mastitis control in dairy herds

Mastitis Control in Dairy Herds, 2nd Edition

The authors would like to thankJane Upton for supplying the line drawings.

Mastitis Control in Dairy Herds,2nd Edition

Roger BloweyBSc, BVSc, FRCVS

Wood Veterinary GroupThe Animal Hospital

GloucesterUK

and

Peter EdmondsonMVB, Cert. CHP, Dip. ECBHM, FRCVS

Shepton Veterinary GroupShepton Mallet

SomersetUK

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First edition published in 1995 by Farming Press Ltd.ISBN 978 085236 314 0

A catalogue record for this book is available from the British Library, London, UK.

Library of Congress Cataloging-in-Publication Data

Blowey, R.W. (Roger William)Mastitis control in dairy herds/Roger Blowey and Peter Edmondson. -- 2nd ed.

p. cm.Includes bibliographical references and index.ISBN 978-1-84593-550-4 (alk. paper)1. Mastitis--Prevention. I. Edmondson, Peter, 1958- II. Title.

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Contents

1 Introduction 12 Structure of Teats and Udder and Mechanisms of Milk Synthesis 53 Teat and Udder Defences Against Mastitis 204 The Mastitis Organisms 335 Milking Machines and Mastitis 606 The Milking Routine and its Effect on Mastitis 957 Teat Disinfection 1168 The Environment and Mastitis 1309 Somatic Cell Count 152

10 Bactoscan and Total Bacterial Count (TBC) 17111 Targets and Monitoring 18412 Treatment and Dry Cow Therapy 19413 Summer Mastitis 21514 Disorders of the Udder and Teats 22015 Residue Avoidance in Milk 23916 Best Practice Guides 248

Appendix: Liner Life Charts 253Appendix: Parlour Audit 255References and Further Reading 256Index 259

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The aim of this book is to explain the manydifferent factors which lead to mastitis andpoor milk quality. If the farmer, vet or herds-man appreciates the way in which mastitisoccurs, then he will be in a much better pos-ition to understand and implement the con-trol measures required. Mastitis can never beeradicated. This is because environmentalinfections such as Escherichia coli (E. coli)will always be present.

It is also highly unlikely that a singleall-embracing vaccine will ever be found tosuppress the multiplicity of types of infec-tion involved. Control must therefore bebased on sound management, and this orig-inates best from a thorough understandingof the principles of the disease involved.

The primary objective of this book is toachieve a thorough understanding of masti-tis. If this results in a reduction in the inci-dence of infection, and in so doing benefitsboth the economics of dairy farming and thewelfare of the cow, then the authors will bewell pleased.

What is Mastitis?

Mastitis simply means ‘inflammation of theudder’. Most farmers associate mastitis withan inflamed quarter together with a changein the appearance of the milk. These changes

are due to the effect of the cow’s inflamma-tory response to infection. However, mastitiscan also occur in the subclinical form. Thismeans that although infection is present inthe udder there are no visible externalchanges to indicate its presence.

Much of the information needed toreduce the incidence of mastitis has beenavailable for the last 30 years. Research workcarried out during the Mastitis FieldExperiment (MFE) trials at the NationalInstitute for Research into Dairying (NIRD)in the 1960s formed the basis of the impor-tant mastitis control measures used today,including the proven five-point plan, whichrecommended:

1. Treating and recording all clinical cases.2. Dipping teats in disinfectant after everymilking.3. Dry cow therapy at the end of lactation.4. Culling chronic mastitis cases.5. Regular milking machine maintenance.

Over the past 40 years, great progress hasbeen made in reducing cell counts, mainlydue to the uptake of the five-point plan bydairy farmers. In the UK, the clinical inci-dence of mastitis has decreased from 121cases per 100 cows per year in 1968, tobetween 40 to 50 in 2009. One case is onequarter affected once.

1©CAB International 2010. Mastitis Control in Dairy Herds (R. Blowey and P. Edmondson)

1 Introduction

What is Mastitis? 1Economics of Mastitis 2What are Realistic Production Targets for the Future? 3

There are two basic types of mastitis:contagious and environmental. The greatestprogress has been in reducing the incidenceof contagious mastitis. Cell counts (alsoreferred to as somatic cell counts, or SCCs)relate to the level of contagious infection andso the effect of this progress can be seen inthe decrease in the national average cellcount of milk in England and Wales from571,000 (571,000/ml) to around 240,000 in2009. This is shown in Fig. 1.1.

The aim now is to further reduce conta-gious mastitis and cell counts, and also toreduce environmental infections. The inci-dence of environmental mastitis hasremained unchanged since 1960. This islargely due to an increase in herd size andhigher milk yields. Milk yield is correlated tothe speed of milking, and flow rates havedoubled over the past 40 years. Over the sameperiod, faster milking speeds have led to a 12-fold increase in mastitis susceptibility.

It is therefore a credit to farmers thatthey have improved the cow’s environmentand hygiene sufficiently to have preventedan increase in the clinical mastitis incidenceover this period. As yields are likely toincrease further in the future, the risk of newinfections will continue to rise.

Mastitis leads to a reduction in the use-ful components of milk and increases thelevel of undesirable elements. This is, ofcourse, exactly the opposite of what thedairy farmer is trying to achieve. Overall,mastitis results in a less acceptable product

and so the value of this milk is muchreduced.

Table 1.1 shows the effect of subclinicalmastitis (i.e. raised cell count) on variousmilk components. It indicates that the yieldof lactose and casein is reduced substan-tially. While the total protein level remainslittle changed, the level of casein isdecreased by up to 20%. This is of great sig-nificance to dairy manufacturers, especiallycheese makers, as it reduces the manufac-turing yield from milk. The changes in but-terfat and lactose levels are of greateconomic significance to the farmer as theymake up the basis of his milk price. Mastitismay cause a reduction in butterfat and pro-tein, lowering the price of milk by up to15%. This will have quite an effect on profit.

Mastitis also produces increased levelsof the enzymes lipase and plasmin, whichbreak down milk fat and casein respectivelyand therefore have a significant effect onmanufacturing yield and keeping quality.These elements are of utmost concern tomilk buyers and in the future it is possiblethat milk will be tested for plasmin andlipase and producers penalized for high lev-els of these enzymes.

Economics of Mastitis

Mastitis affects the farmer economically intwo ways: through direct costs and indirectcosts.

2 Chapter 1

100

1970 1975 1980 1985 1990 1995 2000 2005 2009

200

300

400

SC

C x

100

0/m

l

500

600

Fig. 1.1. Annual average cell count (level of contagious mastitis) for England and Wales, 1970–2009.

Direct costs:

1. Discarded milk.2. Drug and veterinary costs.

Indirect costs:

1. Penalties because of increased cell count.2. Decreased milk yield during remainder of

lactation due to udder damage and/orsubclinical infection.

3. Extra labour requirements for treatingand nursing.

4. Higher culling and replacement rates,leading to loss of genetic potential.

5. Deaths.

The costs of a clinical case of mastitis havebeen quantified: in 2009 it was estimated thatthe average cost of one case of mastitis wasbetween £100 and £200. An average cost of£125 is a well-accepted figure for 2009.

This work assumed that there were threecategories of mastitis: mild, severe and fatal.The most common form of mastitis is themild case, which responds quickly to farmertreatment. The costs here include intramam-mary tubes, discarded milk and a reducedyield for the remainder of the lactation. Asevere case of mastitis requires veterinarytreatment, while not only does a fatal case ofmastitis require veterinary treatment but alsothe cow never returns to the milking herd.

In addition to the cost of mastitis, thereare extra risk factors that should be consid-ered. These include high total bacterial counts(TBCs) or Bactoscans, and the risk of antibi-otic residues entering the bulk milk supply.Both of these incur financial penalties.

The majority of the losses in high cellcount herds are from subclinical infectionresulting in depressed production andreduced yields of lactose, casein and butter-fat. It is generally accepted that herds with acell count of 200,000 or less will have no sig-nificant production losses due to subclinicalinfection. For every 100,000 increase in cellcount above 200,000, there will be a reduc-tion in yield of 2.5%. This reduction,together with financial penalties imposed forelevated cell counts, can be quite substantial.

The average incidence of clinical masti-tis in the United Kingdom in 2009 wasbetween 40 and 50 cases per 100 cows peryear, ranging from some herds with levels aslow as ten to others with up to 150 cases per100 cows per year.

What are Realistic Production Targets forthe Future?

The consumer and the dairy companies arerequiring milk of increasing quality. In thefuture, dairy companies will continue to

Introduction 3

Table 1.1. The effect of mastitis on milk components. (From Philpot and Nickerson, 1991.)

Components Effect of subclinical mastitis

Desirable Total proteins Decreased slightlyCasein Decreased between 6 and 20%Lactose Decreased between 5 and 20%Solids not fat (SNF) Decreased by up to 8%Butterfat Decreased between 4 and 12%Calcium DecreasedPhosphorus DecreasedPotassium DecreasedStability and keeping quality DecreasedTaste Deteriorates and becomes bitterYogurt starter cultures Inhibited

Undesirable Plasmin (degrades casein) IncreasedLipase (breaks down fat) IncreasedImmunoglobulins IncreasedSodium Increased – hence the ʻbitterʼ taste

want low Bactoscan and cell counts, abovewhich producers will incur financial penal-ties. The importance of cell counts to thedairy companies can be seen from the largefinancial penalties that they are imposing.There is an escalating scale of penaltiesimposed for producers with high cell countmilk, with most companies penalizing farm-ers with cell counts over 200,000. Somecompanies penalize farmers up to £300 percow per year for cell counts over 300,000.Producers with a cell count over 400,000 areunable to sell their milk as it exceeds the EUthresholds for milk quality.

The farmer is therefore encouraged tokeep reducing the herd cell count and

Bactoscan, and in so doing will ensure thathe receives the premium price for his milk.This also benefits the consumer and thedairy industry, which will have a qualityproduct with a good shelf life, suitable formanufacturing.

With good herd management it is possi-ble to have an incidence of clinical mastitisbelow 30 cases per 100 cows per year, a herdcell count of under 150,000 and Bactoscansunder 20,000/ml. For ‘problem’ herds thismay take several years to achieve. Meetingthese goals will improve profitability whileensuring a healthy future for both the dairyfarmer and his cows.

4 Chapter 1

This chapter examines the development andstructure of the udder, the structure andfunction of the teats, and mechanisms ofmilk synthesis. The aspects of teat functionthat prevent new infections are discussed inChapter 3.

Structure of the Udder

As shown in Figs 2.1 and 2.9, milk is pro-duced by the cuboidal cells lining the mam-

mary alveoli deep within the mammary gland.Surrounding the alveoli are myoepithelial ormuscle cells (Fig. 2.1).When the stimulus formilk let-down occurs, these cells contract, andthis squeezes milk from the alveoli into theducts. From there milk flows into the glandand teat cisterns where it is ready to be drawnfrom the udder. In higher-yielding cows par-ticularly, there will, of course, be some milkstored in the ducts, cisterns and teats betweenmilkings. The mechanisms of milk synthesisare described on page 15.


2 Structure of Teats and Udder andMechanisms of Milk Synthesis

Structure of the Udder 5Development of the Udder 6

First isometric phase 6First allometric phase 6Second isometric phase 7Second allometric phase 7

Suspension of the Udder 7Rupture of the suspensory apparatus 8

Structure and Function of the Teats 9Supernumerary teats 9Functions of the teats 11Teat size 11The teat wall 11Milk let-down 13Poor milk let-down in heifers 14

Milk Sythesisis and How it is Affected by Mastitis 15Lactose 15Protein 16Milk fat 16Minerals 17

Control of Milk Synthesis 17Milking frequency 18Environmental temperature 18Length of dry period 18

Development of the Udder

The udder (or mammary gland) is derivedfrom a highly modified sweat gland. Assuch, the inside lining of the teats and ductsof the mammary gland is essentially modi-fied skin.

The development of the udder from thebirth of the calf to the start of its first lacta-tion can be divided into four phases:

� First isometric phase.� First allometric phase.� Second isometric phase.� Second allometric phase.

First isometric phase

In the young calf, the growth and develop-ment of the udder proceed at the same rateas the rest of the body, and hence the term‘isometric’, i.e. growing at the same rate.

First allometric phase

There is then a sudden increase in the growth ofthe udder, which as a result begins to developmore rapidly than the rest of the body. Thisphase occurs at approximately 4 to 8 monthsold, i.e. around puberty, and is particularly asso-ciated with peaks of oestrogen occurring eachtime the heifer comes on heat. Development at

6 Chapter 2

Fig. 2.1. The structure of the udder and teat.

Udder

Teat

this stage is primarily of the ducts, whichlengthen and penetrate the pad of fat that occu-pies the site of the udder in the prepubertal calf.Overfeeding at this stage, and prior to it, leads toan excessive pad of fat being laid down at thesite of the future udder. This can causedepressed yields later in life. For example, inone trial (Harrison et al., 1983), two groups ofheifers were reared to produce liveweight gainsof 1.1 kg per day (high) and 0.74 kg per day (con-ventional). Not only did the mammary glandsof the conventionally reared heifers weigh more(40% more) but they also contained much moresecretory tissue (68% more). Gross overfeedingof young heifers is therefore to be avoided. It isthought that a diet high in forage during rearingstimulates greater rumen development andhigher appetite capacity at maturity. Proteinintakes should be high (for example, 18% crudeprotein) and of good quality to promote udderdevelopment, but excess intakes of starchshould be avoided.

Second isometric phase

From after the onset of puberty until thebeginning of pregnancy, the udder againgrows at the same rate as the other bodyorgans.

Second allometric phase

Following conception, udder developmentonce again becomes rapid, with the highestgrowth rate occurring from mid-pregnancyonwards. During this phase the cells of thealveoli especially become more developedand change into a tissue type that is able tosecrete milk.

Suspension of the Udder

The udder consists of four separate mam-mary glands, each with its own distinct teat.There is no flow of milk from one quarter toanother, neither is there any significant directblood flow from one quarter to another. Theblood supply to the udder is massive, withsome 400 litres of blood flowing through the

udder to produce each litre of milk. Add tothis the weight of the secretory tissue and theweight of milk stored and it is easy to seehow total udder weights of 50 to 75 kg areobtained. The reason why all milk should bediscarded when treating one quarter withantibiotics is that antibiotics may beabsorbed from that quarter into the blood-stream, travel around the body and then bedeposited back into one of the otheruntreated quarters. The amount of antibioticinvolved is, of course, relatively small, but itmay be enough to lead to a bulk tank failure.

The suspension of the udder is veryimportant. It is shown in Fig. 2.2 and con-sists of the skin, the superficial lateral liga-ments, the deep lateral ligaments and themedian ligament.

� The skin. This plays only a very minorrole.

� The superficial lateral ligaments. Theseoriginate from the bony floor of the pelvisand pass down the outside of the udder,especially at the front and the sides of the

Structure of Teats and Udder 7

Fig. 2.2. The suspension of the udder.

udder. They branch forwards attaching tothe abdomen (in front) and in the upperleg area to the inner thighs.

� The deep lateral ligaments. These alsooriginate from the floor of the pelvis.Passing down the outside of the udder(but inside the superficial ligaments), theysend small ‘cups’ across within the mam-mary gland and these eventually connectto similar branches from the centralmedian ligament. The largest branchsweeps under the base of the udder, justabove the teats, to join the median liga-ment and provides the major suspensoryapparatus for the udder.

� The median ligaments. There are twomedian ligaments (Fig. 2.2). Both originatefrom the pelvic floor and associatedabdominal wall. They pass down the cen-tre of the udder and the base, where theyseparate and join the lateral ligaments atthe left and right sides. Branches also con-nect to connective tissue that separates thefore and hind quarters. The median liga-ments contain elastic fibres, which allow adegree of ‘give’, providing a shock-absorber effect and allowing the udder toexpand as milk accumulates betweenmilkings.

Rupture of the suspensory apparatus

Rupture of the ligaments may occur gradu-ally or spontaneously. The ligaments thatmost commonly rupture are:

� the median ligaments.� the deep lateral ligaments.� the anterior ligaments (i.e. the front part of

the superficial and deep ligaments).

On occasion, rupture of the anterior liga-ment can lead to a large accumulation ofblood under the skin just in front of theudder. This is known as a haematoma. Somebecome infected and lead to a large, stinkingabscess.

Rupture of the ligaments may be associ-ated with a variety of factors, the mostimportant of which are the following:

� Age: the elastic tissue in the median liga-

ments especially deteriorates with age.� Over-engorgement and oedema of the

udder (see pages 223–224 for the manycauses of udder oedema). This is one goodreason why heifers and cows should notbe ‘steamed up’ (fed extra concentrates)excessively or be kept overfat before calv-ing.

� Poor conformation: it is important toselect for a ‘type’ that has good udderattachment and evenly placed front andrear teats.

Rupture of the median ligaments is probablythe most common reason for poor udder sus-pension. It leads to loss of the ‘cleavage’between quarters, causing the teats to splayoutwards (see Fig. 2.3 and Plate 2.1), mak-ing it difficult to attach the milking units. Italso often leads to air leakage during milk-ing, especially when the unit is first applied,thus producing teat-end impacts (see pages79–80) and increasing the mastitis risk.Rupture of the deep lateral ligaments isinvariably associated with concurrent rup-ture of the superficial ligaments and leads toa total drop of the whole udder (see Fig. 2.4and Plate 2.2). The teats drop to well belowhock level and can easily become injured asthe cow walks.

Rupture of the anterior ligaments (thefront portions of the superficial and deep

8 Chapter 2

Fig. 2.3. Rupture of the median udder ligaments(right) leads to splaying of the teats and loss ofnormal udder cleavage (left).

ligaments) occurs less frequently. It is seenas a gross enlargement at the front of theudder (see Fig. 2.5 and Plate 2.3), whichoften (but not always) leads to a dropping ofthe front teats. The characteristic feature isthat the normal depression at the front of theudder, where the udder joins the abdominalwall, disappears and is replaced with aswelling. Conditions such as haematomas(which are large accumulations of bloodunder the skin) and rupture of the abdomi-nal wall can sometimes be confused withrupture of the anterior udder ligament.Stretching of the udder suspension is one

reason why around 60% of cows have visu-ally uneven quarters.

Structure and Function of the Teats

As described in the section above, the udderconsists of a pad of fat containing manyinterconnecting tubes, all of which terminateat the same point, namely the teat and glandcisterns. The structure could be compared toa tree. The trunk is the teat and gland cis-tern, the branches are the lactiferous ducts,and the small leaves at the ends of twigs arethe secretory alveoli, small sac-like struc-tures deep within the mammary gland. Thisis shown in Fig. 2.1. Milk is produced by thecells lining the mammary alveoli, and muchof the milk is stored here between milkings.

This section describes the structure andfunction of the teats, and discusses milk let-The cow has four main teats, with 60% ofproduction coming from the two hind teats.There may be varying numbers of super-numerary teats (extra teats).

Supernumerary teats

Also known as accessory teats, supernumer-aries are congenital, i.e. they are present at


Fig. 2.4. Rupture of the deep lateral udder ligamentsleads to the udder dropping to well below hocklevel.

Plate 2.1. Rupture of the median udder ligament,leading to splaying of the teats.

Plate 2.2. Rupture of the median and lateral udderligaments, leading to a total ‘drop’ of the udder.

birth and often inherited. Hence it is advis-able not to select heifers from cows withlarge numbers of supernumerary teats.

These teats are most commonly foundat the rear of the udder, behind the two hindteats (Plate 2.4), although they may also befound between the front and rear teats (Plate2.5), and occasionally attached to an exist-ing teat (Plate 2.6). Supernumerariesattached to full teats need handling withcare, as often they have a confluent teatsinus, and removal of the supernumerarycan lead to milk leakage from the main teat.Supernumeraries should be removed at thesame time as the calf is disbudded. The calfneeds to be sitting upright in order to allowa thorough inspection of the udder. If sim-

ply looked at from between the hind legswhile standing, it is very easy to miss thoseaccessory teats which are situated betweenthe main teats. If in any doubt over which

10 Chapter 2

Plate 2.4. Supernumerary teats are most commonlyfound behind the back teats.

Plate 2.6. Occasionally a supernumerary teat isattached to a primary teat. The sinus of both teatsmay be conjoined at the base, making removalmore difficult.

Plate 2.3. Rupture of the anterior udder ligament – alarge swelling appears at the front of the udder.

Fig. 2.5. Rupture of the anterior portion of the deeplateral udder ligament is seen less commonly thanthat of the other ligaments. It leads to a swelling inthe front of the udder and the front teats drop.

Plate 2.5. Supernumerary teats may also occurbetween front and back teats, as in this calf.

are the supernumeraries, simply roll the teatbetween your finger and thumb. The super-numerary is much thicker and has no palp-able teat cistern. It is most easily removed bylifting the skin under its base with your fin-ger (Plate 2.7), and simply cutting it off,using curved scissors. No anaesthetic isrequired in animals less than 2 months old.Failure to remove accessory teats has severaldisadvantages: they are unsightly andaffected animals are less saleable; the ani-mals may develop mastitis (especially sum-mer mastitis – see Chapter 13), and also anabscess on the udder; and if situated verynear to or at the base of a true teat, supernu-meraries may interfere with milking andlead to air leakage, with resulting teat-endimpacts (see pages 79–80).

Functions of the teats

The most important function of the teat is toconvey milk to the young calf. Its use has, ofcourse, been modified to allow hand andmachine milking to produce food for man.The teat has an erectile venous plexus at itsbase, which assists milk flow, and, asdescribed in Chapter 3, the teat, and espe-cially the teat canal, have very importantfunctions in preventing the entry of infec-tion into the udder. Finally, the teat is richlyinnervated and hence can rapidly conveysuckling stimuli to the brain, thus inducinggood milk let-down. This rich innervationcan occasionally make handling cows with

highly sensitive cut teats somewhat haz-ardous.

Teat size

As one would expect, this varies enormously,with lengths ranging from 3 to 14 cm.The diameter also varies, from 2 to 4 cm.Teat length increases from the first to thethird lactation and then remains constant.On both small, short teats and long, wideteats it may be difficult to get good linerattachment and hence there is an increasedrisk of liner slippage and teat-end impacts.Teats may be cone-shaped and pointed orcylindrical with a flat tip (Fig. 2.6).Cylindrical teats are said to be less prone tomastitis and are certainly the most common.

During milking the teat lengthens bysome 30 to 40% and also gets thinner. It issuggested that postmilking teat dip shouldbe applied immediately after unit removal,while the teat is still stretched, as then thedip will penetrate the small cracks and foldsin the teat before it reduces to its pre-milkinglength.

The teat wall

The teat wall consists of four layers, eachhaving an important function in mastitiscontrol and/or milk let-down. These layers,passing from the outside of the teat, are theepidermis, the dermis, the muscle andfinally the endothelium lining the teat cis-tern. These structures are all shown inFig. 2.7.


Plate 2.7. To remove a supernumerary teat, sit thecalf upright, lift the teat with a finger under a fold ofskin and then cut with sharp curved scissors.

Fig. 2.6. Teats may be cone-shaped (left) orcylindrical. Cylindrical teats are said to be lessprone to mastitis.

The epidermis

This is the thick outer lining of the skin. Itssurface consists of a layer of dead, kera-tinized cells (Fig. 2.7) which produce a hos-tile environment for bacterial growth.Keratin is a sulfur-containing protein thatimpregnates cells, thereby increasing theirstrength. It is also present in hair, horn andhoof.

All skin is lined with a keratinized epi-dermis, but teat skin has a particularly thicklayer, some four or five times thicker thanthat of normal skin. It is also very firmlyanchored to the underlying dermis (or sec-ond layer of skin) by deep epidermal pegs,or papillae. If the skin of the udder ispinched between the finger and thumb, itmoves very freely over the underlying tissue.Try doing the same with teat skin: it is firmly

attached. The epidermis of the lips and muz-zle of the cow has a similar structure. It isthought that the firm attachment of theepidermis protects the teat from the shearforces involved in both suckling andmachine milking and also reduces thechances of injury due to physical trauma.Even so, it is surprising how frequently teatsget damaged. Teat skin has no hair follicles,no sweat glands and no sebaceous glands. Inpractical terms this means that teat skin isparticularly susceptible to drying and crack-ing, which is one reason why an emollientis necessary in teat dips (see also pages101–102). It also means that there is little orno flow of sebum over teat skin and hencefly repellents should be applied directly onto the teats. Ear tags and pour-on prepara-tions give a very poor flow of insecticide onto the teats.

12 Chapter 2

Fig. 2.7. Detailed structure of the teat.

Epidermis Dermis

Epidermis Dermis

Teat Canal

The dermis (and erectile plexus)

This is the second layer of the teat wall andis the tissue that carries the blood vesselsand nerves. However, the fine sensory nerveendings are in the epidermis, which is whyexposure of an eroded epidermis (for exam-ple, a teat sore) can be so painful. At the baseof the teat, adjacent to the udder, the dermiscontains the venous erectile plexus. This isa mass of interconnecting blood vessels,which, under the stimulus of suckling or themilk let-down reflex, become engorged toproduce a more rigid and turgid teat base.The stiff teat is extremely important in bothsuckling and machine milking. Suction on aballoon would lead to its collapse. If the baseof the teat were to collapse, it would impedethe flow of milk from the gland cistern intothe teat cistern and hence slow down themilking process. Many herdsmen have prob-ably seen how much blood the erectilevenous plexus can hold: a cow with a cut atthe tip of the teat bleeds very little, whereasa cut through the venous plexus (Plate 2.8) atthe base bleeds profusely and can occasion-ally lead to serious, or even fatal, blood loss.

The muscles

There is a variety of muscles, which are setin transverse, oblique and longitudinalplanes in the dermis of the teat wall. Themost important muscle in terms of mastitiscontrol is the circular sphincter musclearound the teat canal. During milking, when

the teat elongates, the canal opens butbecomes shorter. After milking, sphinctermuscle contraction leads to a shortening ofthe overall teat and closure of the teatsphincter, but a lengthening of the teat canal.The shortened teats are less prone to phys-ical trauma, and the lengthened and closedcanal reduces the risk of entry of bacteria.These changes are shown in Fig. 2.8. As thecanal closes, interlocking folds in the lumenpress tightly together to provide animproved teat-end seal.

Teat cistern lining

The teat cistern is lined with cuboidalepithelium, that is, a double layer of ‘block’cells (Fig. 2.7). In the normal cow these areheld tightly together; however, in responseto bacterial invasion, they have the ability tomove slightly apart, which allows the entryof infection-fighting white blood cells fromthe small blood vessels beneath (seepage 32).

Milk let-down

As will be discussed in more detail inChapter 6, achieving a good milk let-downprior to unit attachment is essential for rapidparlour throughput. The shorter the time themilking machine is on the cow the better, asthis helps to avoid teat-end damage andhence to reduce mastitis levels. The follow-ing section describes the mechanics of milklet-down. Chapter 6 describes its practicalimportance.

There are three phases of milk let-down.

1. Contraction of the myoepithelial or smallmuscle cells that line the outside of thealveoli (Fig. 2.1). These effectively sur-round the milk-secreting cells, like a tyrearound the rubber inner tube of a carwheel. Contraction of the myoepithelialcells forces milk from the mammary alve-oli into the ducts, and hence into the teatand gland cisterns. The herdsman seesthis as an enlargement of the udder andengorging of the teats.


Plate 2.8. A cut into the venous erectile plexus atthe base of the teat often results in profusehaemorrhage.

2. Engorgement of erectile tissue. Figure 2.7shows that there is an erectile venousplexus at the base of the teat. When thisbecomes engorged, it prevents the base ofthe teat from collapsing during milk flow.If the teat had the structure of a limp,elongated balloon, then one suck from acalf or a milking machine liner and theteat would collapse, leading to a cessa-tion of milk flow. The engorged erectiletissue holds the teat ‘open’ between theteat cistern and gland cistern, and thisallows milk to flow.

3. Relaxation of the teat canal. Betweenmilkings, the circular sphincter musclesurrounding the teat canal pulls it closedand this helps to prevent leakage of milkand entry of infection. The third phase ofmilk let-down is relaxation of thismuscle, to allow milk to flow. Studieshave shown that it takes around 15 kPaof pressure to force milk through aclosed teat, but only 4–6 kPa when thecanal is relaxed for milk let-down. Milkcan then flow without causing teat-enddamage.

Poor milk let-down in heifers

Poor milk let-down in heifers can be a majorproblem in some herds, and herdsmen mayfind that they need to use quite large quanti-ties of oxytocin by injection. This should notbe necessary. The following section outlinessome of the factors that may be involved.

It is important to make milking a pleas-ant experience, and not a process associatedwith fear or pain. The heifers need to knowwhat to expect. If fear is involved, adrenalinwill be produced and the let-down mecha-nisms will be inhibited. For example, it maybe a good idea to bring heifers through theparlour before calving so that they know theroutine. Applying a good teat dip at thisstage will also get them used to being han-dled, as well as reducing the incidence ofdry period infections and subsequent clini-cal mastitis in early lactation. Do not chasethem around the collecting yard to get theminto the parlour. They are often last in, whenthe milker’s patience may be waning, soextra care is needed. Make sure that the par-lour stall work is the correct size, i.e. that theheifer is not squashed in to the parlourbetween large cows, making her becomeuncomfortable.

14 Chapter 2

Fig. 2.8. Teat changes during milking. After milking, the teat shortens, the canal lengthens and the foldsinterdigitate to form a tight lipid seal.

Take care with the backing gate. Theheifers are often at the back of the collectingyard, so if they are being pushed by the back-ing gate, or, even worse, if it is electrified,then this will inhibit milk let-down whenthey enter the parlour. Some farms use a sep-arate heifer group, where there will then beless stress from mixing with other animals.Heifers that have a hereditary nervous pre-disposition may be worse affected. It may bethat leaving the calf suckling for too longmay make the heifer fret. However, the con-verse may also be true for some animals,namely that leaving the calf for long enoughgets the heifer used to milk let-down and tobeing milked, even if it is only by the calf.

Excess udder oedema can be a problem,as this is painful and will reduce milk let-down. Overfeeding and insufficient exerciseprecalving are predisposing factors. Someconsider that feeding the heifer will help totake her mind off the milking machine, butmany farms no longer do this. It is, ofcourse, vital to ensure that udder prepara-tion has been maximized and that the heiferis well stimulated before unit application.This means going through the full proce-dure of predip, foremilk, wipe and dry,described in Chapter 6, before the unit isapplied. Some farms claim that an initialudder massage with a warm cloth helps,and others that extra comfort from rubberflooring in the parlour may help. Onemachine manufacturer has an initial rapid‘stimulation pulsation’ phase, run at lowervacuum, to try to stimulate milk let-downbefore unit application.

It is difficult to know how long to leavethe unit on a freshly calved heifer if she isnot letting her milk down. A suggested rou-tine for the first few milkings is:

1. Heifer taken gently into parlour, applyfull udder prep routine, and then unit on.If no milk, take off after 1–2 min max.

2. Repeat for next two milkings, doing yourbest to optimize the let-down response,perhaps by manual massage of the udder.

3. If there is still no milk let-down, at thefourth milking inject oxytocin as soon asshe enters the parlour, so that she associ-ates milk let-down with udder prep, andnot with unit on.

4. Many farms try 2.0 ml (depending on itsstrength) oxytocin for four milkings, then

1.0 ml for the next two milkings, then 0.5ml for two (provided this low dose stillworks), then try without.

Poor let-down in heifers is a very variablecondition, at least partly associated with thetemperament of the heifer herself, and,although the above protocol may be adheredto quite carefully, there will always be oneor two animals that do not seem to respond.There will be no ‘one size fits all’ effect, andit may be necessary to try a range ofapproaches before one works with a partic-ular batch of heifers.

Milk Synthesis and How it is Affected byMastitis

Milk is synthesized in cells lining the alve-oli, the small sacs at the very end of theducts deep within the udder (see Figs 2.1and 2.9). The average composition of milk isshown in Table 2.1.

Colostrum is much more concentratedthan milk, having twice the level of totalsolids (25%) and a very much higher levelof protein (15%) due to the high level ofantibody present. This is why heatingcolostrum leads to its coagulation and whyDairy Regulations state that milk should bediscarded for the first 4 days after calving.

Table 2.1. Approximate composition of milk fromFriesian/Holstein cows.

Component Amount

Total solids 12.5%Protein 3.3%Casein 2.9%Lactose 4.8%Ash 0.7%Calcium 0.12%Phosphorus 0.09%Immunoglobulins 1.0%Vitamin A (μg/g fat) 8Vitamin D (μg/g fat) 15Vitamin E (μg/g fat) 20Water 87.5%

Lactose

Glucose is produced in the liver, primarilyfrom propionate, a product of rumen fer-


mentation. After it is transferred to theudder, part of the glucose is converted intoanother simple sugar, galactose. Next, onemolecule of glucose combines with one ofgalactose to produce lactose. Lactose isknown as a disaccharide (i.e. two monosac-charide sugars conjoined). In summary:

� Liver: propionate to glucose.� Udder: glucose to galactose.� Udder: glucose + galactose = lactose.

Lactose is the main osmotic determin-ant of milk (the factor governing the con-centration of its components in solution). Tomaintain milk at the same concentration asblood, lactose increases and decreases as theconcentration of the other milk componentsvaries. However, the pH of milk is slightlylower than that of blood (i.e. more acidic):

� pH of blood = 7.4� pH of milk = 6.7

This difference may be used to attract drugssuch as erythromycin, trimethoprim, tylosinand penethamate into the mammary gland,as lower pH solutions are drawn to thosewith higher pH. If lactose concentrations inthe udder fall (as occurs with mastitis), thensodium and chloride levels increase to main-tain the osmotic pressure of the milk. Thisis one of the causes of the bitter and slightlysalty taste of mastitic milk. (Some farmersoccasionally taste the milk of cows they areintending to purchase, in an attempt to iden-tify the slightly salty flavour of mastitis.)

These changes can also be used to helpassess mastitis status by electrical conduct-ivity measurements, since sodium and chlor-ide are much better conductors of electricitythan lactose.

Protein

The majority of protein in milk is in the formof casein. Amino acids are transported to theudder via the bloodstream and transformedinto casein by the mammary alveolar cells.Once formed, casein is extruded from thesecells in a mechanism similar to the fatdroplets shown in Fig. 2.9.

Surprisingly, it is the energy content ofthe diet that has the major effect on thecasein content of milk. Dietary protein hasrelatively little influence on milk proteincontent. Other types of protein present inmilk in small quantities are albumin andglobulins. These are transferred directly fromthe blood into milk. Mastitic milk has areduced casein content but increased levelsof albumin and globulin. The total proteincontent of the milk may remain constanttherefore, but the milk is of much poorerquality, particularly for manufacture. This isbecause the coagulation of casein is veryimportant as part of the starting process forcheese and yogurt production. In addition,mastitic milk contains increased levels of theenzyme plasmin, which decomposes caseinin stored milk. Unfortunately, plasmin is notdestroyed by pasteurization and it remainsactive even at 4°C (the storage temperature insupermarkets). Mastitic milk will thereforecontinue to be degraded even following pas-teurization and storage at 4°C; this explainswhy manufacturers are prepared to pay a pre-mium for low cell count milk.

Milk fat

Milk fat is formed in the udder secretorycells when fatty acids are combined withglycerol and converted into a neutral formof fat called triglyceride.

Glycerol + 3 fatty acids = triglyceride

16 Chapter 2

Fig. 2.9. The synthesis of milk fat droplets in theaveolus.

Fatty acids are derived from three mainsources:

� Body fat (50% of total fatty acids). Hencebody condition score is an importantdeterminant of milk fat levels, especiallyin early lactation.

� Dietary fat, especially long-chain fattyacids (those which are solid at room tem-perature and are components of butter andlard). The use of protected fat (i.e. fat thathas been treated so that it can passthrough the rumen unchanged) can there-fore increase the butterfat content of milk.Conversely, short-chain and polyunsat-urated fatty acids in the diet can lead to adecrease in milk fat content.

� Finally, fatty acids are synthesized in theudder from acetate, which is absorbed as aproduct of rumen fermentation. High-fibrediets, which promote increased levels ofacetate in the rumen, will therefore lead toan increase in milk fat production.

Small particles of milk fat (triglyc-eride) are extruded from the secretory cellsin the alveoli and are covered by a thinprotein membrane before passing into themilk (Fig. 2.9).

Besides the enzyme plasmin, mastiticmilk also has an increased level of theenzyme lipase. This leads to degradation ofthe milk fat into its fatty acid componentsand thus imparts a rancid flavour to themilk. Increased levels of fatty acids caninhibit starter cultures used in cheese andyoghurt manufacture, and can also impart arancid flavour to these products.

In summary, mastitic and high cellcount milk is of poorer quality because:

1. Its casein content is lower, and hencecheese manufacture yield per 1000 kg ofmilk is reduced.

2. Plasmin (which degrades casein) levelsare higher, and plasmin remains activeafter pasteurization.

3. Lipase levels increase, inhibiting yogurtstarter cultures, and may impart anadverse flavour.

Minerals

The minerals in milk are derived directlyfrom the blood. Calcium is actively secretedin association with casein.

Control of Milk Synthesis

The rate of milk synthesis, and hence thelevel of yield, is controlled by a number offactors. These include: diet and factors thatinfluence feed intake; hormones, such asprolactin and BST (bovine somatotrophin);and frequency of removal of milk from theudder, i.e. milking frequency. Diet and man-agement factors affecting feed intake clearlydetermine the rate at which nutrients arriveat the udder to be used for milk synthesis,and are major determinants of milk produc-tion. A discussion of these factors is outsidethe scope of this book.

In most mammals, initiation of lactationand continued milk production are con-trolled by the hormone prolactin. In the cow,however, continued milk secretion is influ-enced by a complex interaction of steroids,thyroid hormone and growth hormone, thelatter being more commonly known asbovine somatotrophin (BST). BST is anatural hormone synthesized by thepituitary gland, a small organ at the baseof the brain. Higher-yielding cows havemore BST circulating in their blood thanlower-yielding cows, and cows at peakyield more than late lactation animals.BST can now be produced syntheticallyand, at the dose rate currently being sug-gested, increases yields by 10–20%, i.e.4–6 litres per day. BST alters the cow’smetabolism so that a greater proportion ofher food is used for milk production, thusmaking her more efficient. Some 4–6 weeksafter starting dosing and after an initialincrease in yield, there is an increase in foodintake and appetite. In many countries, theuse of BST has been prohibited as a result ofconsumer pressure, or on the grounds offood safety.


Milking frequency

Increased frequency of milking alsoincreases yield. Changing from twice tothree times daily will increase production byaround 10–15% in cows and 15–20% inheifers. Because of the flatter lactation curveit produces, three times a day milking has tobe continued to the end of lactation to obtainits full beneficial effect. Reducing milkingfrequency decreases yield. For example, ifcows are only milked once a day, yields mayfall by up to 40%. The majority of farms milkat intervals of 10 hours and 14 hours. Trialshave suggested that this does not producesignificantly lower production than precise12-hourly milking in anything but thehighest-yielding cows. The influence ofmilking frequency on milk yield appears tobe controlled by local mechanisms actingwithin the udder. This is thought to be truebecause if two quarters are milked twicedaily and the other two are milked fourtimes daily, only the four times daily quar-ters show an increase in yield. Initially itwas thought that back-pressure of milkwithin the alveoli was responsible.However, if the milk withdrawn from thefour times daily quarters is replaced by anequal volume of saline (i.e. to restore thepressure within the alveoli), yields stillincrease. It has now been shown that milknaturally contains an inhibitor protein andit is the presence of this inhibitor, actingdirectly on the secretory cells within thealveoli, which influences yield. More fre-quent milking leads to more frequentremoval of the inhibitor protein, and hencemore milk is produced. Not only doesfrequent removal of the inhibitor proteinstimulate increased activity of secretorytissue (and hence increased yields), italso slowly increases the amount ofsecretory tissue present, producing a longer-term effect. Finally, and after 2–3 monthsof three times daily milking, the numberof secretory cells increases. This gives alonger-term response, which will persistwhen milking returns to twice daily.The extent of these effects depends partlyon the internal anatomy of the udder.An udder with large teat and gland

cisterns and large ducts will store lessmilk in the alveoli between milkings. Thereis then less contact between milk inhibitorprotein and the secretory tissue, and hencethe cow, will be a higher-yielding animal. Inthe average cow, approximately 60% of thetotal milk is stored in the alveoli and smallducts, and 40% in the cisterns and largeducts.

Although not yet feasible, vaccin-ation of cows against their own inhibitorprotein raises interesting possibilities, asthis could be a further way of increasingyields.

Environmental temperature

Under very cold conditions, waterconsumption and therefore milk yieldfall. When the weather is very hot, food,and especially forage, intakes fall and thiscan depress both milk yield and milk fat lev-els. High environmental humidity exacer-bates the effects of both hot and coldweather.

Length of dry period

Towards the end of lactation, the number ofactive alveolar secretory cells slowlydeclines, reaching a minimum during theearly dry period. The alveolar cells do notdie, but simply collapse, so that the spacewithin the alveolus disappears and theudder consists of a greater proportion of con-nective tissue. New secretory tissue is laiddown when the cow starts to ‘freshen’ readyfor the next calving, and hence the totalamount of secretory tissue (and thereforeyield) increases from one lactation to thenext. A dry period of between 4 and 8 weeksis ideal. If the cow is not dried off at all, thenext lactation yield may be as much as25–30% lower. This may occur, for example,following an abortion, or if a bull is runningwith the herd and no pregnancy diagnosis(PD) is carried out. Cows with excessivelylong dry periods often get overfat and meta-bolically inactive. This produces metabolicdisorders around calving, and increases the

18 Chapter 2

risk of mastitis. Conversely, very short dryperiods have, under some situations, beenassociated with increased cell counts, but

this effect is not large, and generally cowsare more affected by prolonged than byexcessively short dry periods.


Apart from very few exceptions, for exampletuberculosis and leptospirosis, infectionscausing mastitis enter through the teat canal.The cow has very effective ways of reducingthe risk of entry of infection through the teat,and even those infections that do succeed inpenetrating the teat canal defences are com-monly overcome by defences within theudder. Considering how often the teats, andespecially the teat ends, become contami-nated with bacteria, the overall incidence ofmastitis in most herds remains relativelylow, although no doubt most farms wouldprefer it to be even lower. This chapter stud-ies the many ways in which the cow repels

infection. It will then be easier to understandthe reason for carrying out some of the in-parlour control measures discussed in laterchapters.

Defence mechanisms involve both theteat and udder and can be summarized asfollows:

Teat defences act by preventing entry ofinfection into the udder.

� Intact skin provides a hostile environmentfor bacterial multiplication.

� Teat canal closure mechanisms reduce therisk of entry between milkings.

20 ©CAB International 2010. Mastitis Control in Dairy Herds (R. Blowey and P. Edmondson)

3 Teat and Udder Defences AgainstMastitis

Teat Defences 21The teat skin 21The teat canal 22The keratin flush 22The keratin plug 22Teat closure 22Teat canal dimensions and speed of milking 23Mastitis and milking frequency 24Teat-end damage and mastitis 25

Defences within the Udder 25Intrinsic defence mechanisms 25Inducible defence mechanisms 27Poor response in the freshly calved cow 30Individual cow variation 31Can cell counts get too low? 31Effect of low selenium and/or vitamin E 31Reduced PMN activity in milk 32

� Bacteria adherent to keratin in the teatcanal are flushed out at the next milking.

Udder defences act by removing infectionsthat have been able to pass through the teatcanal. They are:

� Intrinsic, i.e. mechanisms that are alwayspresent.

� Induced, i.e. those mechanisms that comeinto operation in response to bacterialinvasion.

Teat Defences

The teat skin

Teat skin has a thick covering of stratifiedsquamous epithelium (Fig. 2.7), the surface ofwhich consists of dead cells filled with kera-tin. When intact, this provides a hostile envir-onment for bacteria, thus preventing theirgrowth. In addition, there are fatty acids pres-ent on skin that are bacteriostatic, that is, theyprevent bacterial growth. However, these bac-teriostatic properties can be removed by con-tinual washing, especially using detergents,and this is why the premilking teat sanitizershould be chosen carefully.

The normally intact surface of the skinmay also become compromised by cuts,cracks, chaps, bruising, warts, pox lesions,etc. Bacteria can then multiply on the sur-

face of the skin and become a reservoir formastitis infections. This is particularly thecase for organisms such as Streptococcusdysgalactiae and Staphylococcus aureus. Anexample is shown in Plate 3.1. Not onlywould this teat act as a reservoir of mastitisorganisms, but it would also reduce milkingspeed. Trials have shown that cows withbadly dry and cracked teat skin are muchslower milkers (Fig. 3.1). They may havedouble the ‘unit on’ time to achieve the samelevel of yield, and, of course, this increasedtime can lead to teat-end damage.

Maintaining an intact and healthy teatskin is one of the important functions of theemollient present in postmilking teat dips.

Teat and Udder Defences 21

8

7

6

5

4

3

2–1 1 3 6 9

Average teat conditionAverage milkout

Ave

rage

milk

out t

ime

(min

utes

)

Ave

rage

teat

sco

re (

end

+sk

in+

area

)

11 13 15 174

4.5

5

5.5

6

6.5

Fig. 3.1. Teat condition and milkout time. In this experiment, cows’ teats were artificially damaged at timezero, leading to an increase in teat score. Note how this is followed by milkout time increasing from 4minutes to 6.5 minutes by day 6.

Plate 3.1. The very dry skin on this teat would notonly act as a potential reservoir for staphylococciand other mastitis organisms, but also reduce milkflow rates and hence speed of milking.

The teat canal

The teat canal is 9 mm long (range 5–13 mm)and is lined with folds of keratinized skinepidermis, covered by a thin film of lipid.This has similar antibacterial properties toteat skin (Figs 2.1 and 2.7). These propertiesare most effective when contraction of thesphincter muscle leads to canal closure. Atteat closure, the sphincter muscle contracts,the folds interdigitate to form a tight seal andthe hydrophobic lipid lining ensures that noresidual continuous column of milk persists,which could otherwise act as a ‘wick’ forbacterial entry. A few droplets remain, some-times referred to as ‘milk lakes’. These oftencontain bacteria, which must be flushed outat the next milking.

Damage to the canal lining and lipidseal could result in a persistent residual col-umn of milk, while fissures and serum oozefrom a cracked epidermis would predisposeto bacterial proliferation.

The rosette of Furstenberg (Fig. 2.1), onthe inner side of the teat canal, is a ring oflymphocyte cells that detect invading bac-teria and stimulate an immune response.

It takes at least 20–30 minutes for theteat end to become fully closed and hence,in order to protect teats from bacterial con-tamination, advice is often given that ani-mals should not be allowed to lie down untilat least 30 minutes after milking. Cowsshould not be left just standing doing noth-ing, however, as the extra standing timesmight increase the incidence of lameness. Inaddition, if they are left standing in an over-crowded, dirty or draughty passageway, theresulting increased teat skin damage and/orteat contamination might actually increasethe risk of mastitis. The majority of farmswould now simply encourage cows to walkback along clean passageways, past freshfood and into clean cubicles, and those cowsthat fail to stop to eat are probably so bad ontheir feet that they are best allowed to liedown to rest. Foot baths are commonly situ-ated a short distance from the parlour exit.These should not be too deep, i.e. 70 mmmaximum, to avoid splashing of the openteat ends, and the bath solution should bechanged on a regular basis.

The keratin flush

Many bacteria entering the teat betweenmilkings become trapped by the layer of ker-atin and lipid lining the teat canal. They arethen flushed out at the start of the next milk-ing by the first flow of milk, as this removesthe superficial layers of keratin lining theteat canal. This is known as ‘the keratinflush’. It is very important to ensure thatudder preparation and unit attachment aresuch that milk flows out of the teat when thecluster is applied, and that there are noreverse flow mechanisms that might lead tomilk and infection being propelled back upinto the udder. Foremilking will help in theremoval of these trapped organisms.

The keratin plug

During the dry period a mixture of wax andkeratin accumulates in the teat canal to forma physical plug. This mechanism isextremely important in preventing newinfections, although as discussed in the sec-tion on dry period infections in Chapter 4, itis by no means always effective. This isespecially the case for cows with ‘open’ teatends that are fast milkers.

Teat closure

Figures 3.2a and b show the importance ofteat sphincter closure in relation to E. colimastitis. Teats were dipped in a broth cul-ture of E. coli at varying times after milking.Of the teats dipped and exposed to E. coli inthe first 10 min after milking, 35% devel-oped mastitis. However, if the teats were notdipped into the E. coli broth until a fewhours before the next milking, then only 5%developed mastitis.

It is particularly important to preventliner slippage and resultant teat-end impactsat the end of milking (see Chapter 5). This isbecause: (i) the canal is more ‘open’ at theend of milking; and (ii) there may be no milkremaining in the quarter to flush out theorganisms that have penetrated the teatcanal by reverse flow.

22 Chapter 3

The degree of closure of the teat canalcan be quantified in terms of the pressurerequired to force fluid back up through theteat canal, and is shown graphically inFig. 3.2b.

Teat canal dimensions and speed of milking

Cows with short teat canals (i.e. short verti-cal length) and those with a wide cross-section diameter are more susceptible tomastitis. Cows with ‘open’ teat canalsalso milk faster. As this is likely to be an


Fig.3.2. (a) The importance of teat sphincter closure in relation to E. coli mastitis: if teats were dipped in abroth culture of E. coli 0–10 min after milking, 35% of quarters developed mastitis. This reduced to 5% ifteats were dipped in E. coli broth immediately prior to the next milking. (From Bramley et al., 1981.) (b) Pressure required to force fluid through the teat canal before, during and after milking. (From Bramleyet al., 1981.)

a

Nextmilking

10 minutesafter milking

0

5

35

% o

f dip

ped

quar

ters

whi

chde

velo

ped

mas

titis

Beforemilking

0

5

10

Pre

ssur

e (k

Pa)

15

b

End ofmilking

20 minutesafter milking

Pressure required to forcebacteria through teat canal (kPa)

Before milkingDuring milking20–30 min. after milking

154–615

(a)

(b)

inherited feature, there will be a genetic sus-ceptibility to mastitis. Conversely, providedthat teat-end lesions do not develop, ‘hard’milkers, with slow milk flow rates, will havea lower infection rate than fast milkers.

However, speed of milking is correlatedwith yield (the greater the yield the greaterthe milk flow rate) and hence increasingselection for yield has led to an overallincrease in milk flow rates. Table 3.1 showsthat the average milk flow rate for a fastmilker doubled between 1950 and 1990.

Table 3.1. Average milk flow rates of fast milkers(kg/min). (From Grindal et al., 1991.)

Per quarter Per cow

1950 0.8 3.21990 1.6 6.4

This has led to a 12-fold increase in sus-ceptibility to mastitis over the same period.Yields have undoubtedly increased furthersince 1990, and hence we can expect to seea corresponding increase in mastitis suscep-tibility. It will be a challenge to us all to pro-vide optimum conditions of housing,machine function and management to con-trol these infections.

Table 3.2 shows the numerical relation-ship between flow rate and mastitis inci-dence when teats were experimentallyexposed to a high bacterial challenge. Threedifferent machine conditions and varyingflow rates were used. Initial results wereobtained with a well-functioning machinewhere the liners were fitted with teat shields

(see Fig. 5.7). If there was no pulsation or,even worse, if teat-end impacts were a prob-lem, then the mastitis risk (expressed as thepercentage of quarters becoming infected)became greater, reaching 100% in cows withvery high milk flow rates. (Milking machinefunction is discussed in Chapter 5.)

Cows with high flow rates are also muchmore susceptible to contracting new infec-tions during the dry period.

Mastitis and milking frequency

The flushing action of milking removes thesuperficial layers of keratin lining the teatcanal and in so doing removes bacteria thatare adherent to the keratin. This is some-times referred to as ‘the keratin flush’ (seepage 22), and it is particularly important forthe removal of Streptococcus agalactiae andStaphyloccoccus aureus, which invade byslow growth through the teat canal. Hence,cows milked three times daily are generallyless susceptible to mastitis than cows milkedtwice daily, and, provided there is noadverse effect of machine milking, they tendto have lower cell counts.

Increased frequency of milking alsodecreases the volume and pressure of milkwithin the udder, and hence reduces the riskof milk leakage on to cubicle beds, whichfurther decreases mastitis risk. Both factorsfurther decrease the susceptibility to masti-tis organisms invading the udder.

This all assumes optimum functioningof the milking equipment. If machine func-tion is poor, with defective pulsation and/orteat-end impacts, then increased frequency

24 Chapter 3

Table 3.2. The influence of milk flow rate from the teat end on the percentage of quarters becominginfected following experimental challenge. A poorly functioning machine dramatically increases theinfection rate. (From Grindal et al., 1991.)

Quarter flow rate (kg/min)

<0.8 0.8–1.2 1.2–1.6 >1.6

Milking conditions Percentage infection

Good pulsation + shields 3 4 7 36No pulsation 15 20 38 92Pulsation + impacts 36 37 55 100

<0.8 0.8–1.2 1.2–1.6 >1.6

of milking would lead to an increased riskof mastitis.

Teat-end damage and mastitis

The teat canal is obviously of vital impor-tance in the prevention of new cases of mas-titis and clearly it follows that any damage tothe teat end will compromise the defencemechanisms. Examples of teat-end damageare described in detail in Chapter 14 andinclude:

� Hyperkeratosis (a protrusion of kera-tinized skin at the teat sphincter) andsphincter eversion, both of which arecaused primarily by adverse effects ofmachine milking.

� Physical trauma: cuts, crushing or bruis-ing.

� ‘Black spot’: a lesion, probably traumaticin origin, with secondary infection causedby the bacterium Fusobacteriumnecrophorum.

� Milking machine damage: teat-endoedema, haemorrhage, sphincter eversion,etc.

� Excessive dilatation of the canal, for exam-ple, when administering intramammaryantibiotics or when inserting a teat can-nula. This can produce cracks in the kera-tin and lipid lining, thereby providing anopportunity for bacterial multiplication.

The way that teat cannulae are used is par-ticularly critical, since it is often 1–2 daysafter withdrawal of the cannula (especiallyafter it has been in situ for several days) thatmastitis occurs. This is presumably becausethe tightly fitting cannula prevents bacterialentry while it is in position, but afterremoval the stretched canal has lost both itsability to close and its bacterial defences,allowing easy entry of infection. For this rea-son many recommend infusing a smallquantity of antibiotic after each milking forthe first 3–4 days following removal of thecannula.

Defences within the Udder

Even when bacteria have managed to over-come the defence mechanisms of the teatcanal and have either grown through it orbeen forced through by the milking machine,clinical or subclinical udder infections areby no means a certainty. There are severalhighly efficient systems within the udderthat assist in the removal of bacteriaand often prevent infections becomingestablished. These can be categorized asintrinsic defence mechanisms, which aresystems continually present in the udder,and inducible systems, which comeinto operation in response to bacterialinvasion.

Intrinsic defence mechanisms

Lactoferrin

Iron is required for bacterial growth, andespecially for the growth of E. coli. In thedry, non-lactating udder, lactoferrin removesthe iron from udder secretions and in sodoing minimizes bacterial multiplication.Although the risk of new E. coli infectionsduring the dry period is four times greaterthan in lactation, the presence of lactoferrinensures that clinical disease (i.e. clinicalE. coli mastitis from these infections) is rareuntil the next lactation (see Table 3.3).

Table 3.3. Experimental E. coli infection in lactat-ing and dry cows. (From Hill, 1981.)

No. of quartersNo. of quarters developing clinical

challenged mastitis

Lactating cows 16 121

Dry cows 12 22

1 Of the four quarters that did not show clinical mastitis,two had a high cell count and two had subclinical masti-tis.

2 Both cases were in cows challenged only a few daysprior to calving, when the lactoferrin in milk had alreadyfallen to a low level.


The bacteriostatic effects of lactoferrinare lost during lactation because:

� Lactoferrin is present in only low concen-trations.

� High citrate levels in milk compete withlactoferrin for iron, producing iron citrate.This can be utilized by the bacteria duringtheir growth processes.

Lactoperoxidase

All milk contains the enzyme lactoperox-idase (LP). In the presence of thiocyanate(SCN) and hydrogen peroxide (H2O2),lactoperoxidase can inhibit the growth ofsome bacteria (Gram-positive organisms, seepage 57) and kill others (Gram-negatives).The level of thiocyanate in milk varies withthe diet, being particularly high when bras-sicas and legumes are fed. Hydrogen perox-ide can be produced by bacteria themselves.Gram-negative bacteria produce very littleH2O2, and so the lactoperoxidase system isprobably not important in their control.There is some evidence that Gram-positivebacteria such as Streptococcus uberis mayproduce sufficient H2O2 for the lactoperoxi-dase system to be partially effective in theircontrol.

Complement

Complement is the general term for a seriesof proteins which, when acting together,produce a cascade effect that results in thekilling of certain strains of Gram-negativebacteria, such as E. coli. E. coli is one of anumber of coliforms that can be groupedinto serum-sensitive strains (killed by com-plement) and serum-resistant strains (not

killed). It has been shown that only the lat-ter are likely to produce mastitis. If a serum-sensitive strain of E. coli is isolated from amilk sample therefore, it is likely to be a con-taminant only and not a cause of mastitis.

