina bifida. Arthrogryposis can be either teratogenic in origin, e.g. in utero infection with Schmallenberg, or inherited.

Plate 1.13 Strabismus (squint). Note how the eyeball is protruding and pointing in towards the nose. Both eyes were affected. This is a progressive condition which can eventually lead to blindness.

Cataracts are an opacity of the lens. They can be hereditary or caused by BVD infection of the dam during late pregnancy. Most cataracts are left untreated and calves seem to manage with very limited or zero vision, although the cataract is often in the centre of the lens only, so that as the eye enlarges with growth the animals may well develop some peripheral vision. Treatment is possible. A very fine knife is inserted between the cornea and sclera (the clear and white parts of the eye) and one or two cuts are made across the front of the lens. The aqueous humour (the liquid in the front part of the eyeball) then slowly dissolves away the lens until sight has been restored.

Plate 1.14 A cataract is an opacity of the lens. The centre of the eye has a blue appearance, as in this calf.

Plate 1.15 Microphthalmia. In this Gloucester calf, born with the eye almost totally absent, the defect was related to a particular bull.

See Chapter 4 for other eye disorders.

Defences against Disease

Animals (and also man) are continually exposed to a range of infectious and other agents which could potentially cause disease, but fortunately disease occurs relatively rarely, i.e. we may become infected with a disease agent, but not affected by it. This is because we all have a range of excellent defence mechanisms which afford a degree of protection against moderate challenge. These defences will be outlined briefly in the following section and can be subdivided into:

Physical barriers

– skin

– respiratory passages

– digestive tract

– eye mechanisms

– commensal bacteria

Chemical barriers

– acid in the stomach

– alkaline in the intestine


The body has an excellent ability to recognise materials which are ‘foreign’ – that is, materials which are not part of itself – and to control them. At the same time it has to recognise those tissues which are part of itself and leave them alone. The mechanism for dealing with ‘foreign invaders’ or ‘non-self’ materials has two components, namely:

– cellular mechanisms: certain cells, e.g. lymphocytes and macrophages, are able to recognise and engulf infectious and other foreign agents

– humoral mechanisms: a system of ‘active’ proteins, most commonly known as antibodies, assist in the detection and destruction of non-self tissue

In addition, there are two categories of both cellular and humoral defence systems:

– innate systems: these exist in all animals and do not rely on previous exposure to an infection

– induced or acquired systems: these come into play after an animal has been exposed to an infection

Following exposure, the precise characteristics of the invading organism are remembered and the body produces specific defences against it, using both cells and antibodies. These are then preformed and ready to attack the invader if it manages to gain entry into the body for a second time. This is the nature of vaccines. They give the unexposed animal a mild or dead form of the infection. The animal then manufactures huge quantities of specific defence materials (both antibodies and cells) and is able to repel an invasion by that infection. Different vaccines are needed for each disease.

Physical and chemical defences

The skin must be the best example of a physical barrier. It consists of a thick layer of epithelial cells, with a dead and keratinised (or reinforced) surface. It is certainly a hostile environment for viral or bacterial multiplication. Should the skin get very wet or dirty, however, or if it is broken by physical damage, then bacteria may gain entry, the infection may become established and pus or abscesses may form. Bacteria retard healing and this is why wounds and cuts should always be cleaned and washed with antiseptic, thus preventing the bacteria from multiplying. Pus is an accumulation of dead white blood cells, dead body cells and fluid from animal tissue and bacteria. Skin is also covered by a film of fatty acids which help to prevent bacterial multiplication. Excessive washing, especially with detergents, removes these acids and thus renders the skin more susceptible to infection. This is of particular relevance to teats, and is one reason why chapping is so common unless emollients are added to the teat dip.

The air passages (trachea, bronchi, etc.) and the intestine can be termed external surfaces because they come into contact with materials (air and food) from outside the animal’s body. In the nose there are hairs which prevent large particles from being inhaled into the lungs. Their function is supported by a microscopic layer of cilia. These small, finger-like projections, which line the surface of the trachea, move in a wave motion to propel bacteria and other smaller particles back up towards the mouth (a process known as the mucociliary escalator), where they can be swallowed or coughed away. In addition mucus glands produce a sticky secretion to line the airways, thus trapping any bacteria or viruses which happen to land and this prevents them from reaching the susceptible tissues of the lungs. These mechanisms are described in detail in Chapter 3.