Immunoglobulins (antibodies)

Antibodies are unlikely to have a primaryrole in mastitis control since it is well knownthat colostrum contains very high levels ofantibodies, and yet freshly calved cows candevelop peracute mastitis and frequently doget severe mastitis several days after calving.The role of specific antibodies against mas-titic bacteria is unclear. Probably their mainfunction is in the opsonization of bacteriabefore they are engulfed by white blood cellsand macrophages. Opsonization is a processwhereby the bacteria become coated withantibody. A portion of an antibody molecule(the Fab arm) attaches to the bacteria, leav-ing a second arm (the Fc fragment) exposed.White blood cells (PMNs) are activated bythe exposed Fc arm and attach to it.Phagocytosis (engulfing) of the bacteria canthen proceed much more rapidly.

Cellular response

There is a variety of different types of cells innormal milk, but by no means all of themcan kill bacteria. The total number of cellscan be counted and is expressed as thesomatic cell count (SCC). Approximate per-centages are given in Table 3.4, althoughthere is still some dispute concerning whichcell types are present. The proportions willvary with factors such as level of yield, stageof lactation and, of course, the presence ofinfection.

26 Chapter 3

Table 3.4. Percentage of cell types in milk and colostrum. (From Lee et al., 1980.)

Mid-lactation Colostrum

PMNsa (neutrophils) 3 61Vacuolated macrophages 65 8Non-vacuolated macrophages 14 25Lymphocytes 16 3Duct cells 2 3

a PMNs = polymorphonuclear leucocytes, bacteria-killing cells, mainly neutrophils.

The main function of macrophages andlymphocytes is to recognize bacteria andthen trigger alarm systems that induce amore vigorous host response, eventuallyleading to huge numbers of PMNs (poly-morphonuclear leucocytes, mainly neu-trophils) entering the milk. These alarmsystems are the inducible defence mecha-nisms described in the next section.

PMNs are important bacteria-killingcells that originate from blood. However, innormal milk they are present in such lownumbers as to be ineffective against a heavybacterial challenge.

Inducible defence mechanisms

When all else has failed and bacteria havepenetrated the teat canal and overcome theintrinsic defence mechanisms, alarm signalsare sent out to the body of the cow request-ing ‘help’. The response to the alarm is theinduced system of mammary defences. It isboth highly effective and fascinating in itsmechanisms. The various stages will bedescribed in some detail.

The chemotaxin alarm

The macrophages and PMNs (see Table 3.4)already present in the milk recognise andengulf fragments of dead bacteria and theirtoxins in a process known as phagocytosis(Fig. 3.3). Phagocytosis in turn leads to the

release of various chemical mediators,known collectively as chemotaxins. Specificchemotaxins include chemicals such asinterleukin 8 and tumour necrosis factor(TNF). It is these chemicals, plus the toxinsproduced directly from bacteria multiplyingwithin the udder, which act as the alarmsystem.

The inflammatory response

The principal response to chemotaxins is amassive inflow of PMNs from the capillariesin the teat wall and udder into the cisternsand ducts. This is achieved in a variety ofstages (Fig. 3.4):

� Increased blood flow: blood vessels in theteat wall dilate, thus increasing the bloodflow and the supply of PMNs to theaffected quarter. Thus a quarter with anacute mastitis infection becomes palpablyswollen, hot and painful.

� Margination: small carbohydrate projec-tions (selectins) appear on the inner sur-face of the cells lining the capillary wall.These attract PMNs towards the sides ofthe capillaries and help to force thembetween the capillary cells and outthrough the wall.

� Loosening of endothelial cell junctions:under the influence of specific chemo-taxins, the endothelial cells lining both thecapillaries and the teat and udder cisternsliterally move apart to facilitate a more


Fig. 3.3. The process of phagocytosis, in which a macrophage engulfs and destroys a bacterial cell.

Macrophage Macrophage Bacterial cell Released fragments ofmakes contact surrounds is engulfed bacteria act as ʻalarmwith a bacterial bacterial cell into lysosomal signalsʼ, stimulating thecell vacuole, where mobilization of vast

it is destroyed numbers of PMNs fromblood vessles in thewalls of the teat andudder cisterns

28 Chapter 3

Fig. 3.4. The response to the alarm signals of bacterial invasion.

PMN(bacteria-killingwhite bloodcell, mainlyneutrophils)

Red blood cell

(E) and (F) Huge numbers of PMNs pass into the milk in the teat and udder cisterns, to produce a massive increase in cellcount. They start engulfing and killing bacteria, releasing more by-products, which further activates the alarm system.

rapid passage of PMNs into the infectedmilk. They close again when the PMNshave passed through.

� Diapedesis: PMNs squeeze through thewalls of the capillaries, across the tissueof the teat wall and udder, through theendothelial lining and into the milk,where they are able to engulf thebacteria.

� Damage to epithelial cells: some of thecells lining the teat duct and lactiferoussinuses can be totally destroyed by thetoxins produced by E. coli infections, andthis allows further access of PMNs (andserum) into the area of multiplying bac-teria. Plate 4.8 shows the inside of anormal teat, which can be compared withthe severely inflamed mastitic teat in Plate4.9. (See Chapter 4.)

� Serum ooze from blood vessels: becausethe junctions between endothelial cells inthe capillary walls have opened to allowthe passage of PMNs, serum can also flowinto the tissues. This produces an uncom-fortable swelling of the affected quarter, astissues stretched and dilated by fluid arepainful. In acute E. coli infections partic-ularly, the leakage of serum is so pro-nounced that it flows directly into themilk and produces the yellow, waterysecretion that is so typical of an acute coli-form mastitis. Occasionally serum oozemay even be seen on the skin surface, as inPlate 4.10.

� Phagocytosis. Once they have passed intothe milk, the PMNs released in responseto the chemotaxin alarm start to engulfwhole bacteria (Fig. 3.3) and the majorpart of the bacteria-killing process, knownas phagocytosis, begins. Inside the PMNthe bacteria are destroyed by a systeminvolving hydrogen peroxide. The firstPMNs to arrive are highly active. Theyrelease lysosomal granules from theircytoplasm, and this further amplifies theinflammatory response.

The severity of the inflammation is oftensuch that it persists well after the bacteriahave been destroyed. This explains the com-mon finding of a hard, hot and painful quar-ter with a watery secretion, from whichbacteria cannot be cultured. This is almostcertainly caused by an acute E. coli infectionthat has been rapidly counteracted by thecow’s defence mechanisms.

The increase in the number of cells inmilk due to the inflammatory response canbe enormous. From a base level of only100,000 (105) per ml, i.e. a cell count of 100,it may increase to as many as 100,000,000(108) per ml (a cell count of 100,000) in just afew hours, and many quarters rapidly reach acell count of 10 billion (109). Bacteria are thenrapidly eliminated, as shown in Fig. 3.5a, andso many PMNs may have entered the udderthat the white cell count of the blood falls toalmost zero.


Fig. 3.5a. Good PMN (white cell) response in a mid-lactation cow can lead to rapid elimination of E. coli.Infection at time zero. (From Hill, 1981.)

0

102

104

Cel

l cou

nt

106

108

6 12 18Time (hours)

PMNs

E. coli numbers

24 30 36

(a)

Poor response in the freshly calved cow

The description given above applies tohealthy cows which are able to mount a dra-matic inflammatory response, producing ahard, hot, swollen quarter. Some of thesecows may be sick, others less so. There is, ofcourse, an alternative reaction. For a varietyof reasons, freshly calved cows seem unableto mount an effective PMN response, andwhen E. coli invades the udder it can con-tinue to multiply almost unchecked. In theinstance shown in Fig. 3.5b, as few as tenorganisms (a minute number) may haveinfected the quarter 12–18 hours earlier, butbecause the cow was less able to mount animmune response, the bacteria continued tomultiply, with bacterial levels reaching 108

(100,000,000) per ml.Because there is a very limited inflam-

matory response in these cases, the mastitismay be difficult to detect. The udder maywell remain soft and the changes in the milkcould be minimal, making it almost indis-tinguishable from colostrum. However, thecow herself will be very ill, due to the sys-temic effects of large quantities of endotoxin,which have been produced by the multiply-ing E. coli bacteria. (Not all bacteria produceendotoxins.) Severely affected cows may berecumbent, scouring, dull and not eating.They may or may not have a temperature

(cows with a good inflammatory responseinvariably have an elevated temperature) butwill probably be shivering with a foul-smelling greenish, mucoid diarrhoea.

Cows that do not die may remain ser-iously ill for some considerable time. Thelipopolysaccharide endotoxin produced byE. coli has a generalized effect on all bodyorgans, which may leave the cow in poorcondition, dull and with a poor appetite, forseveral weeks. There is little that can be donefor such cows, since the damage to the uddertissue has already occurred, and it is simplytime, nursing and tissue regeneration thatwill effect a recovery. Associated damage tothe teat lining is shown in Fig. 3.6.

When phagocytic cells eventuallyappear, they are often monocytes, cells thatare much less effective than PMNs, andtherefore coliforms may continue to beexcreted in the milk for 1–2 weeks postinfection. This strongly justifies the use ofantibiotic for the treatment of early lactationcoliform mastitis cases. When healing even-tually occurs, it is often with alveolar kera-tinization and milk production in thatquarter is then lost, although most recoverin the next lactation.

The pronounced immunosuppressionin the periparturient cow (which leads to anincrease in many diseases around calving) isprobably an innate mechanism protecting

30 Chapter 3

PMNs

0

102

104

Cel

l cou

nt

106

108(b)

6 12 18Time (hours)

E. coli numbers

24 30 36

Fig. 3.5b. A poor cellular response seen especially in some freshly calved cows allows E. coli to multiply tovery high numbers in the udder (compare this with the good response shown in Fig. 3.5a). Provided the cowsurvives, bacterial numbers may remain high for several days. Infection at time zero. (From Hill, 1981.)

the dam against an overreaction to potentialrelease of fetal (and therefore paternal) anti-gen into the maternal circulation during par-turition and against antigens released fromuterine trauma. Feeding and managementalso play a part. This is discussed in moredetail in Chapter 4.

Individual cow variation

There is a considerable variation betweenindividual cows in their response to anE. coli challenge, even in cows at the samestage of lactation. For example, when E. colibacteria were experimentally infused intotwo different cows:

� 98% were killed within 6 hours in onecow compared with

� only 80% killed within 6 hours in the sec-ond cow.

Part of this variation is undoubtedly due toan inherent difference in the rate at whichPMNs can kill bacteria. Using test-tubeexperiments, it can be shown that PMNstaken from the blood of different cows willkill (or eliminate) E. coli at different rates.However, the main difference betweencows is the rate at which cells can be mobi-

lized from blood into the teat and uddersinuses.

Can cell counts get too low?

There is a body of opinion which suggeststhat if somatic cell counts are too low, thencows are more prone to developing the per-acute and fatal form of E. coli and othertypes of mastitis. Initial survey work (Greenet al., 1996) showed that herds with lowercell counts had a higher incidence of toxicmastitis than herds with higher cell counts.This was then followed by more detailedwork (Peeler et al., 2002) on individual quar-ters, showing that quarters with a cell countof less than 20,000 had an increased risk ofdeveloping clinical mastitis. However, thesame study showed that quarters with a cellcount of above 100,000 had an increased riskof clinical disease. There are many otherstudies that have shown that herds withraised cell counts have an increased risk ofclinical mastitis, and that bulls producingdaughters with raised cell counts also havean increased risk of mastitis.

The difference between an initial cellcount of 50,000 or 150,000 cells per ml isalmost insignificant when, with clinicalmastitis, cell counts could rise to100,000,000 per ml within a few hours. Itappears to be the speed at which cells canbe mobilized into the udder, rather than thenumber present initially, which is the criti-cal factor.

Effect of low selenium and/or vitamin E

Macrophages and PMNs engulf bacteria anddestroy them. One of the methods ofdestruction is the release of lysozymes(destructive enzymes) within the PMN vac-uole, with the resultant production of hydro-gen peroxide. A vacuole is simply acompartment within a cell. The hydrogenperoxide thus produced needs to bedestroyed immediately, and this is done bythe action of glutathione peroxidase, (GSH-PX), a selenium-dependent enzyme. Failureto destroy the hydrogen peroxide can quite


Fig. 3.6. Damage to teat canal lining following anacute E. coli infection.

rapidly result in the death of the phago-cytosing cell itself.

Vitamin E reduces the rate of hydrogenperoxide formation within the PMN and sta-bilizes its cell membranes against its attack,while selenium increases the activity ofGSH-PX. Workers in North America havedemonstrated a correlation between dietarylevels of selenium and vitamin E and mas-titis, and recommend supplementation of1000 IU vitamin E per cow per day duringthe dry period and 400–600 IU per cow perday during lactation. British diets contain-ing a higher proportion of grass silage areless likely to be vitamin E deficient, butall-maize diets and diets containing moregluten or high fat, especially polyunsatur-rated fatty acids (PUFAs), require supple-mentation. One British survey showed thatin low mastitis incidence herds there was acorrelation between increased cell count andlow GSH-PX levels: those herds low invitamin E/selenium had higher counts.

Reduced PMN activity in milk

Unfortunately PMNs are less active in milkthan in blood and this is a further reasonwhy peracute mastitis and endotoxic shock

may occur. The reduced PMN activity isthought to be associated with a variety of fac-tors, including the following:

� They may become coated with casein,which reduces their activity.

� PMNs are unable to distinguish fat andcasein globules from bacteria. The glob-ules may be continually engulfed, therebyexhausting PMNs.

� Oxygen levels are naturally lower inmilk than in blood, and are reduced evenfurther by bacterial multiplication in mas-titic secretions. This limits the ability ofthe PMN to destroy the phagocytosedbacteria.

When PMNs leave the capillaries, they effec-tively need to take their food stores (glyco-gen) with them. This is sometimes referredto as ‘taking their packed lunch’. Once thefood has been exhausted, the PMNs becomerelatively inactive.

Although the above factors limit theactivity of PMNs, the system is still highlyeffective, probably because of the very largenumbers of PMNs present. In fact, a cowwith acute mastitis may pour so many whitecells into the mammary gland that blood lev-els may fall almost to zero.

32 Chapter 3


4 The Mastitis Organisms

Mastitis Definitions 34Development of a New Infection 34

Arrival of a reservoir of infection 34Transfer of the infection from the reservoir to the teat end 34Penetration of the teat canal 34Host response 35Dry period versus lactation infections 36

Strategy for Mastitis Control 36Contagious and Environmental Organisms 36

Epidemiology of contagious organisms 37Epidemiology of environmental organisms 37

Specific Organisms Causing Mastitis 37Staphylococcus aureus 38Coagulase-negative staphylococci (CNS) 42Streptococcus agalactiae 42Streptococcus dysgalactiae 43Mycoplasma species 44

Environmental Organisms 44Coliforms, including Escherichia coli 44Other coliforms 46Streptococcus uberis 47Sources of infection 47Spread within the herd 49

Dry Period Infections 50Phases of the dry period 50The host immune response 53The influence of dry matter intake 53Short dry periods 54

Less Common Causes of Mastitis 54Bacillus species 54Yeasts, fungi and moulds 55Relatively rare causes of mastitis 55

Culturing Milk for Bacteria 56Taking a milk sample 56Laboratory plating and incubation 56Antibiotic sensitivity testing 57Interpretation of results 58

Total Bacterial Count, Laboratory Pasteurized Count and Coliforms 58Methodology 59

34 Chapter 4

This chapter examines mastitis in generalterms, discusses the organisms involvedand provides an overview of controlmeasures.

Some diseases, for example, foot-and-mouth, can be totally eliminated by a testand cull policy and strict biosecurity. Otherdiseases, for example, the bacterial infectionblackleg, can be totally controlled by vaccin-ation. Mastitis is different. It will never beeradicated, because there are too many dif-ferent bacteria involved, and many of theseare always present in the environment.Antibiotic treatment has varying degrees ofeffectiveness and, for a variety of reasons,vaccination can only ever produce a partialreduction in incidence. The approach tomastitis must therefore be one of controland, with increased milk flow rates produc-ing ever higher mastitis susceptibility (seepage 24), control will become increasinglyimportant in the future.

Mastitis Definitions

Mastitis is commonly referred to under thefollowing categories:

� Clinical mastitis: an udder infection thatcan be seen, e.g. by clots in the milk, hard-ness, swelling, etc.

� Subclinical mastitis: an udder infectionthat shows no external changes.

Clinical mastitis can be:

� Acute mastitis: sudden in onset and showssevere signs.

� Chronic mastitis: persists for a long time,but is not severe.

Development of a New Infection

To be able to appreciate the importance ofthe various control measures discussed later,it is first necessary to understand how andwhen a new case of mastitis occurs. Thiswill be dealt with under the following head-ings: (i) arrival of a reservoir of infection; (ii)transfer of infection from the reservoir to the

teat end; (iii) penetration of the teat canal;(iv) host response; and (v) dry period versuslactation infections. The ‘cow factors’, i.e.the mechanics of teat and udder defencemechanisms, were described in the previouschapter.

Arrival of a reservoir of infection

Some of the bacteria that cause mastitis arealways present in the environment and aretherefore called ‘environmental organisms’.For these, ‘arrival of a reservoir’ simplymeans a change in environmental condi-tions, leading to an increased challenge ofinfection at the teat end. Many studies haveshown that teats that are soiled with mastiticbacteria are more liable to develop environ-mental mastitis.

Other infections (e.g. Streptococcusagalactiae) are normally only present in theudder of infected cows and ‘arrival of areservoir’ indicates either the purchase of aninfected cow or perhaps an infected cowcalving down into a herd. In this instance,the infection is ‘contagious’ because it passesfrom cow to cow.

Transfer of infection from the reservoir to theteat end

This will generally occur between milk-ings for environmental organisms, sincethe first stage in the establishment ofa new infection is the transfer of bacteriafrom the environment to the teat end.However, for contagious organisms, transferoccurs during the milking process anda vector is needed to carry the bacteria fromthe infected to the non-infected cow (orinfected to non-infected quarter). Examplesof vectors include the milker’s hands, uddercloths (if the same cloth is used on more thanone cow) and the milking machine liner.

Penetration of the teat canal

There appear to be two ways in which bac-teria commonly penetrate the teat canal:

The Mastitis Organisms 35

� First, growth through the canal. Aftertransfer to the teat end, contagious organ-isms, especially Staphylococcus aureusand Streptococcus agalactiae, have strongadhesive factors and begin their ‘attack’ onthe udder by first establishing a colony atthe teat end, i.e. they multiply. Aftercolonising the teat end, bacteria literallygrow up through the teat canal and moveinto the teat sinus.

� Second, propulsion through the canal.Pathogens, particularly environmentalbacteria such as E. coli, do not have adhe-sive properties and hence are often forcedthrough the canal, usually with a reverseflow of milk, such as occurs with teat-endimpacts (see pages 79–80). The exceptionto this is infections that develop duringthe dry period.

This difference between the two groups oforganisms is shown in Table 4.1. A culture ofeither Staphylococcus aureus or of E. coliwas applied to the teat ends. Swabs werethen taken on a daily basis and the percent-age of swabs positive for the organism eachday was monitored.

Although there was a high recovery ratefor E. coli on days 1 and 2, the organism hadbeen eliminated by day 4. Because thestaphylococci form a colony, the number oforganisms multiplies and graduallyincreases with time. In this experiment, teatswere not disinfected after milking. If postdiphad been applied, then the infection ratewith staphylococci would have been muchlower.

One of the other reasons for differencesin the way organisms penetrate the teat canalis the variation in their inherent ability toadhere to epithelial surfaces. Contagiousorganisms such as Staphylococcus aureus

and Streptococcus agalactiae have strongadhesive properties. They therefore stick tosurfaces and become established as chronicconditions. The environmental organismE. coli has virtually no adhesive properties.Hence, during lactation, transfer into theudder is most commonly associated withreverse flow of milk through the teat canal,often by teat-end impacts (pages 79–80).However, new infections during the dryperiod are an extremely important part of thepathogenesis for both E. coli andStreptococcus uberis, and these new infec-tions are clearly not propelled through theteat canal via a reverse flow of milk. Dryperiod infections are dealt with in detaillater in this chapter.

Although it has been stated that conta-gious organisms grow up through the teatcanal and environmental organisms are pro-pelled, it should be appreciated that the dis-tinction is by no means as precise as this.Clearly a reverse flow of milk will assistmovement of contagious pathogens throughthe canal, while there are occasions (e.g.exposure to high teat-end challenge imme-diately after milking) when E. coli seems topenetrate without reverse flow of milk.Streptococcus uberis, which has both envir-onmental and contagious properties, canenter by both routes.

Host response

Even when bacteria have penetrated the teatcanal and entered the udder, establishmentof infection is by no means a certainty. Thereare a variety of ways in which the udder canovercome infection, and the effectiveness ofthese mechanisms can vary enormouslybetween cows. This was discussed in

Table 4.1. A comparison of the pathogenesis of contagious and environmental organisms followingexperimental infection. Staphylococcus aureus (contagious) establishes a colony at the teat end andhence represents a continuous risk. E. coli is present for a much shorter period of time.

% teat swabs % infectedpositive each day Day 1 Day 2 Day 5 Day 10 quarters

S. aureus 50 68 75 73 4E. coli 93 34 10 0 0

Chapter 3. There is also variation in hostresponse to the different organisms, espe-cially between the dry period and lactation.

Dry period versus lactation infections

The previous paragraphs refer primarily tothose new infections that occur during lac-tation. It is now known that many new infec-tions occur during the dry period. Theseinfections often remain dormant in theudder, and do not appear as clinical mastitisuntil the first 3 to 4 months of lactation.Their precise mechanism of entry throughthe teat canal is unknown, but it must be byslow growth. This is discussed later in thischapter.

Strategy for Mastitis Control

Having seen how a new case of mastitis isestablished, it is now possible to define astrategy for control. This can be subdividedinto three parts:

1. Reduce the reservoirs of infection. Thismeans keeping the environment as cleanas possible and reducing the number ofcows carrying contagious organisms, e.g.by dry cow therapy, postmilking teat dis-infection and culling.

2. Control spread by vectors. This is partic-ularly important for contagious organismsand is discussed in detail in Chapter 6.

3. Optimize host defences. The host defencemechanisms were described in Chapter 3.Keeping teats and teat ends in good con-dition is obviously a vital component ofmastitis control and is, once again, influ-enced by milking machine function,which is described in detail in Chapter 5.

Contagious and EnvironmentalOrganisms

It is not the purpose of this book to go intoprecise details of every organism that couldcause mastitis: over 200 different organisms

have been recorded in scientific literature asbeing causes of bovine mastitis. They can begrouped as follows – organisms in bold typecause the majority of mastitis cases.

� ContagiousStaphylococcus aureusStreptococcus agalactiaeCoagulase-negative staphylococciStreptococcus dysgalactiaeCorynebacterium bovisMycoplasma

� EnvironmentalStreptococcus uberisColiforms:

E. coliCitrobacterEnterobacterKlebsiellaPseudomonas aeruginosa

Bacillus cereusBacillus licheniformisPasteurellaStreptococcus faecalisFungiYeasts

There are a number of other, less com-mon causes of mastitis that are more difficultto categorize into contagious or environ-mental. These are listed on page 55.Although it is possible for this wide numberof organisms to be involved, the majority ofmastitis cases are caused by a few commonbacteria. Table 4.2 shows the incidence ofmastitis infection by different types of organ-ism in 1968 compared with that in 1995 and2007. Note the enormous decrease in thepercentage of Staphylococcus aureus cases,and the proportional rise in the percentageof environmental cases (E. coli andStreptococcus uberis). The overall incidenceof clinical mastitis has in fact declined dra-matically, from 121 cases per 100 cows ayear in 1968 to only 50 cases per 100 cows ayear in 1995 and 47 in 2007. This decreasewas largely due to the dramatic effects ofcontrol measures, such as postmilking teatdisinfection, dry cow therapy and culling,on contagious mastitis.

36 Chapter 4

Table 4.2. The results of one survey showing thedecline in the incidence of contagious mastitisbetween 1968, 1995, and 2007 and the propor-tional rise in importance of the environmentalinfections E. coli and Streptococcus uberis.(Adapted from Hill, 1990; Booth, 1993; Bradley etal., 2007.)

Cases of clinical mastitis %

Type 1968 1995 2007

Coliforms 5.4 26 19.8Streptococcus agalactiae 3 0 0Staphylococcus aureus 37.5 15.4 3.3Streptococcus dysgalactiae 20.1 10.8 1.5Streptococcus uberis 17.7 32 23.5Others 16.3 15.8 0No growth 0 0 26.5

No. of cases per cow per year 121 50 47

Although the percentage of environ-mental cases has increased therefore, fromapproximately 23% in 1968 to 43% in 1995,this is due to a decline in the contagiousinfections (Staphylococcus aureus, Strepto-coccus agalactiae and Streptococcus dys-galactiae), rather than a rise in the number ofenvironmental cases.

The major change that has occurredover the past few years in the UK is the bigincrease in Streptococcus uberis infections.There are many species of Streptococcus,and combined, they show both environ-mental and contagious properties, in that thefirst case may arise from an environmentalinfection, especially during the dry period,but because of a poor response to treatment,further cases occur as a result of cow-to-cowspread during the milking routine.

The following section shows that conta-gious and environmental organisms havemarked differences in their epidemiology.

Epidemiology of contagious organisms

� The mammary gland and/or teat skin arereservoirs of infection.

� Organisms are transmitted from the carriercow or quarter to the teats of non-infectedcows/quarters during the milking process.

� Colonies become established at the teatend and slowly grow through the canalover 1–3 days.

� Dry cow therapy (see Chapter 12) andpostmilking teat disinfection (see Chapter7) are important means of control.

� The dry period is not an important timefor new infections.

� Herds with a high incidence of contagiousinfections often have high cell counts buta normal TBC/Bactoscan (see Chapter 10).

� Herds that only have a problem with con-tagious infections typically have a highcell count but often a low incidence ofclinical mastitis.

Epidemiology of environmental organisms

� The environment is the reservoir of infec-tion.

� Organisms are transferred from the reser-voir to the teats between milkings.

� Penetration of the teat canal occurs bypropulsion on a reverse flow of milk.

� Dry cow therapy, to eliminate existingcoliform infections, is of limited value asenvironmental infections do not persistsubclinically and are not carried from onelactation to the next.

� Many new infections occur during the dryperiod, and here dry cow therapy andinternal teat seals are important preven-tive measures.

� Premilking teat disinfection is importantin control, postmilking disinfection lessso.

� Herds with a high incidence of environ-mental infections may have an acceptablecell count but a high level of clinical casesand a raised TBC/Bactoscan.

The differences in the epidemiology of con-tagious and environmental organisms aresummarised in Table 4.3.

Specific Organisms Causing Mastitis

This section gives a short descriptionof some of the major organisms causing


mastitis, their appearance in culture andthe type of mastitis they produce. It is cer-tainly not in any way intended to be a com-prehensive guide to the bacteriology ofmastitis.

It should also be noted that it is not con-sistently possible to determine the organismproducing mastitis from clinical signs alone.While there may be a few classic guidelines– for example, the serum-coloured waterysecretion produced by an acute E. coli infec-tion – these are by no means consistent. E.coli can also cause a very mild mastitis, witha few clots seen at one milking, which willhave totally disappeared to give a normaludder at the next milking, or even occasion-ally a recurrent mastitis with a high cellcount. The organisms described in somedetail in the following sections are the con-tagious organisms Staphylococcus aureus,other staphylococci, Streptococcusagalactiae, Streptococcus dysgalactiae andMycoplasma, and the environmental organ-isms E. coli and Streptococcus uberis.

Staphylococcus aureus

Staphylococcus aureus organisms arehaemolytic gram-positive cocci, seen ascreamy yellow/white colonies on blood agar(Plate 4.1).

They are coagulase-positive (i.e. theyagglutinate with rabbit serum) and are some-times referred to as coagulase-positivestaphylococci, although not all S. aureuscolonies are coagulase-positive. (More detail

of culture techniques is given later in thischapter.)

The primary reservoir for S. aureus iswithin the mammary gland. Staphylococciare notoriously difficult to treat and, onceinfection has become established, it isextremely hard to eliminate. Table 4.4 showsthat treatment of clinical cases of staphylo-coccal mastitis with cloxacillin gives only a25% cure rate and in subclinical cases only40%. Treatment of primary infections inheifers should result in much betterresponse rates, however, and conversely

38 Chapter 4

Table 4.3. A summary of the major differences between contagious and environmental organisms. The dis-tinction between the two groups is not always precise.

Contagious Environmental

Source of infection Teats and udder Contaminated environmentTransfer of infection into During milking Between milkings and during the dry periodthe udderClinical mastitis Most cases are subclinical A higher proportion are clinical

(Streptococcus uberis can be subclinical)Control by Postmilking teat dipping Environmental hygiene

Dry cow therapy PredippingMilking hygiene Dry period teat sealantsCulling

Plate 4.1. Staphylococci growing on a blood agarplate. Each small creamy-white dot represents acolony of staphylococci containing literally millionsof bacteria. The slightly lighter ring around theoutside of the colony is the ring of haemolysis(broken-down blood).

chronically infected older cows may havebacteriological cure rates as low as 10%.This is discussed in more detail in the treat-ment section of Chapter 12.

The reasons for this poor response totreatment are as follows:

� Once established within the udder,staphylococci often become ‘walled off’ byfibrous tissue, allowing only poor pene-tration by antibiotics. The cow in Plate 4.2is obviously affected, with large fibrouslumps protruding from the rear of herudder. She had a cell count of over 3 mil-lion cells/ml and suffered from recurrentbouts of mastitis.

� S. aureus is able to live withinmacrophages, PMNs (see page 26) andepithelial cells, out of the reach of anti-biotics. Antibiotics can circulate withinbody fluids but are largely unable to pen-etrate cells. Other reasons for poorresponse are given in Chapter 12.

These two factors also partly explain thevery variable cell count and bacterial excre-tion rates of cows chronically infected withS. aureus, as shown in Table 4.5. Theseresults show very clearly that it would bemost unwise to take action (e.g. culling)against a cow on the basis of a single cellcount or milk culture result. A negative cul-ture result does not necessarily mean thatthe cow is free of S. aureus; it just means thaton that day no organisms were isolated.Conversely, due to intermittent excretionand to excretion in low numbers, onlyaround one-third of milk samples frominfected cows are culture-positive. The poorresponse to treatment also emphasises theimportance of ensuring that cows do notbecome infected with S. aureus, and hencethe importance of strict hygiene in the milk-ing parlour. Dry cow therapy is vital, andalthough response to treatment is disap-pointing (see Table 4.4), at least its use low-ers the level of infection in a herd, and it isone further method of reducing the level ofchallenge to uninfected cows.

Table 4.5. Variation in cell count and bacterialexcretion rate of a mammary gland infected withStaphylococcus aureus. (From Bramley, 1992.)

Day sampled Bacteria/ml Cell count (× 1000/ml)

1 2,800 8802 6,000 1444 7,000 1045 10,000 896

13 >10,000 15214 1,200 1,00015 >10,000 168


Table 4.4. Bacteriological cure rates (as percentages) for Gram-positive intramammary infections usingthe antibiotic cloxacillin. (From Tyler and Baggot, 1992.)

Lactation

Organism Clinical infection Subclinical infection At drying off

Staphylococcus aureus 25 40 65Streptococcus agalactiae 85 >90 >95Streptococcus dysgalactiae 90 >90 >95Streptococcus uberis 70 85 85

Plate 4.2. Chronic staphylococcal mastitis. Note thelumps in the udder.

40 Chapter 4

Table 4.6 shows the effects on the nextcows to be milked of milking a cow knownto be infected with S. aureus in her udder.The control cows had been tested previouslyand shown to be free of S. aureus on theirteat skin. Note how the level of contamina-tion increases each time the teats are han-dled, and, even when strict hygiene ispractised (gloves, disinfectant in the washwater and paper towel wipes), contamina-tion still occurs.

Trials have shown that a cow sheddingS. aureus in her milk may contaminate theteats of the next six to eight cows to bemilked. The possible level of contaminationis therefore enormous and will depend onfactors such as the quality of the liners(avoid rough rubber, etc.), the initial amountof infection shed and the efficiency of themilking machine. We are, of course, talkingabout the degree of contamination of the teatskin and not about of actual udder infection.Most infections are killed by postdipping.

It is clear that, if S. aureus is present ina herd:

� Postmilking teat disinfection is vital. Evenwith optimal milking hygiene, it will beimpossible to totally prevent the transferof infection from cow to cow, but postdip-ping should destroy much of that infectionon the teats before it can penetrate the teatcanal.

� Ideally, infected cows should be milkedlast and in a separate group. Where this isimpractical, milking known infected cowsthrough a separate cluster, which can thenbe disinfected between uses, will consid-erably reduce the risk of spread from cowto cow.

� Consideration could be given to disinfect-

ing clusters between all cows. This is dis-cussed in Chapter 6.

� Teat skin should be maintained in opti-mum condition. S. aureus is quite a resist-ant organism. It can live outside themammary gland in sites such as uddercloths, the milker’s hands and teat skin.Infections of the teat skin are particularlycommon if the skin is cracked or chapped,or if it has been damaged by pox virusinfections, malfunction of the machine,warts, etc. This is another important rea-son for using a postmilking dip containingan emollient.

Acute gangrenous staphylococcal mastitis

Under certain circumstances, S. aureus cancause an acute gangrenous mastitis. Thisoccurs following the production of largeamounts of toxin. As shown in Table 4.7, thecondition can be replicated experimentallyby removing all immunity from the mam-mary gland, e.g. by infusing anti-bovineleucocyte antiserum, which eliminates allthe white cells. A cow that may have beencarrying a chronic S. aureus infection formonths, or even years, can developStaphylococcal gangrenous mastitis over justa few days. Gangrenous mastitis is notcaused by a specific acute strain ofStaphylococcus therefore, but ratherby a change in the immune status of theudder.

The clinical appearance of gangrenousmastitis is shown in Plates 4.3 to 4.6. Theskin of the teat and of lower parts of theudder, adjacent to the teat, develops ablue/black discoloration. It will probably beclammy and cold to the touch and may havea slightly sticky feel, due to a surface dis-

Table 4.6. Stages in the transfer of Staphylococcus aureus, following the milking of an infected cow, tothe teats of uninfected cows, using different hygiene routines. (From Bramley, 1981a.)

% swabs positive for S. aureus from

Hygiene Teats before Teats after Teats after Teats afterapplied foremilking foremilking udder wash milking

Water 0 29 63 97Disinfectant, paper towel and gloves 0 16 39 79


Table 4.7. Gangrenous Staphylococcus mastitis results from a reduced immune response and not a spe-cific organism. Note how removing defensive white blood cells (PMNs, by infusing antiserum) leads to ahuge rise in bacterial numbers and the rapid death of the cow.

Time (days) PMN count (million/ml) S. aureus count

1 3.5 102 5.0 22

Infuse antiserum

3 9.0 374 0 14,0005 (Died) 170,000

Plate 4.3. Acute gangrenous staphyloccocal mastitis– note the blue/black discoloration. Otherorganisms such as Bacillus cereus and occasionallyE. coli can produce similar changes.

Plate 4.4. Blistered teat skin associated withgangrenous mastitis.

Plate 4.5. The reddish brown, watery secretion, oftenmixed with gas, which is characteristic ofgangrenous mastitis.

Plate 4.6. Severe gangrenous mastitis, leading to anudder slough. This cow should be culled.

charge. In some cases the surface of the skinforms small blisters, as in Plate 4.4.

Stripping the teat produces a dark, port-wine-coloured secretion (Plate 4.5), oftenmixed with gas. If the cow is very sick, thenthe prognosis is hopeless. Even in cows thatare not seriously ill, there is a risk that at alater date the udder may slough and dis-charge the affected quarter (as in Plate 4.6).Badly affected cows are therefore bestculled, although, if only a smaller part of theudder is necrotic, the necrotic tissue willeventually discharge and complete healingcan be achieved.

However, one word of warning. Cowscan also develop a bruised udder (Plate 4.7),causing blood to accumulate under the skin,resulting in a blue/black discoloration.These cows will be healthy in themselves,their milk will be normal, the quarter warm,not cold, and they will recover without anytreatment. They should certainly not betreated or culled as a case of gangrenousmastitis.

Coagulase-negative staphylococci (CNS)

Coagulase-negative staphylococci (CNSorganisms) have been identified as a cause

of clinical and subclinical mastitis and ris-ing cell counts. They are Gram-positivecocci that do not form clots with the tubecoagulase test. They may be haemolytic ornon-haemolytic, but this does not appear toaffect their pathogenicity. Examples of coag-ulase-negative staphylococci are: S. xylosus,S. intermedius, S. hyicus and S. epidermis.They commonly colonize the teat skin, teatend and teat canal; hence it is difficult to besure whether they are a cause of clinical orsubclinical mastitis, or simply a teat-endcontaminant. However, if milk culture froma cow with a raised cell count produces apure growth of CNS, then these organismsare likely to be the cause of an udder infec-tion producing the cell count response. It isvery important to discard the first four to sixsquirts of milk before taking a sample forbacteriology. If this is not done, any CNS iso-lated may have originated from the teat canalonly.

Increased bulk tank levels of CNS mayresult from poor postmilking teat disinfec-tion or from poor teat skin condition. Suchorganisms are known to be present inmaiden and pregnant heifers, and someauthors have shown that this can lead toreduced yields post-partum. There are evendata to show that intramammary treatmentof heifers 6 months pre-partum will increaseyields, but there are great dangers in doingthis, namely the removal of the natural ker-atin plug and the introduction of new infec-tions, e.g. coliforms, yeasts or moulds, whentubing.

Streptococcus agalactiae

Streptococcus agalactiae is a Gram-positive,alpha-haemolytic coccus. Its very smallcolonies have a bluish appearance onEdwards medium.

Streptococcus agalactiae is a highlycontagious cause of mastitis and is easilytransmitted from cow to cow during themilking process. Its primary reservoir ofinfection is in the udder, although it mayoccasionally colonize the teat canal andeven the teat skin, especially if these sur-faces are cracked. Its response to antibiotic

42 Chapter 4

Plate 4.7. Udder bruising. This must not beconfused with gangrenous mastitis.

therapy is very good (see Table 4.4) andhence it should be possible to eliminateinfection from a herd, provided that carefulattention is also paid to the following sixcontrol points:

� Hygiene during milking.� Postmilking teat disinfection.� Dry cow therapy.� Culling of chronic recurrent cases.� Optimum milking machine function.� Careful selection of replacement animals

Hence, if S. agalactiae is isolated from aherd, it is a good indication that there hasbeen a breakdown in the basic hygiene of themilking routine.

Milk from infected quarters may containmassive numbers of bacteria, in some casesup to 100,000,000 (108) per ml. This can leadto an elevated and fluctuating TBC/Bactoscan in badly infected herds. In suchherds, a dramatic response can be obtainedby a system of blitz therapy. This involvestreating all cows by infusing antibiotic intoeach quarter at three consecutive milkings.Almost all antibiotics are effective againstS. agalactiae, allowing short withdrawalproducts, if commercially available, to beused. Because response to therapy is goodand because milk was only discarded for 24hours after treatment, this used to be an eco-nomic procedure in badly infected herds.However, it must be carried out with strictattention to hygiene. Blitz therapy is dis-cussed in more detail in Chapter 12 undertreatment.

The level of S. agalactiae infection in anindividual cow is much more closely asso-ciated with cell count than isStaphylococcus aureus infection. For thisreason, it is possible to carry out partial blitztherapy, where only cows above a certaincell count are treated. This has also pro-duced good results.

Streptococcus agalactiae is thought topenetrate the teat canal by slowly growingthrough it. Undermilking, which reduces theamount of flushing (‘keratin stripping’) ofthe canal, is hence thought to promote newinfections. Although mainly an udderpathogen, S. agalactiae can also survive in

the environment. For example, it has beenshown to persist on milkers’ hands, particu-larly when the hands are badly cracked (asin Plate 6.1) and in this way it can be spreadfrom farm to farm.

Subclinical infections are common, andthese often lead to raised cell counts.Clinical signs may also be transient. Forexample, in one experiment, infusion oflarge numbers of S. agalactiae into a quartercaused severe clinical signs within 8 hours,but by 24 hours all clinical signs were goneand infection had become subclinical(Mackie et al., 1983). Such cows will then beculture-0negative but antibody positive andclearly represent a potential source of infec-tion to other cows (Logan et al., 1982). Incontrast to Staphylococcus aureus, mostinfections lead to high levels of bacterialshedding, and culture is a therefore a gooddiagnostic tool.

Streptococcus dysgalactiae

Streptococcus dysgalactiae is a Gram-positive haemolytic coccus that producesvery small colonies and a greendiscoloration of Edwards medium.

Streptococcus dysgalactiae is the fourthmajor cause of contagious mastitis. As suchit shares many of the properties and controlmethods applicable to Staphylococcusaureus and Streptococcus agalactiae. How-ever, there are a few specific differences.

Streptococcus dysgalactiae surviveswell in the environment and has been con-sidered by some to be halfway between con-tagious and environmental organisms. It iscommonly found on teat skin, particularlywhen the surface integrity is compromisedby chaps, cuts, machine damage, pox viruslesions, etc., and as such its presence in bulkmilk samples is sometimes used as an indi-cator of teat skin damage. Mammary glandcarriers are less important. Streptococcusdysgalactiae is also present on the tonsilsand hence licking could transmit infectionto teats. This could explain why S. dys-galactiae is a common cause of mastitis inheifers, including heifer calves, and drycows. Teat irritation associated with flies or


44 Chapter 4

chapping due to cold weather, might encour-age an animal to lick its teats and hencetransfer infection, which gradually colonizesthe teat canal, until clinical mastitis occurs.

Finally, S. dysgalactiae is commonlyfound as part of the summer mastitis com-plex (see Chapter 13) and can be isolatedfrom the carrier fly, the sheep-head flyHydrotea irritans.

Mycoplasma species

Mycoplasma colonies are slow-growing(10 days) and are said to have a typical‘poached egg’ shape when grown on bloodagar. Mycoplasma needs special culturingfacilities and cannot be grown using thetechniques described on pages 56–57.

There are two common species ofMycoplasma that cause mastitis:Mycoplasma bovis and Mycoplasma califor-nicum. They are highly contagious and canrapidly spread in an infected herd. Responseto antibiotics is poor and, once identified,infected cows should be milked last, in aseparate group, and monitored until self-cure has occurred. However, most cows haveto be culled. Although infected cows maynot be clinically ill, infection can lead to apronounced drop in yield, often referred toas agalactia (meaning ‘no milk’). Affectedquarters may be swollen and produce only ascant ‘gritty’ or sandy, watery secretion.

As this is a highly contagious organism,strict attention must be paid to hygiene atmilking. This should include flushing oreven pasteurization of the clusters betweencows (see Chapter 6). Both clinicallyinfected and subclinical carriers shed largenumbers of the organism.

Mycoplasma bovis can also be a causeof joint infections and of pneumonia incalves.

Environmental Organisms

This section describes the coliforms, includ-ing E. coli, and, of course, Streptococcusuberis. As the dry period plays such an

important part in the epidemiology of envir-onmental organisms, a description of theorganisms is followed by a section on theimportance of dry period infections.

Coliforms including Escherichia coli

Escherichia coli is a Gram-negative bacillusthat produces grey mucoid colonies onblood agar. There are haemolytic and non-haemolytic strains.

After S. uberis, E. coli is the most preva-lent environmental organism causing mas-titis. It is present in large numbers in faecesand hence infection occurs primarily inhoused cows, when conditions are wet andhumid and when hygiene is poor.Environmental factors are discussed in moredetail in Chapter 8. During lactation, E. coliis thought to penetrate the teat canal bypropulsion and hence increased mastitis isseen with dirty teats, suboptimal machinefunction or techniques that lead to teat-endimpacts. Penetration of the open teat canalimmediately postmilking may also be a fac-tor.

E. coli penetration of the teat canal byno means always causes clinical mastitis; infact, quite high numbers (80–90%) of infec-tions undergo self-cure. In some cows, theonly detectable change is a rise in cell countand in bacterial numbers. In others, veryslight damage to the endothelial lining ofthe teat wall produces just a few whiteflaky clots, which have disappeared bythe next milking. The symptoms oftypical E. coli mastitis are a hard, hotswollen quarter, with a watery discharge. Aproportion of cows develop a severe shockreaction and can die within hours. This vari-ation in the response of the cow to invadingE. coli and the reasons for the wide differ-ences in clinical signs are discussed inChapter 3.

Unlike Staphyloccoccus aureus andStreptococcus agalactiae, E. coli does notadhere to the endothelial lining of the teatand udder cisterns. This is probably one rea-son why chronic carrier cows with recurrentbouts of E. coli mastitis are rare.

Escherichia coli toxins

The toxic effects of E. coli mastitis are dueto the release of an endotoxin that is alipopolysaccharide (LPS) derived from thebacterial cell wall the LPS is removed byphagocytosing PMNs (see page 27), which inturn release lysosomal granules, furtherexacerbating the shock reaction.

Plate 4.8 shows a normal teat in cross-section, with a creamy-pink-coloured teatcistern wall. Contrast this with the intensehaemorrhage of the endothelial lining of theteat wall in Plate 4.9, which was taken froma cow that died as a result of E. coli mastitis.If E. coli reaches the smaller ducts and lact-iferous sinuses of the main gland, then amassive multiplication of bacteria occurs,and this leads to a severe response in thecow. Sometimes damage to blood vessels isso great that serum ooze is seen on the sur-face of the udder and teat, as in Plate 4.10.

Such cases can lead to extensive gangreneand resultant sloughing of udder tissue, asseen in Plate 4.6.

Dry period coliform infections

Although lactoferrin prevents clinical drycow coliform mastitis, many new subclin-ical infections are contracted during the dryperiod, especially in the first and last2 weeks. These infections remain dormantin the udder and commonly produce clini-cal mastitis during the first 100 days of lac-tation. Dry period infections are common forboth E. coli and S. uberis, and are dealt within detail later in this chapter.

Variation in strains of Escherichia coli

When a herd outbreak of severe E. coli mas-titis occurs, it is unlikely to be caused by thesame strain of E. coli in every cow, eventhough clinically this may appear to be thecase. There are usually a number of strainsinvolved in a severe challenge. For example,in one survey of 290 isolates from cases ofacute E. coli mastitis:

� 82% were typed as 63 different strains ofE. coli.

� 18% could not be typed.

Cow-to-cow transmission, as occurs withcontagious mastitis, is therefore unlikely tobe important. A severe outbreak of coliform


Plate 4.9. A teat infected with E. coli mastitis. Notethe intense haemorrhage on the teat wall.

Plate 4.8. A normal teat in cross-section.

Plate 4.10. E. coli mastitis. Damage to blood vesselsmay be so extensive that serum oozes through thesurface of the udder skin, as well as into themammary gland.

mastitis is likely to be caused either by aheavy environmental challenge, e.g.increased exposure from the environment,dry period and/or milking machine functionproducing high teat-end contamination, or adecreased immune response.

Vaccination against Escherichia coli

The toxic effects of E. coli are produced byan endotoxin that chemically is an LPSderived from the cell wall. Each time one E.coli divides into two (and this happensevery 20 minutes under the ideal conditionsof warm milk within the mammary gland), acertain amount of LPS is released. In addi-tion, when the E. coli die, further quantitiesof LPS are released. Although the LPSs pro-duced by the various strains of E. coli are alldifferent, there is one strain known as a‘rough mutant’, that produces LPS whichhas a fragment that is common to all LPSsproduced by all other strains. This forms thebasis of what is known as the J5 vaccine. Themanufacturers claim 80% protection fol-lowing three subcutaneous injections of anoil adjuvant vaccine given at drying off, 28days later and within 2 weeks after calving.The results of one field trial, in which halfof each herd was vaccinated and the otherhalf was left as a control, are shown in Table4.8. The vaccine does not result in any fewernew infections. There is a reduction in clin-ical cases, and a marked reduction in acutetoxic cases, which become particularly rare.

Table 4.8. Response to J5 E. coli vaccine. (FromA.W. Hill, personal communication, 1922.)

No. Cases of %of cows conform mastitis infected

Vaccinated 233 6 2.6Non-vaccinated 227 29 12.8

However, it is interesting that the vac-cine does not protect against experimentalchallenge by E. coli, and a good deal of workhas attempted to explain this difference. Alogical explanation would be that the vac-cine in some way alters the method by

which E. coli infections penetrate the teatcanal or become established in the udder.This has still to be clarified.

Chronic recurrent coliforms

In the majority of herds, response to E. coliinfection is very prompt and the organismsare rapidly eliminated through the naturalresponse of the cows, e.g. within12–36 hours. These cows have a hardswollen quarter with a brown watery secre-tion, but often there are no residual bacteriapresent when the quarter is sampled. Cowsthat mount a poor inflammatory response(see pages 27–29) become very sick and E.coli may persist within the udder for 10–14days, despite the use of antibiotics. This per-sistent presence of E. coli can act as achronic irritant, leading to hyperplasia(abnormal cell growth) and keratinization ofthe gland, and the quarter then dries up.Many such quarters become productiveagain in the next lactation.

In a Dutch study, 5% of all clinical col-iform infections resulted in chronic recur-rent mastitis, and this figure may be greaterwith high initial E. coli numbers and whenantibiotics are not used. In a UK study(Bradley and Green, 1998), 35% of coliformcases (20 cases in 13 quarters) recurredif infections originated during the dryperiod, and 17% (18 cases in 15 quarters)recurred if they originated during lactation.It would therefore appear that chronic infec-tions are more likely to arise from the dryperiod.

Other coliforms

There are a range of other organisms, inaddition to E. coli, which fall into the gen-eral category of coliform mastitis and may beisolated from time to time. These include thefollowing:

� Enterobacter aerogenes.� Citrobacter.� Klebsiella pneumoniae. This organism

may be found in damp, stored sawdustfrom freshly felled wood. It can produce a

46 Chapter 4

severe, toxic mastitis if the sawdust orwood product is used for cubicle (free-stall) bedding.

� Pseudomonas aeruginosa. Typically,Pseudomonas originates from contami-nated water, found, for example, in udderwash header tanks that are maintained ata low, warm heat and that do not have lidsover them or sanitizer added to them.Pseudomonas may also be found in waterfrom boreholes. The clinical signs varyenormously, from acute toxic mastitis tochronic recurrent cases. Response to treat-ment is poor, probably because the organ-ism can live inside cells where it is notaccessible to antibiotics. Hence, chron-ically infected cows with high cell countsmay have to be culled, since they repre-sent a source of infection to other cows(though it is perhaps not too serious, asonly low numbers of organisms are shed).

� Non-lactose-fermenting coliforms, oftenreferred to as NLFs, have become anincreasingly common cause of clinicalmastitis. Many of these are also environ-mental, i.e. non-enteric Pseudomonasspecies.

Streptococcus uberis

Streptococcus uberis grows as a non-haemolytic, Gram-positive coccus, produc-ing brown colonies on an Edwards plate,due to splitting of aesculin. Some workerscategorize all aesculin-splitting streptococcias S. uberis. However, this is incorrect asthere are many other examples, includingStreptococcus faecium and Streptococcusbovis.

A typical case of S. uberis mastitis isoften sudden in onset, and produces a hard,swollen quarter, with large white clots in themilk, and sometimes with a high, or veryhigh, body temperature.

Variation in strains of Streptococcus uberis

DNA fingerprinting studies have shown thatS. uberis is not a single organism, but a rangeof organisms. Some strains of S. uberis aremuch more resistant to opsonization (coat-

ing of the bacteria with antibody: seeChapter 3), and hence phagocytosis (engulf-ing) and destruction of these strains of bac-teria by white cells is also poor. This isparticularly so in the presence of the milkprotein casein (see Fig. 4.1). AlthoughS. uberis was initially considered to be anenvironmental organism, it is now alsoknown that some strains can be a cause ofchronic, recurrent and subclinical mastitis,with a poor response to antibiotics.

Prompt antibiotic therapy is there-fore important, although for reasonsgiven later, response to treatment isoften poor. This results in subclinicallyinfected cases, which then spread furtherinfection from cow to cow during the milk-ing process.

Sources of infection

Streptococcus uberis is currently the mostcommon environmental organism causingmastitis in the UK. It is particularly associ-ated with straw yards, where a very highlevel of infection may occur. Up to 1,000,000(106) organisms/g of straw bedding havebeen reported. Fig. 4.2 shows the correlationbetween the level of S. uberis/g of straw bed-ding and incidence of S. uberis mastitis inthe herds surveyed. Note that the majority ofproblem herds were associated with highlevels of S. uberis in the bedding. This hasled to a move away from straw and espe-cially straw yards, and into sand-beddedcubicles. Clean sand supports only a lowlevel of S. uberis and E. coli, and, if the pHof the bedding can be kept high, for exampleusing lime or ash from power station waste,this further reduces bacterial growth.Contaminated sand, e.g. with milk, urine orfaeces, will, of course, support bacterialgrowth.

In addition to being in the environment,S. uberis can also be found on a wide rangeof sites on an animal, such as the mouth,vulva, groin and axilla, as shown inTable 4.9.

Although present in faeces, levels arenot particularly high, and in this respectS. uberis differs from E. coli.


48 Chapter 4

S. uberis problem herds

Other herds

Number of S. uberis per g of straw

101–

1000

Less

than

100

1001

–10,

000

10,0

01–1

00,0

00

100,

001–

1,00

0,00

0

Mor

e th

en 1

,000

,000

80

60

40

% o

f sam

ples

20

0

Fig. 4.2. Levels of Streptococcus uberis in straw bedding in S. uberis problem herds compared with otherherds. (From Hill, 1992a.)

No supplement

0140J

0

20

40

60

% s

urvi

val

80

100

ST10 C221Strain

EF20 C197C

Added casein

Fig. 4.1. Phagocytic resistance of Streptococcus uberis grown with and without casein. Most strains appearto be protected from phagocytosis in the presence of casein. (From Hill, 1992b.)

Spread within the herd

The initial infection may be from the envi-ronment or from the purchase of an infectedcow, but S. uberis can rapidly spread withinthe herd. Following infection, S. uberis isknown to remain refractory in the udder forquite a long period. In one study, this was anaverage of 11⁄2 months after infection andtreatment. This poor treatment response rateand the long refractory period within theudder are thought to be due to a number offactors, for example:

� Its resistance to phagocytosis, caused bypoor opsonization.

� It can exist inside cells, where it is pro-tected from the action of many antibiotics.

� It can enter the mammary lymph node,from where it maintains a reservoir ofinfection.

In one experimental infection, S. uberis hadreached the lymph node in as little as 6 dayspost inoculation. Hence, in herds whereS. uberis is a problem, treatment of clinicalcases needs to be long and aggressive, to tryto avoid the carrier state.

Some cows experimentally infectedwith S. uberis recover, but only after pro-longed treatment with antibiotics, for exam-ple, 5–7 days of combined parenteral (byinjection) and intramammary therapy. Theseare presumably the ‘chronic mastitic’ strains,which are related more closely to contagiousthan to environmental pathogens.

As further evidence of the contagiousnature of S. uberis, it has been shown thatthe prevalence of infected quarters in a herdis a good predictor for the incidence of new

infections. Hence, if the level of S. uberisinfected quarters is low, then the future clin-ical incidence will remain low. However, asthe level of infected quarters rises (possiblyinitially from an environmental or dryperiod source), so will the future number ofclinical cases. This is commonly seen inpractice. There will be an initial outbreakand the source of the outbreak may be iden-tified and corrected, but clinical cases con-tinue for several months due to recycling ofinfection within the herd. Often culling ofthese ‘reservoir’ cases is the only controloption. As the organism shows both conta-gious and environmental properties, thenboth predip and postdip are relevant forcontrol.

Although most herds already havemany different strains of S. uberis present,the introduction of another new strain canstill cause a severe outbreak, all of the samenew strain. This suggests that strain cross-protection is limited, and shows the impor-tance of biosecurity. Bulk tank levels ofS. uberis give a reasonable assessment ofherd status, because strains in the udder aregenerally the same as those found in thebulk tank, i.e. they come from the udder andnot from the environment.

Streptococcus uberis in the dry period

Streptococcus uberis is the most commonnew infection of dry cows, especially duringthe first and last 2 weeks of the dry period.These infections lie dormant in the udder toproduce clinical disease in early lactation.Dry cow therapy and environmental hygieneare therefore very important in control. Onestudy (Williamson et al., 1995) showed that12.3% of control cows were infected with S.uberis at calving, compared with only 1.2%of quarters given antibiotic dry cow therapy.Dry period infections are dealt with in detailin the next section.

Outbreaks at pasture

Streptococcus uberis mastitis outbreakssometimes occur in cows at pasture, espe-cially in late summer. The most probablecause is that, during the summer especially,


Table 4.9. Isolation of Streptococcus uberis from 53in-calf heifers kept at pasture under dry sunnyconditions. (From Bramley, 1981b.)

Site examined No. positive % positive

Escutcheon 48 90Legs 46 86Hind teats 49 92Lips 12 22Total 155 73

cows often tend to lie on the same area atnight, which could then develop a build-upof infection. It is advisable to move cowsevery 2 weeks, to avoid this build-upof infection, and not let them back to thesame paddock for at least 2 and preferably4 weeks. Other factors leading to outbreaksat pasture include the contagious transmis-sion of ‘chronic’ strains, or perhaps cowstransmitting oral infections by licking teatsirritated by flies.

Vaccination against Streptococcus uberis

Because there is such a wide range of strainsof S. uberis, it is important to find a singleantigen that is present in all strains. Leigh(2000) found that most strains produce theenzyme PauA, which activates plasminogenthus releasing casein and other nutrientsfrom milk to allow the organism to grow. Anexperimental vaccine against PauA has beenfound to be multi-strain effective, withoutleading to increase in mammary PMNs,although to date there are no commercialproducts available.

Dry Period Infections

Dry period infections are an extremelyimportant part of the epidemiology of envir-onmental pathogens such as E. coli andS. uberis. These infections often remain dor-mant, i.e. subclinical, throughout the dryperiod, but are then an important cause ofclinical mastitis in the first few months ofthe next lactation. To fully understand thisprocess, it is necessary to examine what hap-pens in the dry period in some detail.

The following section examines thechanges that take place during the dryperiod, when infections occur, environmen-tal and other factors leading to an increasedlevel of new infections, and finally theimmune response, i.e. the way in which thecow modulates the outcome of these newinfections.

Phases of the dry period

There are three phases of the dry period:

1. The first 2 weeks. The teat canal slowlycloses, and a plug of keratin and lipid isexcreted into the lumen of the canal toform a teat seal. Mammary alveoli (milk-secreting tissue) slowly regress.

2. The rest phase during the mid dry period.The secretory tissue is dormant at thisstage, and there is a build-up of naturalinhibitory substances, such as lactoferrin,neutrophils, NAGase (N-acetyl-glucosaminidase) and, of course, im-munoglobulins, especially towards theend of the rest phase.

3. The last 2 weeks before calving. Newsecretory tissue forms, i.e. new mammaryalveoli, and the keratin plug slowly dis-solves ready for the start of the next lac-tation.

It is during the first and last 2 weeks of thedry period, i.e. when the teat canal keratinplug is forming and then dissolving, that thecow is especially susceptible to new infec-tions. This is shown in Fig. 4.3. This graphshows that cows in late lactation (a) onlydevelop a low level of new infections, butimmediately after drying off there is a bigincrease in new infections, namely at (b).These infections do not develop into clini-cal cases at this stage however. During thecentral dry period (c), the level of new infec-tions is very low and many residual infec-tions from the previous lactation areeliminated. The maximum level of newinfections occurs at (d), just before and justafter calving, which is when the teat canalkeratin plug is dissolving and milk is start-ing to accumulate in the udder. The periodjust before and just after calving is thereforethe time of major risk for new dry periodinfections, and this is when management ofthe cow should be at its highest.

As stated above, these new infections donot appear as disease, i.e. as clinical mastitis,during the dry period. The majority remaindormant in the udder, and do not appearas clinical disease until early lactation. InFig. 4.4 it can be seen that most new cases of

50 Chapter 4


Rat

e of

new

infe

ctio

n

DryingoffCalving

Dryingoff

Lactation

ac

d

bb

Dryperiod

1 2 3 4 5 6Month

7 8 9 10 11 12

0

5

10

15

20

25

30

35

40

45

1 2 3 4 5 6 7 8 9

Month of lactation

% H

erd

mas

titis

Fig. 4.3. This figure shows the incidence of new intramammary infections (IMIs) over a lactation. There is alow level in late lactation. This dramatically increases just after drying off, falls again in the mid dry periodand reaches a peak around calving (Green et al., 2002).

Fig. 4.4. New infections contracted during the dry period lead to clinical mastitis during the first4 months after calving. The light blue bars represent clinical mastitis arising from lactation infections, andthe dark blue bars are from dry period infections (Green et al., 2002).

mastitis occur in the first 4 weeks of lactation,and, of these clinical cases, some 60% origi-nate from infections that have become estab-lished during the dry period. This wasdespite the use of dry cow antibiotic therapy.It should also be noted that dry period infec-tions continued to cause clinical mastitis upuntil the fifth month after calving.

The process whereby a keratin plug isformed in the teat canal during the first2 weeks after drying off was describedabove. Unfortunately, many cows do notform an effective teat seal, and in these cowsthe risk of new infections is even greater.Woolford et al. (1998) in New Zealandshowed that 97% of dry period mastitisinfections were in ‘open’ quarters, i.e. quar-ters that had not developed a good teat seal.The slow development of the teat seal isshown in Fig. 4.5. Even at 45 days after dry-ing off, 25% of teats had not formed an effec-tive teat seal, i.e. they were still ‘open’.

The effectiveness of the teat seal varieswith factors such as the following:

� Overall production. Cows with highertotal lactation yields form a less effectiveseal.

� Milk flow rates. Fast milkers form a lesseffective seal, and they are more likely toleak milk. For example, in a trial in theNetherlands, Schukken et al. (1993)showed that cows that leak milk are four

times more likely to develop mastitis inthe dry period.

� Milk yield at drying off. The higher theyield at drying off, the higher will be therisk of an ineffective keratin plug forming.Dingwell et al. (2004) in the USA showedthat new infections developed in 26% ofcows with drying off yields of greater than21 kg, but in only 16% of cows where thedrying off yield was less than 13 kg.Bradley and Green (1998) have shown thatevery 1 litre increase in yield at drying offproduces a 6% increase in the risk of anew dry period infection. It is thereforeessential that the level of yield isdecreased before drying off. This can beachieved by either feeding or manage-ment, but it should not be done by milkingonce a day or alternate-day milking.

� Teat-end damage. Dingwell et al. (2004)showed that cows with a significant levelof teat-end damage were 1.7 times morelikely to develop a new dry period infec-tion. Teat end damage is a risk factor formastitis in both the dry period and lacta-tion therefore.

� Dry cow therapy. Woolford et al. (1998)showed that cows given dry cow therapy(DCT) were twice as likely to form a goodseal. Presumably this is because teat canalorganisms degrade keratin, and theirremoval with DCT leads to a more effec-tive seal.

52 Chapter 4

00

20

40

60

% q

uart

ers

‘ope

n’

80

> 21 litres < 21 litres

100

1 2 3

Weeks of dry period

4 5 6

Fig. 4.5. Keratin plug formation. Although the keratin plug is a very effective teat closure mechanism,unfortunately many cows do not form an effective seal. This is especially the case in higher-yielding animals,cows with teat-end damage and cows with high yields at drying off (Dingwell et al., 2002).

The correct procedure for drying off cows isgiven in Chapter 12. In addition to the abovefactors, the major methods of reducing dryperiod infections are: (i) dry period antibi-otic therapy; (ii) internal and external syn-thetic teat sealants; and (iii) environmentalmanagement. These are discussed in moredetail in Chapters 8 and 12.

The host immune response

In their work, Bradley and Green (1998)found that from 1200 quarters sampled dur-ing the dry period there were 154 dry quar-ters that developed coliform infections, andof these 13 (8.4%) developed clinical col-iform mastitis with the same organism dur-ing the next lactation. In contrast, of the1043 quarters that were not infected duringthe dry period, only 15 (1.4%) developedclinical coliform mastitis in the next lacta-tion.

Quarters subclinically or latentlyinfected with coliforms in the dry period aretherefore almost six times more likely todevelop clinical mastitis during lactation.DNA fingerprinting studies showed that itwas the same organism that carried overinto lactation. In fact, over 50% of all clini-cal coliform mastitis cases seen in early lac-tation are as a result of infections in the dryperiod, so, when investigating a herd out-break, attention to dry cow environ-ment, management and hygiene at dry cowtubing is essential. It would also seem logi-cal to select a dry cow antibiotic that is effec-tive against coliforms, and there are somedata to show that framycetin may be moreeffective.

However, perhaps one of the most inter-esting features of dry period infections is notthe number of clinical cases of mastitis thatoriginate from the dry period, but rather thenumber of new infections that undergospontaneous recovery. From the above, itcan be seen that only 8.4% of quartersinfected during the dry period developedclinical mastitis during lactation, i.e. over90% of cases recovered. An important factorfor the dairy farmer is to understand whatmodulates the immune response, i.e. what

makes the 91.6% of cows recover. There isno doubt that management and stress play apart. In a study of cases of toxic mastitis inNorthern Ireland, Menzies et al. (2003)showed that cows with milk fever are 23times more likely to get toxic mastitis, andthat cows with assisted calvings are 11 timesmore likely to get toxic mastitis.

It is also well known that all cowsundergo a suppression of the immune sys-tem during the 2 weeks before and the2 weeks after calving, and this renders themmuch more susceptible to disease over thisperiod. The extent of the immune suppres-sion can be estimated by measures such asthe speed of the neutrophil response to bac-terial invasion and the efficiency with whichselectins pull neutrophils through the capil-lary wall in response to inflammation (seeFig. 3.4). The evolutionary reasons suggestedfor this reduction in the immune responseinclude the following:

� As the fetus is antigenically different fromthe dam, there is a risk that ‘leakage’ offetal fluid into maternal circulation wouldlead to a hypersensitivity reaction.

� A reduced immune response will reducereaction to trauma that might occur in thebirth canal during parturition.

� Transfer of antibodies into colostrummay decrease circulating maternal anti-body.

The influence of dry matter intake

All dairy farmers know the importance ofgetting a cow to eat after calving, and one ofthe major factors influencing the expressionof the immune system is the level of foodintake at this stage. Dry matter intake (DMI)starts to fall approximately 2 weeks precalv-ing, reducing from around 2.5% of bodyweight to less than 2%, e.g. down to only 10to 12 kg for a 600 kg cow (Fig. 4.6). On theday of calving, the rate of rumination slowsor almost stops, and this further decreasesfood intake. Ample long fibre in the dietstimulates the resumption of rumen activityand hence feed intake. Cows that maintain areasonable feed intake and those that


quickly regain food intake after calving areless likely to develop metabolic disorderssuch as milk fever, metritis, ketosis, dis-placed abomasums, cystic ovaries, and ofcourse, mastitis. Cows that are overfathave lower DMIs and are more likely todevelop metabolic disorders and mastitis.On this definition, therefore, mastitis mighteven be considered to be a metabolic disor-der, in that many cows become infected withmastitis pathogens but only a few areaffected, i.e. progress to develop clinicaldisease.

Short dry periods

All dairy farmers also know that, if a cowhas been dry for a very long time, she has anincreased risk of developing mastitis andother metabolic disorders when she doeseventually calve. A dry period of 8 weekswas originally considered ideal, but recentwork has shown benefits from dropping thisto 5–6 weeks or less. Shorter dry periodsmean that the cow has an additional2–3 weeks of lactation, and that she does notprogress into the same level of ‘metabolicshutdown’. There is some evidence thatcows with both shorter and longer dryperiods have increased cell counts in thenext lactation, but cows with shorter dryperiods have less risk of developing clinicalmastitis.

Less Common Causes of Mastitis

Bacillus species

Bacillus species are seen as both haemolyticand non-haemolytic Gram-positive bacilliwith characteristic large, rough, dry, flakycolonies on blood agar.

There are two common Bacillus speciescausing mastitis: B. cereus and B. licheni-formis. Great care must be taken with sam-pling, since Bacillus species can also be acontaminant of the teat canal and not asso-ciated with mastitis. It is essential to discardfour to six squirts of foremilk before taking asample.

Bacillus cereus

This is classically associated with infectedbrewers’ grains and may produce an acute,gangrenous mastitis (see Plates 4.3 to 4.6). Itcan also occur as a contaminant on dry cowsyringes, warmed in a bucket of contami-nated water for ease of administration.Bacteria (including Pseudomonas) infusedat this stage may persist in the udder toproduce acute mastitis after drying off oroccasionally at the next calving.

Bacillus licheniformis

This is an environmental organism to whichcows are particularly vulnerable if they lie

54 Chapter 4

Fig. 4.6. Depression of intake at calving. All cows experience a fall in dry matter intake (DMI) around thetime of calving (↑). The cows with a larger fall in DMI and those slower to recover intakes in early lactationare more likely to experience metabolic disorders such as milk fever, retained placenta, ketosis, displacedabomasum and mastitis.

0

1

2

3

4

–14 –8 –4 0 3 7 11 16 20

Days

DM

I (%

bod

y w

eigh

t)Healthy cows

Sick cows

on waste silage left beside feed troughs. Thisis especially the case with maize silage,which undergoes more rapid secondary fer-mentation than other types and thereforeproduces a warm bed. Poor cubicle comfort,leading to increased numbers of cows lyingoutside, may also be involved. Bacilluslicheniformis infections ascending into thevagina may also lead to an increase inendometritis (‘whites’), low conception ratesand abortions later in pregnancy.

Clinically, Bacillus species mastitis isoften presented as a hard quarter with whiteclots. Although sensitivity tests often indi-cate that a wide range of antibiotics shouldbe effective for treatment, response is oftendisappointing.

Yeasts, fungi and moulds

Yeasts, fungi and moulds grow slowly onblood agar and are best cultured onSabouraud’s media. Examples of yeastsinclude Candida and Prototheca, andAspergillus is a common fungal infection.Yeasts will be seen as Gram-positive bottle-shaped organisms on smear.

Yeasts and moulds are common envi-ronmental organisms. They may cause mas-titis if the straw or other bedding is wetand/or mouldy, for example from beingstored outside. Yeast mastitis may occur if alarge number of cows are lying out of thecubicles (free-stalls) or if the milker washesthe teats but does not wipe them dry beforeapplying the milking units. This is particu-larly the case if the water is contaminatedand non-sanitized. On farms where wet teatsare a problem, heavy contamination of teatskin leads to infection in bulk milk. It maybe possible to culture Candida species(yeasts), Aspergillus fumigatus (moulds) orPrototheca zopfii (algae) from both bulk milkand cases of clinical mastitis.

Clinically, the mastitis is most com-monly seen as a hard, hot and swollen quar-ter, with thick white clots. The cow mayhave an elevated temperature, especiallywith yeast (Candida) mastitis. Treatmentwith antibiotics is totally ineffective, asyeasts and fungi do not respond to anti-

biotics. Significant success has beenreported from infusing 60–100 ml of a mix-ture of 1.8 g iodine crystals in 2 litres liquidparaffin, plus 23 ml ether, into the quarter,daily for 2–3 days. On each occasion, theinfusion should be stripped out after 6–8hours, otherwise the iodine can produceexcessive irritation and be a cause of in-flammation in itself. Intravenous sodiumiodide or oral potassium iodide given con-currently sometimes improves response totreatment.

As the mixture is unlicensed, i.e. it is an‘off label’ treatment, standard milk with-drawal times apply.

Relatively rare causes of mastitis

The following list includes some of theminor species causing mastitis:

� Arcanobacterium pyogenes. This is dis-cussed in Chapter 13 under summer mas-titis.

� Corynebacterium bovis: can cause sub-clinical mastitis and raised cell counts.Has been associated with poor/delayedpostmilking teat disinfection. May also beisolated from the teat canal and not asso-ciated with mastitis.

� Streptococcus faecalis: present in faecesand a common contaminant in samples.Could be a cause of mastitis if isolated inpure culture.

� Leptospira hardjo: seen in conjunctionwith abortions and milk drop as part of theleptospirosis complex. Very difficult toculture.

� Nocardia asteroides: very hard quarter.Poor response to antibiotics.

� Streptococcus zooepidemicus.� Pasteurella/Mannheimia species: envir-

onmental organisms. Have been associ-ated with warming drying off tubes incontaminated water prior to infusion.

� Serratia species: can cause mastitis inboth dry and lactating cows. Severalspecies but S. marcescens is the mostcommon. Non-pigmented strains arethought to be more pathogenic than pig-mented strains.


� Salmonella: has possible human healthimplications.

� Corynebacterium ulcerans: has possiblehuman health implications (sore throats).

� Listeria monocytogenes: has possiblehuman health implications and has beenassociated with soft cheese.

� Mycobacterium smegmatis.� Yersinia pseudotuberculosis: common

infection of wild birds, especially star-lings.

� Haemophilus somnus.

Specialist texts should be consulted for moredetails of these organisms. (See ‘FurtherReading’ section.)

Culturing Milk for Bacteria

Culturing a pretreatment mastitic milk sam-ple is a standard procedure in the investiga-tion of mastitis. The major reasons for doingthis are:

1. It is obviously important to know whichorganism(s) you are dealing with beforetackling a mastitis problem. This isbecause of the differences in the epi-demiology and subsequent control meth-ods required for contagious andenvironmental mastitis.

2. A knowledge of the organism will alsohelp to determine treatment strategies.For example with extensive Strepto-coc-cus agalactiae infection, blitz therapymight be considered and, with chronicStaphylococcus aureus infection, cullingwould be the likely option. This is dealtwith in more detail in the treatment sec-tion in Chapter 12.

3. Knowledge of the organism involved willalso help to determine if mastitis organ-isms are part of a concurrent TBC/Bactoscan problem.

Taking a milk sample

The quality of the results (and hence valuefor money) obtained from submitting a milksample to the laboratory is to a very large

extent determined by the quality of the ini-tial sample. The teat end is often heavilycontaminated by a range of environmentalbacteria, and by normal commensal teat-endorganisms, but, of course, they are not nec-essarily the cause of the mastitis. Some mayeven penetrate the outer areas of the teatcanal. To determine which bacteria are thecauses of mastitis, samples must be takenvery carefully. The following procedureshould give good results:

1. Make sure the operator has clean hands.Wash and dry if necessary, or wear cleangloves.

2. Wash and thoroughly dry the teat if itappears dirty.

3. Strip out and discard the first four to sixsquirts, thus flushing out non-mastiticbacteria from the teat canal.

4. Predip and wipe.5. Thoroughly scrub the teat end with a swab

soaked in surgical spirit or similar, untilthe swab remains clean. Only then shouldthe top be removed from the sample bottle.

6. Hold the bottle at an angle of 45° or lessand draw out one squirt of milk in a diag-onal direction. If the bottle is held verti-cally there is a much greater risk of dustand debris falling into the sample duringstripping. One good ‘draw’ of milk issufficient. It is not necessary to fill thebottle.

7. Replace the cap and label the bottle withcow identity, quarter, date and farm name.

8. Store the sample in the fridge (+4°C) untilit can be transported to a laboratory.Ideally, samples should be plated outwithin 60–90 minutes, as this gives thebest results. Storage for up to 72 hours at4°C is acceptable. Freezing reduces bac-terial numbers for some organisms (espe-cially for coliforms) but can still giveuseful results. If possible, transport to thelaboratory in ice packs.

Laboratory plating and incubation

Milk samples are cultured on agar plates.These contain special media (e.g. blood) thatprovide food for bacterial growth.

56 Chapter 4

There is a wide range of techniquesavailable, the variation suiting differentneeds. The method described in the follow-ing protocol is currently used by the authors,as it suits their requirements in veterinarypractice. Although not the cheapest method,it allows fairly rapid identification of themajor groups of mastitic organisms.

1. Preheat samples to at least room temper-ature to break down the fat globules, thusreleasing trapped bacteria.

2. Use a sterile cotton wool swab to streakthe initial plate. A standard 7.0 mm bac-teriological loop contains only 0.05 mlmilk and such a low volume could missmastitic organisms that are only presentin low numbers in the milk (e.g. less than20/ml).

3. Plate out on to the following media:� Sheep blood agar (Columbia).� MacConkey.� Edwards.� Sabouraud, especially if yeasts and

fungi/moulds are suspected (althoughthese organisms will also grow slowlyon blood agar).

4. Incubate plates at 37°C and examine after24 hours and again at 48 hours.

5. Gram-stain colonies to determine theorganism morphology (structure) and todetermine whether it is Gram-positive orGram-negative.

Bacteria are differentiated in manydifferent ways: from their appearance onculture plates, their size, their shape andtheir reaction to a stain known as theGram stain. For example:� Shape: most bacteria are shaped as

either� spheres (cocci), e.g. Staphylococcus

or Streptococcus; or� or rods (bacilli), e.g. Bacillus cereus.

� Gram stain: bacteria stain either� Gram-positive: dark purple, e.g.

Staphylococcus or Streptococcus; or� Gram-negative: pink, e.g. E. coli,

Pasteurella or Pseudomonas.Bacilli are often Gram-negative (but

not always: Bacillus species are Gram-positive) and cocci are often Gram-positive. This distinction between

Gram-positive and Gram-negative bac-teria is quite important when compar-ing the antibiotic sensitivity of differentorganisms.

� Haemolysis: some bacteria break downblood, to give a ring of haemolysis or‘clearing’ of the blood around coloniesgrowing on the agar plate, as seen inPlate 4.1.

6. Carry out other useful bacteriological dif-ferentiation tests, which include thosefor:� Coagulase.� Oxidase.� Catalase.

Antibiotic sensitivity testing

A single colony is taken from the originalculture plate, added to a bottle of liquid cul-ture medium (broth) and incubated for 4–6hours, to increase bacterial numbers. It isthen poured over the surface of a secondagar plate. Bacteria should grow evenly overthe surface of this second plate.

Small paper discs, each one containinga different antibiotic, are then placed ontothe surface and the plate is incubated for afurther 24 hours. If the bacteria grow up tothe very edge of the disc (as with the anti-biotic on the left of Plate 4.11), then thisantibiotic will not be effective in treating thebacteria. On the right, the antibiotic has dif-fused out from the disc onto the agar


Plate 4.11. Antibiotic sensitivity plate. Only theantibiotic that causes a zone of inhibition aroundthe disc (right) would be effective in the treatment ofthis infection.

58 Chapter 4

surrounding the disc. Hence the clear zoneof growth inhibition around the outside ofthe disc. The size of the zone of inhibitiondoes not represent the likely efficacy of theanti-biotic used in the cow, but rather theconcentration of the antibiotic in the discand the ease with which it can diffusethrough the agar. Other factors relating toefficacy of antibiotics are discussed inChapter 12.

Interpretation of results

Even when bacteria have been grown andidentified, often a mixture of organisms isobtained and there may still be difficultiesin determining what is significant. The fol-lowing are general guidelines:

1. A pure culture of any mastitis pathogen– highly probable cause of the mastitis.

2. A mixed culture, for example:� Staphylococcus aureus and Strepto-

coccus agalactiae, plus other organismssuch as Streptococcus faecalis; or

� E. coli and Streptococcus uberis, plusother organisms.In the above examples of mixed cul-

tures, Staphylococcus aureus andStreptococcus agalactiae, or E. coli andStreptococcus uberis are the most prob-able cause of mastitis, and the otherorganisms are contaminants. In any sam-ple containing a significant level ofStaphylococcus aureus or Streptococcusagalactiae colonies, these organismsshould be considered significant.

3. A contaminated culture, for example,E. coli, Bacillus species, Proteus andS. faecalis. These are all environmentalorganisms. There are so many bacteriapresent that the sample is obviouslyheavily contaminated and no usefulinformation can be gained.

4. No growth. In any laboratory, one mightexpect as many as 25–35% of samplesgiving no growth, or no significantgrowth. This is often frustrating to theherdsman, who may have taken the sam-ple very carefully from a cow obviouslyaffected by clinical mastitis, e.g. with a

hard and swollen quarter, or recurrentmilk clots. Possible causes of no growthinclude the following:� E. coli infection – host response is so

effective that all the bacteria have beendestroyed by the time udder changesbecome visible (see page 29). This hasbeen shown to be by far the most com-mon cause of ‘no growth’.

� Intermittent excreter, e.g. with chronicstaphylococcal or Streptococcus uberisinfection the numbers of bacteria pres-ent at different times can fluctuategreatly, i.e. when the sample was takenthe organism may only have been pres-ent in very low or undetectable num-bers (see Table 4.5).

� Residual antibiotic from previous treat-ment is still present, inhibiting bacter-ial growth in the lab.

� Excessive delay between taking thesample and plating it out.

� Loop too hot.� Sample volume too small (use a swab).� Unusual organisms, not detectable fol-

lowing standard techniques, e.g.Mycoplasma or Leptospira.

� Traumatic or hypersensitivity mastitis,i.e. where no infectious cause isinvolved. Probably rare.

Total Bacterial Count, LaboratoryPasteurised Count and Coliforms

It is unlikely that farmers reading this textwill want to carry out their own bacteriol-ogy. However, for those involved in labora-tory and mastitis investigational work, theability to perform total bacterial, laboratorypasteurized and coliform counts is invalu-able. Details of interpretation of results aregiven in Chapter 10 (on TBC/Bactoscan).

Total bacterial count (TBC)

This is the total number of living bacteria perml of milk, sometimes also referred to as theTVC, or total viable count. Some Britishdairy companies now require milk with aBactoscan under 30,000 bacteria per ml:otherwise they impose penalties. The TBC

of milk consists of thermodurics, coliformsand many other organisms. Causes of highTBCs in milk and the organisms involvedare discussed in detail in Chapter 10.

Laboratory pasteurized count (LPC)

Also known as the thermoduric (TD) count,this is a measure of the number of living bac-teria present after heating the milk sample.High thermoduric counts are indicative ofpoor plant washing.

Coliform counts (CC)

The number of coliforms per ml of milk. Highcoliform counts are usually associated withdirty (faecally contaminated) teats. Valuesmay be increased when there is poor housingand poor premilking teat preparation.

Pseudomonad count

Pseudomonad species are environmentalcoliforms, sometimes referred to as non lac-tose fermenting coliforms, or NLFs. Theycan be used as an indicator of environmen-tal as opposed to faecal contamination.

Streptococcus uberis count

Raised levels of S. uberis can be associatedeither with environmental contamination or,and more likely, mastitic milk entering thebulk tank. The latter may be due to subclin-ical infections or to poor detection of clinicalcases.

Total Staphylococcal and Staphylococcusaureus counts

High levels of staphylococci may be due tochronic infection, poor postmilking teat dis-infection or poor teat skin quality.

Differential count

This is a semi-quantitative assessment of theproportion of different types of mastitis bac-teria present in the sample. It can help in theinvestigation of both mastitis and TBC

problems. For example, if Streptococcusagalactiae is present in bulk milk it could bethe cause of both a high TBC and a highsomatic cell count.

However, a word of warning: theabsence of S. agalactiae (or any other mas-titis organism) from the bulk milk does notmean that it is not present in the herd. It sim-ply means that it has not been cultured onthis occasion.

Methodology

It is vital that samples remain refrigeratedduring transport to the laboratory, otherwiseTBCs and other counts will increase dra-matically. In order to obtain the results carryout the following procedures:

Total bacterial count

Dilute the milk sample 1:1000 by adding0.01 ml of milk to 10 ml Ringer’s solution,then pipette 1.0 ml into a Petri dish. Pour on20 ml milk agar, cooled to 45°C. Allow tosolidify and then incubate at 37°C for48 hours. Count the colonies. The TBC is thenumber of colonies on the plate × 1000.

Thermoduric count

Heat 10.0 ml milk for 35 minutes at64°C ± 0.5°C. Cool and dilute 1:10 withRinger’s solution. Pipette 1.0 ml of dilutedmilk into a Petri dish and add 20 ml milkagar cooled to 45°C. Incubate at 37°C for 48hours and count as above. The thermoduriccount is the total number of colonies × 10.Values over 200 per ml suggest a wash-upproblem.

Coliform count

Pipette 1.0 ml of undiluted milk into twoPetri dishes. Pour 20 ml of violet red bile agar(cooled to 45°C) into each. Incubate at 37°Cand count the colonies at 24 and 48 hours.Ideally coliform counts should be less than10 colonies per ml of milk, although valuesof up to 20 colonies/ml are acceptable.



5 Milking Machines and Mastitis

History of the Milking Machine 61Function of the Milking Machine 61

Vacuum pump 62Interceptor vessel 63Balance tank 63Regulator 64Sanitary trap 65Vacuum gauge 65Pipelines 65Cluster 66Receiver vessel 67Recorder jar 68Automatic cluster removers 68

Pulsation 68Pulsation chamber 68Pulsation rate and ratio 70Pulsators 70Liner 71Liner shields 73

Robotic Milking 74Maintenance and Machine Testing 74

Daily checks by milkers 74Weekly checks by the manager or owner 75Routine specialist testing 75Static test 76Dynamic test 76

The Milking Machine and its Relationship to Mastitis 78Acting as a vector 78Damage to the teat end 78Colonization of the teat canal 79Liner slip and impact forces 79Undermilking 81Overmilking 81Stray voltage 81

Simple Machine Checks that can be Carried Out Without Specialist Equipment 82Vacuum level 82Vacuum reserve 82Regulator function 82Pulsation system 83Liners and rubberware 83Other checks 83Observations to be carried out during milking 84

Wash-up routines 84Butterfat 85

This chapter explains the function of themilking machine and how it can affect mas-titis. It also describes simple machine checksthat can be carried out without any special-ist testing equipment to assess performance.Milking machine testing and maintenanceare explained, along with common faultsthat are found. How to wash the plant aftermilking and common wash-up problems arediscussed.

The milking machine is the dairyfarmer’s equivalent of a combine harvester.It is a unique piece of equipment as it is theonly machine that harvests food from a liv-ing animal on a regular basis. Milkingmachines are used more than any otherpiece of equipment on the farm. Even so,they are frequently neglected, despite thefact that they are responsible for generatingthe majority of the dairy farmer’s income.Milking machines can have an influenceboth on mastitis and on milk quality, partic-ularly Bactoscan or TBCs.

History of the Milking Machine

In the early 1800s, a number of pioneerstried to devise a machine capable of milkingcows. These people were not farmers, whohad little interest in mechanization whilelabour was cheap, but plumbers, doctors,inventors and engineers. The first machinewas patented in 1836 and consisted of fourmetal cannulae connected to a milk pail sus-pended under the cow. Needless to say, thisdesign must have caused considerable dam-

age to the teat ends and also spread of infec-tion from cow to cow. In 1851, two Britishinventors had the idea of using vacuum tomilk cows. In 1895, the Thistle milkingmachine was developed. It used a steamengine to drive a massive vacuum pump andwas the first machine to include a device(the pulsator) to relieve constant pressure onthe teat.

In the early 1940s, only 30% of dairyfarmers in England and 10% in the USAwere milking by machine. Real developmentonly started in the mid-1940s, when thepost-war shortage of labour stimulated aconcerted drive to develop a commercialmilking machine that was cost-efficient. Thedevelopment of the milking machine con-tinues even now, with the introduction ofmore sophisticated electronics to furtherimprove performance.

Function of the Milking Machine

The basic principles of machine milkingare identical in all milking systems, fromthe sophisticated robotic milker or rotaryparlour down to the milking bale: milkshould be removed swiftly from the udderwith minimal risk to udder health. Milkoutoccurs by applying reduced pressure, i.e.vacuum, to the teat end, which causes theteat canal to open, letting the milk flowout. This is assisted by the oxytocin-induced let-down reflex, which increasesthe pressure within the udder. A constantvacuum level should be maintained

Milking Machines and Mastitis 61

Protein 85Minerals 85Bulk tanks 86Air lines 86

Circulation Cleaning 86Rinse cycle 86Wash cycle 86Disinfection cycle 88Summary of common problems associated with circulation cleaning 88

Acid Boiling Wash (ABW) 90Manual Washing 91If a Wash-up Problem is Suspected 91Common Faults Found with Milking Machines 91

throughout milking. The pulsation system isresponsible for ensuring adequate blood cir-culation around the teat. In order to under-stand how the milking machine operates, itis important to know how and where thevarious components fit into the system.When trying to identify any component, it isadvisable to work your way from the vac-uum pump forwards so as to avoid confu-sion. The components of the milking systemare described below, and this section shouldbe read in conjunction with Fig. 5.1.

Vacuum pump

This is the heart of the milking plant. Itcreates vacuum by extracting air fromthe milking system. Air is removed from allthe pipes, jars, claws and liners. Vacuumlevels are measured in kilopascals (kPa) orinches of mercury (″Hg). One kPa is equiva-lent to 0.3 ″Hg or 1.0 ″Hg is equivalent to3.33 kPa.

Vacuum pumps are rated according tothe amount of air that they can extract at aset vacuum level, normally 50 kPa (15 “Hg).This measurement is expressed in litres ofdisplaced air per minute (l/min), and in theUSA is expressed in cubic feet per minute(c.f.m.). The vacuum pump must always befitted with a belt guard to protect against

injury. Plate 5.1 shows a vacuum pump withno belt guard.

The vacuum pump needs to extractmore air than is necessary to operate themilking system. This overproduction canbe measured and is called the vacuumreserve. Vacuum reserve is needed to allowfor air admission, such as when units areput on or taken off, to ensure the machine

62 Chapter 5

Fig. 5.1. A simple milking system. There is a huge variety of layouts in milking systems. This depends onfactors such as age of the system, whether it has been modified, the amount of space available,manufacturer of the machine, etc.

Plate 5.1. The vacuum pump shown has no beltguard to protect against injury and leaves staff at riskof becoming entangled in the belts (A).

A

Table 5.1. Air admission during milking (in litres ofair/min), showing the importance of havingadequate vacuum reserve if constant vacuum lev-els are to be maintained throughout milking.

Item Air admission (l/min)

ACRs (per unit) 5–25Air bleed per unit 4–12Feeders (per feeder) 5–30Gates (per gate) 10–42Liner slip 28–170Unit attachment 3–225Unit fall-off (per fall) 570–1400

maintains a stable vacuum level duringmilking. Table 5.1 shows some examples ofair admission that occur during milking.

The amount of vacuum reserve requiredfor a milking plant will depend on the num-ber of milking units and any other equip-ment that uses vacuum, such as ACRs(automatic cluster removers), pneumaticgates, feeders and teat dip sprayers.Allowance should also be made if more thanone milker operates the plant. There must besufficient vacuum reserve present to main-tain vacuum stability throughout the wholeof milking. For smaller milking systems, alarge vacuum reserve will be required toensure there is an adequate wash cycle.

Interceptor vessel

This is located close to the vacuum pump.Its function is to prevent any liquids or for-eign matter from entering and damaging thepump. There is a drain valve at the base ofthe interceptor vessel, as shown in Plate 5.2,so that when the machine is turned off anyliquids drain away under gravity.

Balance tank

This is found in some installations and islocated between the interceptor vessel andthe sanitary trap. It is a large hollow vesselup to 200 litres in capacity that acts as a vac-uum reservoir (Plate 5.3). It is designed to


Plate 5.2. The interceptor vessel with drain valve atthe bottom.

Plate 5.3. The regulator should always be fitted tothe balance tank if one is present in the system.

improve vacuum stability during milking.Each balance tank has a drain valve at thebase. In most installations, the vacuum linesfor milking and pulsation feed directly offthe balance tank.

Regulator

The vacuum pump extracts a fixed amountof air from the milking system. However, thedemand for vacuum is variable, dependingon how much air enters the system duringmilking, and so there must be some form ofregulation to maintain stability. The vacuumregulator, sometimes called the vacuum con-troller, is responsible for maintaining vac-uum stability. The regulator leaks air into thesystem as and when necessary so that a con-stant preset vacuum level is maintained atall times. The regulator should be sited in adust-free location where it is easy to cleanand inspect when necessary, as shown inPlate 5.4. Many regulators are now fittedwith a clean air system, as shown in Plate5.5, that draws air from the external envi-ronment. This avoids dust contaminatingthe regulator and entering the milking sys-tem.

The regulator filter should be cleanedregularly because if it becomes blocked itmay be unable to respond rapidly to vacuumchanges in the system. This will result inpoor vacuum stability and increase the riskof fluctuations and thereby new infections.

The regulator should be located on the bal-ance tank, if one is present in the system.The balance tank acts as a reservoir for vac-uum so there should be more stability andless turbulence at this point than on thepipes that feed in and out of the tank.

Regulators are rated according to theamount of air that they can admit into thesystem. Regulator capacity is measured inlitres of air per minute (c.f.m. – cubicfeet/minute – in the USA) and should equalthe capacity of the vacuum pump. Anydefect in regulator function may result invacuum fluctuations during milking. Theregulator should always be leaking air intothe system. If this does not occur, it indicatesthat the plant is unable to maintain a stablevacuum level (i.e. inadequate vacuumreserve) or the regulator is faulty.

There are three types of regulator:weight-, spring- and servo-operated. Weight-and spring-operated regulators measure thevacuum level at the place where the air isadmitted. For this reason, they do notrespond very quickly to pressure changes.Servo regulators have a vacuum sensor fittedaway from the air inlet valve and can correctvacuum fluctuations within milliseconds.Servo regulators are highly efficient and arenow installed in all new parlours.

In some systems, it is the speed of themotor that partly controls vacuum, i.e. as

64 Chapter 5

Plate 5.5. Regulators fitted with a clean air systemare surrounded by a case (A). A pipe (B) feeds airfrom the external environment through the regulatorand into the milking system. Although thesurrounding area is dirty the system should preventthis dirt from entering the pipelines.

A

B

Plate 5.4. The regulator should always be sited in aclean dust-free environment.

more vacuum is needed, the vacuum pumpspeeds up. If this energy-saving device hasbeen installed, the regulator does not alwaysleak in air.

Sanitary trap

This is located at the junction of the milkand air systems and is shown in Plate 5.6. Itsfunction is to prevent any milk or liquidsfrom entering those pipelines that carry onlyair, such as the line to the vacuum pump orto the pulsation system.

The sanitary trap should be made of atransparent material such as glass or pyrexand be located where the milker can keep aneye on it during milking. The trap is fittedwith a floating ball valve so that if fluidsbuild up, the valve rises and shuts off thevacuum supply. This causes all the milkingunits to fall off the cows, and in so doingprotects the vacuum pump and air linesfrom becoming contaminated with milk.

Vacuum gauge

This should be located in the parlour so thatit is visible to the milker throughout milk-ing. Clearly gauges should be large enoughto be read anywhere in the parlour (see Plate5.7). Always check where zero (atmosphericpressure) is on the gauge. Older gauges moveclockwise, while most new gauges moveanticlockwise.

Pipelines

During milking, pipelines carry vacuum,milk or a mixture of the two. There shouldbe as few bends as possible and no constric-tions, as these will interfere with air or liq-uid movement. The free passage of air andliquids helps maintain vacuum stability.Dead ends must be avoided as they are diffi-cult to clean and can lead to Bactoscan orTBC problems (see Chapter 10). Pipelinesthat carry milk must be made of materialsuch as stainless steel or glass that can becleaned and disinfected.


Plate 5.6. Sanitary trap with a ball shut-off valve tostop liquids entering the air lines.

Plate 5.7. The vacuum gauge must be easy to readand visible throughout milking.

Large-bore pipes are now fitted to mostnew milking installations. The effect of pipesize on internal volume is shown in Fig. 5.2.Four pipe sizes filled with an equal volumeof milk are compared. The extra space in thelarger bore pipe allows better movementof milk and air compared with that inthe narrow pipe, which is flooded withmilk. Large-bore pipes are more difficult toclean, however, and need more hot waterplus air injectors (air blasters) to produce aphysical swirling action that will clean theentire internal surface of the pipe (seeChapter 10).

Cluster

This consists of a clawpiece and four teatcups, each with its shell and liner, plus ashort milk and a short pulsation tube. Inmany systems, the short milk tube is an inte-gral part of the liner. The liners are con-nected to the long milk tube through theclawpiece (Fig. 5.3). The short pulsationtubes, one from each liner shell, are con-nected to the long pulsation tube on the out-side of the claw. Milk is removed from theudder into the liner and then through theshort milk tube into the clawpiece and outthrough the long milk tube.

An air bleed hole is fitted to each claw-piece. This leaks atmospheric air duringmilking to assist milk flow away from theudder. Air bleed holes admit between 4 and12 litres of air per minute. In some systems,the air bleed hole is sited in the mouth of theliner (see Plate 5.12). This is said to give‘cleaner’ milking, with less soiling of theteat.

The long milk tube is connected toeither a recorder jar or the milk transfer line.It is important that milk is removed swiftly

from the udder. This will stop flooding inthe clawpiece and the short milk tubes.Flooding means that milk from one quartercould pass to any of the other three teats,thus allowing cross-contamination betweenquarters. Flooding also leads to vacuum fluc-tuation. For this reason, the short milk tubes,the clawpiece and the long milk tube shouldbe of sufficient size to make rapid milkremoval possible.

Many years ago, clawpiece capacity wasas low as 50 ml. However, as milk flow rateshave increased, a capacity of up to 500 ml iscommonplace today. The diameter of theshort air tubes and short milk tubes has alsoincreased. The difference in volumebetween a 13 mm and 16 mm long milk tubeis 50%, and this can have a marked effect onvacuum stability at the teat end.

Milk flows through the short milk tubes,clawpiece and long milk tube into therecorder jar (if fitted), down the milk transferline (this may be called the long milk line)and into the receiver vessel. The milk trans-fer line should be gently sloped to assist thepassage of milk to the receiver vessel.Excessive agitation of the milk results indegradation of the fat.

66 Chapter 5

Fig. 5.2. The same volume of milk shown in pipes ofdifferent sizes.

Fig. 5.3. The cluster consists of a clawpiece and fourteat cups, each with its own shell, liner and shortmilk and short pulsation tubes.

Receiver vessel

The receiver (see Plate 5.8) receives milkfrom one or more milk transfer lines. It maybe made from either glass or stainless steel.

When milk builds up in the receiver, ittriggers sensors to start the milk pump,which is connected to the base of thereceiver. Milk is then pumped away from thereceiver vessel by the milk pump through amilk filter, through plate coolers (if fitted)and into the bulk tank, as shown in Plate 5.9.The milk pump is therefore the ‘break’between the vacuum system and the outsideatmosphere.

Milking systems can be divided intotwo types depending on the level of the milktransfer line in relation to the cow: if themilk transfer line is below the level of theudder, then the system is called a low line,and if milk is lifted above the udder it is ahigh line (see Plates 5.10a and b). High linesystems need to operate at a higher vacuumlevel, as they have to physically ‘lift’ milkfrom the udder into the milk transfer line.


Plate 5.8. A stainless steel receiver vessel is resistantto breakage but difficult to inspect.

Plate 5.9. The milk pump pushes milk from thereceiver vessel under atmospheric pressure into thebulk tank.

Plate 5.10a. Low line system, where the milktransfer line is below the level of the udder.

To bulk tank

Receiver

Milk pump

Milk should not be lifted more than 2 mabove the level of a standing cow.

Recorder jar

This is a vessel that holds and stores milkfrom an individual cow in the parlour. Itallows the milker to see how much milkeach cow has given. Milk travels from therecorder jar to the receiver vessel along themilk transfer line. In the majority of modernsystems there are no recorder jars and milkis released from the long milk tube directlyinto the milk transfer line, and then on intothe receiver vessel. This type of milking iscalled a ‘direct to line’ system.

A milk flow meter may be fitted wherethe long milk tube enters the milk transferline and give a digital reading of milk yield.This flow meter will also trigger the ACR.

Automatic cluster removers

More commonly known as ACRs, these areshown in Plate 5.11. ACRs are a labour-saving device intended to increase the effi-ciency of milking. ACRs also benefit the cowby reducing overmilking, which can resultin teat-end damage. They remove the clus-ter automatically once the cow is milked out.Milk flow is measured by a sensor fitted inthe long milk tube or flow meter. When milkflow falls below a certain preset level, thevacuum supply to the cluster is shut off.There is then a delay as air enters into the

claw through the air bleed hole, making thevacuum level drop, and finally a cordremoves the unit from the udder.

Most modern ACRs are adjustableand set to remove the milking unit once theflow rate falls to between 400 and 500ml/min for twice a day milking and between600 and 800 ml/min for three times a daymilking.

Pulsation

Pulsation is responsible for maintainingblood circulation around the teat. This isachieved by making the liner open (milkoutphase) and closed (massage phase) approxi-mately 60 times per minute. The linershould be able to open fully and collapsecompletely below the teat with full and freemovement. This is achieved by alternatingatmospheric air and vacuum in the pulsationchamber, as shown in Fig. 5.4.

Pulsation chamber

This is the space between the liner and theteat cup shell. Air is extracted from the pul-sation chamber through the short and longpulsation tubes. These join on the top of theclawpiece, as shown in Fig. 5.3. Note thatthere is no connection between the milk andpulsation lines on the clawpiece.

68 Chapter 5

Plate 5.10b. High line system, where the milk has tobe ‘lifted’ above the udder.

Plate 5.11. ACRs shut off the vacuum to the clusterat the end of milking. To prevent the unit falling onthe floor and becoming contaminated, a cord isactivated, which gently lifts the cluster off the cow.


During milking, vacuum is constantlyapplied to the base of the teat. When atmos-pheric air enters the pulsation chamber, itforces the liner to collapse around the teat.This happens because the pressure on theoutside of the liner is greater than thatinside. When this occurs, milk flow stops

and blood is able to circulate around the teat.This is called the ‘massage’ phase.

When the atmospheric air is ‘sucked’out of the pulsation chamber and replacedwith vacuum, the liner is ‘pulled’ open. Thisoccurs as there is no pressure differencebetween the pulsation chamber and the

Fig. 5.4. Liner action on the teat. Pulsation is achieved by alternating atmospheric air and vacuum in thepulsation chamber. Each pulsation cycle can be traced on to a graph (above) to show the pressure changesthat occur inside the pulsation chamber.

Phase

a b c d

Pre

ssur

e (k

Pa)

inside of the liner and so the liner opensunder its own elasticity. The elasticity of theliner is therefore very important. When theliner opens, milk flows away from the udder;this is called the ‘milkout’ phase.

One complete liner movement is calleda pulsation cycle. Each pulsation cycle canbe divided into four phases – a, b, c and d, asshown in Table 5.2. Each pulsation cycle canbe traced on to a graph to show the pressurechanges that occur inside the pulsationchamber, as shown in Fig. 5.4. It must beremembered that this is not pulsation. It isjust a graphical representation of the pres-sure changes that are occurring within thepulsation chamber during a pulsation cycle.Pulsation refers to the actual liner movementaround the teat.

Table 5.2. The pulsation cycle. (From Spencer,1990.)

Phase Liner action on the teat

a Openingb (or milkout) Open with full milk flowc Closingd (or massage) Closed: milk flow stops,

blood circulates

Pulsation rate and ratio

The pulsation rate is the number of pulsa-tion cycles per minute, and the rate is nor-mally between 55 and 60 cycles per minute.The pulsation ratio refers to the length ofmilkout (a + b) compared with massage (c +d) and is expressed as a percentage. A pul-sation ratio of 60/40 refers to 60% of thecycle as milkout and 40% as massage.

Pulsation ratio = a + b × 100%c + d

To make matters even more confusing, thereare two different forms of pulsation: singleand dual.

Single pulsation

Single or simultaneous pulsation occurswhen the movement of all four liners in a

cluster act in unison. Single pulsation maybe referred to as 4 × 0 pulsation. All fourquarters are milked out at the same time andthen massaged at the same time. This resultsin ‘slugs’ of milk flowing away from theudder and possibly greater teat-end vacuumfluctuation, but results in a lower teat-endvacuum level during peak milk flow.

Dual pulsation

Dual or alternate pulsation is where themovement of two liners alternates with thatof the other two. Dual pulsation may bereferred to as 2 × 2 pulsation. So, while twoquarters are being milked, the opposite twoare being massaged. This results in a contin-uous flow of milk away from the udder. Dualpulsation results in more efficient milkingthan single pulsation as there are no surgesof milk or airflow in the system during milk-out. In plants with single pulsation, there isusually only one long pulsation tube,whereas with dual pulsation, there mustalways be two.

Pulsators

A pulsator is a device that provides alternatepulses of vacuum and atmospheric air in thepulsation chamber. There are two differenttypes of pulsators: individual and master.

Master pulsation

This is controlled electronically and regu-lates the pulsation throughout the parlour.Each cluster often has its own ‘slave’ pul-sator controlled by the master. They aredesigned to give uniform pulsation, nomatter where a cow is milked in the parlour.If problems occur with master pulsation,then all milking units will be equallyaffected. All modern milking systems arefitted with electronic master pulsation.

Individual pulsation

Individual pulsation refers to a systemwhere each milking unit has its own indi-vidual pulsator. All the pulsators operate

70 Chapter 5


independently of each other and so cowsmay receive different pulsation rates andratios depending on where they are milkedin the parlour. If a problem occurs with anindividual pulsator, then only that milkingunit will be affected. Individual pulsatorscan be expensive and many manufacturersare now ceasing production of these becauseof the benefits of master pulsation.

Liner

The liner is the only piece of the milkingmachine that comes into direct contact withthe cow. Liners are made from complex rub-ber or silicone material and have a mouth-piece and a barrel, and may have anintegrated or separate short milk tube, asshown in Fig. 5.5. The degree of elasticity ina liner has a big effect on its efficiency andhence liners have a limited useful life.

The majority of European rubber linersare expected to last for 2500 milkings or 6months, whichever comes first. Silicone lin-ers have a much longer life of up to 10,000milkings, but are more expensive.

Liners should meet the followingrequirements:

� Have a soft, flexible mouthpiece that formsan airtight seal with the base of the teat,adjacent to the udder. This will minimizeliner slip and unit fall-off.

� Have a barrel long enough to allow theliner to collapse fully around the base ofthe teat.

� Be easy to clean.� Provide a rapid milkout with minimal teat

injury.

Liners with a triangular barrel are used insome parlours. They are said to be beneficialbecause they produce a more even compres-sion on the teat by applying pressure onthree rather than two planes. One type of tri-angular liner has an air bleed at the mouth-piece to improve milk flow.

Liners eventually lose their elasticity andbecome collapsed as shown in Fig. 5.6. Thisoccurs as liners always open and close in thesame plane and explains why ‘wedging’ issometimes seen at the teat end on some cowsafter unit removal (see pages 235–236).

There is one new type of liner that hasan air bleed at the top of the liner (Plate5.12). It is claimed that the benefits of thisfeature are a better milking performance andbetter ACR take-off as the clawpieces ventmore quickly.

Fig. 5.6. Liners deteriorate with age, becomingcollapsed and losing their elasticity, as shown in theliner on the right.

Fig. 5.5. Liners are made from complex rubber orsilicone material and have a mouthpiece and abarrel, and may have an integrated or separate shortmilk tube.

When liners become more worn, it takeslonger for them to open and they will closeearly due to their tendency to collapse. Also,the overall effect is that milking time will beincreased. Many milkers have noticed thatmilking time is reduced as soon as a set ofcollapsed liners is replaced.

Chemicals, especially chlorine prod-ucts, will denature rubber and so reduceliner life. A rough inner surface of the linermay abrade teat skin and will certainly har-bour bacteria. This will increase the risk ofmastitis transmission and may affectBactoscan or TBCs.

Liner usage can easily be checked byusing the formula below. The number ofcows refers to the total number of cows inthe herd, i.e. milking and dry.

Liner usage (no. of milkings) =No. of cows × 2* × liner life in days

No. of milking units

*Change to 3 if milking three times a day.

For example, in a herd of 160 cows milkedtwice a day through an 8 × 16 parlour (8 × 16

refers to 8 milking units with 16 cow stand-ings), and where liners are replaced twice ayear, liners will have milked 7320 cowsbefore being replaced:

Liner usage = 160 cows × 2 × 183 days =8 milking units

= 7320 milkings per liner

In this case the rubber liners have exceededtheir useful life of 2500 milkings (check themanufacturer’s recommendations for usefullife of the type of liner you are using). Theymay need to be changed more frequently.The frequency of change can be worked outusing the following formula:

Liner life in days (i.e. frequency of changerequired) =

2500* × no. of milking unitsNo. of cows × 2**

*Change if manufacturer’s recommendations are different.** Change to 3 if milking three times aday.

So, for this herd:

Liner life in days =2,500 × 8 = 62.5 days or 2 months160 × 2

The frequency of liner change can bechecked quickly using the liner life charts inthe Appendix at the end of the book. All theinformation required for this is the herd size,the number of milking units and the fre-quency of milking.

Liner choice is very important. The cor-rect liner should be chosen to fit the teat cupshell. It must be able to collapse fully aroundthe base of the teat; otherwise blood will beunable to circulate and this may lead to teat-end oedema (see pages 235–236) and otherteat-end damage. Once liners have becomeworn and rough, not only can they causedamage to the teat end but they also becomemore difficult to clean (see Plate 5.13).Despite its appearance, the inside of such aliner is not smooth, as shown in Plate 5.14,which is an electron micrograph of a wornliner, and is magnified many thousand oftimes.

72 Chapter 5

Plate 5.12. An air bleed at the top of the liner isclaimed to give better milkout and smoother ACRfunction.


Liner shields

These may be fitted to the base of the linerbarrel as shown in Fig. 5.7. Their function isto reduce the effect of any impact forces (seepages 79–80). Experimental work has shownthat liner shields have helped to reduce thenew infection rate by up to 12%. However,the siting of shields is critical. If they are sit-uated too high up the liner they may preventtotal liner collapse. There will then be anincomplete massage phase and teat-enddamage may result.

Robotic Milking

Robotic milking has become more popular,and in 2009 there were about 8000 robots onmore than 2400 farms throughout the world.The first robot or automatic milking system

(AMS) was installed in the Netherlands in1992. The vast majority of robots are found innorth-west Europe, with the Netherlands hav-ing the largest installed base and Scandinaviashowing the fastest growth rate in the pastfew years. The principles of machine milkingwith a robot are identical to those of a con-ventional milking machine, with the excep-tion that the robot has to attach the machineautomatically (Plate 5.15).

Plate 5.13. Worn, rough liners are difficult to cleanand may harbour mastitis bacteria.

Plate 5.14. This is an electron micrograph of a wornliner. See how easy it is for bacteria to stick and bespread from cow to cow.

Fig. 5.7. Liner shields help to reduce the effect ofimpact forces.

Plate 5.15. A robotic milking machine attaching ateat cup.

People install robots for a variety of rea-sons, some of which are for personal lifestylefactors to improve the quality of their life, toincrease milk yield, while others hope thatmore frequent milking and removal of teatcups on an individual teat basis willimprove the health of their dairy herd. Someprefer not to have the task of routine milk-ing, but the majority of users will tell youthat the amount of time that is saved fromusing robots is not as great as many peoplethink.

It is very important that the dairy farm-ers build their dairy system around the robotand not vice versa. Some farmers feel thatthey will be able to install a robot into anexisting facility and that it will work effi-ciently. However, the majority of people findthat this does not work.

It is essential that robots are well main-tained and reliable, as they are milking cows24-7. Engineering support has to be available24-7 in the event of any breakdown or mal-function. There are a number of advantageswith this technology (including allowing thecow to choose when she wants to be milked)that will have a positive impact on yield.Most robots will remove the teat cup fromindividual quarters when they are milkedout, thus avoiding overmilking and maxi-mizing teat condition. Electrical conductiv-ity meters can help with early detection ofclinical mastitis, and the liners are disinfec-ted between cows, thereby avoiding cross-contamination.

Maintenance and Machine Testing

Like any other piece of equipment, the milk-ing machine needs to be maintained cor-rectly so that it operates at maximumefficiency. An inefficient machine may atbest slow down milking or at worst decreaseyield and increase the amount of mastitis.

It is important that all the people whouse the plant know what checks need to becarried out. A machine that is not operatingto its full potential will still remove milkfrom the udder although it may well cause apredisposition to mastitis. Problems withmilking machines tend to be gradual in

onset and so checks need to be made regu-larly.

Some checks should be carried out dailyby milkers, others at regular intervals by themanager or owner and others using special-ist testing equipment on a routine basis.Most manufacturers now have a list ofchecks, together with a timetable of whenthese should take place.

The milking machine is a highly com-plex piece of equipment. It is used twice orsometimes three times every day of everyyear. Compare it to a motor car: car manu-facturers recommend servicing every 5000or 10,000 miles. Virtually everyone gets theircar serviced at the correct intervals: if not,the performance of the car starts to decreaseand breakdown is more likely.

The milking machine is no different.The average milking machine runs for2.5 hours every milking. This is equivalentto over 1800 hours of use each year. If youcompare the milking machine to a car trav-elling at 40 miles per hour (64 k.p.h.) over ayear, the plant would have done the sameamount of work as a car travelling 72,000miles (115,200 kilometres).

Daily checks by milkers

The milkers are the first people who mayfeel that the machine is not operating cor-rectly. Milking time may be increased orunits may fall off for no apparent reason.Perished rubberware or parts such as wornvalves, etc., should be replaced as and whenthey are identified. The milker should alsocheck the vacuum level on the gauge duringmilking. If the milker is unable to identifyand correct faults, then the farm manager ormachine dealer should be called in to sortout the problem.

Weekly checks by the manager or owner

It would be unfair to leave all the responsi-bility for the milking machine to the milker.The manager or owner should check theplant regularly for any possible faults.Rubberware should be checked, liner condi-

74 Chapter 5

tion inspected, the air filter on the regulatorlooked at and the oil level and belt tension ofthe vacuum pump checked.

Routine specialist testing

It is important that milking machines aretested by a qualified technician or adviser ona regular basis. Most farmers have their planttested once a year, and some twice a year.There are some dairy farmers who havenever had their plants tested since the day itwas installed – sometimes a gap of up to20 years. Parlours should be tested to meetspecific standards such as those of the ISO(International Organization for Standard-ization), or national standards. These wouldbe the minimum requirement.

All milking machines should be testedevery 6 months. Plants that milk three timesa day should be tested more frequently. InArizona, where three times a day milking isthe norm, all milking plants are checkedevery month to ensure that they are operat-ing at maximum efficiency. They believe thatthe best test report is one where no problemsare identified, meaning that the machine isworking at its optimum performance. Thereare two types of test that can be carried out:a static and a dynamic test.

The static test is carried out betweenmilkings when no cows are being milked.This is equivalent to an MOT or mechanicalinspection of a car. It is very useful in identi-fying certain problems, but it does have limi-tations. The dynamic test is carried outduring milking, and this is equivalent to aroad test of a car. During the dynamic test themachine is tested under ‘load’ to see what, ifany, problems are present. All parloursshould have an annual dynamic test.

Static test

The static test includes the following.

Vacuum levels in the plant

Vacuum levels are checked at various loca-tions throughout the plant to ensure that

there is no significant loss of vacuumbetween the pump and the teat end, and thatthe plant is set at the correct level. A drop invacuum level would indicate that air is leak-ing into the system. The accuracy of the vac-uum gauge is also checked.