The mouth and oesophagus have a similar thick keratinised lining, like skin, and this helps to prevent bacterial penetration. The stomach, on the other hand, produces mucus and acid, partly to assist digestion, but also helping to prevent bacterial growth, whereas the upper small intestine is very alkaline, again inhibiting bacterial growth. These extremes of acid and alkaline conditions should perhaps be considered as chemical rather than physical defence mechanisms. Vaginal secretions are also acid.

The eye has some interesting and rather unique defences. The eyelids close rapidly when an object is approaching, and this protects the eyeball from physical damage. If a foreign body does land on the eye, however, tears are produced to wash it away and rapid blinking helps to move the object to the corner of the eye where it will cause less damage. If the surface of the eye does become damaged, blood vessels grow across the cornea to supply antibodies and rebuilding materials. This is known as pannus formation, and is described in more detail in Chapter 4.

The final type of physical defence is provided by the bacteria that normally live in and on the animal as ‘commensals’; that is, they live there without causing disease. However, they compete with disease-causing (pathogenic) infections for both nutrients and space. If these normal microbe populations are disturbed, for example by a prolonged course of antibiotics by mouth, it is possible that the more serious pathogenic infections may proliferate and cause disease. This is why it is often recommended that yoghurt or other probiotics are given at the end of a course of calf scour treatment – to recolonise the gut with ‘healthy’ bacteria. Similarly the presence of C. bovis and coagulase negative staphylococci (CNS) at the teat end reduce the probability of an E. coli mastitis infection from becoming established.

The immune system

As stated above, the immune system can be subdivided into two parts, cellular immunity and antibodies, although within the animal the two systems will work very much in conjunction with one another to counteract disease. Although I shall be dealing with the immune response to disease-causing organisms, the reader should appreciate that an identical immune reaction is evoked against any material which the animal recognises as being foreign to its system. This is very important in the human fields of allergy and organ transplant rejection. Any material which the animal recognises as foreign is called an antigen, and antigens evoke both a cellular and an antibody response. Immunity consists of both innate and induced components.

Innate immune mechanisms

Cellular responses

The most common cells involved with innate immunity are neutrophils and macrophages. Both engulf and destroy invading infectious agents by a process known as phagocytosis. Neutrophils and macrophages are therefore sometimes collectively known as phagocytic cells, or simply as phagocytes.

The process of phagocytosis is shown diagrammatically in Figure 1.3. Neutrophils are commonly present in blood, whereas macrophages can be found in milk and other secretions. Macrophages are a type of ‘bobby on the beat’. When they see something they don’t like, they ‘arrest it’ (engulf it) and at the same time send out a signal, which mobilises a ‘rapid reaction force’ of highly active neutrophils. The neutrophils then continue with the process of phagocytosis and destruction.

The body’s defences against infection are:

Physical barriers

Chemical barriers

The immune system

– antibodies (humoral mechanisms) and cells

– innate and induced systems

Macrophages (and cancer cells) produce matrix metalloproteinases (MMPs). These enzymes dissolve body tissue and allow the macrophages to pass between the body cells in their search for foreign invaders. MMPs also allow cancer cells to penetrate. Another important function of macro phages is that they can also hold the invading antigen in a very specific manner. They then present it to the lymphocytes (another form of white blood cell) of the induced immunity system, to ensure that the lymphocytes will recognise it in the future.

Figure 1.3 Phagocytosis, the process by which an animal cell recognises and then engulfs and destroys foreign substances such as bacteria and viruses.

Humoral response

The humoral part of the innate immune system consists of proteins such as complement, interferon and lysozyme. Complement coats the outside of invading agents, in a process known as opsonisation. This makes the invading organism more easily engulfed by macrophages. Interferon is best known for its effect against viruses, but it also has a role in neutralising toxins. Lysozyme is a form of ‘natural antibiotic’ and is highly active in killing certain bacteria, for example Strep. uberis.

Induced immune mechanisms

This also has cellular and humoral components, but each cell and each antibody is highly specific to the invading agent. The induced immune system differs from the innate immune system, in that the induced system must have had previous exposure to an antigen in order to be effective, whereas the ‘innate’ system does not require prior exposure for recognition.

Cellular response

The cellular response of the induced immune system is often referred to as cell mediated immunity. The major cells are lymphocytes.

There is a range of different lymphocytes. They all produce antibodies, but some may have additional functions and means of recognising and destroying invading antigens.

T lymphocytes, including killer T cells, recognise foreign cells, for example cancer cells and tissue transplants in man. Cells which are infected with virus will also be recognised and destroyed by the killer T lymphocytes. ‘Helper’ T lymphocytes (also known as T4 cells) hold the invading antigen so that it can be recognised by B lymphocytes. Each B lymphocyte (also known as a plasma cell) has thousands of recognition sites on its surface.

To return to our police force analogy, macrophages and T lymphocytes hold invading antigens (‘suspects’) and present them to B lymphocytes (‘policemen’), thus enabling the suspect’s ‘fingerprints’ to be taken. Each lymphocyte carries up to 100,000 different fingerprints. Considering there are millions of lymphocytes, this makes the total number of combinations almost infinite. Each recognition site is different for every individual invading antigen. When a lymphocyte meets up with its specific antigen, two things happen:

First, that single lymphocyte multiplies rapidly, producing clones of other identical lymphocytes which are immediately able to recognise that specific invader in the future

Secondly, these lymphocyte clones then produce antibodies, namely specific proteins to neutralise the invader

It is interesting to note the numbers of cells which are involved. In an adult dairy cow approximately 8% of its bodyweight is blood; that is, 48 litres for a 600-kilo cow. An average cow has around 7000 white blood cells per millilitre of blood, approximately 35% of which are lymphocytes, which means there are 2450 lymphocytes per millilitre of blood, or 117,600,000 lymphocytes in total! This only counts the lymphocytes in the blood. Lymphocytes are continually able to move out through the walls of the blood vessels into the extracellular fluid space, across to lymph nodes and then back into the blood again, all the time looking for ‘foreign invaders’.

Humoral response

Antibodies are large protein molecules produced by lymphocytes and their derivative plasma cells to combine with, and hence neutralise, the invading agents. The most interesting feature of antibodies is that they are very specific. Whereas the other defence mechanisms we have discussed so far will be effective against any bacteria, viruses or even dust, there has to be a separate and specific antibody for every type of infectious agent. Thus antibodies effective against one type of E. coli bacteria may not have any action against a slightly different strain of E. coli.

Antibodies work by precisely fitting the shape of the invading antigen, for example, bacteria or virus. This is shown in Figure 1.4. The resultant complex neutralises the antigen, rendering it inactive and no longer capable of further invasion of body tissue. In addition, the antigen/antibody complex is more easily phagocytosed by macrophages. The ‘fit’ of antibody to antigen needs to be precise to be effective. Some of the less effective vaccines may produce antibodies which are not exactly the correct shape. Although they may be able to ‘arrest’ some of the invading infection, other ‘invaders’ are able to break free and still cause damage. This is shown in Figure 1.5.

Figure 1.4 Antibodies are proteins. They work by fitting precisely into the shape of an invading antigen, thereby neutralising it.

Antibodies are acquired by the animal in two separate ways known as active and passive. Active immunisation is the process whereby the animal produces its own antibodies following exposure to an antigen. The cow can also produce antibodies and supply them preformed to the calf during the first few hours of its life via colostrum. Because the calf has not produced these antibodies itself, they are called passive and they provide immediate protection against infections present in the environment. There are four classes of antibody, but only one class, the IgG, is absorbed across the gut wall by the calf. The classes are:

IgG – Comprises around 80% of serum antibody. It is the major component to cross the placenta in some mammals (but not in cattle) and is absorbed across the gut wall from colostrum

IgM – Is especially against toxins, e.g. tetanus, anthrax and botulism. It comprises around 20% of serum antibody, and is the first antibody to be produced in response to an antigen