Vacuum reserve

Vacuum reserve has already been describedas being the production of vacuum over andabove that needed to operate the plant.Adequate vacuum reserve is needed toensure that stability of pressure is main-tained in the plant throughout milking.

The ISO has made recommendations forvacuum reserve. It must be remembered thatthese are minimum recommendations, andideally new plants should exceed these lev-els significantly. This will ensure that plantswill still be able to operate to ISO standardsas they get older and when their perform-ance starts to become less efficient.

Systems with a low vacuum reserve willhave difficulty in maintaining stable vacuumlevels during milking. This may result in anincreased number of liner slips and irregu-lar vacuum fluctuations, which may affectthe incidence of mastitis and poor milkout.Research has shown that herds where themilking machine has inadequate vacuumreserve, there is a correlation with high cellcounts due to an increased level of residualmilk left in the udder after milking.

If units or other items that need vacuumare added to the milking system without anyincrease in the size of vacuum pump, thenthe level of vacuum reserve will be reduced.This may affect the degree of vacuum fluc-tuation. The actual level of vacuum reserveis to some extent of academic interest. Theimportant question is whether the vacuumrequirements for milking and cleaning aresatisfied.

Regulator function

It is important that the regulator functionscorrectly so that a stable vacuum level canbe maintained throughout milking.Regulators commonly become blocked withdirt, thereby reducing the amount of air leak-


ing into the system, but occasionally mech-anisms become defective. Regulators shouldbe inspected and cleaned every week.

Pulsation system

The pulsation performance should be meas-ured at each individual milking unit. In sys-tems with master pulsation there should belittle difference between units. In systemswhere there are individual pulsators, thedifferences in performance can be quiteconsiderable.

General condition of the plant, rubberware,etc.

The plant should be examined for any per-ished rubberware, leaky valves, etc., and itsoverall condition noted. Liner conditionshould be assessed and the frequency ofchange checked to ensure that the liners arereplaced at the correct intervals.

Dynamic test

The dynamic test is carried out during milk-ing, as shown in Plate 5.16. Vacuum levelsand fluctuations close to the teat end arerecorded during the milkout of a few high-yielding cows at the furthest end of the milk-ing system, i.e. at the greatest distance fromthe vacuum pump and receiver vessel. Thisis designed to test the plant under ‘load’. Thelength of milking time, together with yield,

is recorded. The vacuum recording may bemeasured where the long milk tube leavesthe milking cluster or in the short milk tubejust below the liner shell. Rear quarters arepreferred as they yield more than the forequarters and this places the system underfurther load. The level and type of vacuumfluctuation are recorded.

There are two types of vacuum fluctua-tion that may occur at the teat end: regularand irregular. Regular vacuum fluctuationtends to be constant throughout milking.Figure 5.8 shows some different types offluctuation that may occur during milking.

Regular fluctuations are caused by pul-sation. Irregular fluctuations occur as a resultof factors such as inadequate vacuumreserve, unit fall-off, liner slip, etc., andoccur intermittently throughout milking.Liner slips are dangerous as they may resultin reverse milk flow, leading to impactforces. Impact forces drive milk droplets upagainst or through the teat canal and are dis-cussed on pages 79–80.

There are no fixed international stan-dards for vacuum fluctuation. However,some researchers have suggested that levelsover 10 kPa (3″Hg) are undesirable and mayincrease the risk of mastitis. Any irregularvacuum fluctuation is undesirable. A con-tinuous recording at the receiver vessel orthe sanitary trap is also made over a pro-longed period to check that there are no vac-uum changes occurring in the plant. If thereis any vacuum fluctuation here, it is likelyto be further exaggerated towards the teatend.

The behaviour of the cows should benoted during milking. Are they comfortableand content, or are they edgy and uncom-fortable? Is there excessive defaecation orurination? The interaction of the machinewith the cow should also be observed, alongwith teat condition assessment postmilking.

It is essential that all the findings fromthe milking machine test are recorded and areport left on the farm. Test reports shouldalways be discussed with both the milkerand the owner, and any faults identifiedrelated back to udder health. The bestmachine test report is the one showing thatno faults have been identified. In some cases

76 Chapter 5

Plate 5.16. A dynamic test recording the vacuumlevels and fluctuation during milking.


Fig. 5.8. (a) Good tracing showing little teat-end fluctuation. (b) When other milking units are attached, thevacuum level at the teat end drops, as shown by the arrows. This suggests insufficient vacuum reserve or aproblem with the regulator. (c) There is a high level of teat-end vacuum fluctuation (20 kPa) from the start ofmilking to peak flow, which reaches a more acceptable fluctuation (7 kPa) towards the end of milking. Theactual vacuum level varies between 13 and 36 kPa at peak flow and between 40 and 50 kPa towards theend of milking. (d) Teat-end vacuum level remains constant throughout, except when there is a high level(17 kPa) of irregular fluctuation caused by liner slip. This may result in impact forces.

(a)

(b)

(c)

(d)

78 Chapter 5

when a test report has been left on the farmrecommending immediate action, the mes-sage is ignored. This may occur because thesignificance of the fault has not been fullyexplained to the farmer and he sees no rea-son to take any action.

The Milking Machine and its Relationshipto Mastitis

The milking machine can have an effect onthe incidence of mastitis in a number ofways. These include the following:

� Acting as a vector.� Damaging the teat end.� Increasing bacterial colonization at the

teat end.� Creating impact forces.� Undermilking.� Overmilking.� Stray voltage.

Acting as a vector

Disease organisms may be physically trans-mitted from the machine to cows, and in thisway mastitis bacteria can be passed fromcow to cow. This can occur through con-taminated milk remaining on the linerbetween milkings (Plate 5.17). Research

work has shown that following the milkingof an infected cow, Staphylococcus aureusinfection can be spread to the next six toeight cows milked through the contaminatedliner. The risk of this occurring is increasedif worn liners are used because bacteria areable to adhere more easily to their rough-ened surface.

Infection may also spread between quar-ters during milking if there is flooding ofmilk back up the short milk tubes. If thisoccurs milk from all quarters will mix,allowing bacteria to contaminate uninfectedteats. The amount of contamination willdepend on how quickly milk is removedfrom the liner. Large-capacity claws helplimit this effect.

Mycoplasma infections are also spreadvia the liner. While Mycoplasma is not acommon pathogen in Europe, it is prevalentin hot desert areas. Affected animals are gen-erally culled, as treatment is ineffective. Forthis reason, many milking installations havean automatic back-flushing unit that disin-fects the milking unit between cows withboiling water. Back-flush units are being fit-ted in Europe to reduce cow-to-cow trans-mission of staphylococci and streptococciand also to ensure that the liner is cleanbefore being put on the next cow.

Damage to the teat end

The teat canal is the primary defence mech-anism in preventing new intramammaryinfections. Milking cows through a faultymachine that damages the teat skin or teatend will increase the risk of new infections.Damage to the teat skin, especially cuts andchaps, provides an ideal environment for thegrowth of mastitis organisms such asS. aureus and Streptococcus dysgalactiae.Damage to the teat end will allow bacterialcolonization and give bacteria easy accessinto the udder.

One of the commonest and most signifi-cant forms of damage is hyperkeratosis.Hyperkeratosis is caused by overmilking,poor pulsation, high vacuum levels, milkingwith worn liners and/or rough removal ofthe cluster.

Plate 5.17. Infected milk remaining on the liner mayspread infection to the next six to eight cowsmilked.

Any damage to the teat canal is likely toincrease the new infection rate. Figure 5.9shows that quarters with high scores ofhyperkeratosis have higher somatic cellcounts and therefore higher levels of sub-clinical infection. Almost 50% of cows atscore 5 were infected (CMT positive).

Colonisation of the teat canal

Pulsation is important as it allows regularremoval of excess keratin from the teat canalduring milking. Keratin acts as a type of blot-ting paper, mopping up any bacteria presentand, as on the skin, natural sloughing(removal) of superficial cells helps in theremoval of bacteria.

If there are problems with pulsation andthe excess keratin is not removed, then therewill be a build-up of bacteria in the teatcanal. This accumulation is due to reducedmilk flow rates, meaning that the excesskeratin and bacteria are not ‘stripped’ awayfrom the teat duct. These bacteria will be

able to colonize the canal and, if they pene-trate the udder, the risk of mastitis isincreased.

A worn or an incorrect design of liner,small-volume clawpieces, narrow-bore pul-sation tubes and many other factors mayaffect pulsation. Problems with pulsationmay also occur with short-barrelled liners,as the short barrel may cause there to beinsufficient space for the liner to collapsefully around the tip of the teat.

Liner slip and impact forces

Impact forces result in milk particles beingpropelled from the short milk tube or claw-piece up against the teat end, as shown inFig. 5.10.

Impacts occur when there is a pressuredifference between the teat end and the clus-ter, often due to liner slip. This differenceneeds only to occur for milliseconds to cre-ate impacts. Milk may be driven at speeds ofup to 40 miles per hour (64 k.p.h.). This


Fig. 5.9. The percentage of teats associated with a high cell count quarter according to the severity ofhyperkeratosis. CMT = California Mastitis Test. HK1–HK5 = degree of hyperkeratosis scored on a scale of 0(normal) to 5 (severe). (Lewis, 2000.)

Normal0

5

10

15

20

25

30

35

% C

MT

+ve

qua

rter

s

40

45

50

HK1 HK2 HK3

Teat lesion

HK4 HK5

80 Chapter 5

force is such that penetration of the canal,which is open during milking (see page 23),may occur. If the milk is contaminated withmastitis bacteria then infection may follow.Pulling the milking unit off the cow withoutfirst shutting off the vacuum, machine strip-ping (see page 113) or liner slip (see Plate5.18) may all result in impact forces.

Impact forces combined with poor pre-milking teat preparation can result in a highincidence of environmental mastitis. Thisrisk will be increased when cows with dirtyteats are washed but not dried, or whenwater contaminated with environmentalbacteria collects around the top of the liner.If the cause of the liner slip is identified andresolved, and premilking teat preparationimproved, the reduction in clinical mastitiscan be immediate and very significant.

Liner slip may occur due to one or moreof the following reasons:

� Poor unit alignment.� Inadequate plant vacuum reserve.� Cows with small, very large or splayed

teats resulting in poor mouthpiececontact.

� Nervous cows that fidget.� Excessively large liner mouthpiece.� Low vacuum levels.� Poor liner design.� Heavy cluster weight.� High vacuum fluctuation during

milking.� Machine stripping at end of milking.

The majority of liner slips result in ‘squawk-ing’ of air as it enters through the top of theliner. As most liner slips occur towards theend of milking, they pose two dangers. First,there is little resistance at the teat endbecause the teat canal is at its most openphase (see page 23). Second, if milk doespenetrate the teat canal, because there is lit-tle milk left to be removed, it is more likelythat bacteria will remain in the udder untilthe next milking, and this will increase therisk of mastitis developing.

There has been a considerable reductionin the incidence of impact forces over thepast 20 or so years. This is due to manyimprovements in milking machines includ-ing:

� Larger pump capacity.� Improved vacuum stability.� Larger-volume clawpieces.� Larger-diameter short milk tube.� Larger air bleed holes.� Liner shields.

Plate 5.18. Liner slip creates impact forces thatdrive milk against the teat end.

Fig. 5.10. Teat-end impacts are caused when airenters between the teat and the liner, leading to animbalance of pressure between the teat end and theclawpiece.

A high incidence of liner slip can havea major impact on the incidence of clinicalmastitis, especially if premilking teat prep-aration is poor.

Undermilking

At the end of milking about 0.5 litres of milkwill remain in heifers and 0.75 litres incows. In some instances, cows may beundermilked, and several litres of milkremain. In these circumstances, undermilk-ing may affect somatic cell count due to theincrease in the volume of residual milk andbacteria. These bacteria multiply to greaternumbers, with an associated increase insomatic cell count. There may be anincreased risk of clinical mastitis.Streptococcus agalactiae infections increasesignificantly if there is undermilkingbecause of the high number of these bac-teria shed compared with other mastitispathogens.

Overmilking

Overmilking may lead to increased levels ofmastitis due to the effect on teat damage.Research shows that there is more teat con-gestion and teat-end damage with overmilk-ing, which results in more clinical mastitisand higher cell counts. Overmilking can beeasily assessed by looking at cows towardsthe end of milking. If there is no milk flow-ing away from the cluster, cows are beingovermilked (Plate 5.19).

If the clawpiece is empty at take-off, thisalso suggests overmilking. Units should beremoved when milk flow drops to 400 mlper minute or before. Overmilking can alsooccur at the start of milking if there is poorteat preparation, resulting in a poor let-downreflex. This results in ‘biphasic’ let-down(see page 106).

Stray voltage

Stray voltage is where you have small elec-trical currents passing through the cow’s

body. Stray voltage may occur as a result ofpoor or faulty wiring, faulty equipmentand/or improper earthing. Most researchersagree that levels over 1 volt are significant toudder health.

The reactions of animals to stray voltagevary and depend on the path through theanimal and the magnitude of the voltage.Stray voltage problems may be continuousor intermittent and often may be very diffi-cult to detect. There are three general effects:behavioural changes, changes in milkingcharacteristics and reduced production.

Often the first sign of stray voltage isthat cows are reluctant to come in to bemilked. When stray voltage is a problem,cows become nervous during milking. Theyare restless, fidgeting during the milkingprocess, and may have to be pushed into theparlour. They may leave the parlour in greathaste. This is because cows are frightenedand realize that they may be subjected tostray voltage or tingling while they are beingmilked. There will be an increased numberof defaecations and urinations. If cows arehappy to come in to be milked and are calmthroughout milking, stray voltage is unlikelyto be a problem.

A poor milk let-down reflex occurs,resulting in incomplete milking and increas-ing residual milk in one or more quarters.This is because the cows are frightened, andthis reduces the let-down reflex. The num-ber of cows affected and the effect on the let-down reflex depends on the level of stray


Plate 5.19. Overmilking. There is no milk in theclawpiece.

voltage and the reaction of individual cows.Cows are more likely to kick the milkingunit off, which can result in impact forcesand incomplete milking, which results inmore clinical mastitis and a rise in cellcount. Incomplete milking will also reducemilk yield.

Simple Machine Checks that can beCarried Out Without Testing Equipment

There are a variety of simple tests that canbe carried out to help identify possiblemachine problems without using sophisti-cated testing equipment. These aredescribed in the following section and aredesigned to help identify possible problems.They are intended to complement but notreplace routine machine testing, whichremains an essential part of any mastitis con-trol programme. Specialist testing pro-cedures will not be discussed.

Vacuum level

� Check that the vacuum gauge reads zerobefore the machine is switched on.Vacuum gauges are frequently faulty.

� When the machine is turned on, watch theneedle rise. Most plants should reachoperating vacuum level within about10 seconds. If it takes a long time to reachthe operating level, then check that novalves have been left open – they may beleaking air into the plant.

� Tap the gauge to check it is not sticking.� What is the operating vacuum level

according to the gauge? Check this againstthe last milking machine test report.

Vacuum reserve

� Set up the plant for milking. For every fivemilking units, open one so that it sucks airinto the system. If the vacuum level falls bymore than 2 kPa (0.6″Hg), it suggests thatthere may be insufficient vacuum reserve.So, for a 20 × 20 parlour, you should be ableto leak air in through four milking units.

� Stand in the pit so that you have a clearview of the vacuum gauge. Leak air intothe system through one milking unit for5 seconds. Check if the vacuum level hasdropped. Close the unit and record thetime it takes for vacuum to return to thenormal operating level. This is called thevacuum recovery time. It should notexceed 3 seconds. In any system, leakingair in through one unit is equivalent toattaching a cluster to a cow. There shouldbe no fall in vacuum level. If the vacuumdrops, it indicates that there is a signifi-cant problem – possibly inadequate vac-uum reserve or perhaps the regulator isfaulty or dirty. The plant vacuum levelshould never drop when leaking air inthrough one unit.

� Now repeat the test, leaking air in throughtwo milking units for 5 seconds. How fardid the level drop and how long did it taketo return to normal this time? When twounits leak air into the system in smallplants, there may be a small drop in vac-uum. This should not exceed 2 kPa.

� In large milking systems, there should beno drop in vacuum level if you leak in airthrough two units.

� A crude test of vacuum reserve is to leakair in through one unit in five (four unitsin a 20 × 20 parlour) and watch the vac-uum gauge. If there is plenty of reserve,the vacuum level will remain steady.

Regulator function

� First check that the regulator is clean.� Stand close to the regulator during milk-

ing and listen. Can you hear air beingadmitted? The regulator should be contin-uously sucking atmospheric air into thesystem, as there should always be surplusvacuum (reserve) available throughoutmilking. What happens when units areput on, feeders cut in, etc.? If the regulatorstops leaking in air, this indicates that theplant is unable to maintain a stable vac-uum level, which may be due to inade-quate vacuum reserve or a faulty regulator.

� Leak air into the system so that the vac-uum level drops by 2 or 3 kPa. Listen to

82 Chapter 5


the regulator. If it is working correctly, itshould not admit air as the regulator isattempting to raise the working vacuumlevel back to normal. If it is sucking in air,then the regulator is faulty.

� Watch the gauge rise to normal after low-ering the plant vacuum level. If the gauge‘overshoots’ and rises to above the normaloperating level and then settles down, itsuggests that it is either dirty or faulty.

Pulsation system

� First check if the pulsation is master orindividual, single or dual.

� Listen to each pulsator and check that it isworking.

� Place a finger into a liner of each clusterand check that it is moving. In the case ofdual pulsation, you will need to check twoliners with alternate movement. If nomovement is felt, it suggests that theremay be defective pulsation in this unit.

� Measure the pulsation rate. Check thisresult against the last machine test report.

� Check the condition of the short and longpulsation tubes. A hole in a pulsation tubewill affect liner movement. The liner mayonly partially open or may not open at all,as it will be unable to create a full vacuumin the pulsation chamber. This will dependon the size and the location of the hole.

It is easy to demonstrate the effect of inad-equate pulsation to the milker: place bungsin two liners and ask the milker to put theirthumbs inside the two open liners. Turn onthe vacuum supply as for milking and kinkthe long pulsation tube. This will mimiccontinuous milkout without pulsation andwill stop blood circulation around the teator thumb. Watch the effect on the milker andsee their red and swollen thumb afterwards,as shown in Plate 5.20.

Liners and rubberware

� While checking the pulsator action, feelthe inside of the liner. Is it soft andsmooth, or rough and cracked?

� If you have a pencil torch, shine it insidethe liner and have a look.

� How often are the liners changed?� How many milkings have they done

between changes?� How frequently should they be

changed?� Take a liner out of its shell: is it collapsed

or round?� Split the liner lengthways and look at its

condition. (Always make sure that youhave a replacement liner before you dothis or milking will be difficult!) Is theliner clean?

� Check the condition of the rest ofthe rubberware for cracks, holes orsplits.

Other checks

� Check the air bleed hole on the cluster. Ifit is blocked, milk will not flow away fromthe cluster easily. If milk runs back outfrom the liners when the cluster isremoved, it indicates that the air bleedhole may be blocked.

� When was the machine last tested?� What tests were carried out?� Have all the problems identified at previ-

ous visits been corrected?� Was a report left and were the results dis-

cussed fully?� Who usually tests the plant?

Plate 5.20. If there is no pulsation, blood circulationstops as shown in the ‘thumb test’.

84 Chapter 5

Observations to be carried out during milking

� Check that the units sit on the udder com-fortably.

� Is there any evidence of liner slip?� Are cows happy during milking or kicking

and restless?� Check the functioning of the ACRs.� Are units pulled off while still under vac-

uum?� Are cows under- or over-milked?� Do cows kick at the clusters at the end of

milking?� Check that the vacuum gauge remains

static during milking.� Check teat condition after the unit is

removed. Look for evidence of teat dam-age, such as small haemorrhages, sphinc-ter eversion, distortion and cyanosis of theteat skin as soon as the cluster is removedfrom the cow.

� Is the regulator leaking air in throughoutmilking?

� Do units fall off for no apparent reason?� Count the number of biphasic let-downs,

which is an indication of poor let-down.

Further details are given in the parlour auditsection at the end of this book.

Wash-up Routines

An efficient parlour wash-up routine willremove milk residues and bacteria from theplant. This will maintain milk quality,improve the appearance of the parlour andprolong the life of milking equipment.Problems with the wash-up routine willresult in milk residue and bacterial build-upwithin the system. This will increase theBactoscan and TBC (see Chapter 10).

The milking system is washed by thephysical cleaning action of air and water,assisted by temperature and detergent chem-icals, and then the plant is disinfected. Nomatter what system is used, the machinewill not be adequately cleaned unless wash-up solutions come into contact with allsoiled parts of the plant. All too often, poorcleaning is due to poor circulation of solu-

tions, blocked jetters, low temperature or aninadequate volume of wash solution.

The following will be required, irre-spective of the type of milking system:

� A supply of potable water (water free fromfaecal contamination).

� An efficient water heater.� A thermometer.� Chemicals.� Protective clothing.� For circulation cleaning, one, if not two,

wash troughs.

British Standards require a minimum of 18litres (4 gallons) of hot water per milking unitfor circulation cleaning or acid boiling wash.Less than this and the Bactoscan or TBCsmay increase. Remember that some hot watermay be used for other purposes, such as feed-ing calves, etc. Recorder plants (where thereis an individual glass jar for each milkingunit) or large-bore pipelines may need over18 litres of boiler capacity per unit.

The milking system should be cleanedimmediately after milking while the plantis warm and before milk deposits start toform on pipes. Two forms of cleaning areused: circulation cleaning and the acidboiling wash (ABW). Circulation cleaningis the most common method in the UK.

The milking system is designed to pro-duce minimal turbulence of milk duringmilking because excess turbulence may leadto impact forces or ‘buttering’ of milk.However, during the wash-up routine, max-imum turbulence is required to make surethat all internal surfaces of the plant arethoroughly cleaned. In some parlours, morevacuum reserve will be needed to drawwash solutions through the plant than isneeded to provide stable vacuum duringmilking.

Direct to line and some other plants arefitted with air injectors, which admit ‘slugs’of air to increase turbulence by bubbling andswirling water all around the pipes. Airinjectors are essential in large-bore systemsso that the entire surface of each line can bephysically cleaned. Plate 5.21 shows an airinjector sited at the junction of the wash lineand the milk transfer line.


It is essential that all dairy chemicalsare stored safely and used correctly.Protective clothing (goggles, gloves andaprons) should be worn when handlingchemicals to avoid accidental injury.Chemicals must not be stored in the sameroom as the bulk tank to avoid any risk ofmilk taint occurring.

If problems occur with the wash-uproutine, then milk films can build up, asshown in Fig. 5.11. These films providenutrients for bacteria, which can then mul-tiply and increase the Bactoscan or TBC(see Chapter 10).

There are two types of milk soil: organicand inorganic. Organic soils are composedof milk fat (butterfat), protein and sugar. Ifthese residues are left in the plant, they willharden as they dry. Inorganic soils resultfrom mineral deposits, such as calcium,magnesium and iron, and are often referredto as ‘milkstone’.

Butterfat

The temperature and pH of the cleaningsolution must be right in order to ensure thatall butterfat is removed. Butterfat starts tosolidify at temperatures under 35°C. This isan important consideration for the rinsecycle of circulation cleaning. Alkaline deter-gents are used to remove butterfat and mustbe capable of emulsifying (breaking down)the fat globules so that they can be removedfrom the system. If butterfat solutions buildup in the plant, they trap other forms of milksoil and also have a detrimental effect onrubber components.

Protein

Protein films are hard to see. They adherestrongly to pipes and are difficult to remove.Alkaline detergents with chlorine added (i.e.chlorinated) can break down protein so thatit can be removed from the plant. However,water at high temperatures can bind proteindeposits back on to milk pipes.

Minerals

Calcium, magnesium and iron may causeproblems if allowed to precipitate, particu-larly in hard water areas, where milkstonecan easily build up on the pipes. This is seenas a chalky film. Acid solutions are used toremove and prevent the accumulation ofmineral deposits and most dairy farmers runan acid wash (milkstone remover) throughthe plant on a regular basis. These washesusually contain phosphoric acid. This isusually carried out weekly in areas withhard water.

Fig. 5.11. If problems occur with the wash-uproutine, milk films will build up in the plant. Thisdiagram shows how milk films develop.

Plate 5.21. Air injectors are fitted to the milktransfer line to maximize agitation of wash solutionsto ensure that large-volume lines are cleaned.

86 Chapter 5

Bulk tanks

The bulk tank must be cleaned every timemilk is emptied from it. Most tanks are nowcleaned by automatic washers that rely onchemicals and jetters to complete theprocess. All internal parts of the tank thatcan come into contact with milk must becleaned and disinfected. It is essential thatthe milker checks that this process has beencarried out efficiently before milking.

While automatic washers do a good job,there is the risk that, because they are auto-matic, things can go wrong. The milkerrarely looks at the tank to check on cleanli-ness. Occasionally problems do occur, suchas when a wash jetter becomes blocked andso part of the tank is not cleaned. Anothercommon fault is when chemicals that arefeeding the automatic washer run out. Thiscauses a build-up of milk film, in whichpsychrotrophic bacteria can multiply, result-ing an in increased Bactoscan or TBCs.Psychrotrophs are bacteria that thrive underrefrigerated conditions.

Air lines

Occasionally, milk enters the air lines. Forexample, this can occur if there is a splitliner. In this case, milk will be sucked upthrough the pulsation chamber into the pul-sation tubes and into the main pulsationline. If milk does enter the air lines, then thisneeds to be cleaned out. All air lines shouldbe washed twice a year as a minimum.

Circulation Cleaning

Circulation cleaning is divided into threecycles.

� Rinse: removes excess soil.� Wash: cleans the plant.� Disinfect: removes residual bacteria from

the cleaned plant.

When milking is completed, any milk in thereceiver vessel and the milk pump should bedrained. The milk pipe should then be dis-

connected from the bulk tank. The externalsurfaces of clusters and milking units shouldbe rinsed clean (ideally with warm water)and the plant set up for the wash-up routine.This consists of attaching jetters to the clus-ters and then transferring vacuum to thewash lines so that wash water is drawn intothe wash lines, through the cluster and backthrough the return wash line, as shown inFig. 5.12.

Rinse cycle

Warm water at body temperature (38–43°C)should be rinsed through the milking systemand run to waste until the water appears clearimmediately after milking. This will removethe majority of any residual milk left in theplant. Many dairy farmers use a cold waterrinse. Under no circumstances should coldwater be used as it will congeal butterfat ontoglass and stainless steel fittings and cooldown the plant before the hot wash. Energyin the form of hot water will then be requiredto heat up the pipes before the hot wash. Inaddition, minerals and sugars in milk aremore easily dissolved in warm water.

After the rinse cycle, the wash line valvesshould be shut off to prevent large volumesof air being sucked into the system. This airmay cool down the plant before the hot wash.It is advisable to insulate the milk and washlines in colder climates. This is essentialwhere any of these pipes are exposed to theoutside environment. Not only will it preventexcessive cooling during the wash-upprocess, but it will also prevent milk freezingduring winter milking. An efficient rinsecycle should remove about 95% of all milkresidues in the system and all the milk sugars.The remaining residues are removed duringthe wash cycle by chemical action.

Wash cycle

In circulation cleaning, the wash cycle relieson an alkaline detergent solution to removebutterfat. Chlorine is normally incorporatedinto the detergent to remove protein, but inthis form the chlorine has no disinfectant


Fig. 5.12. With circulation cleaning, water is drawn in the wash lines, through the cluster, back through themilk transfer line and into the wash trough, where it is recirculated.

property. Wash-up solutions are very sensi-tive to temperature. In general, their clean-ing power doubles for each 10°C increase upto a maximum of 71°C. Once they exceedthis temperature, they tend to become un-stable, vaporize and become less effective.There are, however, a few detergent solu-tions that are designed to be circulated incold water, so always follow the manufac-turer’s instructions.

An adequate supply of hot water mustbe available. Maintaining the correct tem-perature of water in the boiler is essential. Itis also important that the boiler has a large-bore tap so that the wash trough can be filledrapidly without heat loss.

The water temperature should bechecked regularly against the boiler gauge toensure that the thermostat and heater elem-ent are functioning correctly (see Plate 5.22).Sometimes the boiler gauge becomes faultyor the heating element becomes caked withmineral deposit. This is especially commonin hard water areas. The best way to checkon boiler efficiency is to fill a trough with hotwater and measure the temperature in the

Plate 5.22. Checking the temperature of the hotwash solutions.

filled trough. This is the temperature thatcounts.

Detergent solutions must be used cor-rectly and to do this you must know the vol-ume of wash water. Check themanufacturer’s instructions on how muchdetergent to use. If the solution is too weakit will be ineffective. If it is too strong, thenit will be wasteful and may even corrode thestainless steel or rubberware in the plant.

Hot water is run into the plant and, as ittravels around, it heats up the pipes and ves-sels. Only then should the correct amount ofdetergent solution be mixed into the circu-lating hot water. It should be circulated at60–70°C for 5–8 minutes, or in accordancewith the manufacturer’s recommendation.

The circulation wash relies on the deter-gent action but also the physical swirlingaction of wash solutions. Air injectors createturbulence that is essential in order to haveeffective cleaning in large direct to line sys-tems.

The milker should not hose down theoutside of the recorder jars with cold waterduring the rinse or wash cycles as this willcool down the temperature of the jars andalso of the circulating solutions.

If the rinse cycle has not been effective,a large amount of milk residue may be leftin the system. This milk will inactivate someof the detergent, which will decrease theeffectiveness of the wash-up routine.

Ideally a thermometer or temperaturerecording strip should be fitted to the returnwash pipe to check that the wash solutionsare being circulated at the correct tempera-ture (see Plate 5.23).

If solutions are circulated for long peri-ods of time, their temperature drops andthen protein may be deposited back onto thepipes. Milkers have been known to let thehot wash cycle run while they go and havebreakfast. At the end of the circulation washcycle, the milking plant should be clean andfree from any milk soil.

Disinfection cycle

The disinfectant rinse reduces the numberof bacteria in the plant and helps maintain

milk quality. Sodium hypochlorite is themost commonly used disinfectant, at astrength of 50 p.p.m. (parts per million).This solution may be circulated and thendumped to waste at the end of the cycle.

If you examine the internal surfaces ofsome rubber components in the plant and ablack deposit marks your finger, as shown inPlate 5.24, this indicates rubber damagecaused by too high a level of hypochlorite.The same effect may be seen in the blackcolour of the disinfection rinse shown inPlate 5.25. Remember that chlorine com-pounds reduce the life of all rubberware andliners.

Summary of common problems associatedwith circulation cleaning

� Water is not hot enough – this will makethe detergent solutions less effective asthey are temperature-sensitive.

88 Chapter 5

(a)

(b)

Plate 5.23. A thermometer (a) and a temperaturestrip (b) attached to the return wash line to checkthat wash solutions are circulated at the correcttemperatures.

� Inadequate wash volumes – water may notcome into contact with all internal sur-faces. This may result in some areas of thesystem not being cleaned, especially thetop part of the milk lines.

� Rinsing the plant with cold water aftermilking – this will cool down the warmplant and congeal butterfat. The hot washsolutions will then have to heat up theplant from cold, and the detergents willhave to remove the butterfat deposits.

� Incorrect strength of detergents used – toolittle is ineffective while too much iscostly and corrosive.

� Wash cycle continued in excess of the rec-ommended time – the solutions will cooldown and may re-deposit material backonto the internal surfaces.

� Build-up of deposits in dead-end areasthat are difficult to clean, as shown in Fig.5.13.

� Insufficient turbulence or flow of washsolutions – cleaning may be ineffectiveand deposits can accumulate on pipes (seePlate 5.26). Build-up of milk soil occurredin this plant due to inadequate flow ofwash solutions.

� Blocked wash-up jetters – this may resultin one liner or a complete milking unit notbeing washed. The effect will depend onwhere the jetter is blocked.

� Faulty air injectors – these will not createthe physical turbulence that is needed toclean large-bore lines.


Fig. 5.13. Deposits frequently build up in dead-endareas as they are difficult to clean.

Plate 5.24. Black deposits from rubber partsindicate too high a level of hypochlorite resulting inrubber corrosion.

Plate 5.25. High levels of hypochlorite in thedisinfection solution strip away rubber.

Plate 5.26. If there is insufficient turbulence or flowof wash solutions, cleaning may be ineffective, asshown.

Acid Boiling Wash (ABW)

An ABW relies primarily on heat for disin-fection. Large amounts (18 litres or 4 gallons)of boiling water over 96°C are needed foreach milking unit. This water is run directlyfrom the boiler around the plant to waste, as

shown in Fig. 5.14. It takes the same path asfor circulation cleaning, the only differencebeing that the solutions are run around theplant to waste rather than circulated.

In order to be effective, all parts of theplant must reach and maintain a tempera-ture of 77°C for the whole cycle, which lastsbetween 5 and 6 minutes. In the first fewminutes of cleaning, a solution of dilutenitric or sulfanilic acid is run in with theboiling water to prevent deposits buildingup on any of the surfaces. See Plate 5.27.

The plant must be capable of with-standing high temperatures and acids. Thereshould be no dead ends and the whole sys-tem should be as compact as possible toavoid excessive heat loss. This form of clean-ing is not very popular as problems occur ifthe water temperature or volume is too low.ABW saves on dairy detergents and is afaster form of washing compared with cir-culation cleaning. However, it requires theboiler to heat the water to a very high tem-perature, which can require considerableamounts of energy.

90 Chapter 5

Fig. 5.14. The route of wash solutions with acid boiling wash. The boiling water and acid are run through theplant to waste.

Plate 5.27. Acid boiling wash (ABW) relies on heatand acid for cleaning. Acid is put into the reservoirand released with the boiling water to run aroundthe plant to waste.

Manual Washing

Dump buckets and their clusters can eitherbe washed as part of the wash-up routine ormanually using chemicals and brushes inany system. While this process is labour-intensive and time-consuming, excellentresults can be achieved and in addition, themilker is able to visually check on the effi-ciency of the process. It is important thatclusters of dump buckets are thoroughlycleaned and disinfected, as they are oftenused to milk colostrums from freshly calvedcows, which are very prone to mastitis (seepage 30).

Some farmers place clusters and otherpieces of milking equipment in troughs withsmall volumes of detergent solutions, asshown in Plate 5.28, and expect good results.This has little effect as the solutions do notcome into contact with all the internal sur-faces and there is no physical cleaningaction. In addition, if this method of clean-ing is used on clusters that milk mastiticcows, then this must increase the risk ofspreading infection, as liners may remaincontaminated with mastitis organisms (seepage 111).

If a Wash-up Problem is Suspected

The efficiency of the wash-up routine can beevaluated through laboratory testing of bulkmilk, as described on pages 176–183. If a

wash-up problem is suspected, the causemust be identified. Much can be gained bymanually inspecting the system after thewash-up routine, for example by removingpipe ends and examining internal surfaceswith a torch.

Look inside the following areas for anyevidence of milk film or milk soil build-up:

� Liners.� Milk transfer lines (especially the top of

the line).� Bungs and valves at the base of jars and

lines.� ACR flow meters and sensors.� Receiver vessel.� Dead-end areas.� Milk pump.� Bulk tank.

Common Faults Found with MilkingMachines

Below are a variety of milking machineproblems and their consequences:

� Mix and match parlours (see Plate 5.29).Some farmers or milking machine fittersdo unusual things with parlours.Plate 5.29 shows a parlour with eight unitsmilking through recorder jars and fourunits milking direct to line. Parlours mustbe either direct to line or a recorder jar sys-tem, not a combination of the two. The


Plate 5.29. A combination of a recorder jar anddirect to line parlour, which had a very poor milkingperformance.

Plate 5.28. Cleaning will be ineffective as there isinsufficient detergent solution to come into contactwith all parts of the cluster.

milking performance in this parlour wasvery poor.

� Excess bends in pipes (Plate 5.30): theseimpede air- and milk flow and may reducethe amount of vacuum available at the teatend, increasing the risk of irregular vac-uum fluctuations in the plant and leadingto an increased infection rate.

� Hole in the short pulse tube (Plate 5.31):atmospheric air is sucked in through theshort pulsation tube. This will prevent fullvacuum levels being attained in the pul-sation chamber, resulting in incompleteliner opening, which will slow downmilking in that quarter. In severe cases theliner may not open at all, resulting in fail-ure of that quarter to milk out.

� Split liner (Plate 5.32): a split liner isunable to open and close normally. Thishas two effects. First, it will result inincomplete milkout and massage, leadingto teat damage, which may lead to anincreased risk of new infections. Second,milk will get sucked into the pulsationchamber, up through the pulsation tubesand into the long pulsation line. This mayaffect pulsation itself.

� Congestion of blood in the teat (Plate5.33): this can occur due to a variety ofreasons, including:

� Absence of pulsation, i.e. full vacuumconstantly applied to the teats.

� Incomplete or defective pulsation.� Excessive vacuum levels.� Poor liner design.� Using incompatible liners and shells.� Overmilking.

92 Chapter 5

Plate 5.31. Hole in the short air tube.

Plate 5.32. Split liner.

Plate 5.30. Excess bends in pipelines.


Plate 5.33. Purple teats after unit removal. This iscaused by congestion of blood in the teat.

Plate 5.34. Dirty regulator. Blocked air filters mayresult in higher vacuum levels.

Plate 5.35. Multiple weight-controlled regulators.

Plate 5.36. A flooded sanitary trap due to a faultymilk pump, which could not remove milk from thereceiver vessel.

Plate 5.37. Poor unit alignment, resulting in thecluster twisting on the udder.

Congestion of the teat causes the cow greatdiscomfort and the milk let-down reflex islikely to be reduced. If teat damage occurs,this will increase the likelihood of mastitis.

� Blocked regulator filter (Plate 5.34): a dirtyregulator may be unable to respond rap-idly to vacuum changes in the system,resulting in poor vacuum stability. Thiscan increase the likelihood of irregularvacuum fluctuations thereby increasingthe risk of new infections.

� Multiple weight-controlled regulators(Plate 5.35), which act independently ofone another. They all try to maintainstable vacuum in the system; however, asthey respond slowly to pressure changes,it is likely that they may work against eachother, resulting in poor vacuum stability.

� Flooded sanitary trap (Plate 5.36): thissanitary trap flooded and the floating ballshut off the vacuum supply and all theunits fell off the cows. This occurred dueto problems with the milk pump, whichcould not pump the milk away from thereceiver vessel quickly enough.

� Poor unit alignment (Plate 5.37) due tolong milk tubes or poor placement of themilking unit in relation to the position ofthe cow in the parlour may result in clus-ters twisting on the udder. This willincrease the risk of liner slip, will slowdown milking as the teats become twistedin the cluster and may also increase therisk of undermilking one or more quarters.Good unit alignment is essential to ensureefficient milkout.

94 Chapter 5

This chapter describes the various processesthat constitute a good milking routine anddiscusses the way in which they can protectherd cell count and reduce clinical mastitis,while at the same time speeding up milking.

A good milking routine will removemilk efficiently from the cow with minimalrisk to udder health. It must include practicesthat limit the spread of contagious mastitis inthe parlour, while minimizing the risk ofenvironmental mastitis. This results in qual-ity milk production with low bacterial con-tamination. The milking routine should bedesigned to achieve these goals but at the

same time it must be practical and labour-efficient. The milker needs to understand thescientific reasoning for each step in the milk-ing process in order to achieve these aims.

It is important that a consistent milkingroutine is practised in the herd. Cows love uni-formity. They are easily stressed and so roughhandling or aggressive milkers are to beavoided. Cows can become nervous and thiscan affect their milk let-down reflex. The con-scientious dairyman will benefit from a goodroutine by reduced levels of mastitis, increasedmilk production and a rapid milkout.

The beneficial effects of good hygiene at

©CAB International 2010. Mastitis Control in Dairy Herds (R. Blowey and P. Edmondson)

6 The Milking Routine and its Effect onMastitis

Minimizing Transfer of Infection 96Foremilking 97Mastitis Detection 98Teat Preparation 100Predipping 101Drying Teats before Milking 103Assessing Teat Preparation 104Milk Let-down Reflex 105Batch Preparation 107Unit Attachment 107Milking the Mastitic Cow 108Unit Removal 111Disinfection of Clusters between Cows 111Residual Milk 112Machine Stripping 113Postmilking Teat Disinfection 113Milking Order 113Frequency of Milking 114Robotic Milking 114Summary of the Milking Procedure 115

milking time are shown in Fig. 6.1., whichdemonstrates how different hygiene prac-tices can result in a reduction in clinicalmastitis and also in the new infection rate.This is to be expected as contagious organ-isms are transferred between cows duringthe milking process.

In this trial there is only a slight reduc-tion in infection levels between ‘partial’ and‘full’ hygiene, indicating that at the time ofthis particular trial, the benefits of pasteur-izing clusters between individual cows werelimited.

Minimizing Transfer of Infection

Infection can be transferred from cow to cowduring the milking process by:

� Liners.� Hands.� Cloths.

Control of transfer is based on wearinggloves, using a separate cloth for each cowand minimizing transfer on liners by main-taining liners in good condition and clusterflushing as necessary.

The milker can spread contagious mas-titis as he handles each cow. It is extremelydifficult to disinfect the rough surface ofhands, let alone keep them clean duringmilking (see Plate 6.1). For this reason it isadvisable to wear clean gloves, but it isessential to keep them clean throughoutmilking.

Trial work in 1966 (Neave et al.) showedthat half of all milkers’ hands were infectedwith mastitis organisms even before milkinghad started. Contamination increased duringmilking so that by the end all milkers’ handswere infected.

In another experiment (Neave et al.,1966), two groups of milkers’ hands werecleaned in different ways. The first groupwere washed with a disinfectant solution,

96 Chapter 6

Fig. 6.1. Effect of different hygiene regimes on new infection rate and clinical mastitis. (From Neave et al.,1969.)

No hygiene0

200

400

600

800All types of new infection*

Staphylococci

Strephococci

Clinical

Partial Full

Hygiene None Partial Full

Disinfectant udder wash – √ √Individual cloths – √ √Rubber gloves – √ √Disinfectant hand dipping – √ √Teat dipping – √ √Pasteurized clusters – – √

∗The number of new infections is higher than the number of clinicalcases as many new infections become subclinical or ʻhiddenʼ or areeliminated from the udder without any outward signs of mastitis.

and afterwards only 30% of hands remainedcontaminated. However, in the secondgroup, whose hands were just washed inwater, 95% remained infected.

Once gloves become worn or torn, theymust be discarded. Many milkers wear dis-posable gloves that are discarded after eachmilking. Gloves themselves do not reducethe spread of infection. They only allow youto disinfect hands. To be effective, glovesmust, of course, be rinsed frequently in a dis-infectant solution during the milkingprocess.

The use of rubber gloves is especiallyimportant when dealing withStaphylococcus aureus or Streptococcusagalactiae infections. S. agalactiae has beenisolated from milkers’ hands up to 10 daysafter their last contact with infected animals.Indeed, some relief milkers are known tohave introduced infection into clean herdsin this way.

Foremilking

Foremilking is the practice of hand milkingeach teat before unit attachment. It is rec-ommended for three reasons. It:

! Stimulates the milk let-down reflex.! Aids detection of mastitis.! Flushes out the milk from the teat canal.

This will remove most bacteria that haveentered the teat since the previous milk-ing.

Early detection of mastitis allows prompttreatment of clinical cases. This not onlyresults in higher cure rates, but, more impor-tantly, reduces the risk of spreading infec-tion to the rest of the herd. It also stopsmastitic milk from entering the bulk tankand this helps to avoid high bacterial andcell counts. In the case of S. agalactiae andStreptococcus uberis infections, up to100,000,000 organisms per ml of milk can beshed from an infected quarter. This canaccount for the fluctuating Bactoscan or TBClevels that are frequently found in herdswith an S. agalactiae or S. uberis problem.

Frequently there are clots in the firsttwo or three strippings from cows but theremainder of the milk appears normal. Thisis probably a response to bacteria in the teatsinus but not in the udder itself. In suchcases, only the foremilk needs to be dis-carded but the cow should be marked andcarefully checked at the next milking.

Internal teat sealants are now com-monly used during the dry period. It isimportant that milkers can differentiatebetween debris from these sealants and clin-ical mastitis. Internal teat sealants have abrighter white colour than mastitis clots;they feel rubbery and break down more eas-ily.

Potentially, foremilking does have somedisadvantages. It is time-consuming andmay spread infection. For example, if youhave a mastitis incidence of 45 cases per100 cows per year, nearly 5500 teats willhave to be foremilked to detect one case ofmastitis when milking twice a day. Thisincreases to over 8000 teats when milkingthree times daily.

Some feel that there is a greater risk ofspreading infection from cow to cow as themilker’s hands or gloves become contami-nated with mastitis organisms, and they con-sider that this outweighs the risk associatedwith a failure to detect mastitis at an earlystage. However, a good milker will be wearingclean gloves and will postdip cows, whichwill partially overcome these risks. Comparedwith the risk from liners, which are in con-tact with teats for very much longer, onewould expect that the risk from regularly dis-infected gloved hands is relatively low.

Milking Routines and Effects on Mastitis 97

Plate 6.1. Hands have rough surfaces that aredifficult to clean compared with the smoothsurfaces of rubber gloves.

More and more farmers now foremilk asthey see a large benefit from having a goodmilk let-down reflex, which speeds up milk-ing and also maximizes yield. Foremilkingis also the only accurate method to detectclinical mastitis.

Foremilking should be carried outbefore the teat preparation. Any milk thatcontaminates the milker’s hands will then beremoved before infection can spread to thenext cow. Milk should be stripped onto theparlour floor rather than into a strip cup (seePlate 6.2) as strip cups tend to become reser-voirs of infection rather than acting as an aidto detection. A black tile built into the par-lour floor under each cow’s udder allowseasier examination of milk. When foremilk-ing, hold the teat between your finger andthumb and not in your whole hand, as thisfurther decreases the risk of infection trans-fer. Some milkers use both hands andforemilk two teats at a time.

Mastitis Detection

Mastitis is inflammation of the udder. Theappearance of the milk changes with the

type of inflammatory response and it maylook clotted, watery or stringy, as shown inPlate 6.3. It is not possible to be sure whichorganism is causing the mastitis simply fromthe appearance of the milk alone.

The milker may detect mastitis by oneor more of the following methods:

� Foremilking.� Change in the behaviour of the cow.� Observation of quarter swelling.� In-line mastitis detectors.� Checking the milk sock or filter at the end

of milking.

The importance of foremilking has alreadybeen discussed and this is the best and mostreliable form of mastitis detection. Someherds rely on the other methods mentionedabove.

When a cow comes into the parlour ona different side or at a different time fromusual, then this suggests that something iswrong. She may be sick or it could be due toother factors, such as bulling. Good stock-manship can help identify early cases ofmastitis by picking out cows that act out ofcharacter.

There are occasions when the cow has avisibly swollen quarter but the milk appearsnormal (see Plate 6.4). If the cow is healthyand the milk is normal, this cow should notbe treated but marked and checked carefullyat the next milking.

If the cow is ill, this may be due to avery high temperature, e.g. from infectionwith Streptococcus uberis, or to toxins pro-duced in the udder by a peracute form ofmastitis, caused by organisms such asStaphylococcus aureus or E. coli. This mayoccur so rapidly that the milk still appearsnormal. In these cases prompt veterinarytreatment will be necessary in order to savethe cow’s life. On other occasions, there isno swelling in the quarter and the milkshows very little change but the cow is againvery sick, due to E. coli mastitis toxaemia;this is discussed in detail in Chapter 3.

In-line mastitis detectors can be fitted tothe long milk tube (Plate 6.5). They have awire mesh filter through which most milkpasses. Any clots present clog the filter. Milk

98 Chapter 6

Plate 6.2. Milk should be stripped on to the parlourfloor rather than into a strip cup. .


Plate 6.3. Various types of mastitic milk; (a) Brown, watery secretion, typical of E. coli infections; (b) Waterymilk with some clots; (c) Viscous red/brown secretion is associated with gangerous mastitis; and (d) Clottedmilk indicating mastitis.

(a) (b)

(c) (d)

Plate 6.4. Udder palpation is useful when quartersbecome hot and inflamed, as shown.

Plate 6.5. In-line mastitis detectors are fitted to thelong milk tube and, if clots are present, they clogthe filter.

should be able to bypass the filter withoutimpeding milk flow. Filters should belocated in the long milk tube either at eyelevel or close to the clawpiece so that theyare easily seen when the units are removed.All too often, they are sited in a locationwhere they are difficult, if not impossible, toobserve.

These detectors can give a false sense ofsecurity to milkers. Some assume that allcases of mastitis can be discovered using thismethod, even if filters are never checked.This is not true. Mastitis cases that producewatery milk or very small flecks can bewashed through the detectors and casesmissed. In-line filters pick up clotted formsof mastitis.

In order to be effective detectors mustbe examined after each cow is milked. Inparlours fitted with recorder jars, theseshould be checked before milk is transferredinto the bulk tank. Problems with Bactoscanor TBC and cell count occur when detectorsare not checked, because mastitis goesunseen and mastitic milk enters the bulksupply. This is particularly the case withdirect to line plants, which rely solely ondetectors for mastitis identification. Heremastitic milk will have reached the bulktank by the time clots are seen on the filter.However, despite their limitations, in-linemastitis detectors can still be an additionalaid in detecting mastitis, but be aware thatthey can cause problems with vacuum sta-bility at the teat end due to interfering withthe milk flow in the long milk tube.

Examining the milk sock or filter aftermilking is also important, especially to checkon the hygiene of the milkers. (The milk sockor filter is located between the milk pumpand the bulk tank.) The presence of clots orlarge amounts of faecal contamination, asshown in Plate 6.6, indicates a poor milkingroutine and/or poor mastitis detection.

Some farmers rely solely on checkingthe milk filter for mastitis detection. Whenclots are found, the procedure is to strip outthe entire herd at the next milking to identifythe infected cows. In some instances, milk-ers stop stripping when one mastitic cowhas been identified. This may leave othermastitis cases undetected. On other occa-

sions, no mastitis may be found as the cowmay have cleared up the infection herself.Even then, it would be best to foremilk theherd again at the next milking.

Clinical mastitis is detected by visualchanges to the milk and udder. Some milk-ers carry out additional tests such as theCMT (California Mastitis Test) to decide if aquarter is clinical based on the CMT result.If a milker has to resort to further tests to tryand detect if a quarter has clinical mastitis,the cow does not have clinical mastitis.

In all cases of clinical mastitis, it isadvisable to collect pretreatment milk sam-ples for bacteriological testing. This willallow the identification of the types of mas-titis present on the farm so that specific con-trol measures can be implemented.

Teat Preparation

One Somerset dairy farmer has a notice upin his dairy for his milkers, ‘If the cows’ teatsare not clean enough to put in your mouth,then they are not clean enough to put thecluster on.’ This sums up premilking teatpreparation perfectly.

Good teat preparation is essential forclean milk production. It also helps toreduce the risk of environmental mastitis.The goal in teat preparation is to ensure thatteats are clean and dry before the milkingunits are attached (see Plate 6.7). The bestway to ensure that the cows are clean as they

100 Chapter 6

Plate 6.6. The presence of clots or large amounts offaecal contamination on the milk sock indicates apoor milking routine and/or poor mastitis detection.


enter the parlour is to make sure that theyare kept in a clean environment. This isespecially important during the housingperiod. If cows enter the parlour with dirtyteats, then problems with environmentalmanagement need to be addressed.

Hairy udders, as shown in Plate 6.8, arelikely to trap dirt and this adds to theamount of work the milker has to do. Uddersshould be clipped or singed. Similarly,excess hair on the end of the cow’s tailshould be cut off (Plate 6.9) and the sides ofthe tail clipped, ideally up to the vulva.

Predipping

Predipping is the best way to prepare teatsand refers to the disinfection of the teatbefore milking. The aim is to reduce thenumber of bacteria present on the teat beforethe milking unit is attached. This willgreatly reduce the number of environmentalbacteria entering the milk, and in so doingwill also reduce the risk of environmentalmastitis.

Predip solutions must be fast in action.Only preparations with a proven rapid speedof kill (under 30 seconds) will be effective.To get the maximum benefit, clean teatsshould be coated in predip solution. A min-imum contact time of 20–30 seconds is nec-essary and then the solution must bethoroughly wiped off the teat before the unitis applied. This ensures that no chemicalcontamination of milk occurs. Many herdshave had a marked reduction in clinicalmastitis, Bactoscan or TBC and improve-ment in teat condition when they predip..Many cows also milk out more completelyand faster when they predip as this furthermaximizes the milk let-down reflex. Predipsare discussed in detail on page 126.

There are many herds that do not wishto pre-dip and so, if the cow enters the par-lour with visibly clean teats, then dry wipingthe quarters with a paper towel should suf-fice (see Plate 6.10). If the teats are dirty, asshown in Plate 6.11, they must be washedand dried. Grossly contaminated teatsshould be soaked before washing to allowthe dirt to soften. This allows easier removal

Plate 6.7. Ensure that the teats are clean and drybefore the milking units are attached.

Plate 6.8. Hairy udders are likely to trap dirt andhence increase the risk of environmental mastitis.

Plate 6.9. Long tails should be trimmed, otherwisethey will spread dirt on to the other and teats.

102 Chapter 6

of soil. Poor washing procedures assist thespread of bacteria rather than removingthem. Washing of teats is best carried outusing water from drop hoses. Warm water isrecommended as it is more comfortable forboth the cow and the milker. However, ifwarm water is used, it is essential thatheader tanks are kept clean and covered andpreferable that a sanitizer is added to thewater.

Contaminated water can be a source of

Pseudomonas infections (see page 47).Washing teats in the winter with cold watercan reduce the milk let-down reflex. It mayalso have an adverse affect on teat skin con-dition. Some people wash the teats andudder with a power hose as the cows enterthe parlour. This is not recommended as itmust be painful to the cow and soaks theudder as well as the teats.

It is important to ensure that only theteats and not the udder are washed; other-wise, when the milking unit is attached,water runs down the wet udder and collectsaround the top of the liner, as shown inPlate 6.12. This is commonly referred to as‘magic water’ because one moment it’s thereand the next it’s gone! If sucked in throughthe top of the liner, at best it contaminatesthe milk (causing increased Bactoscan orTBC) and at worst causes liner slip, creatingimpact forces. Impact forces increase the riskof new mastitis infections (see pages 79–80)as there are likely to be high levels of E. coliand Streptococcus uberis in ‘magic water’.The less water used on teats the better. If

Plate 6.10. Visibly clean teats can be dry wipedwith a paper towel.

Plate 6.11. If the teats are dirty, then they must bewashed and dried or predipped and dried.

Plate 6.12. When the udder gets wet, water drainsdown and collects around the top of the liner andthe teats. This is commonly referred to as ‘magicwater’.


washed, it is essential that teats are driedprior to attachment of the cluster.

The addition to the washing water ofeven low levels of disinfectant, for example,60 p.p.m. of iodine or 200 p.p.m. of sodiumhypochlorite, is beneficial. It helps to keepthe warm water and pipelines free from bac-terial contamination. It also reduces thenumber of bacteria on the teat and helps tokeep the milker’s gloves or hands clean dur-ing the milking process.

In hot climates such as the desert areasof the USA and the Middle East, automaticteat washing in sprinkler pens may be used.Here there are two collecting yards beforecows enter the parlour. The first yard is fittedwith sprinklers at ground level that jet waterup against the udder and teats to remove anydirt, as shown in Plate 6.13. The cows arethen allowed to stand while the udders andteats drip dry before they enter the secondcollecting pen, from which they have imme-diate access to the parlour. Sprinkler pensreduce the amount of washing necessary inthe parlour and so speed up milking.However, as they wet both the udder andteats, it is vital that the cows are thoroughlydry before entering the milking parlour. Thesystem can only be used in hot climates andcare must be taken that it does not signifi-

cantly increase standing times; otherwiselameness might result.

Washing but not drying teats beforemilking will increase the bacterial contami-nation in milk and this will raise Bactoscanor TBC. It also deposits bacteria in suspen-sion on the teat end and in so doingincreases the risk of environmental mastitis.Finally, excessively wet teats increase linerslip. In herds where the teats are washed butnot dried before milking, the coliform count,which is a measure of the level of environ-mental contamination of milk, is high (seepages 173–174).

Drying Teats before Milking

Cows should be dried with a single-servicepaper towel or cloth before the milking unitsare attached. Under no circumstancesshould a communal udder cloth, as shownin Plate 6.14, be used, as this only spreadsinfection from cow to cow. Udder clothsoften become so grossly contaminated thatthey are virtually impossible to disinfect.The only acceptable udder cloth is an indi-vidual cloth per cow that is washed, disin-fected and dried between milkings. Such acloth is easy to use and cleans teats well, but

Plate 6.13. Automatic teat-washing sprinklers jet water up against the udder and teats to remove any dirt.

the uptake of this practice will depend onthe costs of labour and energy.

The risk of spreading infection throughthe use of a communal udder cloth cannotbe underestimated. Many farmers are con-vinced that because their udder cloths areplaced in a bucket of disinfectant solutionduring milking all the organisms are killed.This is not correct.

Trial work has shown that Staphylo-coccus aureus can survive on udder clothssoaked in disinfectant solutions for3 minutes. Streptococcus agalactiae cansurvive on cloths for 7 days and can be iso-lated after soaking for up to 5 hours in a 2%hypochlorite solution. This is much longerthan the few minutes they would besoaked in disinfectant solutions duringmilking.