IgA – Present in low concentrations in serum but higher levels are found in secretions in the respiratory and digestive tract, milk, saliva, bile, tears, etc. It is not absorbed across the gut wall from colostrum

IgE – Responsible for allergic reactions. In response to an allergen it binds to the surface of basophils and mast cells (specialised types of white blood cells), leading to the release of vasoactive amines such as histamine and serotonin

Before an animal can produce its own active antibody against a particular infection, it must have been exposed to that infection at some time in the past, recognised it as foreign (viz as an antigen) and stored the information in a type of memory, ready to produce antibodies to overcome subsequent challenges. This initial exposure may be by vaccination, but it is much more likely to be the result of natural infection. A low dose of disease organ isms, which is not sufficient to cause visible symptoms, will be quite adequate to stimulate antibody production and provide active immunity. This process is occurring throughout the animal’s life, and re-exposure to infections helps to boost immunity levels.

Figure 1.5 If the antibody is a poor fit (i.e. not totally specific) as in B, the antigen may break free and continue to cause damage to the host.


Vaccines will be used when there is a risk of a heavy challenge from a specific infection, and especially if the animal has not had previous exposure to that infection. A vaccine consists of the infectious agent which has been altered in some way. When administered to the animal it stimulates the processes of recognition and antibody production, but it cannot cause disease. Vaccines may either be living, when only one dose may be required, or dead, when two doses will be needed at an interval of approximately four weeks. The presence of passive immunity – that is, antibodies acquired from the mother – may prevent the young animal from responding to the vaccine and this is why the instructions may state that animals under a certain age should not be vaccinated, or perhaps that if young animals are vaccinated, then an additional dose may be necessary at a later date. The period during which passive immunity persists varies enormously and depends on both the amount of colostrum ingested and the type of infection. For example, with gut infections such as rotavirus, passive (= colostral) antibodies persist for 7–14 days; for pneumonia infection passive antibodies persist for two to three months; and for some infections such as BVD and leptospirosis passive antibodies may persist for six months.

Vaccination of the calf should therefore be carried out at an age where the period between passive and active protection is minimal, but not so early that there is a risk of a poor vaccine ‘take’ due to persistence of passive colostral immunity.

Antibody titres

Antibodies are very specific: there is a group of antibodies for infection A, another group for infection B and so on. The level, or concentration, of antibody in the blood is referred to as the antibody titre. This may be expressed as

Clearly the animal with a titre of 1:1500 has more antibodies to a particular disease than the animal with a titre of only 1:50.

The titre tells us nothing about the source of the antibody. It could be

From colostrum – in which case the titre would slowly decline as the antibodies become worn out

From a recent infection – in which case the titre would be rising, with the antibody-producing lymphocytes being in a production mode, having just been exposed to infection

From an old infection – in this case the titre would be slowly declining, unless there was a more recent exposure to the same infection, when the antibodies would start to rise again

Antibody titres are sometimes used to diagnose the cause of disease, for example calf pneumonia. If a blood sample is taken as soon as the calf is seen to be ill, then the antibody level to whatever is causing the disease is likely to be low (unless there is still some colostral antibody remaining). A second blood sample is taken two to three weeks later, by which time the amount of antibody to the infectious agent producing the high temperature should have increased considerably. The two blood samples (often referred to as ‘paired sera’) are then tested for antibody levels to a range of possible infections, for example RSV, IBR and PI3 in the case of respiratory disease. The virus which shows a significant increase in antibody titre between initial infection and three weeks later could be the cause of the disease.

It is because of antibodies and other defence mechanisms that an animal can have bacteria living in it without succumbing to disease. The animal is said to be ‘infected’ but not ‘affected’. The situation can rapidly change, however, for example if we mix groups of calves from different sources. Calves from farm one may be carrying infection A and will have antibodies to A. Calves from farm two may have infection B and the corresponding B antibodies. When the two groups are mixed, calves from farm one will be exposed to infection B, but they only have antibodies to A. If the dose of B infection is large enough (for example if the groups were mixed and crowded into a poorly ventilated building), then B disease may occur in farm one calves before they are able to build up sufficient antibodies against B for protection. This is shown diagrammatically in Figure 1.6.

Stress and the immune system

Environmental stress in cattle (and all farm animals) is a major problem, because it decreases the functional capacity of the immune system. Put another way, we have discussed the many remarkable ways in which an animal is able to counteract invasion by disease agents. However, if an animal is ‘stressed’, then these defence mechanisms simply do not work as effectively. Stress leads to the release of hormones such as adrenalin and cortisone, adrenalin preparing the animal to run away, cortisone specifically reducing the activity of its immune mechanisms. So what is stress? Examples of stress leading to a reduced immune response include:

Poor nutrition, including specific deficiencies of vitamins and minerals

Overcrowding, for example the lack of a loafing area. Animals are unable to move away from one another to find any ‘personal space’

Fear, for example young heifers introduced into a large dairy herd

Uncomfortable accommodation. Perhaps heifers that are not cubicle trained lie outside on hard, wet concrete

Poorly ventilated cubicle buildings, with condensation dripping onto the cows’ backs, are also a stress

Rough and unsympathetic handling: driving cattle hard, using dogs or tractors, all produce fear, and this increases the risk of disease

Excessive noise: this might be important for cows in a milking parlour, although they do become accustomed to loud noises if it’s consistent

Transport. Transport stress is interesting. Experimentally it has been shown to cause an increase in antibodies but a decrease in cytotoxic

T cells, i.e. the lymphocytes that destroy virus-infected cells. This is probably one reason why animals succumb to virus infections after transport

Competition for food or water

Concurrent diseases, e.g. chronic lameness or rumen acidosis

Weather, especially heat stress. Temperatures above 25°C (and especially when humidity is high) have been shown to decrease the white blood cell count and therefore compromise the immune response

Calving. Both the cow and calf have a poor immune response for the first week after calving and should therefore be housed and managed to minimise further stress. Stress in heifers is also discussed in Chapters 6 and 9

Not only will the above environmental influences reduce the animal’s resistance to disease, but, perhaps equally important, they can reduce the effectiveness of vaccines. In other words, a stressed animal will not respond as well to vaccination.

Figure 1.6 Specificity of antibodies. Calf A can exist in the presence of infection A because it has antibodies to A. Similarly calf B can exist with infection B. Problems occur when the calves are mixed. Calf A may be totally overwhelmed by infection B before it has had time to develop antibodies to it.

Inflammation and hypersensitivity

We have seen that when a foreign virus or bacterium invades the body, there is a response in terms of cells and antibodies. To increase the effectiveness of this response the body assists as follows:

Blood flow to the area increases

The blood vessels in the area dilate, so more cells to get to the ‘invader’

Small holes appear in the walls of the blood vessels, allowing cells and plasma (the fluid part of blood) to leak out into the affected area

Plasma contains fibrin, which coagulates to form a ‘sponge’ effect. This is important to prevent blood loss if the animal has been injured, but it is also important in that bacteria and viruses stick to the ‘sponge’, where they are then attacked by the host cells

Externally these changes are seen as inflammation, i.e. heat (increased blood flow), swelling (blood vessel dilation and plasma leaking into the tissue) and discomfort. Although the changes may be beneficial in counteracting infection, the discomfort to the animal may produce further clinical signs, for example inflammation in a leg due to entry of infection produces lameness.

Sometimes the inflammatory response can be so marked that it can be detrimental to the animal, or may even be the cause of death. Probably the best example of this is in the lungs. Infection entering the lungs may produce such a marked inflammatory response, especially in terms of release of plasma, that the animal ‘drowns’ in the excess fluid and suffocates. In this instance we would need to give specific drugs (anti-inflammatory agents) to slow down the inflammatory response and to promote recovery.

On other occasions an animal over-reacts to the presence of a foreign invader, for example to a drug or vaccine injection. The immune system throughout the body may start to react and the animal will be seen shivering and shaking, perhaps frothing at the mouth, and eventually collapsing and possibly dying. This is known as an allergic or anaphylactic reaction and we say that the animal has a hypersensitivity to that particular invading antigen.