It is very simple to show how in-effective disinfectants are at killingorganisms on udder cloths. This can bedemonstrated to farmers who are convincedthat use of these cloths poses no riskin spreading infection during milking.Get the milker to squeeze some liquidfrom an udder cloth onto a blood agarplate during milking. Incubate this for24 hours in the laboratory. The growth ofbacteria shown in Plate 6.15 comes from onesuch udder cloth. The results speak forthemselves.

Paper towels are cheap and disposableand are the ideal choice for drying teats. Insome countries old newspapers are used. It

is important that a separate piece of papertowel is used on each cow or else you maysmear dirt or infection from the first cowonto the second and so on.

Medicated towels are recommended bysome people. These are towels impregnatedwith a disinfectant and are designed for sin-gle use. They are only intended to dry anddisinfect clean teats, not to clean and drydirty teats. If they are used to wash dirtyteats, there will be little, if any, benefit overthe use of paper towels.

Assessing Teat Preparation

Teat preparation can be assessed by a vari-ety of means. Obviously the cleanliness ofthe teats can be observed before the unit isattached. The milk sock (see Plate 6.6) canbe checked after milking to see how muchfaecal matter is present. It is important totake into account the number of cows in theherd. A high level of faecal contamination isfar more significant in a small herd than alarge herd.

Carrying out coliform counts on bulkmilk is another useful screening method.Alternatively, teats that have been preparedfor milking can be wiped with a white towelto see how much dirt remains present, asshown in Plate 6.16. It is also useful to exam-ine the inside of the liners during milking.If they are dirty, this indicates that teatpreparation is suboptimal.

104 Chapter 6

Plate 6.14. Communal udder cloths spread mastitisbacteria from cow to cow.

Plate 6.15. Growth of bacteria from an udder clothsampled during milking.

Milk Let-down Reflex

Milk is extracted from the udder by apply-ing vacuum to the end of the teat. This liter-

ally ‘sucks’ the milk out. It is important thatthe teat does not collapse during milking.This is achieved in two ways. First, thevenous plexus at the base of the teat (seepage 13) becomes engorged with blood, andthis makes the teat become erect. Second,there is an increase in pressure within theudder during milking, which causes the teatto become full and turgid, thus making milkremoval easier.

Release of the hormone oxytocin resultsin increased udder pressure. Stimulation ofthe udder and teats causes the pituitarygland at the base of the brain to secrete oxy-tocin. Oxytocin acts on the alveolar musclesin the udder, which then squeeze milk intothe ducts. This results in a pressure build-up and produces the syndrome called milklet-down.

Oxytocin release occurs through twoforms of milk let-down reflexes: ‘condi-tioned’ and ‘unconditioned’. Conditionedreflexes are those that the cow takes inthrough her eyes, ears and nose, such as thesound of the vacuum pump and the smell ofconcentrates. Unconditioned reflexes occuras a result of teat stimulation, such as wash-ing, predipping, foremilking and drying.

The level of the conditioned reflex gen-erally remains constant and so the aim of agood milking routine is to maximize the levelof the unconditioned reflex (see Figure 6.2).This is where the benefit of a good and


Fig. 6.2. Levels of oxytocin with good and poor udder stimulation.

0

2

4

6

8

10

12

14

16

18

PoorUdder stimulation

Oxy

toxi

n le

vel

Good

Unconditioned

Conditioned

Plate 6.16. Teats can be wiped with a white papertowel after preparation to see how effective teatpreparation has been.

106 Chapter 6

consistent milking routine pays dividends.Farmers report that cows milk out faster

following good teat stimulation fromforemilking and predipping. They also milkout more fully, resulting in higher milkyields.

The key factor in the speed of milkoutis not the level of oxytocin in the blood butrather the timing of the oxytocin release.Studies have shown that teat or udder mas-sage for 30–60 seconds immediately beforeunits are attached results in faster milk flowrates. The oxytocin let-down reflex is rela-tively short-lived and does not extend

beyond 10 minutes. Cows should thereforehave finished milking within 10 minutes ofstimulation. Taking full advantage of themilk let-down reflex will result in fastermilking and reduced teat damage, andensure the most complete removal of milkfrom the udder, thereby improving produc-tion.

The effect of a good let-down reflex canbe seen using a Lactocorder, a device thatmeasures milk flow rates from individualcows. The Lactocorder is fitted in the longmilk tube between the cluster and the milktransfer line or recorder jar (see Plate 6.17),and measures yield against time. Figure 6.3shows the milking pattern of a cow wherethere has been no manual stimulation. It canbe seen that there is an initial milk flow inthe first minute of just over 2 litres perminute. This is the milk from the teats andgland cistern. However, a minute afterattachment the flow rate has dropped downto just below a litre per minute and then,once let-down has occurred, it takes 7 min-utes to harvest 13.7 litres of milk. This iscalled biphasic milk let-down (i.e. initialmilk flow, then flow stops, then peak flow),and it can also be observed by simply watch-ing the bowls in the claw.

Compare Fig. 6.3 with Fig. 6.4 where

Plate 6.17. A Lactocorder measures milk flowthroughout milking.

Fig. 6.3. Lactocorder tracing (solid line) showing biphasic milk let-down and overmilking: 13.7 kg milk in 7minutes.

00

1

2

3

4

Flo

w (

kg/m

in)

5

6

7

1 2 3 4 5 6Time (min)

7 8


the Lactocorder measures a cow that has had20 seconds of manual stimulation and wherethe unit was attached within 1–2 minutesafter stimulation. This shows that milk flowsat a rate of 4 litres per minute once the unitis attached, and this cow milks out in 4 min-utes, having given 13.8 litres of milk, a sav-ing of 3 minutes compared with the cowwith no manual stimulation.

Batch Preparation

The short time spent stimulating cows withforemilking has a large payback in a reducedmilking time. The unit has to be attached atthe right time following stimulation and sobatch preparation of cows is advised. Batchpreparation is where the milker prepares aset number of cows and then attaches theunit within 1–2 minutes so that the cluster isattached to coincide with the oxytocinrelease.

This means that in a herringbone par-lour, cows are prepared in batches so thatthe clusters are attached within 1–2 minutesafter stimulation. An example is a milker

who foremilks and then predips the firstcow, and then follows this routine down abatch of four to six cows. He then returns tothe first cow, dries the teats and attaches thecluster and repeats this action on theremaining cows (see Fig. 6.5). He thenmoves on to the next batch of cows.

In a rotary parlour with two milkerspreparing the udder and teats, it is easy tohave a time delay of 60–90 seconds fromstimulation to attachment. In herringboneparlours where there are two milkers, youcan use the follower and leader principle,where the leader will predip and strip andthe follower dry and attach. Farmers findthat milking cows with a set routine andbatch preparation speeds up milking.

Unit Attachment

An efficient milker will attach the unitswithout leaking large amounts of air into thesystem. This helps to make sure that vacuumlevels remain stable and reduces the risk ofliner slip and impact forces.

Most units should be carefully aligned

Fig. 6.4. Lactocorder tracing (solid line) showing excellent milk flow and rapid milkout: 14 kg in 4.25minutes.

00

1

2

3

4

Flo

w (

kg/m

in)

5

6

7

1 2 3 4 5 6Time (min)

7 8

108 Chapter 6

so that the cluster sits comfortably on theudder without twisting. This ensures thatthe cow will milk out evenly. Clusters thattwist are uncomfortable for the cow, mayresult in the poor milkout of a quarter andwill increase the risk of liner slip and thecow kicking off the unit (see Plate 6.18).They will also increase the risk of air beingadmitted through the top of the liner.

Units are designed to be attached withthe long milk hose extending out through thehind legs or forwards towards the head of

the cow. In the latter case, a support bar, asshown in Plate 6.19, is needed to avoid theunit twisting on the udder. Although com-monly used in Europe and the USA, supportarms are not frequently used in the UK.

On occasion, milkers have been knownto place stones or bricks on top of the claw-piece to try to speed up a slow milker, asshown in Plate 6.20. This practice is not tobe encouraged as it causes excessive pullingon the teats and this further increases anyteat damage already present, and mayindirectly slow milking down even further.

Milking the Mastitic Cow

In an ideal world, as soon as a new case ofmastitis is detected the cow should be held

Fig. 6.5. The first task is to predip and strip the batch of cows (A). The milker then walks back and (B) wipesthe teats dry and attaches the unit down the batch. He then starts on the second batch.

Plate 6.18. Poor unit alignment. Clusters that twistare uncomfortable for the cow and may result in thepoor milkout of a quarter and increase liner slip.

Plate 6.19. A support arm helps to prevent the unitresting on the udder by taking the weight of thelong milk tube.


back and milked last. Unfortunately, thisdoes not always happen as it can be time-consuming and there may be no facilities forseparating and holding back individual ani-mals. Milking infected cows last, or evenbetter, in a separate group, eliminates therisk of mastitic or antibiotic-containing milkentering the bulk tank. (Don’t forget toremove the milk line from the bulk tankfirst.) It also reduces the spread of mastitisto the rest of the herd via the milker’s hands

and contaminated liners, and allows themilker more time to treat cows properlywithout slowing down the milking process.Remember that liner condition is also sig-nificant, as worn, cracked liners will retainmore bacteria than smooth liners.

It is important to disinfect the clusterafter milking mastitic cows. This will reducethe risk of transferring infection to other ani-mals. Many milkers dip the units in a disin-fectant solution for a few seconds. While thisreduces the number of bacteria present, itdoes not kill all the organisms nor does itfully eliminate the possibility of spread.

Table 6.1 compares the efficiency of dif-ferent methods of disinfecting clusters. It canbe seen that after cold water flush for 5 sec-onds many bacteria were still present.Unfortunately, the data do not give the initialnumber of bacteria present. You need to cir-culate water at 74°C for 3 minutes in order todisinfect the cluster, but this is impracticalduring milking. The only effective methodto sterilize the cluster during milking is toflush it with the water at 85°C for 5 seconds.Most farmers disinfect the cluster byimmersing it in a solution of hypochlorite,iodine or peracetic acid solution for severalminutes. While this does not sterilize theunit completely, it does remove the majorityof the infection, minimizing the risk of cross-contamination.

In some of the dairy herds in the hot ordesert areas of the world, where highly con-tagious Mycoplasma mastitis poses a realthreat to udder health, back-flushing unitsare fitted to parlours. These disinfect themilking unit by passing water at 85°C

Table 6.1. Disinfection of teat cup clusters after removal from cows with mastitis. (From Bramley et al.,1981.)

% Clusters No. S. aureus/mlNo. positive after recovered per

Treatment Time tested cleaning cluster

Cold water flush 5 s 19 100 100,000–800,000Circulation of cold hypochlorite (300 p.p.m.) 3 min 19 100 50–2,000Circulation of water @ 66°C 3 min 18 22 0–80Circulation of water @ 74°C 3 min 85 0 0Circulation of water @ 85°C 5 s 530 3 0–15

Plate 6.20. Milkers have been known to placestones or bricks on top of the clawpiece to try andspeed up a slow milker. This is not recommended.

110 Chapter 6

through the liners, as shown in Plate 6.21.These units are very expensive and, pro-vided good mastitis control measures areused, less benefit would be gained fromthem under temperate conditions, whereMycoplasma infections are rarely encoun-tered.

The simplest way to reduce the spread ofinfection is to have a separate cluster for milk-ing mastitic cows (see Plate 6.22). This meansthat they can be milked as and when theyenter the parlour. This cluster can then be ade-quately disinfected between uses withoutslowing down the milking process (see Plate6.23). Clusters can be disinfected in a solutionof peracetic acid, hypochlorite or another suit-able disinfectant. Many farmers have a sepa-rate cluster connected to a ‘dump bucket’. Bycollecting mastitic milk separately, there is norisk of antibiotic contamination.

The dump bucket used on mastitic cowsis also often used to collect colostrum fromfresh calvers. Freshly calved cows are verysusceptible to infection, as their resistanceto disease is low at this time. If the cluster isnot disinfected between uses, this may actas a source of new mastitis infections(see the contaminated liner in Plate 6.24). Itis essential that these units are not neg-lected, that liners are changed frequentlyand that they are thoroughly cleaned aftereach milking.

Many farmers still milk mastitic cowsinto recorder jars and then drain this milkinto a bucket or on to the floor. There are sev-eral dangers in doing this. The milker may

Plate 6.21. Back-flushing units with disinfectantsolution will help to reduce the spread of infectionfrom cow to cow.

Plate 6.22. A separate cluster connected to a dumpbucket will reduce the risk of spreading infection tohealthy cows and eliminate the risk of antibioticresidues entering the bulk supply.

Plate 6.23. After milking a mastitic cow through thedump bucket, it is essential that the cluster isdisinfected before it is attached to the next cow.

forget to dump the milk, so antibioticresidues contaminate the bulk supply. Thevalve at the bottom of the recorder jar maybe faulty and milk may leak past the valveand into the bulk tank. Finally, antibioticsconcentrate in butterfat and so jars that arenot rinsed out thoroughly after milk isreleased may still result in antibiotic con-tamination from butterfat rings around theinside of the jar. Antibiotic residues are dis-cussed in Chapter 15.

Unit Removal

Once cows are milked out, the vacuum sup-ply to the cluster should be shut off.Atmospheric air enters the clawpiecethrough the air bleed hole, releasing the vac-uum and allowing the unit to ‘fall off’ theudder. Where ACRs (automatic clusterremovers) are fitted, they should operate inthe same way. A cluster removed while stillunder vacuum can result in large impactforces and may cause teat sphincter damage.

There are three important adjustmentson the ACR, namely:

� The milk flow rate, which will eventuallytrigger ACR activation.

� A delay between reaching this flow rateand vacuum shut off.

� A further delay between vacuum shut-offand ACR pull.

First, milk flow rates triggering ACR removalwere traditionally set at 200 ml/min, butmore recently this has been increased to400 to 600 ml/min or 600 to 800 ml/min forhigh-yielding cows milked three times a day.Second, there has to be a delay betweenreaching this ‘trigger value’ and vacuumshut-off; otherwise a cow that has had a tem-porary drop in flow rate, e.g. from liner slip,will have the unit removed early.

Third, the delay between vacuum shut-off and ACR pull allows time for vacuumlevels in the claw to vent, thereby reducingthe risk of teat-end damage. If a significantnumber of cows kick at unit removal, it islikely either that the milk flow trigger is toolow or that there is insufficient delaybetween vacuum shut-off and ACR pull.

Overmilking is not to be encouraged asit increases the unit time on, slows downmilking and increases the risk of teat-enddamage, clinical mastitis and high cellcount.

Disinfection of Clusters between Cows

At the end of milking, a small amount ofmilk, about 2–4 ml, is held inside themouthpiece of the liner. When the cluster isattached to the next cow, the milk from theprevious cow will run down the inside ofthe liner and contaminate the teat of the nextcow to be milked. This represents a risk oftransfer of infection.

At one stage, dipping clusters into abucket of disinfectant solution between cowswas a popular procedure in the milking rou-tine. It was generally believed that dippingunits in a solution of hypochlorite for a fewseconds would remove all bacteria from con-taminated liners. The difficulty of completelydisinfecting clusters has been shown in Table6.1. Although cluster dipping will help toreduce bacteria numbers, it is unlikely to betotally effective in eliminating the spread ofbacteria from cow to cow.


Plate 6.24. The liner of a dump bucket that has notbeen cleaned correctly. You can see the crud andthe deposits inside the liner.

The MFE trial work in the late 1960s(page 1; Fig. 6.1) that showed the effect ofpasteurizing clusters on clinical and sub-clinical infections was marginal, and so itwas not incorporated into the five-point-plan that was recommended. However, itmust be remembered that at this time herdsize was small, yields were low, environ-mental mastitis was not a significant prob-lem, and the major problem was subclinicalmastitis.

Dairy herds have changed significantlysince then. Back-flushing units will helpto remove the both environmental andcontagious bacteria and this can only be ofbenefit, especially in herds where environ-mental management or teat preparation issuboptimal.

A variety of cluster flush systems are inuse. In one, the flush solution is emittedfrom a small nozzle inside the mouth of theliner (see Plate 6.25), while others incorp-orate pulses of air and a sanitized flush solu-tion that enters the long milk tube andflushes through the cluster and out throughthe liners.

While there are ample data to show thatthis reduces the level of all bacteria present

in the liner (staphylococci, streptococci,coliforms, etc.), so far there are no good trialdata to demonstrate a positive benefit interms of cell count or reduced mastitis inci-dence. Liners are always flushed betweencows on robotic systems.

Residual Milk

No matter how long you leave the milkingunit on the cow, not all milk will be removedfrom the udder. The remaining milk is calledresidual milk. The amount of residual milkis usually 0.5 litres for heifers and 0.75 litresin cows.

There are a variety of factors that canincrease the amount of residual milk:

� Disturbing or frightening cows just beforeor during milking, which will affect thelet-down reflex.

� Delay between udder stimulation andattaching the teat cups.

� Irregular milking intervals.� Teat injuries.� Poor unit alignment, leading to incom-

plete milkout in one or more quarters.� Poor ACR adjustment, leading to early

cluster removal.� Milking through a defective parlour.� Liner ‘creep’, leading to poor milkout.

112 Chapter 6

Plate 6.25. The flush solution is emitted from asmall nozzle inside the mouth of the liner tominimize cross-contamination.

Plate 6.26. Machine stripping is the processwhereby a downward pressure is applied to theclawpiece with one hand, while the quarters aremassaged with the other. This is not recommended.

A good milking routine will help to keep theamount of residual milk to a minimum,thereby maximizing yield. If a large amountof milk remains in the udder, this may aggra-vate subclinical mastitis, especially withStreptococcus agalactiae infections. It canalso decrease milk yield.

Machine Stripping

Machine stripping is the process wherebydownward pressure is applied to the claw-piece with one hand, while the quarters aremassaged with the other, as shown inPlate 6.26. The intention is to maximize milkremoval and reduce the amount of residualmilk in the udder.

There is a danger that, if machine strip-ping is carried out with great vigour andenthusiasm, air will be sucked in throughthe top of the liner, resulting in impactforces. Impact forces may cause a massivereverse flow of milk against the teat end (seepages 79–80). If bacteria penetrate the teatcanal, a new infection may become estab-lished. For these reasons, machine strippingis not recommended.

Today’s dairy cow is selected for goodudder and teat conformation. In addition,the ability of modern milking machines toreduce the amount of residual milk hasgreatly improved, due to modifications totheir design.

Postmilking Teat Disinfection

Immediately after the cluster is removed theentire surface of each teat should be coatedin a disinfectant solution, as shown inPlate 6.27. This can be applied as a dip or asa spray.

The aim of postmilking teat disinfectionis to kill any bacteria transferred on to theteat during milking before they have achance to colonize or infiltrate the teat canal.Postmilking teat dipping is an essentialmethod of controlling contagious mastitis. Itis less effective against coliform and otherenvironmental forms of mastitis (for whichpredipping is more important). Teat dippingis discussed in detail in Chapter 7.

After cows leave the parlour, theyshould exit along clean and freshlyscraped passages and move towardsfreshly bedded housing. They shouldhave access to food and water to encouragethem to remain standing for between20 and 30 minutes while the teat canalcloses fully. If cows lie down immediatelyafter milking while the teat canal is open,there is a risk that environmental bacteriamay penetrate the udder, and mastitis mayresult.

In some herds, cows are kept standingin a passageway for prolonged times aftermilking. This can have adverse effects onlameness. A lame or sick cow should be ableto lie down after milking if she so chooses.Cows naturally feed after milking, allowingtime for the teat canal to close; they shouldthen be able to lie down.

Milking Order

If a herd is divided into groups, then milkingorder should be considered. Many farmersgroup their cows, and the types of group willdepend on the management. To help reducethe spread of mastitis cows should bemilked in the following order:

� High yielders.� Low yielders.� High cell count cows.� Mastitic, lame and other treated cows.


Plate 6.27. Immediately after the cluster has beenremoved following each milking, the entire surfaceof each teat should be coated in a disinfectantsolution. Note the brown stain left by the iodine inthe dip.

Late lactation cows are likely to have anincreased amount of subclinical infectiondue to longer exposure to mastitis organismsthroughout lactation. Therefore, the greatestrisk of contagious mastitis will come fromthis group of cows.

A high cell count group can help limitthe spread of infection within a herd, butmost herds that have cell counts under con-trol do not need such a group.

Frequency of Milking

There is a higher yield when the milking fre-quency is increased to three or four times aday, without significant effect on milk com-position. At three times a day, yields can beincreased by up to 15% in heifers and 10%in cows. This is due to the removal of themilk inhibitor protein, resulting in moremilk being synthesized in the udder.

In addition, as milk is removed from theudder more frequently, flushing out any bac-teria in the teat canal and udder (and despitea possible increased risk of new infectionsfrom extra milking), the mastitis incidencein herds that are milked three times a daytends to be lower than in their twice dailymilked counterparts. Herds that are milkedthree times daily also have lower cell countsdue to this flushing action.

Robotic Milking

Robotic milking has become more popular,with large numbers of robots on the conti-nent and in the USA. The robot milks thecow in a very different way from what hap-pens in a conventional parlour, as both teatpreparation and mastitis detection are totallyautomated. Once an individual quarter ismilked out, the liner on that quarter isremoved. This minimizes overmilking onindividual quarters. Disinfection of the linerbetween every cow is automated, along withpostmilking teat disinfection. There are sig-nificant advantages to this technology, pro-vided that it works and that the managementand facilities of the farm suit robotic milking.

However, there are some potential prob-lems. Foremilk is not visually examined andmastitis is detected from electrical conduc-tivity. Any change in conductivity results inthis milk being discarded and a warningmessage about that cow. She must bechecked to decide whether she has clinicalmastitis. Most robots allow farmers to adjustconductivity thresholds so as to reduce thenumber of false alarms relating to mastitis.The new robots compare individual quarterconductivity with results from previousmilkings and look for changes to improvethe accuracy of mastitis detection. This canbe very useful for the early detection of mas-titis.

Teats are cleaned using rotary brushes(see Plate 6.28), which use a combination ofdisinfectant solution and physical action toclean. Teats are not dried, which is a disad-vantage. If teats are grossly contaminatedbefore milking, then teat preparation maynot be adequate, and the wet teats can con-tain large amounts of environmental bacte-ria. This will increase the risk ofenvironmental mastitis and/or raise the TBCor Bactoscan.

Postmilking teat disinfection is usuallyfrom a central spray nozzle, which can onlycoat the inner surfaces of the teats. Outersurfaces may not be fully disinfected.

Not all cows may enter regularly to bemilked. This can result in intermittent milk-ing, and this may increase cell counts of

114 Chapter 6

Plate 6.28. Robotic milking machines use rotatingbrushes to clean teats. Teats are not dried before theunit is attached.


such animals. It is important that cows aremilked at the correct frequency. This mayinvolve some form of feeding to encouragecows to enter the parlour.

Summary of the Milking Procedure

The aim of the milking routine is to milkclean, dry teats with a correctly functioningmilking machine as efficiently as possible,thus posing minimal risk to udder healthwhile maintaining milk quality. This isachieved by the following routine:

� Foremilk cows.� Carry out teat preparation so that teats are

clean and dry. Predipping is the gold stan-dard. Predip, allow a contact time of30 seconds and wipe dry.

� Attach the milking unit within 1–2 min-utes of teat preparation.

� Check machine alignment so that it sitssquarely on the udder.

� When the cow is milked out, shut offthe vacuum and then remove thecluster.

� Coat teats with teat dip.� Allow the cow to exit to a sheltered yard

with access to food and water so that sheis encouraged to remain standing for20–30 minutes.

The additional time spent diligently carry-ing out these procedures will be re-warded by a lower incidence of mastitis,lower cell counts, cleaner milk production,increased milk yield, increased satisfactionfor the milker and greater comfort for thecow.


Postdipping 116Predipping 117Method of Application: Dip or Spray 117

Dipping 117Spraying 117

Preparation and Storage of Dips 119Chemicals Used in Post- and Predipping Disinfectants 120

Iodophors 120Chlorhexidine 120Quaternary ammonium compounds (QACs) 120Dodecyl benzene sulfonic acid (DDBSA) 121Hypochlorite 121Acidified sodium chlorite 121Foam dips 121Viscosity and surfactant 122Barrier dips 122

Postmilking Teat Disinfection 123Removal of mastitis bacteria 123Removal of bacteria from teat sores 124Improving skin quality with dip additives 124Automatic teat disinfection systems 124Limitations of postmilking teat disinfection 125Seasonal use of dips 126

Premilking Teat Disinfection 126When does predipping not work? 127

Iodine Residues 128

7 Teat Disinfection

This chapter examines the reasons for teatdisinfection, the methods of application (dipor spray), the chemicals used, some of theassociated management faults and theimportance of chemical residues. Teatdisinfection can be carried out immediatelybefore milking (predipping) or immediatelyafter (postdipping).

Postdipping

In postdipping (see also page 113), thedisinfectant is applied as soon as the milkingunit is removed. Teats must not be wipeddry after the postdip has been applied.Postmilking teat disinfection is one of themost important preventive measures in

mastitis control and an integral part of the‘five-point plan’ (see page 1). It should becarried out in every herd, after everymilking, throughout the year.

Predipping

In predipping (see also pages 101–102), thedisinfectant is applied to the teats just beforemilking, and teats must be wiped before thecluster is attached. Predipping is a newerconcept, aimed at reducing the incidence ofenvironmental mastitis and reducing theTBC/Bactoscan (see Chapter 10). In mostinstances the disinfectants used for postdipsdiffer from those used as predips, asdifferent speeds of kill are required.

Method of Application: Dip or Spray

Because of the importance of removingbacteria from the entire teat (see page 21), itis essential that the whole teat, and not justthe teat end, is disinfected. This is likely tobe best achieved by dipping, althoughspraying can be effective if carried outconscientiously.

Dipping

Dipping uses less product than spraying(approximately 10 ml per cow per milkingfor dipping versus 15 ml for spraying) and,provided that it is carried out correctly, willprovide excellent teat cover. The teat dip potshould be large enough to contain the teatwithout excessive spillage of dip and, at thesame time, it should be full enough to ensurethat small teats will reach and be covered bythe dip solution (see Fig. 7.1).

Dual compartment anti-spill cups (pots)are also available (Fig. 7.2). When the bottomcompartment is squeezed, dip is forced intothe top. If the pot should then be knockedover (or kicked out of the milker’s hand), it isonly the dip in the top of the pot that isspilled. These cups often have a hook on the

side, allowing them to be attached to themilker’s belt (Plate 7.1) and therefore readilyavailable for use. Whatever type of pot ischosen, it should be applied so that the rimmakes contact with the udder, and the pot isthen shaken to ensure total teat cover.

Teat dip pots should be cleaned regularly,to prevent contamination. Any dip remainingin the pot at the end of milking should bediscarded and the pot cleaned before reuse atthe next milking. If pots are hung in theparlour during milking, take care that they donot become contaminated, as in Plate 7.2.

Spraying

Teat spraying can also be effective, but mustbe carried out conscientiously. It is much

Teat Disinfection 117

Fig. 7.1. (Left) A small, narrow teat dip cup that isoverfull will cause the iodine to be wasted and themilker’s hands to become stained, whereas anexcessively wide cup with only a small quantity ofteat dip (right) may mean that small teats are notadequately dipped.

Fig. 7.2. Anti-spill teat dip cups are available. Onlythe dip in the top chamber is spilled if the cup isknocked over.

easier to achieve only partial cover than withdipping. Spray lances should be ofreasonable length, with the nozzle pointingupwards and not directly out from the end(Fig. 7.3). Spray should be applied frombeneath the teats while rotating the lance ina circular action below the base of the udder.At least two rotations will be needed toachieve full cover, one to the left to cover theleft side of teats, and one to the right to coverthe right side. A single rotation is simply notsufficient.

In herringbone parlours, some milkersopen the gate, releasing the cows, and then tryto apply teat spray as they walk past.Unfortunately, this results in very poor teatcover. If iodine disinfectants are used, it iseasy to see when only one side of the teat hasbeen coated, as in Plate 7.3. The disinfectantmay well run to the end of the teat, thuseliminating teat-end colonies and reducingthe most important aspect of mastitistransmission. However, the absence ofdisinfectant on one side of the teat could allowthe establishment of a reservoir of mastitispathogens on the untreated teat skin. Youshould also regularly check the spray lance.The two most common faults found are:

1. The nozzle becomes partially blocked, sothat the spray is emitted from one side ofthe lance only.

118 Chapter 7

Fig. 7.3. Spray applied from the side using spraylances achieves only partial cover. Spray should beapplied from the bottom of the teat in a circularmotion to ensure total coverage.

Plate 7.2. Teat dip pots should be stored in theparlour in such a way that they do not becomecontaminated.

Plate 7.1. Dip pots for predip and postdip areconveniently attached to the belt during milking.

×

2. The nozzle emits teat disinfectant as a jetrather than a spray, and this results inpoor teat cover.

These faults can be checked by sprayingdisinfectant on to a piece of white papertowel. The pattern on the towel is theemission pattern of the spray lance. Hand-held garden sprayers have been used, butmost do not provide a sufficiently fineaerosol or wide enough spray angle to beeffective.

The best method of checking teat coveris to examine teats immediately afterdisinfectant application, and preferablywhen the milker is not aware that this isbeing done, e.g. during a teat scoring visit. Alamp is needed for this, as shown in thesection on teat scoring in Chapter 14 (seepages 233–234). In this system a ‘missed

cow’ is defined as a cow where the surface ofone or more teats is less than half coveredwith disinfectant, i.e. quite a severe score. Agood herd will achieve only 5% of cows‘missed’. In poor herds, some 90 to 95% ofcows may be ‘missed’. This clearly has amajor effect on the spread of contagiouspathogens.

A comparison between teat dipping andspraying is shown in Table 7.1.

Preparation and Storage of Dips

Some dips are bought ready to use, whileothers are supplied as concentrates and haveto be diluted. Ready-to-use products areoften more stable, as they have beencarefully formulated and diluted with softwater. When diluting a concentrate, theinstructions should be followed closely and,ideally, only enough solution for a few daysshould be made up to avoid deterioration.Hard water on bore hole water may not besuitable.

Unused containers of dip should bestored away from cold areas, since freez-ing may lead to separation of water fromthe chemical. When in use, make surethat the top of the drum is not left open inan area where large quantities of waterare splashed. Water contamination willdilute the teat dip or, even worse, ifcontaminated by circulation cleaner rinsewater, the dip may become denatured andineffective.


Plate 7.3. Poorly applied spray leads to only oneside of the teats being covered.

Table 7.1. Comparison between dipping and spraying.

Dipping Spraying

Teat cover Generally good Good if carefulVolume used 10 ml 15 mlper cow/milkingCost Very cheap More expensive

equipment to installPoints to watch Dirty teat dip cups Blocked nozzles

Keep pot full causing slow flowCows with very ratesshort or long teats Solution running

out during milking

Chemicals Used in Post- and PredippingDisinfectants

There is a range of chemicals used for bothteat dips and sprays. It is not possible to bespecific concerning the most effectivedisinfectant, because their properties vary.In the UK, some products have a MedicinesLicence, i.e. the manufacturer has carriedout field trials to show that the disinfectantis safe and is effective in the controlof mastitis. Other products are simplysold unlicensed as a postmilking teatrinse, making no claims regarding mastitiscontrol. Licensed products are clearlythe safest option. The best dip is theone that fully covers every teat at everymilking.

The most common products used arelisted below.

lodophors

These are probably the most widely usedcompounds in dips. They consist of0.25–0.5% total iodine in association with acomplexing agent, which essentially actsas a ‘reservoir’ of free inert iodine. As thefree iodine is slowly used up by reactingwith bacteria, more free iodine is releasedfrom the complexing agent reservoir tomaintain a constant level of activeingredient in postdips of around 3–5 p.p.m.The problem of iodine residues is discussedon page 128, and a low-iodine residue dipdescribed.

Iodophors have a low water solubilityand require surfactants to bring them intosolution. These are strong acids and this canbe irritating to teat skin, hence mostproducts contain significant levels ofemollients. Like other teat dips, iodophorsare not selective in their action. They havequite a rapid action, although like most otherteat disinfectants, they react with anyorganic matter and so, if teats are badlysoiled or heavily coated with milk or if theteat dip cup becomes contaminated withfaecal material, then efficacy is markedlyreduced.

One advantage of iodine is its colour. Itstains skin and so it is easy to see how wellteats have been covered after milking(though any stain left on the herdsman’shands may not be appreciated). Iodine dipthat has been excessively diluted looks ‘pale’in the pot but can still cause staining. Somemilkers dislike the smell, and inhalation ofthe fumes produced may cause unacceptablerespiratory irritation, especially when teatspraying.

Chlorhexidine

Commonly used at between 0.4 and 0.8%,chlorhexidine has a wide activity againstmost bacteria and, because of its greaterpersistency on the teat, it is especiallyeffective against staphylococci, which iswhy it is commonly used as a teatdisinfectant for goats. It is less affected byorganic material than most otherdisinfectants, although it is relativelycolourless, making it less easy to see thattotal teat cover has been achieved. It iswater-soluble so needs very little surfactant,and non-irritant, so products may be soldwith only a low level of emollient. However,emollient may be added to improve teat skincondition.

Quaternary ammonium compounds (QACs)

These teat dips consist of the quaternaryammonium compound (the bacteria-killingcomponent), a ‘wetting agent’ to assist ingreater penetration of skin and dirt, pHbuffers to stabilize the acidity of the product,emollients and water. Colouring agents maybe added to show that the teats have beendipped, and thickening agents may giveincreased persistence on teat skin.Quaternary ammonium compounds are notirritant to teat skin, although carefulformulation is necessary to maintainefficacy. Effectiveness against Pseudomonasand Nocardia is very doubtful and thesebacteria have even been known to grow inQAC solutions.

120 Chapter 7

Dodecyl benzene sulfonic acid (DDBSA)

Used at a rate 2.0% inclusion rate, DDBSAdips are non-irritant to teats and to theoperator. They have a wide range of activityagainst most bacteria but are ineffectiveagainst bacterial spores. They have a longerlength of action than some dips (and hencemay confer some protection againstcoliforms) and work quite well in thepresence of organic matter.

Hypochlorite

Hypochlorite is by far the cheapest productavailable, and is quite rapid in action. Its maindisadvantage is that it rapidly reacts withorganic material (milk, faeces and skin debris)and becomes ineffective. Used at the usualconcentration of 4.0%, it can also irritate themilker’s hands, cause damage and bleachingof clothing and result in quite marked dryingof teats, especially when first used. Theseeffects are partly caused by the inclusion ofsodium hydroxide (around 0.05%), which issometimes used to stabilize the product.Hypochlorite cannot be safely used as a teatspray, however, as inhalation illness mayresult. It is colourless and hence it is difficultto assess the efficacy of teat cover.

Ideally, hypochlorite should beintroduced at a low concentration and thenslowly built up to 4.0% (40,000 p.p.m.).Provided that weather conditions arefavourable, teat skin often adapts well andthe product can be used without severereaction. There are anecdotal reports that itsstrong oxidizing action improves the rate ofhealing of teat-end damage (e.g. black spot,see page 229) and of viral skin lesions, suchas pseudocowpox (see pages 227–228).

Due to formulation problems, ifemollients are used they must be addedimmediately before to milking. Hypochloritesolutions are relatively unstable. Theyshould be stored under cool conditions andwith the lid closed; otherwise they canevaporate quite quickly and lose theirpotency.

There are hypochlorite deriva-tives available, for example, 5 g per litre

sodium dichloroisocyanurate, which aremore stable and have a less severe skin-drying effect.

Acidified sodium chlorite

Combinations of sodium chlorite with lacticor mandelic acid form the antimicrobialcompounds chlorous acid and chlorinedioxide, which are effective against mostbacteria, yeasts and moulds. Acidifiedsodium chlorite compounds are two-partproducts, an activator and a base that aremixed immediately before use, as are addedemollients and humectants. The final mixcontains around 0.3% sodium chlorite, andbarrier films can be incorporated.

Foam dips

Foams, for both pre- and postdips, arepopular on some farms. The foam may beproduced in a cup attached to a low pressureair line, or it may result simply by squeezingthe base of a specially designed cup(Plate 7.4).

Foams are easier to apply than standardliquid dips, some of which are surprisinglydifficult to repeatedly force into the uppercompartment, and as a consequence maymake your forearm ache. However, foam is,by definition, a liquid with air holes in it, so,although foams may appear to give good teatcover, the amount of chemical applied to theteat skin may be low.


Plate 7.4. A foam teat dip.

Viscosity and surfactant

Teat dips vary considerably in their viscosityand surfactant properties. Surfactant promotesthe ability of the dip to penetrate cracks andcrevices in teat skin, thereby removing teatskin bacteria, and viscosity influences theability of the dip to remain on the teat afterapplication. Plate 7.5 shows the result of usinga cheaper low-viscosity dip – most of theproduct is on the floor under the cow.

Barrier dips

Barrier dips are only used postmilking. Theyare more expensive and thicker thanconventional products, drip less and consistof a disinfectant, a gel and an alcohol – oftenisopropanol – which promotes rapid drying.As the dip dries, it leaves a plastic film

covering the teat end. Barrier dips arepromoted on the basis that they last longerand hence provide protection againstinfection by environmental organismsbetween milkings. The residual plastic filmmay have to be removed when preparingteats premilking, and some barrier dipsspecify that predip must be used to removeresidual barrier film at the next milking.Because of their high viscosity, it is possibleto rapidly immerse a teat in barrier dip andwithdraw the pot with no dip left on the teat.Barrier dips therefore take slightly longer toapply. With their thick film, their presenceon the teat is easily seen (Plate 7.6), and thisperhaps encourages the herdsman to takeextra care with application.

Although they give a striking colourfilm over the teat, there is no evidence thatbarrier dips are any more effective thanconventional products. Anecdotal reports ofreduced mastitis could be due to morediligent application or to the need to usepredip to remove the barrier prior to the nextmilking. There is concern by some that thevery high viscosity of barrier dips mayprevent their penetration into cracks andcrevices in teat skin, and as such they maybe less effective against teat skin organismssuch as staphylococci. This is especially thecase if there is a delay between unit take-offand application of the dip, leading toshortening of the teat canal. Aqueous dipsmight penetrate better because of the

122 Chapter 7

Plate 7.5. Low-viscosity dips may run off the teatsand on to the floor.

Plate 7.6. Barrier dips produce a striking film overthe teat, but the evidence that they are consistentlymore effective is lacking.

hydrostatic pressure applied when the teatis immersed in the dip cup.

External teat sealants for dry cows arediscussed on page 212.

Postmilking Teat Disinfection

There are three major reasons for carryingout postmilking teat disinfection, namely:

� Removal of mastitis bacteria from the teatskin.

� Removal of bacteria from teat sores.� Improvement of teat skin quality.

Removal of mastitis bacteria

During the milking process, contagiousmastitis pathogens can be spread from cowto cow by three vectors. These are:

� Hands.� Cloths.� Liners.

Control of transfer via hands is achieved bywearing gloves and rinsing hands regularly.Control of spread by cloths is by ensuring thatcommunal cloths are not used. It is generallyconsidered acceptable to use a separate clothfor each cow, but even then infection mayhave been spread from teat to teat of the samecow. Control of spread by the liner is by meansof cluster flushing and this is discussed inChapter 6. Despite these measures, it is stilllikely that there will have been some transferof infection from cow to cow.

The liner represents the greatest riskbecause 2–4 ml of milk remains inside thelip of the mouth of the liner after unit take-off. Unless flushed, this milk will run downthe inside of the liner (Plate 7.7) and willcontaminate the teats of the next cow to bemilked. This is why it is important todisinfect the whole of the teat and not justthe teat end.

In addition to infection from othercows, there may be mastitis pathogens at theteat end that have arisen from the teat skin ofthe same cow. There is a risk that the drip ofmilk present in the teat canal at the end of

milking (Plate 7.8) will contain mastitisorganisms, and these could potentially leadto new infections.

Unless removed, these bacteria multiplyto form colonies and slowly penetrate theteat canal. It is the adhesive properties of thecontagious mastitis organisms (see page 36)that allow them to do this. Once they havereached the udder, a new infection may beestablished.

Postmilking teat disinfection removesbacteria deposited during the milkingprocess and, as such, it is an extremelyimportant control measure against


Plate 7.8. The drip of milk seen in the teat canalafter milking represents a risk of establishing a newinfection and needs to be removed by diligentpostmilking teat disinfection.

Plate 7.7. Milk residues in the liner from theprevious cow, which will run on to the teat of thenext cow to be milked.

contagious mastitis. The disinfectant shouldbe applied as soon as the cluster is removed.At this stage, the canal is still open and sosome disinfectant can penetrate the teatorifice. This ensures that those mastitisbacteria that have started to enter the canalwill also be killed.

Removal of bacteria from teat sores

Any skin lesion that is infected will be slowto heal. Teat disinfection removes bacteriafrom the skin surface. This promotes healingand maintains teat skin in optimumcondition. Rough, cracked or chapped teatskin, as in Plate 3.1, can be a reservoir fororganisms such as Staphylococcus aureus,CNS (coagulase-negative staphylococci) orStreptococcus dysgalactiae. Thoroughdisinfection of the whole teat is important toensure that all bacteria are killed.

Improving skin quality with dip additives

Teat skin has relatively few sebaceousglands, and so continual washing followedby exposure of damp teats to a cold andwindy environment can remove protectivefatty acids and lead to cracking. The mostcommon additives to teat dips are:

� Emollients: they form a seal around theskin to prevent further water loss byevaporation. Similar products are used inudder creams.

� Humectants: these assist in drawing waterinto the skin.

Lanolin (emollient) and glycerine(humectant) are the most common additivesand may be included at up to 10%concentration in the dip. As the level ofadditive increases, the proportion ofdisinfectant and hence the bacterial killingability of the final product decrease (see Fig.7.4). For this reason, additives are rarelyincluded above the 10% level. If moreadditive than this is used, then the productmay also become too thick and impossibleto dispense through a spray line.

Automatic teat disinfection systems

Automatic teat disinfection systems, sited atthe exit to the milking parlour, are available.The majority are activated by an electronic‘eye’. As the cow walks past, the ‘eye’triggers a burst of disinfectant spray from anozzle or a raised bar on the floor (Plate 7.9)and directs it on to the udder.

124 Chapter 7

Plate 7.9. Automatic teat disinfection system sited atthe exit of the parlour.

Fig. 7.4. Emollient levels above 10% significantlydepress the bacteria-killing ability of the dip.

0 10

% Emollient in dip

Bac

teria

-kill

ing

abili

ty o

f dip

20

Automatic systems are beingcontinually improved, but as yet none are aseffective as thorough teat dipping. Theirmain disadvantages are as follows:

� Some cows rush past and may onlyreceive a small amount of spray or may bemissed altogether. This is partiallyovercome by trapping each cow in a headyoke as she passes along the spray race.

� Cows with very high udders will besprayed on the inside of the thighs but fullteat cover will not be achieved, whereascows with low udders will get spray onthe inside of the teats only.

� Faeces deposited on the spray jetter byone cow could be sprayed onto thefollowing cow.

� Some spray systems have a jetter bar thatcan make contact with (and contaminate)the teats of cows with very pendulousudders.

� If sited outside the parlour, thedisinfectant spray may be deflected awayfrom the teats during windy weather.

� As most systems are sited at the parlourexit, they apply the teat disinfectantwhen the cows are leaving the parlour.This could be some time after the unit hasbeen removed, when the teat canal hasalready started to close. Because of this,high cell counts associated withorganisms such as Corynebacterium bovishave been reported with automatic teatdisinfection.

� The system could run out of teatdisinfectant without the operatorknowing. Alarm devices should be fitted.

Automated dipping can also be applied frominside the liner (Plate 6.25). Whilst highlylabour efficient, the system needs carefulmonitoring of teat dip cover.

Limitations of postmilking teat disinfection

Although a vital part of every mastitiscontrol programme, postmilking teatdisinfection has some limitations:

� It has no effect on existing infections – ifteat dipping is introduced into a herdalready heavily infected with contagiousorganisms, you cannot expect a rapidreduction in cell count or mastitisincidence. Although dipping prevents thetransfer of bacteria and hence reduces therate of new infections, it has no effect onexisting infections. For example, in onetrial over a 12-month period, a 50%reduction in new infections producedonly a 14% reduction in the overallnumber of quarters infected.

� A herd with a high cell count that startspostdipping should not expect a rapidreduction in cell count. High cell countswill only decrease with treatment, drycow therapy and culling.

� Its main effect is against contagiousorganisms – environmental infections arethought to be transferred on to the teat endbetween milkings and propelled throughthe teat canal by impacts during themilking (see pages 79–80), or they are theresult of dry period infections (see pages50–52). As postmilking disinfectants havea relatively short action e.g. 1–2 hoursafter application, they will have a limitedeffect against environmental mastitis.Premilking disinfection is therefore moreimportant in the control of environmentalmastitis.

� It may cause teat irritation – this isparticularly the case during wet and coldweather. Some chemicals are quite irritant,although their adverse effects can bereduced or avoided by the inclusion ofemollients. Under sub-zero conditions,some farmers discontinue teat disinfection.Disinfectants are temperature-sensitive;hence. during very cold weather, teat dipsnot only are more irritant, but also have alower bacteria-killing power.

� It is inactivated by organic matter – alldisinfectants are less active in thepresence of milk or faeces. For this reason,it may be better to discard residual dipfrom the cup at the end of each milking,to clean the cup and to add new dip beforethe next milking.


Seasonal use of dips

Seasonal postdipping is common in somecountries where it is considered thatinfection only spreads during winter. Someherdsmen have tried stopping postmilkingteat disinfection during the summer, only tofind that cell counts begin to rise due to abuild-up of contagious organisms. Thecontagious mastitis bacteria will spreadduring milking throughout the year. In orderto be effective, all teats must be disinfectedafter every milking, irrespective of theseason.

Premilking Teat Disinfection

Premilking teat disinfection is an importantcontrol measure against environmentalmastitis and reduces bacterial counts in bulkmilk. Predipping also stimulates milk let-down and hence speeds up milking.

Teats should be clean prior to theapplication of the milking machine. Theymay be washed, and the use of a sanitizer inthe water further reduces bacterial burdens.If washed, teats must be dried beforemilking.

Although dry wiping or washing anddrying help to reduce bacterial levels on

teats, they are by no means as effective asapplying a premilking disinfectant. Table 7.2shows the benefits of teat disinfection overand above washing and drying, in anexperiment where teats were first exposed toan experimental challenge of Streptococcusuberis 1–2 hours before milking.

Washing and drying produced a 43%reduction in the percentage of quartersinfected. There was an additional 40%decrease in infected quarters when teatswere dipped in a disinfectant prior tomilking, even though previously the teatshad been washed and wiped.

Predipping, first introduced inCalifornia, is now widely used in NorthAmerica and is becoming increasinglypopular in Europe. Its prime effect is againstenvironmental mastitis.

One large field trial in the USA (seeTable 7.3) involved four herds over a 3-yearperiod. The cows were individuallydesignated 50:50 as predip and controlanimals, although all were housed, fedand milked as a single group in eachherd. Results showed a 46% reductionin the incidence of environmental infec-tions caused by Streptococcus uberis andE. coli in those cows on which predip wasused.

126 Chapter 7

Table 7.2. Comparison of the effectiveness of different methods of premilking teat preparations. (FromGalton et al., 1988.)

Teat preparation No. of quarters infected % reduction % further reduction

No preparation 27 – –Wash and dry 15 43 –Wash, dry, then predip and dry 9 67 40

Table 7.3. The effect of predipping on the reduction of new intramammary environmental infections infour commercial dairy herds. (From Pankey et al., 1987.)

Number ofquarters Number of infected quarters %

Treatment at risk S. uberis Coliforms total reduction

Control 553 31 41 72 –Predip 619 18 21 39 46

Results from field trials in the UK havebeen similar, with one trial (Blowey andCollis, 1992) showing almost a 50%reduction in clinical mastitis incidence andanother a 30% reduction. Predip should beapplied before the application of the milkingunits. If the teats are grossly soiled, theymust be washed and dried before the predipis applied. Predip needs a minimum contacttime of around 30 seconds and then must bewiped off prior to the application of themachine. To achieve this many milkersadopt the following routine:

� Predip.� Forestrip.� Wipe.� Apply.

This has the advantage of a longer period ofpredip contact time with the teat, and alsothe teat is damp when foremilked, makingstripping easier. Others say that, for hygieneand teat cleanliness reasons, predip andwipe should be the last procedures prior tounit application. Whichever sequence isused, it is important to fully wipe the teatend to get full benefit from predipping. It iseasy to wipe the barrel of the teat but leavea residue of dip and bacteria on the tip at thecanal.

Clearly speed of action is important forpredips. One novel licensed product with ahigh (50 p.p.m.) free iodine but low(0.1%) total iodine content is currently soldas having a very rapid action, with a99.99% kill of teat surface bacteria within30 seconds. This product is stable at pH 6.5(most iodophor dips are acid) and hence canbe used without an emollient.

Not only can predipping reduceenvironmental mastitis, but, if teatcontamination is the cause of a highTBC/Bactoscan, then predipping will reducebacterial counts. Improving housingconditions to avoid excessive soiling of theteats between milkings is clearly alsoimportant. It seems logical that, if the teat isleft soaking in disinfectant for a period oftime and then wiped, this must be a veryeffective method of removing dirt anddebris. The effectiveness of predipping is

seen in some herds where coliform countsin milk may reach zero. As withpostdipping, care should be taken to ensurethat the pot does not become contaminatedwith faeces.

A further claim by the proponents ofpremilking teat dipping is that the teats aremore moist and supple when the milkingmachine is applied, and this leads to lessliner slip. Some say that teat condition willalso improve, but this will clearly depend onthe type of postdip used (e.g. high or lowemollient). A marked improvement in teatskin condition could explain the anecdotalreports of predipping also leading to animprovement in cell count.

A few farmers have used standardpostdip products as a predip, sometimes bydiluting the postdip 50:50 with water. Thisshould be avoided for three reasons:

� Postdips may not have the very rapidspeed of kill required of a predip.

� The high iodine concentrations used inpostdips could lead to residues if thepostdip is used as a predip.

� If a diluted postdip is used as a predip, itis essential that full-strength solution isstill retained for postdipping, otherwisepostdip efficacy will be reduced.

The ideal situation would be to have a singleproduct that could be used as both a pre-andpostdip.

In summary, a comparison of the majorpoints of predipping and postdipping isgiven in Table 7.4.

There will be some exceptions to thepoints in this table. For example, predippingwill reduce initial Streptococcus uberisinfections, and as such may help to reducecell counts. Similarly, postdipping willprevent further spread of S. uberis and thismay reduce the TBC/Bactoscan.

When does predipping not work?

Predipping is commonly implemented as acontrol measure against environmentalmastitis. If it is going to be effective, then aresponse would be expected within a few


weeks (compared with postdipping, whichmay take several months before an effect isseen). There are however, circumstanceswhere predip does not appear to be effective.These are:

� Environmental infections arising from thedry period.

� Mastitis due to heavy teat-endcontamination immediately postmilking.The effects of this are shown in Table 7.5.

Table 7.5. The effect of an E. coli broth on newinfection rates. Broth was applied to 20 teats either1 hour before milking or immediately after milking.

Culture of One hourE. coli applied before Immediatelyto teat ends milking after milking

Number of 2 in 40 14 in 40infected quarters (5%) (35%)Effect of predip Good Poor

Note that predipping would be less effective if the teatsare contaminated immediately after milking.

Iodine Residues

Concern has been expressed about thewidespread use of iodine products leadingto increased milk iodine levels. Milk iscertainly an important source of iodine forman. Most milks contain around 350 μg/litreof iodine. As the adult human daily dietary

iodine requirement is 150 μg, this would beobtained from the consumption of 430 ml(0.75 pints) of average milk. The majority ofiodine in milk (around 70–80%) comes fromthe cow’s diet (see Fig. 7.5). Widely differingdiets can lead to great variation in milkiodine content. For example, in one trial(Blowey and Collis, 1992), bulk milk iodineranged from 200 to 4000 μg/litre. Very smallamounts of iodine may come from bulk tankcleaners and possibly from sanitizers addedto teat washing water.

Perhaps surprisingly, more iodineresidues are derived from postmilking teatdisinfection than from predipping. This isdue to a combination of factors:

� Premilking teat disinfectants are wipedfrom the teats before the cluster isattached.

� Iodine applied immediately postmilkingwill penetrate the teat canal.

� In herds where teats are only dry-wipedbefore milking, postdipping iodineresidues will still be present on the teatsat the next milking.

� There is good evidence that iodinecan penetrate skin and then the teatwall and can pass into milk in the teatcistern.

Products are available with a low (0.1%) totaliodine content but a higher (50 p.p.m.) freeiodine level. This gives lower residues (andmore rapid bacterial kill) than conventional

128 Chapter 7

Table 7.4. Comparison of predipping and postdipping.

Predip Postdip

Season Particularly during Essentialhousing periods, throughout thedepending on yearclimate

Speed of action Must be rapid Not important

Main effect Environmental Contagiousagainst mastitis mastitis

Effect on:Cell count Limited Decreases SCC

TBC/Bactoscan Decreases TBC No effect on TBC(if dirty teats arecontributory)

iodine dips with 0.5% total iodine and 2p.p.m. ‘free’ iodine and, as such, it is idealfor predipping. It is also stable at pH 6.5 andcan be used without an emollient.

When iodine teat disinfectant is appliedby spray, there is an increase in atmosphericiodine. Levels do not reach values highenough to represent a human health hazard(Blowey and Collis, 1992), although thevapour may irritate some herdsmen.

Suggested maximum dietary iodineintake limits for the UK are 2000 μg/day (13times the dietary requirement). A dailyintake of only 500 ml/day (less than a pint)of some extreme farm milks would beneeded to reach these limits. Most of themilk consumed is from mixed sources,however, and it is therefore unlikely thatthese extremes would occur with purchasedmilk.


Fig. 7.5. The relative importance of different sources of iodine in milk. There is an enormous variationbetween farms in the amount of iodine from the diet.

0

100

Tot

al io

dine

in m

ilk

Iodi

ne fr

omdi

et

Iodi

ne fr

ompo

stdi

ppin

g

Iodi

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8 The Environment and Mastitis

Variation in Environments 131Bedding Types 131

Straw 132Sawdust and shavings 133Sand 133Ash 133Shredded paper 134Mats and mattresses 134Bedding amounts 135Cubicle sanitizers 135Space allowances 135

Importance of Ventilation 136Cubicle (Free-stall) Systems 138

Size 138Division height 140Cubicle length 140Neck rails 141Brisket boards 141Cubicle base 142Management 144

Straw Yards 144Stocking density 145Bedding 145Yard design 146

Sand Yards 147General Environmental Considerations 148

Avoid high stocking densities 148Clear away waste food 148Handle cows gently 149Rubber parlour floor surface 149Avoid draughts 149Heat stress 150Establish a postcalving group 150Dry cow hygiene 151

The Environment and Mastitis 131

Maintaining a clean and comfortable envir-onment for cows is of major importance inboth mastitis control and in the productionof clean, quality milk. Comfort and cleanli-ness also influence the incidence of lame-ness. It is well known that the incidence ofmastitis is related to the degree of bacterialcontamination of the teat, and especially theteat end. This chapter is primarily con-cerned with those factors that help to keepcows clean.

Variation in Environments

Dairy cows are kept under a very wide rangeof conditions. They may be grazing pasturesduring a dry summer, or plodding throughmuddy gateways during a wet spring orautumn. They may be housed in open yards(Plate 8.1) in the hotter climates of Arizona,California, Israel or Saudi Arabia, or in cu-bicles (free-stalls), cowsheds or straw yards(Plate 8.2) in Europe and the more northernparts of North America.

Whatever the environment, the twomajor factors that can lead to an increase inmastitis and bacterial contamination of milkare:

� Housing – confinement leads to muchcloser cow-to-cow contact and therefore agreater opportunity for faecal contamin-ation.

� Humidity – damp conditions facilitate themovement of faeces on to udders and

allow greater multiplication of environ-mental organisms.

Often when cows are housed in winter frompasture, there is an increase in mastitis. Partof this will be associated with cow-to-cowcontact, and part will be because, in the UKat least, housing probably coincides withincreasingly damp weather.

Large numbers of E. coli (1000 (103) pergram) are normally excreted in the faeces.This can increase considerably (up to 106 pergram) in a freshly calved cow fed on a high-concentrate ration. Even worse than this isthe warm mixture of milk, bedding and fae-ces that can sometimes accumulate at therear of the cubicle of a high-yielding cowleaking milk. Bedding like this may containup to 1000 million (109) E. coli per gram andrepresents a serious challenge to the mam-mary gland, especially during milk leakagewhen the teat canal is open and highly sus-ceptible to mastitis. Milk leakage is a majorproblem for high-yielding dairy cows.

Bedding Types

Growth of bacteria is dependent on the pres-ence of four major requirements:

1. Food.2. Warmth.3. Moisture.4. Mid range pH.

Plate 8.1. Cows in an open sand yard, typical ofhotter climates.

Plate 8.2. Straw yard, typical winter housing fortemperate climates. Although very comfortable forthe cows, a high degree of management is requiredto avoid mastitis.

132 Chapter 8

If any one of these requirements is absent,then bacterial growth is restricted. Forexample, if the bed is very dry, it willreduce mastitis, as will the use of productsthat lead to a very high pH. If the beddingis inorganic material, e.g. sand, it shouldbe ideal because it is inert and does notsupport bacterial growth.

Both the type of bedding and the wayin which the bedding is managed can havea marked effect on coliform levels. This isshown in Table 8.1, which compares fourhousing systems. It is interesting to notethat no cases of coliform mastitis were seenin the 150 cows housed over the winter insystems 1, 2 and 3 (sand, straw and well-stored sawdust) but seven cases occurredin 3 months in only 24 cows housed in sys-tem 4 (damp sawdust). Table 8.2 showshow different types of bedding support thegrowth of different organisms on teats.Sawdust was the worst bedding for bothtotal coliforms and Klebsiella, while strawproduced very high numbers of environ-mental streptococci on teat skin. Thisagrees with clinical, on-farm experiences,where Streptococcus uberis mastitis is

commonly associated with straw yards.Damp and badly stored sawdust may havea high coliform count. However, providedthat it is stored dry (i.e. not allowed to fer-ment) and is kept dry on the cubicle beds,there is no reason why sawdust or shavingsshould not be used as bedding material.They can be particularly useful when rub-ber mats and automatic scrapers are in use.Cubicles bedded with sand and ash areprobably ideal and will reduce the inci-dence of both E. coli and S. uberis, butsand may cause problems with slurry sys-tems.

The following section describes themain properties of each bedding type.

Straw

Straw is an organic material and hencesupports bacterial growth. This is espe-cially the case if the straw is damp. Normalstraw has around 12% moisture (88% drymatter (DM)), but this can reach 30% if thestraw is baled at a time of sea mist, storedunder plastic sheet which prevents air

Table 8.2. Comparison of growth of mastitis organisms in three different types of bedding. (From Rendoset al., 1975.)

Bacterial counts (geometric means)Sawdust Shavings Straw

Beddinga Teatb Bedding Teat Bedding Teat

Total coliforms 5.2 127 6.6 12 3.1 8Klebsiella 4.4 11 6.6 2 6.5 1Streptococci 1.1 38 8.6 717 5.3 2064

aCount per g/used bedding (× 106).bCount from teat swab.

Table 8.1. Coliform levels using different housing systems. (From Bramley et al., 1981.)

Group Housing system Number of coliforms/g bedding Cases of coliform mastitis

1 Sand cubicles 37,000 02 Straw yards 47,000 03 Well-managed 44,000 0

sawdust yards4 Poorly managed 66,000–69,000 7

sawdust yards

flow, or stored outside (see Plate 8.3). Notonly does wet straw absorb less moisture,but it might contain yeasts and moulds thatcould cause mastitis. Damp straw is espe-cially associated with outbreaks of S. uberismastitis (Fig. 4.2), and hence straw to beused as bedding should always be storedunder cover.

Sawdust and shavings

Sawdust and shavings are also organic and,like straw, support bacterial growth. If saw-dust is used it should be kiln-dried and notfrom fresh-cut wood. Kiln-dried shavings arearound 90% dry matter, whereas sawdustfrom recently felled wood may have as lowas 70% dry matter, or even lower if it hasbeen stored outside in the wet. There isclearly little point in using bedding thatalready contains 30% moisture. If it feelswarm in the pile it is dangerous to use. Somemanufacturers are now producing a finewood chip from waste pallets, etc., to beused as bedding. This should drain well, butwill support bacterial growth.

Sand

Sand is probably the ideal bedding.Provided it is deep enough (ideally 4 to 6″),it provides and produces good comfortableclean bedding and hence reduces both mas-titis and lameness (Plate 8.4). Being inor-

ganic, provided that it is clean, it does notsupport bacterial growth. However, if thesand at the rear of the cubicle goes black anddamp, then it should be dug out andreplaced with clean sand. This happenswhen the sand has become contaminatedwith urine, milk or faeces; then, with thewarmth of the cow lying on it, quite highbacterial levels can be produced. A sandcubicle will always have a rear lip. This isan advantage to the cow as she will be ableto push against the lip with her hind feetwhen rising to stand, and this increasescubicle comfort.

The type of sand used must also bechosen carefully. If the clay content is toohigh, the sand will become compacted andgo hard, especially at the rear of the bed,where there is often more moisture. Thisleads to cow discomfort, pooling of moistureat the back of the cubicle and hence anincreased risk of mastitis. Squeeze a sampleof sand in your hand. If it is compacted intoa ball and retains its shape when released,the clay content is too high. Like most otherbedding types, sand is best stored undercover, otherwise it may be too wet before itis even used as bedding.

Ash

Ash, a waste product from paper-, card-board- and wood-fired power stations, has


Plate 8.3. Straw bales that are not stored undercover get damp and predispose to mastitis if usedfor bedding.

Plate 8.4. This sand cubicle (which has a lip) givesgood comfort, but note that, in the adjacent cubicle,it is damp at the back. If the sand in this area goesblack, then it should be dug out and replaced withclean sand.

recently been introduced as a bedding mater-ial and seems to have some significant bene-fits. In addition to its intense drying andwater-absorbing properties, ash has a veryhigh pH of 9 to 11, and this in itself reducesbacterial growth, including that of S. uberis.Care must be taken that teats do not becomeexcessively dry or affected by superficialburns, especially if a ‘barrier’ postdip isbeing used, because the ash tends to stick tothe film of barrier dip. Most farms use ash incombination with other bedding. It mixeswith sand especially well (Plate 8.5), pro-ducing a dry material that does not becomecompacted. Ash can also be used as a2–4 inch layer on the base of a yard to retardthe rate of fermentation of the straw bed, andash on concrete provides a good, firm, non-slip surface.

Shredded paper

Shredded paper has been used as bedding,but has not become popular. It is not partic-ularly absorbent and when wet it tends tobecome matted and solid. It may also stickto cows’ flanks where it looks untidy.Mixtures of cardboard and wood chip arebetter, as is shredded waste plasterboardfrom the building industry.

Mats and mattresses

The ideal bedding should be soft and yield-ing, to encourage the cow to lie down, but atthe same time strong enough to preventdamage from the movements of the cow. Itshould also be clean and hygienic.Mattresses (Plate 8.6) and rubber mats aregood, and represent both increased comfortand a saving in bedding costs, but they mustbe kept dry and lightly bedded, as inPlate 8.6, otherwise there is a risk of masti-tis and hock sores and of cubicle rejection.Some bedding should always be used, theamount depending on the softness of thebed. This is for two reasons. First, it is tokeep the bed dry; otherwise the sweaty skinwill leave a damp area and predispose tomastitis. This is especially the case if therehas also been milk leakage on to the cubiclebed. Second, a small covering of bedding isneeded to provide an anti-friction surface, asthe cow slides across the bed when she islying down. Inadequate bedding leads tohock sores.

If the rear edge of the cubicle mattressis slippery, then the cow may slip as shepushes with the toes of her hind feet tostand, and this can increase the incidence oflameness. This has led to many farmersreturning to cubicles with a rear lip.Mattresses are often softer and more com-fortable than mats, and should ideally

134 Chapter 8

Plate 8.5. Ash from wood- and paper-fired powerstations can be mixed with sand to produceexcellent bedding. Its high pH prevents bacterialgrowth, especially of Streptococcus uberis.

Plate 8.6. Cow mattresses are often formed fromcanvas sacks filled with rubber chippings. Themattress must have sufficient bedding; otherwise therear of the cubicle will be both damp and slippery.

extend to the rear of the cubicle; otherwisethe hock may be uncomfortable due to lyingon a ridge.

Bedding amounts

Clearly it is not just the type of bedding thatinfluences mastitis; the quantity of the bed-ding used and the frequency of renewing itare also important. Ample bedding, espe-cially with dry materials such as straw orshavings, is essential to keep cows clean.The absolute amounts required will dependon cubicle design, the presence or absenceof mats or mattresses and the space withinthe building. If space is limited, e.g. the cu-bicle passages are narrow, or there is lessloafing (relaxation) area, then more beddingwill be required. A very rough guideline tothe amounts of bedding required (kg per cowper day) is given in Table 8.3.

The amounts given in Table 8.3 areapproximate figures only. Clearly the morebedding that is used the greater will be thecleanliness of the cows. For example, inPlate 8.7 straw use was 5.0 kg per cowper day, giving a good covering evenacross the passage. The cows were veryclean, and lameness and mastitis were low,although with straw the risk of S. uberisremains.

Table 8.3. Approximate bedding and sanitizer(lime) requirements (kg/cow/day) for cubicles andyards. Amounts will vary enormously with factorssuch as stocking density, ventilation, weather anddiet.

Cubicles withBedding mats ormaterial Cubicles mattresses Yards

Straw 2.5 1.0 15Sawdust 2.0 1.0 nua

Sand 8.0 1.0 10Ash 4.0 1.5 nuCardboard 2.0 1.0 nuLime 0.05 0.025 nu

anu = not used

Cubicle sanitizers

Addition of small quantities of lime (seeTable 8.3) or other proprietary cubicle sani-tizer powder will help to dry the beds, andits high pH acts as a disinfectant. S. uberiscan multiply at up to pH 9.5, however, sosignificant quantities need to be used. Makesure that it is hydrated or slaked lime (cal-cium hydroxide, Ca(OH)2) or even groundlimestone (calcium carbonate, CaCO3) andnot quicklime (calcium oxide, CaO), as thelatter will cause severe teat burns. Limeshould be added to the cubicle bed first, thenthe bedding placed on top, as this will fur-ther reduce the risk of excessive teat drying.This has not been done in Plate 8.6. A rangeof other proprietary cubicle sanitizers areavailable, their main claim being that theyare less likely to cause teat skin burns.

Space allowances

In the introduction to this chapter, it wasstated that housing cows increased theirdegree of contact and that this predisposedto mastitis. It follows, therefore, that provid-ing more space, in terms of both air volumeand floor area, will be beneficial. Originalcubicle buildings were only 10 ft to theeaves, the roof was supported by the cubicledivision, and the passageway between cubi-cles was only 8 ft in width. Modern cows


Plate 8.7. A wide passage and high levels of strawbedding help to keep cows clean and reduce bothmastitis and lameness.

are, of course, much higher-yielding, butbuildings are now erected at 20 ft to theeaves and with passage width between thebacks of cubicles up to 15 ft wide. Thischange from 8 ft to 15 ft passages gives thecows almost double the space and, of course,there is half the amount of slurry in thepassageway.

Most farms are stocked at no more than90 to 95% cubicle occupancy, i.e. there are 5to 10% more cubicles than cows in thebuilding. This is especially for the high-yielding group, and is often a requirement offarm assurance audit schemes. There is con-siderable discussion over whether buildingsshould be two-row or three-row barns, asthis affects the feed space allowance, andwill have an indirect effect on mastitis andlameness. If the cubicles are 4 ft in width,then a two-row barn has 2 ft of feeding spaceper cow, which is ideal, whereas a three-rowbarn has only 1.3 ft per cow feed space. Ifspace is limited, cubicles are uncomfortableor the building is poorly ventilated, thencows will lie outside on concrete (Plate 8.8),with the obvious hygiene and mastitis con-sequences.

Space allowance is also important instraw yards, particularly for transition cowsand fresh calvers, the two groups that are atgreatest risk of contracting new infections(see section on dry period infections onpages 50–52). A generous allowance wouldbe 8 sq.m of bedded area per cow, increas-

ing to 10 sq.m for fresh calvers. If housingoptions are limited, then in the short termincreased space allowance can be providedby outside loafing areas, although provisionmay need to be made for shelter and/orshade in periods of inclement or very hotweather.

Importance of Ventilation

Cows are extremely wet animals (Plate 8.9).The fluid produced by a high-yielding dairycow consuming large quantities of food isenormous. Approximate figures are:

� 4–5 litres per day from skin and respira-tory tract (treble this on a very hot day).

� 20 litres per day in urine.� 30 litres per day in faeces.

High-yielding cows also produce largeamounts of heat, around 1.5 to 2.0 kW/hour,depending on the level of yield. It is there-fore vitally important that buildings aredesigned to be well ventilated in order toremove this heat and humidity, and thatstocking densities are kept in reasonableproportions, to avoid a build-up of heat andmoisture. Under current UK conditions, it isunlikely that cows will get too cold. Themajor reason for housing them is for ease offeeding and to protect the land (from footpoaching, i.e. foot damage to the pasture)

136 Chapter 8

Plate 8.8. A combination of uncomfortable cubiclesand warm weather encouraged a large number ofcows to lie outside, with a consequent increase inmastitis.

Plate 8.9. As can be seen from the amount ofmoisture being exhaled, cows are extremely ‘wet’animals. They excrete over 50 litres of water per dayin the urine, faeces, breath and sweat, in addition tothe milk that they produce.

and not to protect the cows. Hence, if cowscan be kept as close to lower environmentaltemperatures as possible and protected fromthe direct effects of driving rain or directsunlight, this should be ideal. Damp, hot andhumid conditions predispose to mastitis.Heat stress leads to excess standing, pre-disposing to mastitis, and is discussed at theend of this chapter.

Long, narrow, blind-ended straw yardswhere you can ‘feel’ the humidity and staleair at the far end are particularly dangerous(see Fig. 8.15). Poorly ventilated cubiclebuildings with a low roof, where condensa-tion drips on to both cows and bedding on acold morning, will predispose to mastitisand respiratory diseases such as IBR (infec-tious bovine rhinotracheitis) . If you can’tsee the far end of the shed because of con-densation and mist or if condensation isdripping from the roof on to the cows’ backs(Plate 8.10) then ventilation is totally inade-quate.

Some suggested ways of ensuring ade-quate ventilation include:

� Ensure an adequate apex outlet at the roof.Air will only flow into a building if it canget in and get out again. This is bestachieved by having a 23–30.5 cm gap(approx. 9–12″), plus a 15 cm (approx. 6″)‘upstand’ on the final sheet of roofingmaterial (see Fig. 8.1). A cross-flow of airacross the upstand produces an extractoreffect. The conventional roofing cowlswith a narrow outlet simply do not allowsufficient air flow.

� If a new building is being constructed,turn the roofing sheets upside down andleave a 1.3–1.9 cm (approx. 0.5–0.75″) gapbetween each run of sheets (Fig. 8.2aand b). Provided that there are sufficientanimals in the building to produce heatand an upward flow of air, under mostconditions this seems to prevent rain fromentering and improves ventilation. It alsoreduces roofing costs, as fewer sheets areused.

� A similar effect may be obtained in exist-ing buildings by using an angle grinder to


Plate 8.10. Condensation dripping from the roofjoists is considered to be a sign of poor ventilation.

Fig. 8.1. Leaving a 23–30.5 cm gap at the apex ofthe roof and adding a 15 cm upstand improvesventilation.

Fig. 8.2. (a) Conventional roof sheeting in which theedges are faced downwards and adjacent sheetsoverlap. (b) It has been suggested that ventilationcan be improved by reversing the sheets so that theedges face upwards and a gap of 1.3–1.9 cm is leftbetween each sheet.

(b)

(a)

cut narrow slots into the top of everyfourth to sixth ridge of the roofing sheets(Fig. 8.3). If this is done close to the apexof the roof, it will have a particularly goodeffect.

� Clad the sides and gable ends of the build-ings with Yorkshire boarding (spaced ver-tical boarding), leaving a 12.7 cm (approx.5″) gap between boards. In many build-ings, alternate boards are adequate, espe-cially if facing a feed passage, or, if thearea is reasonably sheltered from rain,then the building is best with no sides atall.

� Avoid multiple-span buildings (Fig. 8.4).By far the best air flow is achieved whenbuildings stand singly. Also avoid build-ings of excessive span, e.g. more than18.3 m wide (approx. 60′).

� Ensure adequate drainage. Standing waterincreases the humidity within a buildingand further predisposes to mastitis. Strawyards with earth or sand floors and cubiclehouses with good drainage or slatted pas-sageways both reduce the amount ofstanding water.

� In older wooden buildings air flow canoften be improved by cutting out part ofthe fronts, as in Plate 8.11. Provided that

there is a rail or similar to stop the cowpassing through and that there is no directexposure to rain, this will be a bigimprovement.

Cubicle (Free-stall) Systems

The most important features of cubicle sys-tems are their design and management.Cubicles should be designed to be comfort-able for cows and to be in constant use, butto stay reasonably clean.

Uncomfortable cubicles will often stayclean, simply because the cows do not usethem, but so many cows then lie outside onthe concrete that mastitis (and lameness)becomes a problem. Plate 8.8 shows a typi-cal example. In this instance, a combinationof warm weather and uncomfortable cubi-cles led to a large number of cows lying out-side, with a resultant increase in mastitis.

One of the most important factors deter-mining cubicle acceptance is pre-partumheifer training. Although training is vital,cubicle design is also important, and is dis-cussed in the following section.

Size

This must depend on the size of the cow,but for modern large Holsteins cubicles

138 Chapter 8

Plate 8.11. As this wooden cubicle house was closeto an adjacent building, removal of most of the frontnot only improved cow comfort but also improvedair flow and overall ventilation.

Fig. 8.3. Ventilation can be improved in existingbuildings by cutting slots into the top of every fourthto sixth ridge of the roofing sheets.

Fig. 8.4. Avoid a multiple-span building such as this.The best ventilation is obtained from a single-spanbuilding that is not excessively wide.

2.3–2.4 m long by 1.2 m wide (7′ 6″–8′ longby 4′ wide) are reasonable dimensions (seeFig. 8.5). Length seems to be the most impor-tant dimension affecting cubicle acceptance.If cubicles are too wide, then cows may notlie straight, and this leads to soiling of thebed, as in Plate 8.12 . Lying diagonally canalso be a result of the lower edge of the metalcubicle division being too high, e.g. morethan 22″ above the cubicle bed.

Where there is a double row of facingcubicles (Fig. 8.5, right), space-sharing at thefront makes a 2.3 m length acceptable. The

cubicle should be such that a cow can sit init, with her head held extended forwards toruminate. If the cubicle is too short, she hasto sit with her neck flexed (Fig. 8.6), whichmakes it difficult for her to regurgitate thecud. In addition, there is insufficient lungespace for her to regain the standing position.

Cubicle discomfort also encouragescows to stand for excessive periods of timeand predisposes to lameness. Cubicles thatare too narrow, or which have excessivelyrigid divisions, can lead to compression ofthe rumen when the cow is lying down. Thiscan further impede rumination, as well asdiscouraging cubicle acceptance. Figure 8.7shows one such design. Note how the rumenof a large cow would be directly compressedby the cubicle division. By removing boththe upright bar AB and the horizontal CD,and replacing them with a length of ropeunder tension, as in Fig. 8.8, the cubiclebecomes much more comfortable.


Fig. 8.5. A single row of cubicles needs to be 2.4 m(8’) long (above). Two facing rows can be 2.3 m (7′6”) long (right).

Plate 8.12. If the cubicle is too wide, or if the loweredge of the rear cubicle division is too high, cowsmay lie diagonally, leading to soiling of the bed.

140 Chapter 8

Division height

The height of the division is also important,especially at the front of the cubicle. Ifheight PQ (Fig. 8.7) is too short, it will beuncomfortable for the cow when she isstanding and she may also have to depressher neck when sitting ‘space-sharing’ withthe adjacent or opposite cubicle. This furtherreduces comfort and impedes rumination.Clearly optimum height varies with cowsize, but 1.32 m (4′3″) for Holsteins has beensuggested. The rear upright above R (Fig. 8.7)is best eliminated to give the cantilever div-ision seen in Fig. 8.10.

Cubicle length

Cows may get too far forward with long cu-bicles and defaecate on the bed when lyingor standing. Some animals also occasionallyshuffle far forward on their knees, finishingup so close to the front wall (as in Fig. 8.9)that they either have great difficulty instanding or are totally unable to rise. Thismost commonly occurs with an uncomfort-able base. Ideally, a cow should have at least1.2 m (4 ft) of forward lunging space toenable her to stand easily.

Fig. 8.7. Cubicles with excessively rigid divisionscan be uncomfortable. Pressure is exerted on therumen (circled).

Fig. 8.9. Some cows move so far forward in thecubicle that they are unable to lunge forward andtherefore find it very difficult to stand up.

Fig. 8.6. (Left) A cubicle that is too short forces thecow to sit with her neck excessively flexed, thusimpeding rumination. (Right) Space is needed at thefront of the cubicle to allow the cow to extend herneck during regurgitation of the cud, and to allowforward lunging when rising to stand.

Fig. 8.8. A flexible division gives greater cowcomfort. The lower cubicle rail can be replaced by arope under tension. A two-stranded rope is broughtunder tension by rotating a piece of wood (seearrows) fixed between two strands. When the ropeis taut, the wood is tied to the top cubicle rail.

Neck rails

Encouraging the cow to remain in the cor-rect position in the cubicle can be achievedby using either brisket boards or neck railsor both. Neck rails can either be attached tothe top of the cubicle divisions, or sus-pended above, as shown in Fig. 8.10. Ineither case, they should be positionedapproximately 30–45 cm (approx. 1′–1′ 6″)from the front of the cubicle, although thisvaries enormously depending on cubiclelength. The suspended rail, positioned to be7.5–10 cm (approx. 3–4″) below the neckheight of a standing animal, is preferable,since rails attached to the cubicle divisionmay be so low as to discourage cubicleacceptance. Both have the same disad-vantage, however, in that once she islying down, there is nothing to prevent thecow shuffling into the position shown inFig. 8.9. However, when she stands up, the

presence of the rail on her neck will encour-age her to reverse to the rear of the cubicleand thereby urinate and defaecate into thepassage.

Brisket boards

Brisket boards sited 1.72 m (5′ 8″) from theback of the cubicle (Fig. 8.11) will certainlystop the cow shuffling too far forward.However, when she stands up she can stilleasily stand over the front of the board anddefaecate onto the rear of the cubicle. A neckrail is therefore needed in conjunction witha brisket board.

Brisket boards should have roundededges rather than the sharp square edgeshown in Fig. 8.11. Soft, moulded, pillow-shaped, plastic tubes are ideal. They mustnot be too high, however, or they mayprevent the natural ‘one front leg forward’position adopted by a proportion of sittingcows.

A long, pyramidal concrete shape,0.38 m (15″) high was once used betweentwo facing rows of cubicles (Fig. 8.12 andPlate 8.13), as a means of correctly position-ing cows in the cubicle. When seated, thecow could no longer go too far forward in thecubicle and yet the height CD meant that shecould extend her neck over the top of the


Fig. 8.10. (a) Neck rails may either be fixed to thetop of the cubicle divisions or (b) preferablysuspended above the divisions.

Fig. 8.11. A brisket board prevents the cow shufflingtoo far forward. It should be angled forward towardsthe front of the cubicle to reduce knee damage.

(a)

(b)

142 Chapter 8

pyramid into facing rows of cubicles. Whenfully standing she had to keep her feet backbehind B and hence defaecated into thedunging channel. However, when rising to

stand, one foot had to be placed on T, theslope of the concrete, to push herselfupright, and many cows found this uncom-fortable. The system is still in use in somehousing situations, but is not popular.

Cubicle base

Limestone, earth, sand and concrete have allbeen used for cubicle bases. The first threeall suffer the disadvantage that they gradu-ally become eroded to form pits, which atthe rear of the cubicle can become filled withdamp, soiled bedding, which will then rep-resent a source of mastitis infection.Plate 8.14 shows a typical example.

Figure 8.13 shows the three majorpoints of contact when a cow is lying in acubicle. These are the positions of the twoknees (A and B) and either the right hock (asin Fig. 8.13) or the left hock, according towhich side the cow is lying on (C). Thesethree contact points are clearly recognizablein many cubicles: look for the three areaswhere straw bedding has been scuffed away,often exposing bare concrete. Unless a con-crete base is used, cows continually liftingthemselves eventually erode depressions atthe front or back of the cubicle, leading todiscomfort. The rear depression can alsobecome soiled with faeces and wet bedding,as in Plate 8.14. If sand is in use, it needs tobe deep enough to remain spread over the

Fig. 8.12. A pyramid of concrete between two facing rows of cubicles (or a triangle against a wall) preventscows moving too far forward, while at the same time allowing sufficient space for chewing the cud andlunging forward to stand. This is no longer popular as it may lead to cubicle rejection.

Plate 8.13. A concrete pyramid 0.38 m highbetween two facing rows of cubicles was once usedto prevent cows going too far forward. It is nolonger popular.

whole cubicle base. Mats and mattresses willprevent this unevenness developing,although bedding is still needed to preventhock abrasions.

An example of an advanced case ofhock abrasion is shown in Plate 8.15. Thelesion is first seen as hair loss over thebruised skin, which is followed by fluidaccumulating in the hock bursa. (A bursa isa small ‘shock-absorber’ pouch, which actsto protect a protruding portion of bone andallows skin, muscles, tendons, etc., to glideover the bony surface.) Only when the skinis broken would the swellings shown inPlate 8.15 become infected.

The majority of farms now have con-crete bases in their cubicles. Although theseare certainly easier to keep clean, they canbe hard and uncomfortable and this maylead to cubicle rejection. Mats, mattresses ordeep bedding are essential.

Animals accustomed to cubicles with alip often touch the lip with their toe beforestepping into the dunging passage. Removalof this lip (for example by concreting thecubicle base) can induce apprehension insome cows because they do not know whenand where to step down and this too canlead to cubicle rejection. Increasingly peo-ple prefer cubicles with a lip (such as thatshown in Plate 8.4). Additional effort maybe needed to keep the rear of the cubicleclean (and correct positioning of the cow isvital), but a lip positions the animal better:her tail lies inside the cubicle and not in theslurry passage, and the lip is used as a pointof contact for the hind feet when the cowpushes to stand up.

Cubicles with a high kerb (e.g. greaterthan 12.5–15 cm or 5–6″) were once thoughtto be a problem, as heifers especially mayhave been nervous about reversing from ahigh step. However, provided animals havebeen trained in advance, step height is prob-ably not a major factor for comfort, and stepsof 250 mm (10″) are acceptable.

The slope of the cubicle floor is impor-tant and should be 10–13 cm (4–5″) fromfront to rear, that is from Q to R in Fig. 8.7. A


Plate 8.14. Badly soiled cubicle beds represent amastitis risk.

Fig. 8.13. A, B and C are the major contact pointsbetween the cow and the cubicle base and must bewell bedded.

Plate 8.15. Gross hock swellings, the result of lyingon a hard surface. The hair loss and scab on the skinsurface show the major points of abrasion.

cow much prefers to lie uphill. A level or,even worse, downward-sloping cubiclecould lead to rejection.

Management

Cleaning and renewing the bedding of thecubicles and yards should ideally be carriedout during milking, so that as cows exit fromthe parlour they are able to walk back alongclean passageways, past fresh food, and thenlie down in clean cubicles. Ideally, all soiledareas should be scraped from the backs ofthe cubicles at least twice daily (and prefer-ably every time the herdsman walks past). Ifusing straw, sawdust or shavings, fresh bed-ding should be added daily, although, ifstraw usage is liberal, it may be sufficient{but not ideal) to bed the cubicles twiceweekly, scraping fresh straw from the frontto the rear of the cubicle every day, asrequired. A small quantity of hydrated lime(Ca(OH)2) or even ground limestone(CaCO3) sprinkled on to the rear of the cu-bicles once or twice a week (as in Plate 8.16)also helps to keep the bed dry, as limeabsorbs moisture. Lime should be appliedand then covered with fresh bedding (e.g.

straw or sawdust). This prevents direct andexcessive contact of lime with teats, whichcould otherwise lead to cracking. Do not usequicklime, as this will produce severe teatburns.

The importance of regularly renewingthe bedding is shown in Fig. 8.14. Whensawdust was added to cubicles on aweekly basis (A), coliform levels werequite high. Levels declined when dailybedding was carried out (B), but the situa-tion soon de-teriorated when there was areturn to the original system of weeklybedding (C).

Cubicle passages should be scraped ateach milking, and ideally this should be car-ried out before the cows return to the cu-bicles (Plate 8.17). This keeps the teats asclean as possible during the first critical20–30 minutes after milking, when the cowis more susceptible to mastitis, because theteat sphincter has not fully closed. It alsoreduces the amount of faeces carried back onto the cubicle beds by soiled feet.

Straw Yards

Straw (loose) yards (Plate 8.2) are certainlygood for cow comfort and, if given thechoice, cows would opt for yards rather than

144 Chapter 8

Plate 8.16. Hydrated lime both dries and disinfectscubicle beds. However, do not use an excess as itcan also produce drying and cracking of the teats.

Plate 8.17. A semi-automated system. The tractor isscraping slurry from the passageway, a brush hasremoved soiled material from the rear of the cubicleon the right, and clean sawdust is being added tothe cubicles on the left. The building is then readyfor the cows to enter after milking.

cubicles. However, they are not withoutproblems. Whereas with cubicles cows canbe positioned to drop urine and faeces intothe passageway and hence keep the teats andudder clean, with straw yards there is agreater chance of faecal soiling of the udder.Hence there is generally an increased mas-titis risk, especially when yards are badlydesigned or poorly managed, but, becausethey are more comfortable, there is usually alower incidence of lameness. Straw usage ismuch higher (almost ten times more) than incubicles and hence both bedding and labourcosts are higher.

Stocking density

Stocking densities tend to be lower, becausefewer cows can be housed in a strawyard than if the same building were usedfor cu-bicles. Current recommendationsare that cows need at least 6 sq. m (65 sq.ftper cow) of bedded area, plus a further1.8 sq. m (20 sq. ft) for feeding and loafing,i.e. 8 sq. m (85 sq ft ) per cow in total, andthat fresh calvers and transition cows begiven 10 sq. m (110 sq. ft) per cow. Higherfigures than this may be needed for largecows.

Bedding

Yards should be bedded at least once a day,preferably during morning milking, and, aswith cubicles:

� Cows should be encouraged to stand andeat for 30 minutes after milking (but not ifthis means locking them into an over-crowded and draughty passageway).

� Passageways leading back to the yardsshould be scraped clean before the cowswalk along them.

The straw used for bedding must be clean,dry and free from fungi and moulds. Strawstored outside will significantly increasemastitis risks, and herd outbreaks will occurwith damp and mouldy straw, even if liberalquantities are used. Mastitis caused byyeasts and moulds is a particular problem,because of its poor response to treatment.

Straw beds tend to heat up. Fortunately,the anaerobic fermentation that occurs in thecompacted lower levels does not support thegrowth of E. coli, but surface temperaturesin normal yards are around 40°C and thispromotes bacterial growth (Plate 8.18). Thereis some suggestion that the use of excessivequantities of straw can lead to overheatingand that this can increase coliform counts.Yards should be cleaned out frequently, at


Fig. 8.14. The importance of regular renewal of cubicle bedding. E. coli numbers were high when freshsawdust was added weekly (A), fell rapidly when daily bedding was introduced (B), but soon deteriorated onreturn to weekly bedding (C). (From Bramley, 1992.)

00.1

E. c

oli n

umbe

rs(m

illio

ns p

er g

saw

dust

)

1.0

10

100

A B C1000

4 8 12 16

Time (days)

20 24 28 32

146 Chapter 8

least every five weeks. If left longer, there isan increased risk of mastitis. Some farmsclean out as frequently as every 2–3 weeksand suggest that this uses less straw. Aftercleaning out, hydrated lime or power stationash can be spread over the floor beforerenewal of bedding. This reduces the rate offermentation and increases the time beforethe next batch of bedding in the yards startsto heat up.

A hard-core base may be better thanconcrete, in that it permits better drainage.However, this is only likely to be of majorimportance in yards where the concrete base

is flat and poorly drained. If the strawsquelches when you stand on the bed, thenit’s too wet.

Yard design

One of the most important aspects of strawyards in relation to mastitis is the design ofthe yard. Long, narrow yards (as in Fig. 8.15,on the left) are more easily soiled, becausecows have to walk across a greater distanceto get to the rear. The positioning of thewater troughs (W) in the example shown isalso very poor as the only access to them isthrough the bedded area.

The design shown on the right is far bet-ter. Access to the water troughs (W) shouldonly be from the feeding passage (P) andhence this avoids excessive soiling of thebedded area (and it is less important whenthe water trough overflows).

Opinions differ on the value of the bar-rier BC. By restricting access, areas AB andCD become more soiled, but the area behindBC (H) stays cleaner, and cows prefer to lieagainst a wall if possible. Some systems havea continuous step approximately 30 cm high(12″) running from A to D. This helps toretain the straw bedding and gives fullaccess to the yard. The depth of the yard

Fig. 8.15. Design of straw yards: long, narrow, poorly ventilated yards with badly placed water troughsshould be avoided (left). A more useful design is shown on the right.

Plate 8.18. Muck from a straw yard ferments andheats to around 40°C. Only the upper layers arelikely to contain mastitis organisms.

Key

==

====

(AE) should be at least 7.3 m and, preferably,no greater than 9.1 m (24–30 ft), with a feedpassage (P) of 3.5 m (approx. 12 ft) mimi-mum and a food trough (or floor area) (F) of0.76 m (2′ 6″) per cow. Scraping the passage(P) twice daily further reduces faecal soilingof the bed.

Ventilation is equally important in strawyards to that in cubicle houses and cow-sheds, and can be improved by providingroof insulation. However, this is rarely done,because of cost. The ideal humidity for dairycows is around 70%, whereas many build-ings reach 85% or higher in the UK duringwinter. High humidity also increases theheat stress in cows kept in hotter climatesand should be avoided if possible.

Sand Yards

In hotter climates and desert regions cowsare housed on sand corrals or yards and mayhave access to cubicles or a slatted areaunder cover. Shaded areas are vital and inthe absence of specific shade cows tend tocongregate and shelter along the edges ofbuildings, as seen in Plate 8.19. More com-monly, tall constructions providing shadeare erected, and cows will lie in their shad-ows. The dimensions and siting of suchshaded areas are vital. Ideally they shouldprovide shade over different parts of thesand yard throughout the day, so that allareas under shadow are also exposed to thedrying influence of the sun at least once eachday. Plate 8.20 shows cows lying under asun shelter.

During the dry season, corrals should becleaned out every 6–8 weeks. The top sur-face of the sand is scraped off and removed.In the Middle East, soiled sand (sand anddry faeces) is a valuable commodity for hor-ticulture. Fresh sand is brought in to top upthe yard (Plate 8.21). Sand provides gooddrainage and the heat of the sun dries thefaecal pats, which are then broken up eachday by a tractor and scraper (Plate 8.22).

During wet weather sand yards becomevery muddy (see Plate 8.23) and cleaningteats prior to milking becomes a major task.The risk of environmental mastitis increases


Plate 8.20. Artificial shade from the sun in hotterclimates. Note how the cows specifically lie in theareas under shadow.

Plate 8.21. Yards should be cleaned and fresh sandprovided every 6–8 weeks.

Plate 8.19. In the absence of specific shelters, cowscongregate along the sides of buildings to obtainshade.

substantially. If possible, cows should bekept in cubicle areas, preferably with fans asa cooling system, until the yards dry out.

General Environmental Considerations

There are certain points of general manage-ment that are applicable to all housing sys-tems.

Avoid high stocking densities

Tightly packed cows create high humidityand are often under stress, especiallyyounger heifers. Whenever possible, a largeloafing area should be provided (Plate 8.24).In many parts of the world this need not betotally under cover, since cows are preparedto go outside in quite low temperatures, aslong as it is neither raining heavily norextremely windy. In hotter climates, loafingareas can be used at night.

The provision of adequate loafing (andfeeding) areas also aids in heat detection andhelps to reduce the incidence of lameness.This is because cows that have enough spaceto walk around are likely to suffer less dam-age to their feet than cows that stand still forlong periods of time. In addition, if they areable to move away from other cows, not onlyare they more likely to show better signs ofoestrus (heat) behaviour, but it will be eas-ier to identify such cows.

Clear away waste food

Waste silage or other food left lying besidethe trough encourages cows to lie outside(see Plate 8.25). It can also be a good culturemedium for environmental mastitis bacteria,particularly E. coli, B. licheniformis andB. cereus, and by contaminating the teats canproduce high TBC/Bactoscans. Areas aroundthe feed troughs should therefore be cleanedregularly.

148 Chapter 8

Plate 8.24. In temperate climates, access to clean,open loafing and feeding areas helps in mastitiscontrol, reduces lameness and improves heatdetection.

Plate 8.22. Sand yards need to be scraped daily tobreak up dried faecal pats.

Plate 8.23. Under wet conditions, open sand yardsbecome a real problem.

Handle cows gently

There is now a considerable volume of evi-dence to show that stressed cows are moreprone to infections, and this includes masti-tis. If rushed along roads and through door-ways, they may injure or excessively soiltheir teats. If forcibly driven into the milk-ing parlour, the cows’ let-down is likely tobe inhibited, with the consequences oflonger milking times, increased teat-enddamage and depressed yields (see section onheifer milk let-down, pages 14–15). Makesure the backing gate allows them plenty ofroom in the collecting yard, and allow thecows to flow into the parlour at their ownspeed. If the gate is pushing the cows for-ward too hard, they will become stressedand then more difficult to handle in the par-lour, with poor milk let-down. The differ-ence between quietly and roughly handledcows very soon becomes apparent from theirreaction to visitors.

Most farms now have a foot bath afterthe parlour exit. To avoid contamination of‘open’ teats, the bath should not be too deep(around 70 mm), the solution should bechanged daily to avoid excess contaminationand, for large herds, it should be wideenough to allow two cows to pass at thesame time.

Rubber parlour floor surface

Increasing numbers of dairy farms now haverubber matting fixed to the parlour floor(Plate 8.26). Although primarily aimed atlameness, a rubber floor also has someadvantages in mastitis control. Because it ismore comfortable, cows stand more quietlyand fidget less, and this is reported to leadto reduced liner slip. Cows are said to flowinto the parlour better, thus reducing over-all milking times. This should reduce bothmastitis and lameness. Another potentialadvantage is that rubber flooring overcomesthe erosive damage caused by some barrierdips. Plate 8.27 shows how the cement sur-face of a parlour floor has been eroded byone commercial dip. The presence of a whiteaggregate on the surface makes it quite diffi-

cult to identify mastitis during foremilking,whereas milk is much more easily inspectedwith black rubber flooring.

Avoid draughts

Chilling of the udder may reduce theimmune response and hence the cow’s abil-ity to counteract infections that havepenetrated the teat canal. Chilling of teatswill undoubtedly lead to cracking andchapping, and this further predisposes tomastitis. Cows must not be left standing for20–30 minutes (to allow the teat canal to


Plate 8.26. Rubber flooring in the milking parlour isclaimed to have advantages for both lameness andmastitis control.

Plate 8.27. The cement surface of this parlour floorhas been eroded by a barrier teat dip, exposing awhite aggregate. This makes detection of mastitis inthe foremilk more difficult.

150 Chapter 8

close) in exposed yards or draughty pas-sageways, especially when the teats are stillwet with teat dip. It is better to allow them toreturn to feed.

Heat stress

At the other end of the spectrum, it is alsoimportant to keep dairy cows cool, and evenin the UK heat stress can become an issue,leading to increased mastitis. Heat stress canaffect cows at surprisingly low temperatures,for example, early changes may be seen at aslow a temperature as 24°C, especially if thehumidity is high. This has led to the use ofthe temperature humidity index (THI),which is described by the equation:

THI = temperature + (0.36 × dew point) + 41.2

Buildings can reach high temperaturesin the middle of summer, especially if thereis a high number of translucent roof sheets,effectively turning the building into a green-house. No more than 10% of the roof shouldbe Perspex sheeting to avoid this effect. Thesituation is made worse by the heat pro-duced by high-yielding cows. A 40-litre cowproduces 1.7 kW heat per day, rising to2.2 kW at 60 litres.

There are a range of clinical signs forheat stress, including panting, sweating, tailswishing and decreased feed intake. Cowsget very dirty because they stand for longerperiods and stand in groups, especially nearwater troughs, where they splash water withtheir tongues. This combination of damp,excess standing, close cow contact and dirtycoats leads to increased mastitis.

A wide range of control options areavailable, all aimed at reducing the buildingtemperature and increasing air flow.Removal of internal walls helps to improveair flow through the building, and Yorkshireboarding can be removed from around theoutside of the building. Fans are of greatvalue as they produce a cooling effect byincreasing air movement. If humidity is nottoo high, misters will provide an additionalcooling effect

Perspex roof sheets can be painted toreduce the greenhouse effect, and cubicle

occupancy rates should be reduced, e.g. byturning the ‘lows’ outside, maybe at night,and allowing the ‘highs’ to run into the‘lows’ area. This will also allow the buildingto cool.

Other control options include plantingtrees to provide shade; the evaporation fromtheir leaves also reduces air temperature. Asfood intakes will fall, maximize the palata-bility of the ration and provide an ampleflow of cool water. In Florida, cows areallowed to walk into deep cooling ponds.

Cross-breeding, e.g. with Jersey orBrown Swiss, may help in the longer term

Establish a postcalving group

All cows undergo a period of immunosup-pression during the periparturient period,rendering them more susceptible to a wholerange of diseases, including mastitis. Thiswas discussed in detail in Chapter 3 (pages26–28). The immunosuppression will beeven more pronounced if the cow is concur-rently subjected to high levels of environ-mental stress from defects in housing,feeding or management. For this reason,many larger herds now have an immediatepostcalving or maternity group of cows,which are retained in a more ‘gentle’ envi-ronment than the remainder of the herd.This can be done by keeping them in a smallgroup, at a lower stocking density and per-haps in a straw yard for the first 1–2 weeksafter calving and before introducing them tothe main herd and to cubicles.

It has been found that this can increaseyields and decrease lameness. Perhaps sur-prisingly, cubicle acceptance is improvedwhen the change from straw yards to cubi-cles occurs. Of course, it is vitally importantthat this group should be retained in a cleanand well-bedded yard, at a low stocking den-sity, otherwise mastitis problems could beexacerbated. Predipping should definitely becarried out in this group, if it is not alreadyin routine use.

The disadvantage of the system is thatfor the milker it means an additional groupto bring into the parlour, and for the cow itintroduces an additional group change.


Frequent changes of social grouping arestressful for the cow. It has been estimatedthat when a cow is introduced into a newsocial group she suffers ten aggressive inter-actions every hour for the first few days, i.e.240 interactions every 24 hours.

Dry cow hygiene

The hygiene of dry cows is often overlooked.As discussed in Chapter 4 (pages 50–54), thecritical periods are the first 2 weeks afterdrying off and the 2 weeks prior to calving.If more than one in 12 cows or heifers thatare calving develop mastitis in the first 4weeks of their lactation, or if cell counts arehigh (more than 15% above 200,000) infresh-calved heifers, then this is said to indi-cate an environmental dry period infection.Control measures to be considered includeimproved environment (Plate 8.28), hygieneat dry cow tubing, use of internal teatsealants, reducing yields prior to drying offand minimizing teat-end damage.Environmental hygiene at these times isvital, and stocking densities should prefer-ably be even lower than for milking cows. Ifat pasture, it has been recommended thatcows close to calving should be moved to aclean paddock every 2 weeks and notreturned to the same paddock for at least 4weeks (Plate 8.28). This advice can pose con-siderable practical difficulties, however,because there are often only one or two well-drained fields near the parlour where close-to-calving cows can be carefully watched.

Plate 8.28. If dry cows and heifers are being fedfrom a feeder, as in this case, make sure that thefeeder is regularly moved so that the cows are nottempted to lie on contaminated ground.

©CAB International 2010. Mastitis Control in Dairy Herds (R. Blowey and P. Edmondson)

9 Somatic Cell Count

Why Cell Counts are Important 153Financial penalties 153Legal compliance 153Reduction in milk yield 153The suitability of milk for manufacturing or liquid milk consumption 154

Measurement of Cell Counts 154Automated testing 154DCC cell count tester 155California Mastitis Test (CMT) 155Agitation of the bulk tank before sampling 155

Factors that Affect Somatic Cell Counts 155Mastitis 157Type of mastitis organism 157Age 157Stage of lactation 157Diurnal and seasonal and variations 158Stress 158Milking frequency 159Day-to-day variations and management factors 159

Herd Somatic Cell Counts 159Very low herd cell counts 160

Individual Cow Somatic Cell Counts (ICSCCs) 162Interpretation and Use of Cell Count Data 163

Culture 163Early dry cow therapy 163Drying off an individual quarter 164Treatment during lactation 164Milking order 165Culling 165Withholding milk from the bulk supply 165Evaluating treatment efficacy 166

Study Herd 166

Somatic Cell Count 153

This chapter describes why cell counts areimportant, how they can be measured, thefactors that result in raised counts and actionon high cell count cows, along with anexample of how individual cell count datacan be used.

The somatic cell count (SCC) is thenumber of cells present in milk (‘body’ cellsas distinguished from invading bacterialcells). It is used as one indicator of udderinfection. Somatic cells are made up of acombination of white blood cells and epithe-lial cells. White blood cells enter milk inresponse to inflammation, which may occurdue to disease (see pages 27–28), or occa-sionally to injury. Epithelial cells are shedfrom the lining of the udder tissue. Whiteblood cells make up the majority of thesomatic cells, especially when the cell countis raised.

The SCC is quite a crude measurementand there are a variety of factors that willaffect the result. In general, it is the conta-gious mastitis organisms that are responsi-ble for high cell counts, as they make up themajority of subclinical infections. This isbecause the body continues to send in largenumbers of white cells while attempting toremove this subclinical infection.

The SCC is measured in thousands ofcells per ml of milk. The results are normallyexpressed in thousands to the farmer, e.g. acount of 250 refers to 250,000 cells per ml ofmilk. It is impossible to have a cell count ofzero.

There is no reason why any dairy herdshould not have a mean annual rolling herdcell count under 150,000. This means a lowlevel of subclinical infection and minimaldamage to the milk-producing tissues,thereby maximizing milk yield and ensuringthe production of quality milk that willattract a premium price.

Why Cell Counts are Important

Financial penalties

All dairy companies in the UK have a pay-ment system that penalizes farms with high

cell counts. High cell count milk has lessyield for processing and the shelf life of liq-uid milk is reduced. The penalties vary andthe majority of companies have an escalat-ing scale of penalties once the average cellcount exceeds 250,000. Many companiesalso offer ‘bonus payments’ if the cell countis under 200,000 or 250,000. Farmersrespond positively to these paymentschemes as there is a real financial incentiveto produce low cell count milk.

Legal compliance

Most countries set a maximum cell countlevel above which milk cannot be collectedoff farm. In the EU, once the 3-month geo-metric mean cell count exceeds 400,000 formore than 3 months, milk cannot be col-lected off farm. In the USA, this thresholdwas 750,000 in 2009.

Nearly every dairy company now hassome system of financial penalty that isimposed if the cell count or Bactoscan/TBC(total bacterial count; see Chapter 10) of bulkmilk rises above a certain threshold. This isintended to ensure that the milk produced isof the highest quality. Farmers who do notmeet these production standards are finan-cially penalized according to the quality oftheir milk.

The level of penalty will depend on theuse of the milk (cheese, liquid) and on sup-ply. If there is a large supply pool, a cheesemaker is likely to impose cell counts at alower threshold to encourage quality milkfor processing.

Reduction in milk yield

Most farmers are well aware that, as the herdcell count rises, there is a corresponding dropin milk yield. This occurs as a result of dam-age to the milk-producing tissue caused bymastitis bacteria and the toxins they produce.

One Canadian study showed that milkyield drops by 2.5% for every increase incell count of 100,000 above a base figureof 200,000. This is shown in Fig. 9.1. For

example, a herd with an average yield of7000 litres with a count of 360,000 can beexpected to have a 4% loss in yield due tosubclinical mastitis, or 280 litres per cow inlost production.

The suitability of milk for manufacturing orliquid milk consumption

The final and most important concern abouthigh cell counts is the acceptability of milkto retailers and the manufacturing industry.It must be remembered that the quality ofmilk is only as good as when it leaves thefarm. Poor-quality milk always remainspoor-quality milk.

High cell count milk has a reduction incasein, lactose and calcium, and an increasein the enzymes plasmin and lipase (seepage 17). Table 9.1 shows the compositionaldifferences between low and high cell countmilk.

Reduced casein levels result in a reduc-tion of manufactured product. Reduced cal-cium levels result in poorer cheese clotting,higher fat losses and higher moisture reten-tion. Increased plasmin results in loweryields of proteins and affects the stretch

properties in mozzarella cheese, gives aweaker body to yogurts and poorer water-binding properties. Plasmin withstands tem-peratures of pasteurization and continues toact in the final processed product. Lipasebreaks down milk fat, resulting in rancid andoff flavours.

Measurement of Cell Counts

Automated testing

The majority of laboratories use aFossomatic cell counter, which can handle

154 Chapter 9

Fig. 9.1. Effect of herd cell count (SCC) on milk production: milk yield drops by 2.5% for every increase incell count of 100,000 above a base figure of 200,000. (Adjusted from Philpot, 1984.)

Table 9.1. Effect of somatic cell count (SCC) onmilk composition.

Low High % ofConstituent SCC SCC normal

Butterfat 3.90 3.90 100Total protein 3.35 3.32 99Casein 2.6 2.1 82Whey protein 0.75 1.22 162Lactose 4.6 4.2 90Calcium 0.12 0.04 33Sodium 0.057 0.105 184

0200 400 600

SCC x 1000/ml800 1,000

5

10

15%

Pro

duct

ion

loss

20

large numbers of samples per hour. Thereare other automatic testing machines,including the Bentley. There will be a levelof variation in the measurement of milk sam-ples using either of these methods, with adifference of up to ± 5%. Bulk tank and indi-vidual cow samples are all tested using auto-mated methods.

DCC cell count tester

The DCC (DeLaval Cell Counter) is aportable cell count tester that gives a numer-ical result. This allows accurate testing ofindividual cows, quarters or bulk milk onthe farm. These portable DCC testersare used by dairy farmers, veterinarians andlaboratories throughout the world. The testprocedure is simple. Milk is loaded into thetest cassette (one per sample) and theninserted into the DCC machine. After about1 minute a numerical result is displayed.This is a very useful tool for managing milkquality at farm and cow level. Independentstudies by the University of Wisconsin haveshown that the DCC accurately measures cellcount.

California Mastitis Test (CMT)

This is a simple test that is useful in detect-ing subclinical mastitis by crudely estimat-ing the cell count of milk. The CMT test doesnot give a numerical result, but rather anindication whether the count is high or low.Any result over a trace reaction is regardedas suspicious. The benefits of the CMTare:

� It is a cheap test.� It can be carried out by the milker during

milking.� Results are available immediately.� It gives an indication of the level of infec-

tion of each quarter, as compared with anindividual cow cell count, which onlygives an overall udder result.

The test is carried out in the following man-ner (see Fig. 9.2):

� Foremilk is discarded.� One or two squirts of milk from each quar-

ter are drawn into the paddle dish.� The paddle is tilted so that milk is dis-

carded to a fixed volume per sample.� An equal volume of reagent is added to the

milk.� This solution is then mixed and examined

after 30 seconds for the presence of a gelreaction seen on the base of the paddle.The plate must be rinsed before going onto the next cow.

The disadvantages of the CMT include:

� Significant variation in results.� Potential variation between operators.� Changes are only seen at cell counts of

400,000 and over.� No numeric result.� Does not pick up all infected quarters.

The results can be scored into five cat-egories ranging from negative, where themilk and reagent remain watery, up to thehighest cell count, where the milk andreagent mixture almost solidifies. This isdetermined according to the gel reaction.

Agitation of the bulk tank before sampling

Somatic cells concentrate in butterfat and sothe bulk tank must be agitated for at least2 minutes before the milk is sampled to col-lect a representative sample. Otherwise, thecell count result may be higher. Edmondsonfound that the cell count in unagitated milkwas 486,000 compared with 119,000 whenthe tank was agitated for two minutes.

Factors that Affect Somatic Cell Counts

When discussing cell counts, take care withdefinitions. For example, when referring to‘cell count’ it might be:

� The cell count of an individual cow orquarter at one sampling.

� The bulk tank cell count for that day.� The mean bulk cell count over a 3- or

12-month period, etc.


156 Chapter 9

Fig. 9.2. How to carry out the California Mastitis Test (CMT).

Solutions are examined for the presence of a ʻgelʼ orʻslimeʼ reaction: gelatinous ʻstringsʼ indicate a highcell count quarter.

Foremilk is discarded and one or two squirts of milk aredrawn from each quarter into a paddle dish.

The milk and the reagent are mixed.

Positive strings of gel.

Excess milk is discarded.

An equal volume of CMT reagent is added to the milk.


The rest of this section refers to individualcow cell counts. It is then followed by a sec-tion on herd cell counts.

Mastitis

Mastitis is the major factor that causesincreased cell counts. When mastitis organ-isms enter the udder, the defence mecha-nisms of the cow send vast numbers of whitecells into the milk to try and kill bacteria (seepages 27–28). If the infection is eliminated,then the cell count will fall back to its nor-mal level. If the white cells are unable tototally remove the organisms, then a sub-clinical infection is established. White cellsare then continually secreted into milk, lead-ing to a raised cell count.

Type of mastitis organism

Contagious bacteria (see pages 38–44) aremuch more likely to produce subclinicalinfections and therefore high bulk tank herdcell counts than environmental organisms.The exception to this is Streptococcusuberis. Infections caused by environmentalorganisms tend to be rapidly eliminated andthe cell count normally only rises during theperiod of mastitis.

Different bacteria can produce differentimmune responses in the body. In addition,the same organism may produce differingresponses in the same animal. In the case ofacute E. coli infections, there is often a hugevariation in response, as discussed on page30. When the immune system responds well,there will be a massive increase in the num-ber of white cells, for example, up to20,000,000 per ml within 4 hours of E. coliinvading the udder. In other instances, par-ticularly in early-lactation cows, if thedefence mechanism does not react, there isno increase in cell count and the cow will dieno matter how she is treated. This is becausethe organism is free to multiply and producetoxins with no resistance from the cow.

For some organisms, there is a relation-ship between cell count and the level of

infection in the udder. For example, severeStreptococcus agalactiae infections mayproduce counts of up to 12,000,000 ininfected quarters and the count correlateswell with the level of infection. Other mas-titis bacteria, particularly Staphylococcusaureus, which are shed in much lower num-bers, produce a much more variableresponse, as shown in Table 4.5. There is nomethod of identifying the mastitis organismfrom the cell count of an individual quarter.

Age

In S. aureus problem herds, older cows tendto have higher cell counts. This is simplydue to the increased period of exposure ofthe udder over previous lactations. The teatcanals may be damaged, allowing easieraccess for bacteria to enter the mammarygland. Finally, the immune response fromolder animals may be effective.

Figure 9.3 shows the distribution of cellcounts in a herd infected with S. aureus. Thisherd was divided into three groups: first lac-tation heifers, cows in lactation numbers twoto four, and older cows in their fifth and sub-sequent lactation. Only 11% of the heifershad cell counts over 1,000,000, comparedwith 21% of the middle group and 46% ofolder cows in lactation five and upwards.

Freshly calved heifers tend to have cellcounts in the range of 20,000 to 100,000, andin the absence of mastitis counts wouldremain at this level. When analysing indi-vidual cell count data, check the differencesbetween age groups. If the older cows havehigher cell counts, this suggests problemswith S. aureus, which can be confirmed bybacteriology.

Stage of lactation

Cell counts are often high in the first 7 to10 days after calving, although this may notoccur in every cow. Towards the end of lac-tation, as the amount of milk producedreduces, cell counts may rise in animals thathave subclinical mastitis. For example, a

158 Chapter 9

cow producing 10,000,000 cells per day in20 litres of milk will have a cell count of 500.If the same cow were only producing 5 litres,the cell count might increase significantlydue to a concentration effect. This effect isvery marked in animals yielding less than 5litres of milk per day. Cell counts in cowsthat are free from subclinical infection donot alter significantly in late lactation.

Diurnal and seasonal variations

In herds that do not have regular milkingintervals, cell counts tend to be higher in theafternoon milking than the morning milking.This is partly due to a shorter milking inter-val and lower milk yield resulting in a con-centration effect. This can be seen in a herdthat had separate tanks for morning andafternoon milk (see Table 9.2) and wherethere was a 14:10-hour milking interval. Theresults for a month were averaged out andshow that the afternoon milk had a signifi-cantly higher cell count.

In grazing herds, counts can be higherin summer than in the winter, but the reasonfor this is not clearly understood. In season-ally calving herds with subclinical infection,there may be a rise in cell count when most

cows are towards the end of lactation. Figure9.4 shows the monthly and the annual aver-age cell count for an autumn-calving herdover a 4-year period. The monthly resultsfluctuate depending on the time of the year.In the summer, when most cows are in latelactation, the monthly cell counts rise, butthey fall back in the winter.

Stress

Any event that causes stress, such as oestrus(bulling), sickness or events like tuberculintesting may affect the cell count of an indi-vidual animal. In addition to increasing thenumber of white cells in the blood, there isfrequently a reduction in milk yield and thiscauses a further concentration effect. Stresswill not be responsible for an increase inherd cell count.

Table 9.2. Variation in morning and afternoon cellcount in herd with uneven milking interval.

Milking Average cell count Variation

Morning 147,000 ±60,000Afternoon 221,000 ±70,000

Fig. 9.3. Distribution of cell counts by lactation number in a Staphyloccus aureus infected herd.

0

5

10

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erd

35

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–2000 –5000 5000+

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L2–4

L5


Milking frequency

Some farmers reduce the frequency of milk-ing to once daily or even every other daybefore drying off. Research work shows thatcows milked intermittently towards the endof lactation will have dramatically increasedcell counts.

In tests, the average cell count for a groupof non-infected cows yielding over 5 litres perday was 237,000. When these cows were notmilked for 2 days the cell count increased to540,000. Stopping milking for an extra 4 daysincreased the cell count to 7,600,000, withsome of the cows having counts as high as15,000,000. These results clearly show thatcows should be dried off abruptly.

The reason for this increase is that themilk (and bacteria) are not flushed out andso there is a significant increase in the num-ber of bacteria and the cell count rises. Thisalso explains why cell counts usually fall inherds that are milked three times a day.