The Balance of Disease

As we have described the types of infectious agents and the physical and immune defence mechanisms of the animal, their interaction can now be examined and related to the production of disease. Take a case of human typhoid. The disease itself does not matter and the figures used are not accurate, but it serves to illustrate the point very well. Putting one typhoid bacterium on the tongue of a healthy person would probably have no effect on him at all. Give him a hundred bacteria and he may feel rather off-colour and would probably get diarrhoea. Using a dose of a thousand bacteria, our ‘guinea-pig’ would develop a severe illness, with sickness, diarrhoea and generalised symptoms.

Now if this particular man had been drinking heavily, had lost his way home and had spent 24 hours in the cold without food and was suffering from exposure, in this case we would expect different results. Possibly one bacterium would cause mild diarrhoea, a hundred would cause a severe illness and a dose of a thousand might be fatal.

This simple example serves to illustrate two extremely important points, namely that the severity of a disease is dependent upon:

The dose of infection received

The state of health of the infected animal

This is extremely common in animal disease, where there is often a multiplicity of factors affecting the severity and spread of a condition. It is more easily understood by saying that health and disease are on each side of a balance, with the animal acting as the pivot of that balance. One of the best diseases to illustrate this point is enzootic pneumonia (sometimes called virus pneumonia) of calves, although E. coli and the other causes of environmental mastitis would serve as equally good examples. This is illustrated in Figure 1.7. Along each arm of the balance various items can be ‘hung’ which will either boost health or exacerbate disease. Provided the animal can be maintained with the balance in the level position, it can cope quite happily with infection, living with it but suffering relatively few adverse effects. This is the basis of preventive medicine. There is a risk of disease occurring on every farm, and so it is necessary to take various husbandry and other preventive measures to minimise those risks.

Figure 1.7 The balance of disease, using calf pneumonia as an example.

Principles of Treatment

Treatments needed for each condition are given throughout the book. Only outlines of treatment are described, because drug availability changes very quickly and it is likely that any text on treatment will be out of date before it is even published!

This section describes a general approach which could be applied to the treatment of any animal. Treatment may be divided into:

Specific drug treatment

Supportive therapy


Specific drug treatment

If the disease under consideration is caused by an infectious agent, then it is likely that there is a drug is available to kill, or at least neutralise, that agent. For example:

Bacteria – use antibiotics

Viruses – no specific drug therapy is available

Protozoa – use specific antiprotozoal drugs

Fungi (yeasts and moulds) – use specific antifungal drugs

Worms – use anthelmintics

Ectoparasites – use insecticides such as pyrethroids or avermectins


Antibiotics are chemicals which destroy bacteria but have little or no adverse effect on the animal. Some act by actively killing the bacteria (e.g. penicillin, which damages their outer membrane) and these are called bacteriocidal antibiotics. Others simply prevent bacterial growth and multiplication (e.g. tetracyclines interfere with bacterial protein synthesis) and the bacteria then either die at a normal rate or are killed by the animal’s defence mechanisms. These are known as bacteriostatic antibiotics.

Theoretically bacteriocidal and bacteriostatic antibiotics should not be used simultaneously in an animal, since one might counteract the effects of the other. This is because the bacteriocidals work best against rapidly growing and dividing bacteria, whereas bacteriostatics actually inhibit bacterial growth and multiplication. The animal’s immune defence mechanisms are likely to be severely impaired and unable to destroy bacteria, for example after calving or as a result of toxaemia, then it is probably best to use a bacteriocidal rather than a bacteriostatic drug. Bacteriocidal antibiotics are also used in the treatment of endocarditis. However, the distinction is not that precise, in that some antibiotics are bacteriostatic when used at low doses, but are bacteriocidal when given in large amounts.

Different antibiotics are effective against different types of bacteria. Some, for example the tetracyclines, flouroquinolones, cephalosporins and chloramphenicol, are known as broad-spectrum antibiotics and are effective against most organisms. Others, such as penicillin, are only effective against staphylococci, streptococci and a few other groups. Even then, certain strains of staphylococci produce penicillinase which destroys penicillin and thus prevents its action. These strains of staphylococci are called penicillin resistant. (This is discussed in more detail in Chapter 7.) Even when the correct antibiotic has

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