Day-to-day variations and managementfactors

Cell counts vary from day to day. This is dueto a variety of all the factors listed previ-

ously, together with management factorssuch as nutrition, calving patterns, sourcesof replacements and milking machine func-tion. Research work has established that, asthe level of vacuum reserve in a milkingplant decreases, the herd cell count willincrease. Hence, it is essential to ensure thatthe machine is well maintained to help keepcell counts low.

Herd Somatic Cell Counts

The factors listed above explain the varia-tion in individual cow cell counts. Within aherd, many of these variations are averagedout. By far the greatest influence on herd cellcount is the level of subclinical mastitis. Asthis rises, so does the cell count. A herd witha cell count under 200,000 will have littlecontagious mastitis present compared witha herd with a count over 500,000, which hasa serious problem.

However, herd cell counts are not nec-essarily linked to the number of clinicalcases, since this could be due to a high levelof environmental mastitis, which will havelittle effect on cell count. In effect, clinicalmastitis and subclinical mastitis (high cellcount) are two separate conditions.

Fig. 9.4. Annual average and monthly bulk somatic tank cell count found in a seasonally calving herd.

100

Month

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300

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600

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atic

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l cou

nt (

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Aug OctDec Feb Apl

Jun

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160 Chapter 9

Farmers may receive a variety of differ-ent sorts of herd bulk tank cell count results:

� Individual tank results.� Monthly figures.� Three-month geometric rolling mean.� Annual rolling mean count.

These may all give different results andtrends that can be misleading. Specificresults will vary greatly, depending on whatis happening within the herd on that date.The more samples that are measured, thegreater the amount of variation.

In herds with rising cell counts, two orthree sets of low bulk tank results may sug-gest that the problem has disappeared. Insome situations this may be the case, as theoffending cow or cows may have been driedoff or sold. In the majority of cases, however,it is just a temporary fall and will rise again.

Figure 9.5 shows the individual,monthly, 3-monthly and annual rollingmean bulk milk cell counts for a 150-cowherd over a period of 13 months. It can beseen that there is a high individual bulkresult marked ‘A’ at the beginning of May.The next six individual results are signifi-cantly lower, and many farmers may con-sider that the problem has disappeared.However, it can be seen that over the fol-lowing 3 months, all the cell count parame-ters increase, indicating that there has beenan increase in subclinical infection and thatresult ‘A’ was not a one-off incident. It isessential to examine the cell count trend tosee what is happening in the herd.

In this herd it can be seen that there wasa significant improvement in herd cell countfrom August until December and that themonthly and 3-monthly average cell countsfell. The annual average hardly changed andreflects very slow changes in this cell countmeasurement parameter.

High herd cell counts can only bereduced over a short period of time by ruth-less culling of the animals responsible forthe increase, or by withholding milk fromthe bulk tank. However, in the long term,this is unlikely to solve the underlying mas-titis problem. The dairy farmer who expectsthat he can reduce a cell count of 350,000 to

150,000 in a matter of a couple of monthswith minimal effort is likely to be disap-pointed, as infection is in the udder and canonly be removed by culling, drying off cowsor treating during lactation. The speed ofdecline in most cases will depend on:

� The type of infection present.� The proportion of the herd infected.� How well control measures have been

implemented.� Culling policy.� Financial situation of the farmer.� The willingness to follow recommen-

dations.� Action taken for individual problem cows.

Very low herd cell counts

Can cell counts get too low? The simpleanswer to this is no. At one time, it was feltthat, if the herd cell count was too low, thencows would lose their ability to fight offinfection that entered the udder and wouldtherefore become more susceptible to envi-ronmental mastitis.

This is not the case. It is the speed ofmovement of the white cells into the milk,not the number of white blood cells presentbefore infection occurs, that determineswhether or not bacteria will be eliminated.

There are plenty of data available toshow that herds with cell counts under100,000 can have less clinical mastitis thanherds with higher counts. Data from 11herds in a Somerset veterinary practice withcell counts under 70,000 had a low mastitisrate of between seven and 21 clinical casesof mastitis per 100 cows per year. This iswell below the target figure of 30 cases (seepage 186). However, it is important toremember that some low cell count herdsmay have more clinical cases of mastitisthan a herd with a high cell count. Thiswould be due to a high level of environ-mental mastitis. Table 9.3 shows some hypo-thetical examples of this.

Herd A has good control of both conta-gious and environmental mastitis and so hasan overall mastitis rate (cases per 100 cowsper year) of 17, well below the target of 30.


Fig. 9.5. Daily bulk milk, monthly, 3-monthly and annual rolling mean bulk milk cell count (SCC) over a 13-month period.

Jan

100

100

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/ml

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Monthly SCC

3-monthly SCC

Annual rolling mean SCC

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/ml

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600

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Dec Jan

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Feb

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A

162 Chapter 9

Herd B has major problems with environ-mental mastitis, which could be due to dirtycows or a poor milking routine, etc., but stillhas good control of contagious mastitis.Herd B therefore has a high mastitis rate buta low cell count.

Herd C has a high cell count but noproblems with environmental mastitis andso the mastitis rate is still below target lev-els, at 29. Herd D has problems with bothtypes of mastitis and a mastitis rate of 66.

All a herd cell count tells us is that thereis good control of contagious mastitis. Theabove examples show that there is no asso-ciation between herd cell count and clinicalcase incidence. Herds can have a high or lowcell count, and a high or low level of clinicalmastitis. However, as most low cell countherds are well managed, the risk of environ-mental mastitis is often lower. It all comesdown to attention to detail.

Individual Cow Somatic Cell Counts(ICSCCs)

Individual cow cell counts are the best way toidentify high cell count cows. A count of over200,000 indicates subclinical infection.Individual cell counts are calculated from amixed sample from all four quarters. This mayalso be called a composite sample. Quartercell counts refer to results from individualquarters. Samples for cell count testing need

not be collected in a sterile manner. However,lumps of faecal matter may cause problemswith electronic testing, and foremilk shouldbe discarded as it may have a higher count.

In herds where the cows are regularlysampled, individual cow cell counts aretested electronically and it can take timefrom collection to the results getting back, sowhen the farmer receives them they are his-torical data. This is to say that the results donot necessarily relate to current udder status.

In order to get the maximum benefit,cows should be sampled monthly so thattrends can be studied rather than individualresults only. A single high cell count indi-cates current infection status. However, sub-sequent tests may be low.

The danger of taking action on a singleresult has already been discussed earlier inthis chapter. Many farmers with a high cellcount have culled cows on the basis of a one-off screening of their herd, only to find thatthe herd count has remained unchanged.Culling should never be considered on thebasis of a single cell count.

The big problem with individual cowresults is that they do not identify which orhow many of the quarters are infected or thelevel of any infection. This is shown in Table9.4. From the composite result and interpre-tation guidelines shown in Table 9.4, wewould expect Cow 2 to have no subclinicalinfection. The quarter results, however,show that there is significant infection pres-ent in the left hind quarter. Individualresults and their interpretation from Cows60 and 140 are correct.

Table 9.3. The incidence of contagious andenvironmental clinical mastitis over a 12-monthperiod in four herds with differing mastitis controland environmental management.

Herdsa A B C D

Somatic cell count 125 125 300 300(× 1000/ml)

Control of contagious Good Good Poor PoormastitisEnvironmental mastitis Good Poor Good PoormanagementContagious cases 7 6 25 24Environmental cases 10 43 4 42Total mastitis cases 17 49 29 66

aAll herds contained 100 cows.

Table 9.4. The effect of quarter and individual cowcell counts (× 1000/ml) in three cows.

Cow 2 Cow 60 Cow 140

Individual cell count 139 314 582

Interpretation Not Infection Infectioninfected present present

Quarter cell count results:LF (left fore) 20 600 425RF 52 31 673LH (left hind) 570 573 423RH 33 51 807

Interpretation and Use of Cell CountData

Individual cow cell count data need to becarefully analysed. For problem herds, thepercentage contribution to the bulk tank isan important figure. In some herds, a smallproportion of cows can make up a significantproportion of the bulk tank cells. Some farm-ers decide to cull these animals without see-ing any long-term benefit. This is becausethese cows are symptoms of a subclinicalinfection and, if all that is being done isremoving the symptom, then the disease willcontinue to spread throughout the herd.

Many farmers receive monthly cellcount data but this information is not alwaysused to maximum benefit. Looking at indi-vidual cell count data for the lactation isimportant. How many tests were over200,000? Did this cow have problems in theprevious lactation, in which case it may sug-gest a chronic infection such asStaphylococcus aureus or Streptococcusuberis. If it is the older cows that have thehighest cell counts, then this suggests aproblem with Staphylococcus aureus infec-tion. If the end of lactation cows have thehighest cell counts, then these cows can bedried off with antibiotic dry cow therapy totry and remove infection. If more than 15%of the herd have cell counts over 200,000,this suggests widespread subclinical infec-tion.

Having accumulated and studied yourcell count results over a period of 3–4 months,you need to know what action can be taken.There are a variety of options.

Culture

By sampling high cell count cows, the con-tagious mastitis organisms present in theherd can be identified and specific controlmeasures implemented. Sterile samplesmust be collected carefully and submitted tothe laboratory in the correct manner.

As there is no method of knowing howmany or which quarters are infected from anindividual cow cell count result, it is rec-ommended to carry out a CMT and only col-

lect milk samples from high count quartersto maximize success.

Select a range of cows for sampling.Animals with persistently high countsshould be chosen, and use a mix of youngand old. It makes no difference if ananimal is going to be culled or dried off, allthat is needed is to identify the cause ofinfection.

Having identified the organism present,the control options for the high cell countare:

� Treatment.� Dry off quarter.� Dry off early.� Culling.� Milk last.

Early dry cow therapy

Early dry cow therapy should be consideredif a high count cow is in late lactation. Thiswill remove her milk from the bulk supply,which will have an immediate effect inreducing the herd cell count. It will alsoremove the risk of spreading infection toclean cows.

Unfortunately, dry cow therapy will noteliminate all infections. Staphylococcusaureus is the classic example (see page 210).If the infection is due to Streptococcusagalactiae, then dry cow therapy is veryeffective. However, there is a risk that cowswith an extended dry period may becomeoverfat, leading to calving problems and anincrease in the number of metabolic prob-lems during the next lactation.

The benefits of dry cow therapy in elim-inating subclinical infection can be demon-strated using individual cell counts. In oneexperiment, 38 cows were sampled in thelast 2 months before they were dried off,using dry cow therapy. They were resampled14 days after calving. The results are shownin Fig. 9.6. Over 60% of cows had a cellcount over 500,000 before drying off, com-pared with only 9% after calving, indicatingthat the dry cow therapy had removed thebulk of the subclinical infection at the endof lactation.


164 Chapter 9

Drying off an individual quarter

Some farmers just dry off one infected quar-ter, which they identified by using the CMTtest or individual quarter cell counts. It isadvisable to carry out a CMT on the cow forthree or four milkings to ensure that the cor-rect infected quarters are identified. It ispractical to dry off one quarter, but less so iftwo or more are infected. It is important thatno dry cow antibiotic treatment is adminis-tered to this quarter, as it may lead to anti-biotic failure. More details of drying offquarters and trial results are given inChapter 12.

Treatment during lactation

Treatment of chronic subclinical Staphylo-coccus aureus mastitis during lactation isgenerally unsuccessful. This is because ittends to be chronic and well established. It isimportant to know which bacteria you areattempting to treat. Cure rates are very lowwith S. aureus infections (see pages 197,205–206), often under 25% during lactation,and, when combined with the high treat-ment costs (intramammary antibiotics, dis-carded milk and extra labour), this line ofaction becomes very expensive. The only

time when treatment of S. aureus during lac-tation may be considered is with an excep-tional cow and if the farmer is prepared toaccept that this form of treatment may wellbe unsuccessful.

If the high cell count is due toStreptococcus agalactiae, therapy may cer-tainly be worthwhile. Unfortunately, chronicinfections due to Streptococcus uberis canalso be very difficult to treat.

These considerations show the impor-tance of bacteriology results to work out iftreatment is a viable option, and what treat-ment regime should be used.

Some vets and farmers recommend theCMT to decide which quarter should betreated. This is a logical and responsibleapproach to treatment; however, two prob-lems can be encountered. First, the CMTonly gives a positive reaction once cellcounts go over 400,000, whereas infection ispresent once the cell count is over 200,000.This means that not all infected quarters areidentified and treated. Second, bacteria suchas Staphylococcus aureus are shed intermit-tently and this means that cell counts ofquarters can vary from milking to milking.The best success for treating high cell countcows comes from treating all four quarterswith intrammammary tubes and combiningthis with parenteral antibiotics. A prolonged

Fig. 9.6. Individual cow cell count found in late lactation and 14 days postcalving showing effect of dry cowtherapy.

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s (%

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Somatic cell count (SCC) x 1000/ml

1001–2000

2001–5000

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Late lactation

14 days postcalving

course of treatment will further maximizesuccess.

Milking order

High cell count cows act as a reservoir ofinfection. Milking these animals last shouldhelp to reduce the spread of infection. Insome herds, the big problem is the prac-ticality of segregating these cows and keep-ing them separate. At best, it is difficult, ifnot impossible, in many herds. Researchwork shows that this can be a relativelyeffective method of reducing diseasetransmission.

In problem high cell count herds, form-ing a high cell count group that is milkedlast reduces the transfer of infection. Once acow enters this group, she should remainthere until the end of her lactation or untilthe cell count drops for two consecutivemonths. These groups may be used when itis practical, e.g. during housing, or as ashort-term measure to assist control of dis-ease. It is possible to disinfect the clusterafter milking high cell count cows to reducetransfer. If herds are grouped then the milk-ing order is important.

Culling

This is a method of eliminating problemcows permanently, but it is costly due to themarked difference between the sale value ofa cull cow and replacement costs. In addi-tion, if the cull cow is replaced with a cowpurchased at market, you may end up backwhere you started – with another high cellcount animal. Few cows are sold through themarket because they give too much milk,have persistently low cell counts or havenever had a case of mastitis.

Culling should never be based on cellcount data in isolation. Factors such as thetype of infection present should always beconsidered. For example, if a high cell countis due to Streptococcus agalactiae, thentreatment will be successful in reducingthe count. In this case, culling these cowswould be a very expensive way of reducing

the herd cell count. Of course, if infectionis due to Staphylococcus aureus, and thecow has a chronic infection and is con-tributing a high percentage of cells to thebulk tank, then culling is a sound course ofaction.

Cows with persistently high cell countsfor three or more consecutive tests might beconsidered for culling but it is essential totake other factors into account. Theseinclude:

� Percent contribution to the bulk tank.� Bacteriology results.� The herd cell count and financial

penalties.� The number of cows in this category.� The number of cases of mastitis that each

animal has had.� Milk yield.� Fertility status.� General health.� Source of replacements.

Before deciding to cull any cow, the otheroptions such as treatment, drying off earlyor drying off the infected quarter should becarefully considered.

Withholding milk from the bulk supply

The herd cell count can be reduced by with-holding milk from high cell count cows fromthe bulk supply. This will have an immedi-ate effect in improving the situation andallows the farmer time to consider whichline of action he wishes to take, but it is acostly option. In herds that are over quotalimits, this temporary line of action canprove invaluable.

Some farmers will then feed this milk tocalves. This is a controversial course ofaction – some suggest that mastitic milk maycause infection of the immature udder.Mastitis organisms may gain entry to theudder either by calves sucking the teats ofother calves or they may be spread by flies.For this reason, some people recommendonly feeding this mastitic milk to bullcalves.


166 Chapter 9

Evaluating treatment efficacy

Cows with mastitis will have increased cellcounts. These counts will decline after suc-cessful treatment. In cases where there hasbeen a bacteriological cure, i.e. all the bac-teria have been eliminated from the udder,then cell counts would be expected todecline to below 400,000, but this may takeup to 4 to 6 weeks. If infection remains pres-ent and becomes subclinical, then countswill remain elevated.

Study Herd

Table 9.5 shows individual cow cell countresults for a herd of 140 cows that recordswith National Milk Records in the UK.These data have been imported into theINTERHERD computer program, whichallows in-depth analysis.

These data show that the currentmonth’s average cell count was 396,000 andthat the rolling annual average for the herdwas 305,000. A cell count of 396,000 indi-cates very high levels of subclinical masti-tis, and the farmer is losing 10% of his milkprice in cell count penalties. The annualaverage cell count changes very slowly, but,if it is increasing, it suggests that the prob-lem is deteriorating. The cell count figure of396,000 is from monthly milk-recordingrecords, which will differ from those of themilk buyer, who will be testing bulk tankmore frequently.

The lactation breakdown for Augustshows that the 29 heifers had an average cellcount of 115,000 which suggests that theyare free of infection. However, the result forthe 14 cows in lactation 4 shows an averagecell count of over a million, indicating thatthis group of cows have severe levels ofinfection.

Table 9.5. Summary of somatic cell count results.

Rolling annual average of whole herda 305This monthʼs herd averagea 396

Average test for: 3 Jun 3 Jul 3 Aug Total Cows – Aug1st lactation 277 137 115 292nd lactation 725 445 377 283rd lactation 191 189 224 214th lactation 140 886 1002 145th lactation 191 763 566 21

Cow no. Lact.b Days in milk Lact. avg. No.>200c 1 May 2 Jun 3 Jul 3 Aug % of total

1385 4 262 1012 7 498 90 682 9720 140651 2 16 3631 1 795 3631 90331 7 201 474 1 60 18 102 3578 90678 4 13 3414 1 3414 40318 7 153 829 4 485 218 1903 2021 50258 6 140 1360 5 384 645 833 1911 40016 4 291 452 2 50 4120 1472 30117 6 404 92 3 74 59 241 1329 00338 6 66 1710 2 2079 1252 31247 3 77 557 2 345 145 411 1244 20101 4 18 1152 1 1152 30477 4 211 480 5 780 5 761 1021 20612 2 362 201 7 412 290 423 1013 10255 6 308 1054 8 3534 69 1299 875 20028 3 334 607 6 74 90 237 836 1

aSomatic cell count (SCC) × 1000/ml; bLactation; cNumber of SCCs > 200.

Below the lactation summary there is alist showing the cows with the highest con-tribution to the bulk tank for August.Percentage contribution to the bulk tank willbe a combination of cell count and yield. Onthe day of recording, there were 113 cows inmilk. The first six cows, or 5% of milkers,accounted for 45% of the somatic cells.There are another three cows in the list thataccount for a further 9% of somatic cells.This is a prime example of a herd where onthe day of sampling a small proportion ofcows (8%) accounts for a large percentage(54%) of the bulk tank cell count.

Figure 9.7 shows the distribution of cellcount within the herd for the past four milkrecordings. This shows that at the lastrecording there were 13 cows with cellcounts over a million, 11 with countsbetween 500,000 and a million, 11 withcounts between 300,000 and 500,000, and 53with cell counts of under 100,000. Thus,31% of the herd have cell counts of over300,000, indicating widespread subclinicalinfection within the herd.

Table 9.6 shows the cell count by stageof lactation. For August, the average cellcount for the first 100 days of lactation is398,000, from 100 to 199 days it is 324,000,and it is 428,000 for cows calved more than200 days. If the cell count were high in theend of the lactation group, drying off thesecows would be an easy way of helping toreduce the cell count.

This herd has had no samples collectedfor bacteriology and so ten of the highestcontributing cows to the bulk tank should beselected and submitted for culture, alongwith a sample of bulk milk. This will helpto establish the cause of the high cell count.

A farm visit needs to be carried out toassess mastitis management. During thisvisit, control measures can be tightened upand any measures or products that are usedand have no benefit can be stopped. Tacklinghigh cell count cows without addressing thespread of infection in the herd will not resultin long-term benefits. Once this step hasbeen carried out, action on individual cowscan be taken.

Now let us consider the individual cowresults from the cows contributing the high-est percentage contribution to the bulk tankand the possible actions that could be taken.These cows will not necessarily have thehighest cell counts, but, as we need toreduce the herd cell count, the percentagecontribution is the key area to examine.

Cow 1385

This is a lactation 4 cow, contributing 14%of cells to the bulk tank, calved 262 days andgiving 15 litres. She is pregnant and so canbe dried off. An alternative is to dry off the


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5 August

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Fig. 9.7. Individual cow somatic cell count (SCC)distribution over past four milk recordings fromcows at all stages of lactation.

168 Chapter 9

quarter (DOQ) if only one quarter is CMT-positive. This is discussed in Chapter 12.Drying off the cow or drying off a quarterremoves her milk from the bulk tank andhelps to protect the rest of the herd.

Cow 651

This is a lactation 2 animal contributing 9%of herd cells and calved only 16 days. Herlast cell count in the last lactation was 795 (1May recording); this suggests that dry cowtherapy (if given) was ineffective. It is impor-tant to check that this cow does not haveclinical mastitis and, if she does, that she istreated. If not, she should be CMT-tested tosee if she still has a high cell count. TheCMT result for such a high cell count will bevery obvious. If the test reading is high, as ashort-term measure, this milk should be fedto bull calves and a sterile milk sample takento identify the cause of the infection, to helpdecide what action should be taken.

Cow 331

This cow is in lactation 7 and is calved 201days. She has had one cell count over200,000 in this lactation. Her last cell countwas 3,578,000 and she was contributing 9%to the bulk tank. Her lactation average is474,000.

Table 9.7 shows her previous cell counthistory. While this is an old cow, she hasonly had one high cell count reading over200,000 in her lifetime. A jump from102,000 up to almost 4 million suggests thatthis cow may have been developing or hadclinical mastitis at the recording that wasmissed. On questioning the farmer, this cow

was found to have mastitis the day afterrecording. If clinical mastitis treatment hasbeen successful, her cell count shouldreduce at the next recording.

Cow 678

This is a lactation 4 cow, calved 13 days andcontributing 4% of all cells. In her previouslactations, the cell count averages were96,000 and 121,000 with no readings over200,000. Despite her age, this cow does nothave chronic infection and the advice is thesame as for cow 651. It is possible that thisreading is due to her being freshly calved.

Cow 318

This is a lactation 7 cow, calved 153 days,with a cell count of over 2 million con-tributing 5% of all somatic cells. This cowhas had high cell counts for the previous twolactations, 911,000 and over 2 million, and isclearly a chronic high cell count cow thatshould be culled from the herd now.

Cow 258

This cow is in lactation 6 and is calved 140days. She has had five readings over 200,000this lactation; her last cell count was1,911,000 and was contributing 4% to thebulk tank. Her lactation average is 1,360,000.It is very helpful to look at the previous his-tory of this cow to make sound managementdecisions.

Table 9.8 shows her history for the pre-vious lactations. It can be seen that her aver-age cell counts in lactations 4 and 5 were

Table 9.6. Individual cow cell count average by days in milk.

Cell Cell CellDays in milk No. 2 Jun count 3 Jul count Days pp 3 Aug count

<100 29 37.92 kg 124 34.43 kg 289 49 31.73 kg 398100–199 27 33.80 kg 511 29.45 kg 516 168 26.47 kg 324>199 57 30.94 kg 284 24.63 kg 351 281 22.17 kg 428


531,000 and 723,000. In addition, she has 14results over 200,000 in lactation 4 and 13 inlactation 5. This cow had received antibioticdry cow therapy at the end of every lacta-tion. This cell count history indicates thatthe cow most probably has a chronic sub-clinical infection, such as Staphylococcusaureus or Streptococcus uberis, which is notresponding to treatment. This cow should beculled from the herd. As this herd has a very

high cell count, culling this cow and cowno. 318 should take place as soon as possibleas they account for 9% of all somatic cells.

If this cow were in a herd where the cellcount was low and the farmer was not beingpenalized, the cow should still be culled.However, the timing of culling can change.She may not be culled until the end of lac-tation as it is clear that herd mastitis controlmeasures are effective due to the low herd

Table 9.7. Individual cell count history of cow 331.

Table 9.8. Individual cell count history of cow 258.

cell count. She would pose a lower risk toother cows because hygiene is good. Analternative would be to dry off the quarter.

These results show that the interpretation ofindividual cell counts requires careful con-sideration, and action can only be taken ona series of results, not on the basis of a one-off screening.

170 Chapter 9

This chapter describes the sources of bac-teria in milk, compares TBC testing withBactoscan and shows how bulk tank analy-sis of milk can help to identify the cause ofhigh Bactoscan counts.

A high Bactoscan or TBC can affect thedairy farmer in two ways: directly in theform of financial penalties and the possibil-ity of increased levels of mastitis, and indi-rectly through the production of apoor-quality, short shelf life milk that is lessacceptable to the consumer and manufac-turer. Some bacteria can cause ‘off’ flavours,due to increased levels of the enzymes plas-min and lipase, which break down caseinand butterfat. Some producers believe thatpasteurization will not only kill all the bac-teria present in milk, but will also put rightany milk quality problems. This is nottrue.

The total bacterial count (TBC) of milkis a measure of the number of bacteria grown

using a specific culture medium and aspecified temperature, and over a fixedperiod of time. It is sometimes referred to asthe total viable count (TVC).

The Bactoscan test measures the totalnumber of bacteria using an electronicmethod. The test takes 10 minutes comparedwith 72 hours for the TBC. The Bactoscan isfar more accurate and measures all bacteria(dead and live) rather than counting livingcolony-forming units (cfu). It counts all bac-teria, irrespective of their culture mediumand temperature requirements and, as such,measures pyschrotrophs (bacteria that growunder refrigerated conditions) which are notpicked up by the TBC test. Bactoscan testingis a far more accurate and reliable measureof the bacterial count in milk.

For both testing methods, the results aregiven as the total number of bacteria per mlof milk. For simplification, the results arecommonly reported back to the farmer in


10 Bactoscan and Total Bacterial Count(TBC)

The Three Sources of Bacteria in Milk 172Mastitis organisms 172Environmental contamination 173Dirty milking equipment 174

Failure of Refrigeration 174Bulk Tank Analysis (BTA) 176

Common tests carried out on bulk milk 176When to use bulk tank analysis 178Interpretation of bulk samples 179Examples of the use of BTA in problem herds 180

thousands, and so a count of 9 refers to aTBC or Bactoscan of 9000 per ml.

The majority of milk buyers havereplaced the TBC with the Bactoscan test. Acomparison of the two tests is shown inTable 10.1. There is no precise numericalcorrelation between the two tests. An addedadvantage of the Bactoscan is that the farmercan be notified of a high result quickly sothat he can take action.

The 1992 EC Council Directive 92/46/EEC for dairy products required bacterial lev-els to be under 100,000/ml. It must be remem-bered that most dairy companies are onlyinterested in purchasing ‘quality’ milk. Aherd with good hygiene will have a Bactoscanof 20,000 or less. There are many herds thathave counts of around 10,000 and these areoften herds that predip and have meticulousparlour hygiene, as well as excellent wash-uproutines, as seen in Plate 10.1. Dairy compa-nies measure Bactoscans regularly.

However, the benefits of Bactoscan test-ing to the farmer are limited as results do notidentify the bacteria present or the source ofthe organisms. Despite this, the Bactoscanremains an accurate test for measuring thenumber of bacteria in milk. With further test-ing, bulk tank samples can yield valuableinformation in relation to mastitis manage-ment, as described later in this chapter.

Bacterial contamination of milk mayoccur in two ways: directly from the cowwhen mastitis organisms are shed into themilk, or indirectly from the environment ormilking equipment.

The Three Sources of Bacteria in Milk

There are three main causes of highBactoscans. These are:

� Mastitis organisms.� Environmental contaminants.� Dirty milking equipment.

Mastitis organisms

Mastitis organisms should be suspected ifthe Bactoscan fluctuates dramatically. Milkfrom a healthy quarter will have low num-bers of bacteria present, usually under 1000per ml. When quarters become infected withclinical or subclinical mastitis, the numbersof bacteria can increase substantially.Streptococcus agalactiae and Streptococcusuberis are shed in extremely high numbers,for example, up to 100,000,000 per ml, inclinically infected quarters. Large numbersof coliforms may also be shed with E. colimastitis. In herds infected with these organ-isms, it is easy to understand why Bactoscanlevels can fluctuate.

Take a herd producing 1500 litres ofmilk per day with an average Bactoscan of

172 Chapter 10

Plate 10.1. A good wash-up routine will ensure thatfarms maintain a low Bactsocan.

Table 10.1. Comparison of TBC and Bactoscan.

Bactoscan TBC

Measures All bacteria Colony-forming unitsTime 10 minutes 72 hoursAccuracy ± 10% ± 30–50%Psychrotroph measurement Yes NoCorrelation Approx. 4–5 × TBC

5000. The addition of as little as 2 litres ofmastitic milk from a clinical S. uberis cow(shedding 100 million bacteria per ml) canincrease the bulk tank Bactoscan to 138,000.For this reason, it is important to detect clin-ical infections early so that mastitic milkdoes not enter the bulk supply.

Figure 10.1 shows the typical fluctuat-ing effect of an S. agalactiae infection on theBactoscan in a herd of 50 cows. Other mas-titis organisms, for example, staphylococci,tend not to shed bacteria in large enoughnumbers to significantly affect the bulk tankBactoscan (see Table 4.5).

Unfortunately, the milker cannot detectsubclinical mastitis and so it is inevitablethat some mastitis bacteria will enter thebulk supply. The best way to reduce thiseffect is through a mastitis control pro-gramme that will reduce the level of infec-tion in the herd, and ultimately the numberof mastitic organisms entering the milk.

Environmental contamination

The main cause of environmental contami-nation of milk is keeping cows in poor envir-onmental conditions, combined withinadequate teat preparation. The importance

of good udder preparation has been referredto in Chapter 6. It is essential that the milk-ing unit is attached to clean dry teats.Milking dirty teats will not only contaminatethe bulk milk but must also increase the like-lihood of environmental mastitis.

The coliform count measures the num-ber of coliform organisms in milk and givesan indication of the level of environmentalcontamination and the standard of premilk-ing preparation. Coliforms are only onegroup of environmental organisms, of whichthe most important is E. coli, but there aremany others, such as Streptococcus uberis,Streptococcus faecalis, Bacillus species, etc.

The technique for carrying out a col-iform count is described on page 59. The tar-get figure with good milking hygiene is tohave a coliform count under 10 per ml, butlevels under 20 per ml are acceptable. Highlevels of environmental bacteria will reducethe shelf life of milk and increase the risk ofoff flavours and hence its acceptability toprocessors. There are many herds with excel-lent premilking preparation that regularlyhave coliform counts of 5 per ml or less.

Table 10.2 shows a comparison of theTBC and coliform count before and after achange in the milking routine in a herd of1000 dairy cows in Arizona. Initially, teatswere washed but not dried, which resultedin high TBCs and coliform counts. Once themilking routine was modified and teats werewashed and then dried before milking, thecounts reduced significantly. Remember thecoliform count will not measure all envir-onmental organisms. It just gives an indica-tion of whether the level of environmentalcontamination in milk is high or low.

Table 10.2. The effect of different types of teatpreparation on the TBC and coliform count/ml ofmilk. (From T. Fuhrmann, unpublished data,personal communication.)

Washing but not drying: Washing and drying:3 months before 3 months after

Test change in routine change in routine

TBC 50,000 10,000Coliform count 120 20

Bactoscan and Total Bacterial Count 173

Fig. 10.1. The typical effect that a single clinicalcase of Streptococcus agalactiae mastitis can haveon the bulk TBC in a herd of 50 cows.

0

20

5 10Time (days)

15 20

40

60

TB

C x

100

0/m

l

80

100

The type of winter bedding used is alsoimportant: sawdust and wood shavingsbecome rapidly contaminated with bacteriajust 24 hours after bedding down – this isdue to their large surface area and their abil-ity to absorb moisture. Sand is inert anddoes not support bacterial growth.

In well-run dairy herds where there isplenty of clean, dry and well-bedded accom-modation, teats should remain clean. Inpoorly managed herds where there is insuf-ficient or dirty, damp accommodation, forexample, where there are uncomfortablecubicles resulting in cows lying outside, thecondition of the teats of the cows enteringthe parlour will be poor.

A practical way to assess premilking teatpreparation on farm is to check the milksocks or filters after milking. If they are dirty,this is likely to contribute to high coliformcounts. Cows should come in to be milkedwith clean udders and teats. Hairy uddersand long tails can increase the risk of dirtycows. Check inside the liners during milking;they should be free of faecal contamination.

Dirty milking equipment

Inadequately cleaned milking equipmentcan lead to raised Bactoscans, as seen inPlate 10.2. A laboratory assessment of plantcleaning can be made using the laboratorypasteurized count (LPC) or thermoduric (TD)count, where levels over 175 cfu/ml suggesta wash-up problem.

Milkers should look out for the follow-ing, which can cause contamination of thebulk milk:

� Wash-up problems, see pages 88–89.� Dirty bulk tank (see Plate 10.3): it should

be inspected after every wash.

Failure of Refrigeration

Milk should be cooled to 4°C or less as soonas possible after milking to limit the growthof bacteria. This helps to maintain milk qual-ity. In the UK, milk cannot legally be col-lected off farm if it is over 6°C. When there

is a refrigeration problem and milk is notkept cool or not cooled rapidly, bacterialmultiplication will take place.

The importance of efficient refrigerationis becoming greater with a decreasing fre-quency of milk collection from some farms.In some countries, milk for liquid milk con-sumption is collected every second day,while milk for manufacturing can be col-lected every third day, without any significanteffect on Bactoscan or milk quality providedthe refrigeration is efficient and there are goodhygiene and management practices on farm.

174 Chapter 10

Plate 10.2. A dirty receiver vessel will increase theBactoscan.

Plate 10.3. Soil, as shown in the dark line just abovethe milk, allows psychrotrophic bacteria to grow.

The effect of multiplication will dependon the number and type of bacteria, togetherwith the temperature of the milk. Warm milkis an excellent medium for bacterial growth.Some bacteria, such as coliforms, may dou-ble in number every 20 minutes under opti-mum conditions. The increase in bacterialnumbers in raw milk stored at different tem-peratures over a 12-hour period is shown inFig. 10.2. These data refer to ‘clean’ milk, i.e.milk without excess environmental contam-ination. As temperature increases above4.5°C, the rate of bacterial growth increasesexponentially.

Plate coolers are commonly used to coolmilk before it enters the bulk tank (seePlate 10.4). They operate by using a heatexchange mechanism. Large volumes of coldrunning water (as much as seven times thatof the milk) flow in the opposite direction tomilk with the heat from the milk passingthrough to warm the water, as shown inFig. 10.3. Some plate coolers circulatechilled water from the bulk tank, whichdrops the temperature further. The resultanteffect of the heat exchange mechanism (withthe most efficient systems) is to have milkleaving the cooler at a temperature as low as6°C. Tube coolers (tubes surrounding the

milk line through which cold water flows inthe opposite direction to the milk) have thesame effect.

The warm water from the plate coolersmay be used to wash dirty teats before milk-ing. Others divert this water to a drinkingtrough so that cows can have a warm drinkafter milking. Cooling milk before it entersthe bulk tank saves energy as the tank hasless work to do. It also helps to protect milkquality, as the milk reaches 4°C more rap-idly, thus reducing bacterial multiplication.


Fig. 10.2. Effect of storage temperature on bacterialgrowth in raw milk over a 12-hour period. At 21°Cthere is a 700-fold increase in bacterial numbersover a 12-hour period. (From Philpot andNickerson, 1991.)

Plate 10.4. Plate coolers drop the temperature ofmilk quickly and slow down bacterialmultiplication, while saving energy.

Fig. 10.3. Plate cooler. Large volumes of cold waterrun through the plate cooler in the oppositedirection to the milk, resulting in warm water, butcool milk leaving the plate cooler.

0

500

1000

1500

Bac

teria

l gro

wth

rat

e (x

1000

/ml)

2000

2500

3000

5 10 15 20 25 30

Temperature (°C)

The shelf life of pasteurized milk is con-siderably affected by storage temperature, asshown in Fig. 10.4. This is of great impor-tance to retailers, the milkman and, ofcourse, the consumer. It can be seen thatwhen pasteurized milk is stored at 16°C itsshelf life is only 1 day, compared with10 days when stored at 5°C.

Bulk Tank Analysis (BTA)

Bulk tank analysis can offer a variety of teststhat can be carried out, along with a differ-ential bacterial screen. All bacteria in milkhave originated from either the udder, theenvironment or a dirty plant, and commontests for these are described in the nextsection.

Common tests carried out on bulk milk

The somatic cell count (SCC) gives an indi-cation of the level of subclinical mastitis.

The TBC (total bacterial count) gives aquantitative indication of bacteria in milkand, while it is not as accurate as aBactoscan test, it gives an indication of thetotal numbers of bacteria in milk.

The LPC (laboratory pasteurized count),often called a (TD) thermoduric count, meas-ures thermoduric bacteria, which withstandhigh temperatures of pasteurization. Highcounts indicate problems with plant wash-ing. Because thermoduric bacteria can with-stand the temperatures of pasteurization,they can continue to grow in the milkingsystem if the wash-up routine does notremove them.

The coliform count (CC) gives an indi-cation of faecal and environmental contam-ination, which is due to poor teatpreparation or poor hygiene. Coliforms actas a marker for all the other environmentalorganisms, such as faecal streptococci,yeasts and fungi. Increased coliforms canalso arise from mastitis.

The Pseudomonads count gives anotherindication of environmental contamination,although the source of these organisms isvery different. Some Pseudomonads bacte-ria are psychrotrophs and so multiply incold conditions.

Streptococcus uberis, Staphylococcusaureus and the total staphylococci countsgive a measure of these individual bacteria.The total staphylococci count measures allstaphylococci, including S. aureus. Thesecounts are useful in herds with contagiousmastitis problems. Streptococcus uberis ispredominantly an environmental bacteriumassociated with the use of straw bedding andis a common cause of clinical and sub-clinical mastitis in the UK and Europe.

A differential bacteria screen identifiesall bacteria in milk, no matter what their ori-gin. Some laboratories quantify these as + forsmall numbers, up to +++ for high levels. Inthe UK, screening for Mycoplasma is notroutinely carried out, as this is a rare masti-tis pathogen. In parts of the world where thisis a problem, it should be a regular part ofthe bulk tank screening.

The presence of each type of bacteriumin milk each has its own individual signifi-cance.

� Streptococcus agalactiae is a highly con-tagious mastitis bacterium that can resultin very high cell counts.

176 Chapter 10

50

2

4

6

8

10

She

lf lif

e (d

ays)

12

14

16

18

20

22

10 15Temperature (°C)

20 25

Fig. 10.4. Shelf life of pasteurized milk in daysaccording to the storage temperature. (From Philpotand Nickerson, 1991.)

� Streptococcus dysgalactiae is associatedwith poor teat skin condition and possiblemilking machine problems linked to teatdamage and/or injury.

� Corynebacterium bovis is associated withpoor postmilking teat disinfection.

� Pseudomonas aeruginosa is associatedwith contaminated water sources and cancause a severe mastitis.

� Klebsiella is associated with wood prod-ucts, such as sawdust, and can cause clin-ical mastitis.

� Yeasts and fungi are associated withpoor hygiene, as is the presence of S. fae-calis.

Table 10.3 shows the target levels for the dif-ferent test types for bulk tank analysis fromone laboratory. There are many herds thatare consistently under these targets.

Table 10.3. Targets for bulk tank analysis. Dairyfarmers who have a good mastitis managementregularly achieve these targets.

Somatic cell count <150,000Total bacterial count <5,000Laboratory pasteurized count <175Coliform count <20Pseudomonads count <500Streptococcus uberis count <200Total staphylocci count <200Staphylococcus aureus count <50

There is another group of bacteria calledpsychrotrophs. These are bacteria that growwell under cold conditions, as low as 2 to9°C, and so these bacteria continue to multi-ply in the bulk tank. Some organisms arethermoduric psychotrophs; an example isBacillus cereus, which is commonly foundin the environment. If these enter the bulksupply, as may occur if teats are not properlyprepared before milking, then they are notkilled by pasteurization and continue tomultiply in refrigerated pasteurized milk. B.cereus can cause food poisoning in man.Psychrotrophs are not routinely measured inbulk milk, as, provided milk meets the stan-dards for the above tests, they should notcause any problem.

Bulk tank analysis is a useful way toidentify herd and management factors asso-ciated with Bactoscan problems. It may bepossible to eliminate a dirty milking plant orenvironmental contamination as the causeof the high Bactoscan. However, care isneeded with interpretation. For example, ifan organism has been isolated from a bulksample, then we know that this organism ispresent in the herd. However, if a suspectedorganism has not been identified, it does notmean that it is absent from the herd, butrather that it just has not been identifiedfrom that particular sample. It may be thecase that it may be identified, if present, infuture samples.

It is essential that the sample milk fortesting is transported from the farm to thelaboratory within 24 hours, and at no morethan 6°C to minimize any bacterial growth.Milk should be fresh and not frozen,although collection of daily samples over aweek, freezing, and then processing thewhole batch can help to eliminate laboratoryvariation associated with a series of samples.However, freezing will alter the number oforganisms present; for example, there willbe a reduction in the number of coliforms. Iftwo bulk tanks are used, both should be sam-pled and tested individually, and any differ-ences between milkers and wash-uproutines should be recorded.

Bulk tank samples should be collectedin the following way:

� Agitate the bulk tank for at least 2 minutesto ensure that the milk is well mixed, seePlate 10.5.

� Scoop at least 30 ml of milk into a sterilesample pot using a sterile scoop, or wear-ing a clean disposable glove and dippingthe pot into the bulk tank. This ensuresthat the remainder of the milk does notbecome contaminated during sampling.

� Seal the container and label with thedate and farm name, and tank identity (ifsamples are taken from more than onetank).

� Store at 4°C from collection until trans-porting to the lab; the sample can be keptin a fridge and then transported in an ice-box to the laboratory.


Some milk quality labs that test the cellcount and Bactoscan for dairy companies canalso offer bulk tank analysis. The advantageis that they can test a sample with a knownhigh Bactoscan reading, which will help pin-point the origin of the contamination.

When to use bulk tank analysis

Raised Bactoscan (TBC) counts

It is essential to know the source of bacterialcontamination in problem herds to be ableto resolve the problem efficiently. Bulk test-ing can assist with this. In an ideal world,you would only test samples with knownhigh counts, but this is not always practical.In herds with fluctuating Bactoscans, bulksamples can be frozen and then known highBactoscan samples can be sent to the lab fortesting. Freezing can affect the coliformcount but, when the levels are high enoughto influence the Bactoscan, they are wellabove the target levels and this has littleeffect on diagnosing the problem.

Raised somatic cell counts

Some herds do not have any individual cowcell counts or bacteriology results. The BTAcan give a good indication of problem areasthrough the Streptococcus uberis,

Staphylococcus aureus and total staphylo-cocci counts, along with the differential bac-teriological screen. A BTA screen shouldalways be carried out when investigatingproblem herds.

Problems with clinical mastitis

The majority of cases of clinical mastitisin low cell count herds will be due toenvironmental mastitis caused by E. coliand maybe some Streptococcus uberis.In some countries with high somatic cellcount herds, there may also be problemsfrom the contagious bacteria, such asStaphylococcus aureus, Streptococcusagalactiae and S. uberis. BTA provides help-ful insight into hygiene from the coliformcounts. A low count indicates excellent pre-milking teat preparation. But the presence ofhigh coliform counts, along with the pres-ence of faecal streptococci, yeasts and fungi,indicates gross contamination and willincrease the risk of environmental mastitis.High levels of streptococci and staphylo-cocci may also be contributing to theproblems.

Screening tool

Many producers want to have a regularcheck on milk quality so that they can passthese results back to the milking team to pro-vide motivation and encouragement. BTAcan act as an early warning system forimpending problems and allows early inter-vention.

Individual BTA tests

In some herds there may be a problem withteat preparation. Using the coliform countalone as a monitoring tool for individualmilkings can have quite an impact on gettingpeople to improve performance. This may beused as a separate test to monitor milkerswhose hygiene may be marginal. Milkerscan argue with your interpretation of theirhygiene, but it becomes much more difficultto argue with lab tests. These results supportthe decision-making process.

178 Chapter 10

Plate 10.5. Milk samples must be collected from awell-agitated bulk tank and kept cold until theyreach the lab.

Milk quality enhancement programmes

When farmers have Bactoscan results belowthe target levels set by their milk buyer, theremay still be further room for improvement.A Bactoscan enhancement programme wasset up for a dairy company where BTA wascarried out for every milk producer over a2-year period. The milk buyer wanted tohave much lower Bactoscan results for com-mercial advantage and this was a novel wayof persuading farmers to improve. Resultsand interpretation were returned to the farm(see Fig. 10.5).

While many of the farmers may haveconsidered they had no areas for improve-ment, it was surprising to find that only 6%had levels below all the target figures forLPC, coliform and Staphylococcus aureuscounts; 78% had wash-up problems; 35%had high coliform counts, indicating poorpremilking teat preparation; 53% had abovetarget levels of S. aureus; and 8% of herdswere found to have Streptococcus agalactiaeinfections. Over the 2-year period, theBactoscan averages for all purchased milkfell from 38,000 to 20,000/ml. There wasalso a reduction in cell counts by identify-ing and addressing contagious mastitis prob-lems that were previously not identified.

Interpretation of bulk samples

The interpretation of bulk samples requiresknowledge of the various tests and how theyrelate to mastitis management. Frequently,the problems identified may involve morethan one area of mastitis. For the fourproblem study herds discussed below, theresults are given of bulk tank sampleanalyses, together with their interpretations,in conjunction with other findings on thefarm.

When investigating problems, remem-ber that analysis of one bulk tank sample isa snapshot of the milk on that day only. Avariety of factors need to be considered,including: who was milking, were the nor-mal milking and wash-up routines followed,how good was mastitis detection on that daycompared with others, and was the samplecorrectly taken, stored and dispatched to thelaboratory?

Some advisers may read too much fromone sample. A lab result should never beconsidered in isolation from the rest of theherd history. It must be remembered, how-ever, that bulk tank analysis is only an aid toidentifying the possible causes of highBactoscans.


Fig. 10.5. Percentage of farms with problems with wash-up, teat preparation, presence of Streptococcusagalactiae or above target levels of Staphylococcus aureus.

Wash-up

0

10

20

30

40

Farms

(%) 50

60

70

80

Teat prep. Staph. aureus Strep. agalactiae

Examples of the use of BTA in problem herds

The following examples are actual resultstaken from real-life herd problems investi-gated by the authors.

Herd A: somatic cell and clinical mastitisproblems, and the occasional high Bactoscan

result

The presenting problem in herd A is a risingcell count (see Table 10.4) and a high level ofclinical mastitis. Milking cows are housedboth in cubicles and on straw yards. Theowner has a herdsman who is convincedthat he is doing an excellent job. The herdhas expanded by 50% over the past 3 years.Various recommendations have been madebut were rejected due to shortage of time.

The TBC is above target and the highcoliform count result shows major problemswith teat preparation. The presence of yeastsand Streptococcus faecalis further confirmpoor hygiene. There are also high S. uberis,staphylococci and Staphylococcus aureuscounts and high cell count. The presence ofCorynebacterium bovis suggests problemswith postmilking teat disinfection. Thewash-up routine was adequate, as shownfrom the low thermoduric count, or LPC, of50, well below the target of 175.

The following were found during thefarm visit. The coliform count of 312 showsthat teat preparation was poor, as the milkerwas finding it difficult to milk on his own;he had too big a parlour for one milker andwas trying to cut out tasks to ensure he hada fast throughput in the parlour.

Units were applied to dirty teats. Therewas no foremilking and mastitic milk fre-quently entered the bulk tank. As many ofthe cows were bedded on straw yards, acommon cause of clinical mastitis will havebeen Streptococcus uberis which is shed atvery high levels and can increase bulk tankBactoscan results. Straw yards were cleanedout every 6 to 8 weeks instead of every3 to 4 weeks, due to shortage of labour.

There were no separate clusters formilking cows with mastitis and, when a reg-ular cluster was used to milk a cow withclinical mastitis, it was not disinfectedbefore milking the next cow. There were alot of old cows with high cell counts andthese cultured positive to Staphylococcusaureus. The farmer was teat dipping but, dueto reduced profitability, diluted the teat dip1:5 rather than 1:4 to try and save money.This will have contributed to the high levelsof C. bovis.

The bacteriology results helped to per-suade the owner and his milker to makemajor changes to mastitis management andthe problems were slowly resolved.

Herd B: somatic cell and Bactoscan problems

The request for herd B was to investigate ahigh somatic cell count of over 400,000/ml(Table 10.5). The owner had another busi-ness, which has been far more profitablethan the dairy, and he had left control to thedairy staff for many years. Four months ear-lier, the old staff left and two replacementswith little experience of milking wererecruited. They were given minimal training.

180 Chapter 10

Table 10.4. Bulk tank analysis for Herd A.

Streptococcus Total StaphylococcusColiform Pseudomonads uberis staphylococci aureus SCC

Test TBC LPC count count count count count × 1000/ml

Target <5000 <175 <20 <500 <200 <200 <50 <150Result 9000 50 312 250 6500 650 216 338

Differential bacterial screen Yeasts ++Streptococcus faecalis +++Corynebacterium bovis ++

The herd had a new parlour fitted 2 yearsago and since then had never had a lowBactoscan count, with levels always above60,000/ml.

The TBC is well above target and thehigh LPC (950) result shows that there is aplant wash-up problem. The high coliformcount (87) and the presence of Streptococcusfaecalis, yeasts and fungi suggest poorenvironmental conditions and/or premilk-ing teat preparation. The total staphylococciand Staphylococcus aureus counts are veryhigh, indicating that these are likely to becontributing to the high cell count of421,000.

The presence of C. bovis suggests thatthere are problems with postmilking teat dis-infection. That of Streptococcus dysgalac-tiae suggests teat damage or poor teat skincondition.

From further investigation, the follow-ing were identified. Postmilking teat disin-fection had stopped completely a fewmonths previously. Teat skin condition wasvery poor, with quite a few teat lesions. Teatswere dirty on entering the parlour and werewashed but not dried before units wereattached. This effectively suspends environ-mental organisms into a ‘soup’ on the teat,which subsequently passes into the bulktank.

A hot wash after milking was carriedout once daily with inadequate amounts ofhot water, insufficient chemicals andblocked air injectors, and this resulted indeposits in the milk transfer line, as shownin Plate 10.6. The milker also failed to turnoff the plate cooler, which cooled the circu-

lating wash solutions. This accounted for thehigh LPC.

Once the wash cycle was modified, theBactoscan results fell to under 30,000/mlimmediately. The predominant cause of thehigh cell count was Staphylococcus aureus.This was identified from bacteriology of thehigh cell count cows and the fact that it wasthe older cows that had the high cell counts.Over a period of a year the cell count wasreduced to below 150,000 and many chronichigh cell count S. aureus cows were culled.

Herd C: high Bactoscan counts

The presenting problem in herd C was con-sistently high Bactoscan results of over70,000 in a herd that normally had excellentmilk quality and low levels of clinical mas-titis. Prior to being asked to investigate, the


Table 10.5. Bulk tank analysis for Herd B.

Streptococcus Total StaphylococcusColiform Pseudomonads uberis staphylococci aureus SCC


Target <5,000 <175 <20 <500 <200 <200 <50 <150Result 22,000 950 87 590 150 1,600 330 421

Differential bacterial screen Streptococcus faecalis +++Streptococcus dysgalactiae +Corynebacterium bovis ++Yeasts ++, Fungi +

Plate 10.6. Soil can be seen half way up the milktransfer line, caused by lack of turbulence duringthe wash cycle.

owner had stripped the parlour and platecooler and cleaned all areas thoroughly ashe thought it might have been due to a faultwith the wash-up routine after milking. Hehad also replaced all the rubberware in theplant.

The initial results failed to identify anyspecific problem that could be responsiblefor the high Bactoscan result, apart from aslightly raised LPC (190) and raisedPseudomonads, total staphylococci andS. aureus counts (Table 10.6). Also, the factthat the LPC was slightly raised did not seemto support a failure of washing sufficient tocause such a high Bactoscan. This sampledid not seem to support such high readingsas were found on the Bactoscan results.

A farm visit was arranged to check theacid boiling wash procedure; this showedthat the plant temperature was only 71°C,6°C lower than required for effective wash-ing. The boiler was serviced and wash tem-peratures adjusted, but the high Bactoscancounts persisted. Another bulk sample wascollected and showed low thermoduriccounts but a Pseudomonads count of over15,000/ml.

Water samples were collected from allthe water sources in the parlour and dairybut all tested negative. The only possiblesource of high levels of Pseudomonads wasfrom the chilled water from the bulk tankthat circulated around the plate cooler tocool milk rapidly. The plate cooler wasbypassed and the Bactoscan results immedi-ately fell back to their normal level of under10,000/ml.

It transpired that there was a pinpointleak in the plate cooler that allowed small

amounts of the chilled water contaminatedwith Pseudomonads to enter the milk as itpassed through the plate cooler.Pseudomonads are psychrotrophs and con-tinued to multiply in the bulk tank, andwere responsible for the high Bactoscan.This highlights the advantages of the differ-ential tests in diagnosing causes of the prob-lem, but also demonstrates the need to visitthe farm to see what’s happening.

While the herd cell count is 98,000/mland indicates good control of contagiousmastitis, the slightly raised counts forS. aureus and other staphylococci need to becarefully monitored.

Herd D: problems with teat preparation dueto large numbers of milkers

The 600 cows of herd D were milked threetimes daily through two separate parlours.Both groups had a very high mastitis rateand used up to seven different milkers. Poorteat preparation was one of the main prob-lems contributing to the high levels of clin-ical mastitis. Bacteriology results showedthat most clinical cases were environmentalin origin. Milkers blamed each other for fail-ure to prepare teats properly.

Milker schools were carried out duringweek 2 to provide a uniform agreed milkingroutine and to explain why changes werenecessary. Coliform counts were carried outin week 1 without the milkers’ knowledge.This showed that all the milkers, with theexception of Sean, had poor teat preparation.A league table was organized to rank milkersaccording to coliform counts (Table 10.7).This had an impact on most milkers, and

182 Chapter 10

Table 10.6. Bulk tank analysis for Herd C.

Streptococcus Total StreptococcusColiform Pseudomonas uberis staphylococci aureus SCC


Target <5,000 <175 <20 <500 <200 <200 <50 <150Result 11,000 190 3 995 70 325 65 98

Differential bacterial screen Streptococcus faecalis +

any who remained consistently high wereassigned other duties outside the parlour.

This approach stopped milkers blamingeach other, highlighted Sean as a consis-tently good milker and removed Martin from

the milking team. The other three milkershave been shown that their improvementsfollowing the milking school have paid divi-dends in their performance, with a concur-rent reduction in clinical mastitis cases.


Table 10.7. Coliform counts for Herd D.

John Sean Martin Mike James

Week 1 35 8 944 28 142Week 2 24 20 254 22 95Week 3 15 12 165 25 18Week 4 18 16 18 14Week 5 12 9 12 17Comment Improved Always a Stopped Improved Significant

clean milker milking Week 3 improvement

This chapter examines the different ways inwhich mastitis can be recorded and howrecords can be used to help identify thecause of mastitis. Target figures and the eco-nomics of the disease are discussed andsome examples are given of how herdrecords can be used.

Records are an important part inmonitoring the incidence of any disease.Mastitis is no exception. In fact, mastitis is oneof the few diseases where a detailed analysisof the data can be used to help in the controlof infection.

Many farmers rely on their cell countresults to give an indication of their mastitissituation, as their milk buyer providesthis information monthly. Many farmerskeep mastitis records, but these are notanalysed and so the incidence of clini-cal mastitis is often underestimated. Cellcounts do give useful information but havelimitations. High counts indicate the pres-

ence of subclinical mastitis, especially thatdue to Staphylococcus aureus, Strepto-coccus dysgalactiae and Streptococcusagalactiae. Unfortunately, cell countsdo not necessarily bear any relation tothe clinical incidence of mastitis. There-fore, it is important to have and make use ofaccurate clinical records; otherwise there islittle benefit to be gained from keeping thedata.

Mastitis records will enable the farmerto do the following:

� Identify cows whose milk needs to bewithheld from the bulk supply.

� Identify problem cows that should be con-sidered for culling.

� Allow detailed monitoring of the herdmastitis performance to check that it iswithin acceptable limits and to see howthe herd compares with others being mon-itored.


11 Targets and Monitoring

Record Keeping 185Mastitis Targets 185

Mastitis rate 185Percentage of herd affected 185Recurrence rate 187Milking cow tube usage 188Seasonal variation 188Stage of lactation 188

What Does Mastitis Cost in My Herd? 189Herd Examples 190

Herd A 190Herd B 191

� Gain valuable information that can pointtowards the possible cause of mastitis out-breaks and other problems.

Record Keeping

The following should be recorded for eachcase of mastitis:

� Cow number.� Date.� Quarter/s infected.� Treatments given and number of tubes of

antibiotic used.� Bacteriology results (if available).

One case of mastitis is defined as one quar-ter infected once. A cow that calves downwith mastitis in all four quarters thereforecounts as four cases of mastitis. If a treatedquarter clears up but mastitis recurs 7 ormore days after the remission of clinicalsigns, then this is defined as a new case ofmastitis. If mastitis recurs in the same quar-ter less than 7 days after the remission ofclinical signs, then this is defined as a con-tinuing case of mastitis.

Mastitis cases can be recorded in a var-iety of ways (see Fig. 11.1). Ideally, sub-sequent cases of mastitis should be recordedadjacent to the first case so that problemcows are readily identified. In the firstmethod of data layout, shown in Fig. 11.1(a),it can easily be seen that cow 32 has hadrepeat cases of mastitis. Although exactlythe same information is given using the sec-ond method, shown in Fig. 11.1(b) it is notimmediately apparent that cow 32 is such aproblem.

Mastitis records should be checkedregularly and cows with four or more casesshould be considered either for culling fromthe herd or for having the offending quarterdried off.

An alternative, more visual system, canbe used, as shown in Fig. 11.2. Here thecows are recorded on a bar chart on amonthly basis. The cow number and quarterare entered on the chart and a monthly targetcan be added. In this example, it can be seenthat the incidence is above target from

November to April, which coincides withhousing.

Record analysis will allow the mostappropriate control measures to be put intoplace. It is important that these data areanalysed regularly. Every 6 months is ideal,as it will help to identify possible problemsand trends. Economic data can also beincluded to cost the benefits or losses frommastitis, together with Bactoscan and cellcount penalties.

Mastitis Targets

Table 11.1 gives a range of figures thatshould be achievable within a herd, that isthe targets to be aimed for and the level atwhich some action or interference should betaken.

Mastitis rate

The mastitis rate is the number of cases ofmastitis per 100 cows per annum. It is aninvaluable measure of the mastitis incidenceas it allows comparison between herds irre-spective of size. A mastitis rate below targetmeans that the herd has good control of clin-ical mastitis. Of course, this is assuming thatall cases of mastitis have been accuratelyrecorded.

The mastitis rate can be worked outusing the formula below:

Mastitis rate =No. of cases of mastitis per year x 100

Total no. of cows in herd (milking and dry)

A high mastitis rate indicates a high numberof mastitis cases in the herd but does notidentify what type of infection is present, i.e.contagious or environmental.

Percentage of herd affected

The percentage of cows affected per yearrepresents the proportion of the herd thathave had one or more cases of mastitis overa 12-month period. This helps to give some

Targets and Monitoring 185

indication of the type of mastitis present. Onthe one hand, chronic recurring mastitis,caused by Staphylococcus aureus, couldaffect a small percentage of the herd, butthere may still be a high mastitis rate. Thismay occur because the same cows keep get-ting repeat cases of mastitis in the samequarter. On the other hand, an outbreak ofcoliform environmental mastitis is likely to

186 Chapter 11

(a)

Cow Date Quarter

69 22.5 LH32 25.5 LH + RH73 2.6 LF32 3.7 LH4 15.6 LF

17 12.8 LH + RH32 15.8 LH + RH4 17.9 RF

17 21.9 RH + RF166 25.9 RH99 3.10 LF32 23.10 LH37 14.11 LH91 21.11 RH

(b)

Fig.11.1. Two forms of mastitis recording. (a) Thetop system more readily identifies the problem cowsas all information relating to the same cow isrecorded on one line. (b) In the chart belowseparate cases of mastitis in the same cow are notrelated back to each other as they are in the topchart

Table 11.1. Target and interference levels fordifferent mastitis and milk quality parameters.

Parameter Targets Interference

SCC 150,000 200,000Bactoscan 20,000 30,000Mastitis rate (cases per100 cows per year) 30 40Percentage herdaffected 20 25Recurrence rate 10 20Milking cow tubes percow per year 1.4 2.5Milking cow tubesper case 4.5 6.0Percentage drycow mastitis 1.0 2.5

result in a larger percentage of the herdaffected but relatively few repeat treatmentsin the same quarter. Herds with severe prob-lems with environmental mastitis can have35% or more of the herd affected.

The percentage of cows affected peryear can be worked out using the followingformula:

Percentage cows affected =No. of cows that have had mastitis over a

12-month period × 100Total no. of cows in the herd

(milking and dry)

Recurrence rate

The recurrence rate is the percentage ofquarters requiring one or more repeat treat-ments over a 12-month period. A repeattreatment refers to one or more cases of mas-titis recurring in the same quarter. The recur-rence rate can be worked out using thefollowing formula:

Recurrence rate =No. of mastitis quarters requiring

repeat treatment × 100Total no. of quarters affected

For example, in Fig 11.1 cows 32and 17 have both had quarters requiringone or more repeat treatments. Cow 32had two recurring quarters (the leftand right hind (LH and RH)) and cow 17had one (the right hind (RH)). The totalnumber of quarters needing one or morerepeat treatments is therefore three –two (LH and RH) for cow 32 and one forcow 17 (RH).

So, looking at the cows in Fig. 11.1,there have been 18 cases of mastitis ina total of 13 quarters. Three of thesequarters have had one or more repeat treat-ments and so the recurrence rate is3/13 × 100 =23%.

A high recurrence rate may be due toproblems with Staphylococcus aureus orStreptococcus uberis infections, which areoften difficult to treat. High rates can also bedue to poor mastitis detection, where infec-tions are not picked up early and so theresponse to treatment is poor. Likewise, ifthe treatment regime is ineffective, such astoo short a duration of treatment or theincorrect selection of antibiotic, then casesmay also recur.


Fig.11.2. Monthly mastitis records.

Jan Feb Mar Apr May Jun Jul Aug Sep Oct Nov DecMonth

No.

of c

ases

Monthly target

Milking cow tube usage

The number of milking cow tubes used inthe herd will depend on the number ofcases of mastitis, the number of tubesused to treat each case and whether any highcell count cows were treated with intram-mammary tubes during lactation. Althoughmost manufacturers recommend threetubes per case, the average usage is closerto five to six tubes per case. A high numberof tubes used per cow per year, e.g.over 6, could indicate one or more of thefollowing:

� A high incidence of clinical mastitis.� Infection that responds poorly to treat-

ment.� Not all cases of mastitis have been

recorded.� A high number of high cell count cows

treated in lactation.� Mastitis tubes used for reasons other than

for treating mastitis.

As the total tube usage is not collectedfrom farm data (it comes from your vetand/or pharmacist), the tube usage figuregives a useful indication of the accuracy offarm data.

Many veterinary practices now havecomputerized accounting systems that cangive the number and type of intramammarytubes supplied over a given period of time.The number of milking cow tubes used percase of mastitis and per cow is worked outusing the following formulae:

No. milking cow tubes per case =No. tubes used

No. cases mastitis

No. tubes per cow =No. tubes used per yearTotal no. of cows in herd

Seasonal variation

It is useful to examine mastitis incidence bymonth of the year. A high number of casesin the housed period suggests a problem dueto environmental mastitis, while year-roundincidence may suggest a problem with con-tagious mastitis. It is helpful to work out thepercentage of cases that occur during thehoused period, as this is the period of great-est risk of environmental mastitis. Figure11.2 shows the seasonal trends of clinicalmastitis in one herd, clearly with the major-ity of mastitis occurring during the housedperiod.

Stage of lactation

Analysis of mastitis according to stage of lac-tation can be very helpful. This informationis only likely to be able to be extracted fromherds that record on a computer systemwhich can analyse mastitis data.

If there is a peak of mastitis around thetime of calving, this suggests problems withorganisms such as Streptococcus uberis andE. coli, as shown in Fig. 11.3. In this herd, itcan be seen that 15% of all cases occur withina week of calving. These relate to dry periodinfections and the conditions in which thecows are kept during the dry period andaround calving. Also, 25% occur between 61and 100 days, which coincides with peak lac-tation. These figures suggest that there aremany issues with cows in early lactation andfurther investigation is required.

More than half of all cases of mastitisare expected to occur within the first 100days of calving as this relates to the effect ofdry period infections, calving, peak yieldand the highest production stress on thecow. If mastitis occurs all the way throughlactation, then this suggests that there maybe other factors that are influencing mastitis,such as defective milking machine functionor poor hygiene.

188 Chapter 11

What Does Mastitis Cost in my Herd?

Mastitis and milk quality costs are easilyquantified. They include:

� Penalties from cell count.� Penalties from Bactoscan.� Increased clinical mastitis.� Reduced yields.� Any costs relating to a bulk tank antibiotic

failure.

Mastitis is one of the few diseases wherethese losses can easily be calculated, andtwo herd examples are discussed at the endof this chapter. Penalties from the cell countand Bactoscan can easily be added up frommilk statements. Alternatively, you multiplythe penalty by the average yield per cow andthe number of cows in the herd. So a herd of150 cows with an average yield of 8000 litreslosing 0.3 p.p.l. (pence per litre) from thecell count and 0.2 p.p.l. from the Bactoscanis losing a total of 0.5 ppl of milk. If you thenmultiply this by 8000 litres it comes to a lossof £40 per cow per year. The herd cost is £40times 150 cows, which is £6000 per year.

Of course, this does not take intoaccount any effect of reduction of milk yieldfrom the high cell count herds, or the

culling, the treatment of problem cows or thetime spent trying to manage the problem.

For clinical mastitis, the costs are moredifficult to work out. They include:

� Discarded milk.� Medicine costs.� Labour.� Veterinary fees.� Any deaths.� Reduction in yield for the rest of

lactation.� Risk of spread to other cows.� Culling and loss of genetic potential.

The milk discarded is easy to work out byadding the duration of treatment to the with-drawal period and multiplying by the aver-age yield of the cow. For example, if a cowwith clinical mastitis giving 40 litres per dayis treated for 5 days, and then has a milkwithdrawal period of 4 days, then her milkwill be out of the tank for 9 days and thetotal milk loss will be 360 litres. This canthen be multiplied by the milk price. Somefarmers discount these costs, as this milkmay be fed to calves. However, many regardit as inadvisable to feed mastitic milkto replacement heifer calves, as this mightcontribute to problems with antibiotic


Fig.11.3. Incidence of mastitis by days calved.

20

25

30

0

5

10

15

Mas

titis

cas

es (

%)

0–7 8–30 31–60Days calved

61–100 101–200 201 +

resistance, although there are no firm data tosupport the existence of this risk.

Medicine costs and labour should beeasy to quantify. Many farmers estimate thata simple case of mastitis slows down milk-ing. Time is spent milking the cow sepa-rately, administering any medication,completing the farm records and ensuringthat the milk does not enter the bulk supply.

There is a reduction in milk yield fol-lowing mastitis. Mild cases can result in a10% reduction in yield and more severecases 25%, and toxic cases may result incows not producing any milk whatsoever.The cost of this reduction in yield is alwaysunderestimated. If you take a cow with amild case of mastitis in one quarter, in a cowyielding 8000 litres, that quarter will have areduction in yield of 200 litres.

Often average figures are quoted forclinical mastitis, which may be too high ortoo low for some herds. It is always worthworking out the costs of discarded milk,treatment and labour for an average case as abenchmark figure. An allowance then needsto be added to cover the costs of reducedyield for the remainder of lactation, and alsothe culling, death and veterinary fees.

Herd Examples

Herd A

The mastitis data for herd A are shownbelow and relate to a 12-month period. Thefarmer requested help in dealing with hiscell count problem, from which he was los-ing 1 p.p.l. He has kept accurate records andhas used his milking cow tubes only fortreating clinical mastitis.

Herd size: 150 cowsNumber of cases of mastitis: 188Number of cows affected with mastitis: 68Total number of quarters with mastitis:125Number of quarters with one or morerepeat treatments: 42Number of intramammary tubespurchased: 750Average yield per cow: 8000

Mastitis rate =188 (cases of mastitis) × 100

(150 cows in herd)= 125 cases/100 cows/year

Percentage of herd affected =68 (no of cows affected) × 100 = 45%

150 (cows in herd)

Recurrence rate =42 (quarters repeating) × 100 = 34%125 (quarters with mastitis)

No. of milking cow tubes per cow per year =750 (tubes) = 5.0150 (cows)

No. of tubes per case per year =750 (tubes) = 4.0188 (cases)

Mastitis rate 125Percentage of herd affected 45%Recurrence rate 34%No. of tubes/cow/year 5.0No. of tubes/clinical case 4.0Herd cell count 280,000

The mastitis rate of 125 shown aboveindicates major problems with clinical mas-titis and is more than four times the targetlevel of 30. The farmer had no idea of theextent of his clinical mastitis problem. Hedid keep records, but these were neveranalysed. He was very surprised at the levelof infection. This is a common finding inherds in which there is no regular analysis oftheir mastitis records.

As 45% of the herd has had one ormore cases, this suggests that there areissues with environmental mastitis. Furtherrecord analysis shows that 60% of all casesoccured during the housed period – 5months of the year – again suggesting thatclinical mastitis is due more to environ-mental bacteria.

The recurrence rate of 34% is very highand suggests that there is a problem eitherwith Staphylococcus aureus orStreptococcus uberis infections, poor masti-tis detection and/or a poor treatment regime.The herd has a high cell count and so we

190 Chapter 11

know that there are problems with subclini-cal mastitis, suggesting that Staphylococcusaureus or Streptococcus uberis would beprevalent in this herd. The cause of clinicalcases (and, of course, of high cell count) willneed to be confirmed by bacteriology.

Economics of mastitis for herd A

The milk buyer is deducting 1 p.p.l. or 4% ofthe milk price due to the high herd cellcount. If you multiply milk yield (8000litres) times financial penalty (1 p.p.l.) thisworks out at £80 per cow per year. Multiplythis by the number of cows in the herd (150)you get a total loss of £12,000. This is morethan the cost of the farmer’s veterinary billsand medicine costs.

The farmer estimates that each case ofmastitis costs £125. He treats cows for anaverage of 3 days, with a 4-day milk with-drawal period, and so milk is discarded fora total of 7 days. The average yield of cowswith clinical mastitis is 40 litres and so foreach clinical case he is discarding 280 litresat an average cost of 25 p.p.l., which is £70.

Medicine costs for a case average £25 (ashe injects his cows as well as using intra-mammary tubes) and he has allowed £10 forlabour. These three costs alone come to £105and he has not made any allowance for anyreduction in yield for the remainder of lac-tation, or for toxic cases or any culling thatmay result from persistent cases. It is likelythat he has underestimated the cost of clini-cal mastitis.

Clinical mastitis cannot be eradicatedbut, over a period of time, we may be able toattain the target mastitis rate of 30 cases per100 cows per year, or 45 cases in the herdper year (there are 150 cows, so you multiplythe target figure by 1.5). This means that wewould save a total of 143 cases at a saving of£17,875 (143 cases × £125/case). While itmay take some time to achieve this, as theremay be issues with accommodation or themilking parlour, the savings do help thefarmer to focus on the true losses and alsohelp him make any decisions on capitalexpenditure.

So, for this herd, if the cell count andclinical mastitis issues are resolved, there is

a potential to increase profit by £29,875 peryear (£12,000 plus £17,875), which is equiv-alent to almost £200 per cow, or to a milkprice rise of 2.5 p.p.l. (10% of the currentprice). So, while the farmer initially calledfor help for his cell count problem, as thiswas easily identified from his milk state-ment, he was totally unaware that the great-est economic loss came from the high levelsof clinical mastitis in his herd.

Herd B

This is a 200-cow herd yielding close to9000 litres which is housed from Novemberthrough to the end of April. The mastitisdata have been analysed and the results areas follows:

Mastitis rate 73Percentage of herd affected 54%Recurrence rate 12%No. of tubes/cow/year 2.6No. tubes/clinical case 3.5Herd cell count 120,000

Figure 11.4 shows the seasonality ofclinical mastitis, along with a baseline show-ing the average monthly target of five clinicalcases: the target is for a mastitis rate of 30cases per 100 cows per year, and so, as thisherd has 200 cows, this would be 60 casesper year or five per month. Figure 11.5shows the distribution of clinical casesaccording to days calved.

The mastitis rate of 73 shows significantproblems with clinical mastitis. Over 50%of the herd has had clinical mastitis, whichsuggests problems with environmental mas-titis. The herd cell count is 120,000, whichsuggests little problem with contagious mas-titis.

Figure 11.4 confirms environmentalinfections, with 69% of all cases occurr-ing during the 6-month housed period.Figure 11.5 shows that 27% of all clinicalcases occur within the first week of calving,suggesting problems with dry period infec-tions, such as Streptococcus uberis andE. coli, and possibly poor managementaround calving, However, if the herd


had problems with S. uberis, the herdcell count would be higher and so it ismost likely that the problem is due to E. coliand other coliform infections. The farmerhad two cows die with postcalving E. colimastitis, which is the most severe form ofmastitis.

The recurrence rate of 12% is slightlyabove target; however, the herd cell count islow, at 120,000, indicating very good control

of subclinical mastitis. There are likely to befew problems with Staphylococcus aureusor Streptococcus uberis. But there could besome cows in the herd that are infected witheither of these bacteria. An average of 3.5tubes per case are used and this suggests thatthe response to treatment is adequate.Bacteriology is required to confirm thatE. coli is the predominant cause of clinicalmastitis.

192 Chapter 11

Fig.11.4. Monthly mastitis cases in herd B. Blue bars indicate housed period, light blue bars non-housedperiod.

Fig.11.5. Clinical cases by stage of lactation in herd B.

15

Num

ber

of c

ases

20

25

0

5

10

J F M A M J J A S O N D

Monthly target

Month

0

5

10

15

20

25

30

0–7 8–30 31–60 61–100 101–200 201 +

Days calved

Num

ber

of c

ases

(%

)

Economics of mastitis for herd B

There are no cell count or Bactoscan penal-ties for this herd. The herd owner estimatesthat each case of mastitis is costing him £200due to the fact that two cows have died withclinical mastitis in the past year, and fourothers have either dried up or lost quarters.He also realizes that there is a significant pro-

duction loss for the remainder of lactation.Mastitis cannot be eradicated but, in time,

there is no reason why the mastitis rate cannotdrop from 73 down to 30. This is a saving of43 cases per 100 cows. The owner has 200cows and so will save 86 cases of mastitis at£200 each, which is £17,200 each year, or £86per cow per year, equivalent to a milk priceincrease of almost a penny per litre.



12 Treatment and Dry Cow Therapy

Treatment Overview 195Reasons for Treatment 195Treatment During Lactation 195

Separation of the mastitic cow 195Technique for the administration of intramammary antibiotics 196

Antibiotic Therapy 197Is antibiotic treatment worthwhile? 197Choice of Antibiotic 199

Antibiotic sensitivity and udder penetration 199Response of coliforms to antibiotics 201Effectiveness in milk 201Bactericidal and bacteriostatic antibiotics 201Acidity and lipid solubility 202Intracellular effects 202Withdrawal period 202

Benefits of Early Treatment 202Combination Antibiotic Therapy (Concurrent Injection and Tubing,

Aggressive Therapy) 203Drying Off Quarters 204Resistance of Staphylococcus aureus to Treatment 205Blitz Therapy Against Streptococcus agalactiae 206Supportive Therapy 206

Fluid therapy 207Anti-inflammatory drugs 208Administration of calcium 208Administration of glucose 208Continual stripping and oxytocin 208Non-antibiotic intramammary infusions 209Topical preparations 209Homoeopathy 209

Dry Cow Therapy 209Long-acting antibiotics 210Treat all quarters 211Teat sealants 212Administration of dry cow tubes 212Infusion technique 213

While much of this book focuses on the pre-vention and control of mastitis, the textwould not be complete without some refer-ence to treatment. The main objective oftreatment is to reduce or eliminate infectionfrom the udder.

Treatment Overview

Mastitis treatments can be administered at twodifferent stages in the cow’s lactation cycle:

� Lactating cow therapy is administered tocows while they are in milk.

� Dry cow therapy, administered the daythe cow is dried off, attempts to: (i) removethose infections accumulated during thelactation, i.e. to prevent carry-over to thenext lactation; and (ii) to reduce the num-ber of new infections contracted duringthe dry period.

Mastitis treatment can be administered bydifferent routes:

� Intramammary treatment is infused intothe udder through the teat canal.

� Parenteral treatment is given by injection.

Reasons for Treatment

Irrespective of the cause of mastitis, there areseveral reasons why some form of treatment(not necessarily antibiotic) should be insti-gated as soon as a cow is clinically affected.These are:

� To prevent the spread of infection to othercows.

� To restore the productivity of the cow,thereby allowing her milk to be sold.

� To prevent the mastitis from getting anyworse.

� To reduce the probability of recurrentcases.

� To avoid long-term and possibly irre-versible udder damage, which would havea deleterious effect on yield and milk qual-ity (i.e. cell count and TBC/Bactoscan).

� To improve overall cow health and wel-fare.

Treatment During Lactation

It is the milker who will first recognize acase of mastitis and it is usually the milkerwho will make many of the decisions relat-ing to treatment. This chapter is there-fore written with this person very much inmind. Foremilking and other procedures toassist in the prompt recognition of clinicalmastitis are described in Chapter 6, whichshould be read in conjunction with thissection.

Separation of the mastitic cow

Ideally, as soon as a clinical case has beenidentified, the mastitic cow should be separ-ated from others to prevent the spread ofinfection. In large herds, this may consist ofphysically removing the cow to a mastitic or‘hospital’ group, which is then milked last,and where treatment is administered. Insmaller herds, the affected cow should becarefully identified, e.g. by a leg or tail bandor udder spray, and then milked through aseparate cluster and into a dump bucket(Plate 12.1) or dump line.

Treatment and Dry Cow Therapy 195

Plate 12.1. A dump bucket with separate claw.

The advantages of separating the mas-titic cow into a separate group are:

� Treatment can be administered more care-fully and recorded.

� It reduces the risk of transfer of infectionto other cows.

� It reduces the risk of antibiotic contam-ination of the bulk tank.

If the cow is in a separate group, thenthe milker has sufficient time to admini-ster intramammary antibiotics care-fully, record which cow has been treatedand possibly take her temperature tosee if additional parenteral therapy (byinjection) is needed. During milking,there is much more pressure on themilker and a greater risk that mistakes willbe made.

An infected cow (and especially oneinfected with Staphylococcus aureus) willcontaminate teat liners and can transmitinfection to the next six to eight cowsmilked. Milking her last, or through aseparate cluster, avoids this, providedthat the mastitic cluster is disinfected,e.g. by soaking it in hypochlorite solution,before milking the next mastitic cow; other-wise infection can still be spread. This isoften overlooked and is particularly impor-tant if the same cluster is also used to milkfreshly calved cows, whose milk is beingdiscarded because of colostrum or dry cowantibiotic.

Avoiding antibiotic residues is dis-cussed in Chapter 15. When milking mastiticcows last or using a separate bucket andcluster, there is a lesser (or zero) risk of con-taminating bulk milk with antibiotic fromtreated quarters. Some parlours have a dumpline, as already described, through whichcolostrum and mastitic milk pass into a sep-arate collection vessel. However, they maystill have no separate cluster. This is verydangerous – you would need to avoid onlyone extra case of mastitis to pay for an addi-tional cluster.

Technique for the administration ofintramammary antibiotics

This should be done as carefully and ascleanly as possible. Rough handling can leadto teat canal damage, which in turn predis-poses to mastitis. Administration of antibi-otic through a contaminated teat end mightintroduce a yeast infection, which is partic-ularly difficult to cure. The following proce-dure is suggested:

1. Carefully mark the cow to show that shehas been treated with antibiotic. Mostfarms would put this as the final step,but, having known of cases where thewrong cow has been treated (and then notknown which cow this is), it is recom-mended that this is done first. A varietyof marker sprays, leg tapes and tail bandsare used.

2. Ensure that both the milker’s hands andthe affected teat are clean and dry. Wash,if necessary, and then wipe dry with aclean paper towel.

3. Swab the end of the teat with methylatedspirits or alcohol, until it is clean, i.e.until the swab can be rubbed across theteat end without becoming soiled. Thismay take more than one swab (Plate 12.2).

196 Chapter 12

Plate 12.2. Swab the teat end until it is clean.Ideally gloves should be worn.

4. Remove the cap of the antibiotic tubeand, without touching its tip with yourhand, gently insert it into the teat canal(Plate 12.3). It is not necessary to insertthe nozzle to its full depth: in fact, to doso could dilate the teat canal excessively,thereby cracking its protective keratinand lipid lining (see page 22) and predis-posing the cow to mastitis. Partial inser-tion is also recommended (particularlyfor dry cow therapy) because it enablessome antibiotic to be left in the canalitself. Some manufacturers are now pro-ducing antibiotic tubes with very smallnozzles to achieve partial penetration andreduce teat-end damage (see Fig. 12.1).However, if the cow is nervous or diffi-cult to handle, full penetration may beunavoidable.

5. Hold the tip of the teat between the fin-ger and thumb of one hand and then usethe other hand to massage the antibioticup into the teat and udder cistern.

6. After administration, dip all four teats.This is important for both lactating anddry cow therapy. Tubing the cow, how-ever carefully, dilates the teat canal andhence the extra protection of a dip is veryvaluable. In addition, it is probable that,even if only one quarter has mastitis, dur-ing the milking process infection mayhave spread to the teat orifice of the other

three quarters. This infection can beremoved by thorough teat disinfection.

7. Record the treatment in the medicinesbook (a legal requirement in the UK) andelsewhere as necessary (see pages186 and 242).

Antibiotic Therapy

Is antibiotic treatment worthwhile?

This question has to be answered beforeselecting the antibiotic to be used. There is abody of opinion that considers that anti-biotic treatment of some types of mastitisduring lactation is simply not worthwhile.The reasons given for this are:

1. The response of Staphylococcus aureusinfections to treatment is very disap-pointing (see Table 4.4). Although theclots and other clinical signs may disap-pear, there may be only a 20–35% bac-teriological success rate.

2. Many cases of mastitis undergo self-cure,i.e. the infection is naturally eliminated


Fig. 12.1. Long and short nozzle tubes: the shortnozzle (right) is preferable, as it will preventunnecessary damage of the teat canal.

Plate 12.3. Inserting an intramammary antibiotictube.

by the cow without treatment. This is par-ticularly likely with coliform infections,where the response by the cow can be sodramatic that in some cases all bacteriamay have been eliminated within 4–6hours (see page 29). However, even col-iforms occasionally establish themselves aschronic persistent udder infections.

3. The cost of the discarded antibiotic milkand the risk of antibiotic contaminationof the bulk milk are both so high that theyrender treatment uneconomic.

Many papers have been written on this sub-ject, some in favour of treatment, othersagainst. It is the opinion of the authors thattreatment is worthwhile. The main reasonsfor this are:

1. For certain infections the response toantibiotics is good.

2. Even for S. aureus the response rate isacceptable if the infection is detectedearly.

3. Response to treatment generally giveshigher bacteriological elimination ratesthan self-cure.

Cure rates for streptococci andStaphylococcus aureus

The response of Streptococcus agalactiaeand Streptococcus dysgalactiae infections to

treatment is generally good, although it isaccepted that, as was shown in Table 4.4,complete bacteriological cure rates forStaphylococcus aureus can be poor.However, if it is a first-time infection, thencure rates even for S. aureus may be reason-able. Table 12.1 is taken from NIRD work inthe 1960s and shows the bacteriological curerates for clinical S. aureus mastitis identifiedby the milker and treated with the antibioticcloxacillin. Note that, although overall bac-teriological cure rates were disappointing at38%, when cows were infected for the firsttime the cure rate was as high as 50%. Thiscertainly makes treatment worthwhile. Itwas only those cows that had had previousunsuccessful treatments both during lacta-tion and at drying off where the responserate was so poor, at only 6%. The ‘responserate to all infections’ includes all cowsinfected at the start of the trial plus thoseinfected during the trial, and hence the over-all lower response rate.

Self-cure rates versus antibiotics

The data in Table 12.2 are a summary of arange of clinical trial reports. They showthat, for streptococci, treatment gives a con-siderably better bacterial elimination thanself-cure. Even for S. aureus and coliforms,the cure rate following therapy was higherthan for self-cure. The highest rate of antibi-otic cure (35%) quoted in the table for S.aureus would relate to an average infection

198 Chapter 12

Table 12.1. Response rate of clinical cases of Staphylococcus aureus mastitis to treatment withcloxacillin.

Previous unsuccessful treatments New infections All infections

During lactation At drying off No. treated % eliminated No. treated % eliminated

0 0 283 50 452 411 0 63 22 131 18

>1 0 48 10 102 8

0 One or more 12 25 52 171 One or more 8 12 49 12

>1 One or more 17 6 72 5

Total infections 431 38 858 28

(see Table 12.1), and it is likely that, if allfirst-time clinical cases were treated aggres-sively, response to treatment wouldimprove.

Overall benefits of antibiotic therapy

In summary, it is considered beneficial totreat clinical mastitis using antibiotic ther-apy for the following reasons:

1. It produces a more rapid and higherbacteriological elimination than‘self-cure’.

2. It reduces the probability of chronicrecurrent infections.

3. It reduces the extent of milk yield depres-sion.

4. It results in a more rapid return to anacceptable cell count, and hence tosaleable milk.

If therapy saves one mastitis death, this paysfor many treatments.

Mastitis control is a ‘numbers game’. Itinvolves reducing bacterial challenge at theteat end, rather than totally eliminating it.Although antibiotic treatment may not elim-inate infection totally, it may reduce bac-terial numbers such that the risk returns tomanageable proportions.

Choice of Antibiotic

This is a huge subject and in itself consists ofsufficient material to fill a whole book. Thissection gives simple guidelines only. It doesnot lay down specific rules for treatment, butrather points to the complexity of the sub-

ject and gives examples of a few of the fac-tors involved.

As is the case with the purchase of a car,there are numerous manufacturers, eachwith their own range of products and eachwith its own unique claims of effectiveness.Also, like cars, there are many products onthe market between which there is little tochoose in terms of value for money.

The following criteria should be con-sidered when making a choice of antibioticfor treatment:

� Antibiotic sensitivity of the bacteriainvolved.

� Ability to penetrate the udder.� Ability to persist in the udder at a con-

centration sufficient to kill bacteria fol-lowing single or multiple infusions.

� Effectiveness in the presence of milk.� Whether it is bactericidal (killing) or bac-

teriostatic (arresting growth).� Lipid solubility, plasma protein binding

properties and pH level in solution.� Withdrawal periods.� Cost.

There is an excellent article by MacKellar(1991) that gives much more detailed infor-mation.

Antibiotic sensitivity and udder penetration

The following section discusses some of theproperties of commonly used antibiotics andtheir spectrum of action. These are summa-rized in Table 12.3.

Penicillins

As a general rule, penicillins are effectiveagainst Gram-positive bacteria (staphylo-cocci and streptococci, but not against Gram-negatives (coliforms, etc.). Most penicillinspenetrate the udder reasonably well.Examples include:

� Penicillin G.� Penethamate.� Cloxacillin.� Nafcillin.


Table 12.2. Spontaneous versus antibiotic curerates for mastitis.

Spontaneous Antibioticcures cures

Staphylococcus aureus 20% 20–35%Streptococcus agalactiae 19% 36–95%and S. dysgalactiaeColiforms 70% 71–90%

Penethamate has better udder penetrationthan the rest of the group, and is marketedas a specific treatment against Streptococcusuberis. When in the udder, it undergoes achange to penicillin G before it starts its bac-terial killing. As it is not effective againstcoliforms or beta-lactamase strains ofStaphylococcus aureus, it needs to be usedselectively.

Unfortunately, many (approxi-mately 70%) mastitic strains of S. aureusare now penicillin-resistant, becausethey have adapted to produce the enzymebeta-lactamase. This enzyme breaksdown the beta-lactam ring structureof penicillin. Cloxacillin and nafcillinare effective in the presence of beta-lactamase and, despite widespread usein dry cow therapy preparations overthe past 40 years, to date, no staphy-lococci have been found that are resistantto these drugs. Cloxacillin and nafcillinare therefore suitable treatments for drycow infections caused by staphylococci(see Table 12.6). However, they are noteffective against coliforms, which are Gram-negative.

Some penicillins have been syntheti-cally modified so that they have some effectagainst coliforms, namely:

� Ampicillin.� Amoxycillin.

However, these two drugs are still not effec-tive against beta-lactamase producingstaphylococci. Clavulanic acid is an irre-versible inhibitor of beta-lactamase, and bycombining clavulanic acid with amoxycillin,provides a product which should be effec-tive against the vast majority of mastitic bac-teria. Other combination products thatshould, theoretically, achieve good udderpenetration and be effective against allorganisms are a mixture of cloxacillin (killsGram-positives and beta-lactamase produc-ing staphylococci) plus amoxycillin (killsGram-positives and Gram-negatives) orcloxacillin plus ampicillin.

Aminoglycosides

The aminoglycoside group of antibiotics,are:

� Streptomycin.� Neomycin.� Framycetin.

They are active against coliforms andeffective against beta-lactamase producing

200 Chapter 12

Table 12.3. The spectrum of action of common antibiotics.

Beta-lactamase FastidiousGram-positive Gram-positive Gram-negative Gram-negative

Antibiotic bacteriaa bacteriaa,b bacteriac bacteriad

Penicillin + – – +Penethamate + – – +Cloxacillin + + – +Amoxycillin + – + +Amoxycillin + clavulanic acid + + + +Streptomycin – – + +Erythromycin + + – +Cephalosporins (3rd generation +)e + + + +Tetracyclines + + + +Tylosin + + – +

aGram-positive bacteria include staphylococci, streptococci, Bacillus species.bBeta-lactamase producers include Staphylococcus aureus.cGram-negative bacteria include E. coli, Pseudomonas, Klebsiella.dFastidious Gram-negative bacteria include Pasteurella, Moraxella, Bordetella, Actinobacillus.eCephalosporins include cephoperazone and cefquinome. Third- and fourth-generation cephalosporins have a greatereffect against coliforms.

staphylococci. They have poor penetra-tion of the udder tissue. One of theirstrengths is that they are relatively inexpen-sive. As penicillins achieve good penetrationof the udder, products containing penicillinand streptomycin are often used incombination.

Cephalosporins

Cephalosporins are active against Gram-negative and Gram-positive bacteria, includ-ing beta-lactamase producing staphylococci,although penetration of the udder is not asgood as with the penicillins. ‘Secondgeneration’ cephalosporins, for examplecefuroxine, have improved activity againstGram-negatives, whilst ‘third-generation’products, for example, cefquinome, have theadded advantage of some effect againstPseudomonads.

Tetracyclines

Tetracyclines are broad-spectrum, that is,they are effective against Gram-negative andGram-positive bacteria, with some activityagainst beta-lactamase producing staphylo-cocci. However, penetration of the udder tis-sue is limited (although this can beovercome by using very high dosages) andresistance may occur with coliforms.

Response of coliforms to antibiotics

Coliforms have a variable sensitivity toantibiotics, and standard texts (Tyler andBaggot, 1992) show how wide this can be.For example, in two reports the range ofsensitivity to tetracycline varied from23 to 68%. For ampicillin the range was35–64%. As a herd outbreak of E. coli mas-titis (the most common of the coliform types)always involves a range of different strainsof E. coli, precise guidelines regarding themost effective antibiotic to use on the basisof the sensitivity of a single bacterial isolatecannot be given. Gentamycin is effectiveagainst both E. coli and Klebsiella, but thecost of treatment is usually prohibitive, witha very long withdrawal period.

Whichever preparation is decided uponfor routine use (and this must be a joint deci-sion between the farmer and his vet), the fol-lowing factors are important when selectinga preparation for routine ‘first line’ treat-ments:

� Due to the increasing incidence of coli-form mastitis (see Table 4.2), lactationtreatments should always involve a broad-spectrum antibiotic, e.g. one that is effec-tive against Gram-positive (i.e.staphylococci and streptococci), Gram-negative (e.g. coliforms) and beta-lactamase producing organisms.

� Although preparations used in dry cowtherapy were originally aimed primarily atstaphylococci and streptococci, coveragainst coliforms is an advantage.

Effectiveness in milk

Although the antibiotic sensitivity plate testis used to assess response, many antibioticsare less effective in the presence of milk thanthe test suggests. For example, the ratio foroxytetracycline is 4:1. This means that oxy-tetracycline is four times less effective in thepresence of milk than it is in the plate test.Other examples include streptomycin (5:1),erythromycin (7:1) and trimethoprim/sulfa-diazine (500:1). However, these figures wereobtained in experiments using whole milkand results may not apply to mastitic milk,which has a higher pH than uninfected milk.

Bactericidal and bacteriostatic antibiotics

Antibiotics vary in the way they act. Some,for example, the penicillins, specifically killbacteria (they are bactericidal). However,others, for example, the tetracyclines, sim-ply prevent bacterial growth and multipli-cation (they are bacteriostatic) and rely onthe cow’s own defence mechanisms to over-come the infection. If the cow is freshlycalved or if she is very sick, the activity ofher defence mechanisms may be compro-mised, and bacteriostatic antibiotics may notbe appropriate. In such cases, the use of


bactericidal antibiotics may be preferable, asthe innate immune response is then lessimportant. The counter-argument to this isthat bactericidal antibiotics may lead to sud-den bacterial death and the release of endo-toxins (especially with coliform infection;see page 45), making the clinical conditionmore severe.

Acidity and lipid solubility

Antibiotics are either acidic or basic,depending on their pH when in solution.Because the pH of milk (6.7) is lower thanthe pH of blood (7.4), drugs such as tylosin,erythromycin, trimethoprim and tilmicosin,which are naturally more alkaline, will bedrawn into the mammary gland and pene-trate the udder. They are likely to be mosteffective in the active udder, because duringthe dry period the pH difference is less. It isfor this reason that the use of these productsis recommended more during lactation, atdrying off or at the start of the next lactation,rather than in the dry, inactive udder.

When the udder becomes inflamed, asin severe mastitis, the pH of milk increasestowards the pH of blood, and this pH trapbecomes less important.

The lipid solubility and the degree towhich antibiotics bind to proteins in bloodwill also affect their ability to penetrate theudder, particularly following intravenous orintramuscular injection.

Intracellular effects

Certain bacteria, for example,Staphylococcus aureus and Streptococcusuberis, are able to penetrate and exist insideneutrophils and macrophages, where theyare protected against the action of manyantibiotics. They remain in a quiescent intra-cellular state until they become active at alater date to produce a repeat case of mas-titis. Some manufacturers claim that certainantibiotics can penetrate cells and reachquite high intracellular concentrations,thereby eliminating the carrier state.Examples include tylosin, which is said to

reach an intracellular concentration tentimes higher than that of the surrounding tis-sue fluid.

Withdrawal period

Post-treatment milk- and meat-withholdingperiods are stated on the product and mustalways be observed. Although the majorityof the antibiotic remains in the treated quar-ter, some will diffuse into the bloodstream,pass around the body and be deposited backinto the untreated quarters. This is becausethere is a very high blood flow through theudder (400–500 litres of blood for each litreof milk produced). When the affected quar-ter is inflamed, flow rates may be evenhigher. Milk must therefore be discardedfrom all four quarters, even if only one quar-ter is being treated.

The withdrawal period given on thetube relates to the use of that tube as statedin the instructions. If the herdsman decidesto use an increased frequency of tubing,administers two tubes at the first treatmentor injects the cow with antibiotic in additionto tubing her, then this could affect therequired withdrawal period. Further detailis given in Chapter 15. If in doubt, ask yourvet. In the UK a few products, e.g.cefoquinone, have a licence for combinationtherapy, and milk-withholding periodsare specified. Further details are given onantibiotic residuesin Chapter 15.

The ability of an antibiotic to persist inthe udder at bacteria-killing concentrationsdepends partly on the chemical nature of theantibiotic and partly on its formulation. Forexample, products with a long persistency,as would be required for dry cow therapy, areformulated in slow-release oils or waxes, ormanufactured with a much smaller particlesize. Conversely, aqueous preparations aregenerally shorter-acting, with a low persis-tency but a short milk-withholding period.

Benefits of Early Treatment

If an initial infection can be treated earlypost-infection, then response to therapy is

202 Chapter 12

likely to be improved. This was demon-strated for the field cases of Staphylococcusaureus described in Table 12.1. Early treat-ment has also been shown to be more effec-tive under experimental conditions (Milner1997). Teats were dipped in a culture ofStaphylococcus aureus or Streptococcusuberis, and various methods were used todetect signs of infection. The first evidenceof infection was bacteria cultured from themilk (approximately 1 day after exposure),the second an increase in milk cell count (2days), the third a rise in milk conductivity(3 days) and the fourth as clinical signs (4–5days after infection). It was found that, iftreatment was instigated early, i.e. whenchanges in milk conductivity were detected,then both clinical and bacteriologicalresponse rates improved. Results are shownin Table 12.4. Fewer tubes were used fortreatment, and milk yield depression wasless if treatment was instigated early.

This is good evidence to promote:

� Foremilking, as this enables the earlydetection of clinical cases and hence moreeffective treatment.

� Treatment of cows with rising cell counts,i.e. before they become clinical.

The same experiment also showed that ittook around 2 weeks for the cell count of aconventionally detected and treated infectedquarter to fall below 400,000, despite the fact

that clinical and bacteriological cure hadbeen achieved well prior to this. The signifi-cance of a prolonged milk discard from suchcows is obvious.

Combination Antibiotic Therapy(Concurrent Injection and Tubing,

Aggressive Therapy)

In some countries, mastitis is treated only byparenteral therapy (i.e. by injection), and inthese countries treatment is considered to beequally effective whether antibiotic isadministered as an intramammary tube or byinjection.

In the EU, injections are increasinglyadministered at the same time as intramam-mary tubes. This is known as ‘combinationtherapy’ and, if continued for a longer periodof time, or at a higher dose level, it isreferred to as ‘aggressive therapy’. It hasbeen estimated that the surface area of theudder is 25 sq.m per quarter and, if this iscorrect, then it is perhaps not surprising thatintramammary therapy does not reach allparts of the udder.

Results of a trial demonstrating theadvantages of injecting penicillin at thesame time as using amoxycillin intra-mammary tubes in the treatment ofStaphylococcus aureus mastitis is shown inTable 12.5), where cure rates increased from


Table 12.4. Experimentally it has been shown that early treatment (evidenced by an increase in milkconductivity) of mastitis produces a more effective response than conventional treatment (evidenced byclinical changes in the milk) (Milner, 1997).

Conventional treatment (clots seen) Early treatment (conductivity)

Experimental infection with Streptococcus Staphylococcus Streptococcus Staphylococcusuberis aureus uberis aureus

Clinical cases seen 8/8 6/6 0/8 0/8No. of tubes used to resolve 8 10 6 6.5clinical signs or reduce conductivityNumber of cows with low 7/8 1/6 3/8 1/8yields at 14 days post-treatmentSomatic cell count at treatment 12 million 4 million 2 million 2 millionNumber of milkings (days) 31 (14.5 days) 35 (17.5 days) 17 (8.5 days) 14 (7 days)before cell count of affectedaffected quarter fell to <400,000

25 to 51% when additional parenteraltherapy was used. This treatment would notbe effective against beta-lactamase produc-ing staphylococci.

Aggressive primary therapy certainlyreduces the incidence of recurrent andchronic infections, and will be especiallyused in animals that are pyrexic (have a hightemperature) or sick. Aggressive therapy,e.g. 5–7 days of concurrent intramammarytubes and injectable antibiotic, has also beensuggested for the treatment of chronicallyinfected cows or cows with a high cellcount. Others have suggested 5 days of‘milking cow’ intramammary treatment, fol-lowed by drying off with dry cow antibiotictreatment.

Drying Off Quarters

It is known that in some 5% of quartersexisting infections ‘self-cure’ during the dryperiod, and there is evidence that the longerthe dry period the greater is the probabilityof self-cure. From this, a technique for thetreatment of chronic recurrent cases of mas-titis has developed (Blowey and Deyes,2005). Quarters that have had four or morecases of clinical mastitis in a lactation arebest dried off, so that the cow can continueto be milked on three quarters. While thereare obvious disadvantages of having three-quartered cows in the herd, if the alternativeto drying off a quarter is to cull the cow (avery expensive option), then clearly a three-quartered cow is acceptable.

The main advantages of drying off quar-ters are as follows:

� The cow continues in production.� Infected milk no longer increases the SCC

and TBC/Bactoscan of the bulk milk.� It reduces the risk of spreading infection

to other cows.� Following a prolonged dry period, plus

dry cow antibiotic therapy, the quarteroften returns to normal production in thenext lactation.

� It does not require the cost of antibioticsused in aggressive therapy.

The technique used by most herdsmen is togive the cow one final intramammary treat-ment using lactating tubes, e.g. for her fourthclinical case, then simply stop milking theaffected quarter. Do not use dry cow therapyat this stage because of the risk of antibioticresidues.

When the remaining three quarters arethen dried off at the end of lactation, all fourquarters are given dry cow therapy plus aninternal teat sealant. Some herdsmen alsouse an internal teat sealant when the quar-ter is dried off. In a survey of 4326 cows in16 dairy herds using a variety of techniquesto dry off the quarter, 125 cows had hadquarters dried off, and the overall successrate, defined as cows returning to normalproduction in the next lactation, was 66%(Blowey and Deyes, 2005). However, if onlythose cows that were treated with antibioticat drying off the quarter and then again atdrying off the cow were included, the suc-cess rate rose to 92%. The majority of thesecows also had a low cell count and no majorpathogens in the next lactation.

Partial drying off of quarters has beenattempted as a treatment. A chronic recurringclinical case is treated for 3–5 days and thennot milked for 3–4 weeks. These cows willcome back into production again in the samelactation, although milk needs to be discardedfor the first few days because the initial cellcount will be very high. This technique is lesseffective than the longer dry period.

Temporary cessation of milking is agood technique for cows with teat damage,and is discussed later in this chapter.

Drying off the affected quarter or thewhole cow, or culling, is still the only cer-tain way of removing chronic carriers.

204 Chapter 12

Table 12.5. Advantages of injecting penicillinintramuscularly concurrently with amoxycillinintramammary tubes. (From Owens et al., 1988.)

3 days3 days amoxycillin

amoxycillin intramammary +intramammary penicillin IM

No. of quarters 40 35% cured 25 51

Resistance of Staphylococcus aureus toTreatment

Staphylococcus aureus (also known ascoagulase-positive staphylococci) gives anotoriously poor response to treatment. Thiswas demonstrated in Table 4.4 and again inTable 12.2. Even with dry cow therapy,response is poor (Table 12.7).

This is particularly the case in oldercows, where the infection has been presentin the udder for some time. (Tables 12.1 and12.8).

There are several reasons for the disap-pointing response of staphylococci to treat-ment. These include:

� S. aureus forms abscesses within theudder. A typical example is shown inPlate 4.2. These abscesses are often sur-rounded by a thick fibrous capsule. Thisprevents the antibiotic from reaching thebacteria, or insufficient antibiotic concen-tration is achieved within the abscess tokill bacteria effectively.

� Some strains of S. aureus can live withincells such as macrophages. Most antibi-otics are only able to circulate in the bodyfluids surrounding cells and are not ableto penetrate the cell itself. Those staphy-lococci that live inside the cells are henceprotected from the majority of antibiotics.(A few antibiotics can penetrate cells – seeprevious section – but in the UK these arenot yet available as intramammary prepa-rations.)

� Many strains of S. aureus producebeta-lactamase, making them resistantto certain types of penicillin. Evenwhen effective antibiotics are used, how-ever, response to treatment is still verypoor.

� Some strains of S. aureus can persist in astate of bacterial dormancy with a mucoidcapsule and completely cease multiply-ing. In this state they are not killed byantibiotics, although they can reactivate ata later date.

� L forms of S. aureus may occur. Theseare bacteria that do not have a propercell wall and therefore most antibioticswill not kill them. This includes

cloxacillin and other antibiotics thatare effective against beta-lactamase pro-ducing strains. (The antibiotic novo-biocin is effective.) However, there is somedoubt whether L forms of S. aureus areproduced under the conditions present inthe udder.

One of the difficulties with assessingresponse to treatment for S.aureus is that,following a course of antibiotic therapy,many quarters initially appear to haveresponded and no bacteria are isolated froma milk sample. However, this is simplybecause no S.aureus are present in that par-ticular sample. If the same cow is sampledat a later date, bacteria may have beenreleased from an abscess or an intracellularsite, or they may have been revived fromtheir dormant state, and it is then found thatthe cow is still infected, i.e. treatment wasnot effective.

This is clearly demonstrated inTable 12.6. When cows infected withS. aureus were sampled 16 days after treat-ment, it was found that bacteria were stillpresent in only 43% of treated quarters, sothe success rate was 57%. However, if sam-pled again at 30 days, bacteria were isolatedfrom 56% of the treated cows, and thisincreased to 62% of cows (only a 38%response) if sampled at 60 days post-treatment.

These results were obtained in a trialusing combined intramammary andinjectable antibiotics. If only intramammarytreatment was used, then the response at60 days was even lower (27%).

Table 12.6. The results obtained in trialsassessing the response rate of Staphylococcusaureus to treatment with antibiotics.

% cows withNo. of days Staphylococcus % response toafter treatment aureus treatment

16 43 57

30 56 44

60 62 38


Blitz Therapy Against Streptococcusagalactiae

The response of Streptococcus agalactiae totreatment is totally different from that ofStaphylococcus aureus. Streptococcusagalactiae is very sensitive to many anti-biotics and response to treatment, even dur-ing lactation, is generally very good (Tables12.2 and 12.4). This allows a system knownas ‘blitz therapy’ to be used in the elimina-tion of S. agalactiae from milking herds.Control of S. agalactiae is also discussed onpages 42–43.

Blitz therapy involves the use of intra-mammary antibiotics infused into all fourquarters of every milking cow in the herd.Two forms are used: total – where the entiremilking herd is treated – and partial – whereonly selected animals are treated, e.g. thosethat have a high cell count and are culture-positive. Bacteriology of high cell countcows is essential to confirm that S. agalactiaeis the primary cause of the high cell counts.It is not acceptable to simply rely on posi-tive bulk tank samples, as these do not givesufficient detail on the extent of theinfection.

In order for this technique to be suc-cessful, S. agalactiae must be the major organ-ism responsible for the mastitis problem, andall aspects of milking hygiene must bereviewed. As discussed earlier in this book,the presence of S. agalactiae in a herd is anindication that there is a fault in basichygiene, e.g. inappropriate postdippingand/or dry cow therapy, as these measureswill normally eliminate the infection from aherd.

Future replacement cows may be a pos-sible cause of reinfection, and many recom-mend that newly purchased cows are treatedwith intramammary antibiotics before theyjoin the milking herd. Any dry cows notbeing milked at the time of the ‘blitz’ shouldbe given dry cow therapy if it has not beenadministered previously.

Scrupulous hygiene is needed to ‘blitz’a herd. Extra help is needed in the parlour,and it is essential that teat ends are thor-oughly disinfected before any tubes areadministered. Do not remove the caps of the

intramammary tubes in advance (e.g. forspeed of administration in the parlour) asthis increases the risk of contamination priorto infusion. There have been several docu-mented cases where severe outbreaks ofmastitis have followed blitz therapy, andthese can often be traced back to suboptimalhygiene. If the introduced organisms areyeasts or fungi that do not respond well totreatment, the overall herd situation can bemade much worse.

Blitz therapy is not always successful.There are many reasons for this, for exam-ple:

� Infected cows may be reintroduced intothe herd.

� The milkers become careless with basicparlour hygiene and allow residual infec-tion to spread within the herd.

� Dry cows may not have received dry cowtherapy and so may reintroduce infectioninto the milking herd.

� When using partial or selective blitz ther-apy, some infected cows are not selectedfor treatment and so a reservoir of infec-tion remains within the herd.

� Other organisms, in addition toS. agalactiae, were the cause of mastitis,and the therapy chosen was not effectiveagainst these other organisms, or theyshowed a poor response rate

� A total error in diagnosis, in thatS. agalactiae was not the main pathogenin the herd.

� Infection was introduced during the masstubing, and this led to increasedmastitis.

Although blitz therapy is a useful technique,therefore, it should only be undertaken fol-lowing a thorough investigation of the herdproblem, and even then with strict attentionto aseptic techniques.

Supportive Therapy

In addition to antibiotics, a wide range ofother treatments have been suggested for dif-ferent types of mastitis. These include fluidtherapy and supportive therapy, such as the

206 Chapter 12

use of anti-inflammatory agents and oxy-tocin.

Fluid therapy

Toxins, particularly those produced bycoliform and gangrenous staphylococcalmastitis, can cause a state of shock andaffect many body organs. Blood vesselsdilate and as a result blood pressure starts tofall. Falling blood pressure leads to poor cir-culation and consequently poor tissue per-fusion with blood. The animal appearsdehydrated, as its body fluids are in the tis-sues and not in its circulation. Dehydrationmay frequently reach 7–10% of body weight.This means that, for an average 600 kg cow,40–60 litres of fluid need to be replaced torestore the circulation to normality.Dehydration further increases the feeling ofmalaise and general ill health of the cow.Administration of fluids, especially in ani-mals that will not drink, can be of consider-able benefit.

Fluids may be administered in a varietyof ways.

Intravenous administration

As the rate of intravenous administration isslow, this can be a time-consuming andtherefore expensive exercise. Firm fixationof the intravenous catheter is required, andas such should only be undertaken by vets.Sometimes a small garden pump is used. Aneffective intravenous solution can be pre-pared by mixing a proprietary packet of oralelectrolyte powder with warm tap water.This should help to restore normal meta-bolic activity.

Some people recommend the intra-venous administration of 2.0 litres hyper-tonic (concentrated) salt solution (70 g perlitre NaCl). This stimulates extreme thirst inthe cow and encourages her to drink.However, if the technique is used in recum-bent cows, it is obviously vital that water isfully accessible. Extreme care is needed dur-ing the infusion to monitor for shock.

Oral administration

Provided that the cow will drink, one of thesimplest ways of administering oral fluids isvia a watering can, as in Plate 12.4. If elec-trolyte solutions (that is, calf scour formula-tions) containing bicarbonate are given, theymay stimulate closure of the oesophagealgroove, transferring the fluid directly intothe abomasum, where its absorption is moreeffective.

A faster way of administering large vol-umes of fluid (e.g. 10–20 litres) is by using anoral pump, as shown in Plate 12.5. The tubeis protected from the cow’s teeth by flexiblemetal rings and held in place by nose clips(‘bulldogs’). Fluids are pumped into therumen via a stirrup pump from a bucket.


Plate 12.4. Oral fluids are easily administered usinga watering can.

Plate 12.5. Oral pump fluid apparatus: (A) flexiblemetal tube to insert through mouth and intooesophagus, (B) nose clips hold the tube in position,(C) pump, which is placed into the bucket of oralfluids.

C

BA

Provided that cows will drink volun-tarily, it is difficult to see how addi-tional benefit is obtained from forciblefluid administration. However, onepoint is important and that is that water(preferably warm) should always bereadily available to a sick cow. If she isrecumbent, this means offering her warmwater five to six times daily, within easyreach. Cows will also readily drink elec-trolyte solutions.

Anti-inflammatory drugs

In addition to the use of fluids, shock canalso be counteracted by the use of anti-inflammatory drugs, such as flunixin,meloxicam, aspirin or cortisone. Thesedrugs are not licensed for use in dairy cowsin all countries and therefore the specificinstances for their use should be confirmedwith the regulatory authority. Cortisonegiven locally or parenterally reducesswelling and the inflammatory response, butit may also allow greater bacterial multipli-cation. However, there are no experimentaldata to support this.

Many commercial intramammary prod-ucts contain 10 mg prednisolone (a form ofcortisone), which is aimed at reducing thehardness and swelling in the affected quar-ter. This perhaps permits better antibioticpenetration. Some cows with a typical hardquarter 4 to 5 days after a coliform infectionrespond well to larger doses of cortisone,either by injection or by infusion into theudder. Intramammary infusion of cortisonemay not be legal in some countries and abor-tion may be induced.

Administration of calcium

Some sick cows are naturally hypocalcaemic(have low blood calcium) and, if dealingwith a case of acute mastitis at calving, it isnot always possible to be sure if a concur-rent hypocalcaemia is present. Calcium isalso said to aid detoxification processes inthe liver. For this reason, 400 ml of calciumborogluconate, possibly mixed with glucose

(as dextrose), is sometimes given to sickmastitic cows.

Administration of glucose

Cows with acute E. coli mastitis can behypoglycaemic (have low blood glucose)and may benefit from intravenous dextroseinfusions (oral glucose is of no value, as it isdestroyed in the rumen). In addition, thephagocytic activity of macrophages in theudder, i.e. the way in which white cellsengulf bacteria is relatively poor, due to lowoxygen concentrations in milk.

It has been suggested that the infusionof dextrose into the udder promotes phago-cytic activity. Evidence supporting this islimited. Great care needs to be taken toensure that the teat canal is not damaged andthat yeasts and other organisms are notaccidentally infused, making the mastitisworse.

Continual stripping and oxytocin

The toxins produced by mastitic bacteriaeither are absorbed by the cow (possiblymaking her ill) or can be stripped out of theudder manually. Clearly the latter is prefer-able; hence the importance of regular strip-ping of the affected quarter, maybe six oreight times daily, or more for very sick cows.Some people suggest stripping every 30–60minutes until the cow is better.

The efficiency of stripping can beimproved by giving oxytocin injections,which help to eject milk from the deeperparts of the gland. Natural let-down is highlyunlikely to occur in a sick cow, and even ifthe affected cow is very ill, there is likely tobe a considerable amount of residual milk inthe alveoli and small ducts and this, plus itstoxins, could be removed using oxytocin.Used at a higher dose rate, oxytocin is alsosaid to promote neutrophil movement out ofthe capillaries, and hence aids in the inflam-matory response.

Others have suggested leaving a strongsuckler calf with the cow to do the strippingfor you. However, if the quarter is painful the

208 Chapter 12

cow might resent the calf sucking and onlyallow the normal unaffected quarters to bestripped out. In addition, the calf is lesslikely to suck a quarter containing bittermilk. The value of this technique is thereforea matter of conjecture.

Non-antibiotic intramammary infusions

The use of iodine preparations against yeastand fungal mastitis was described onpage 55. Others have suggested infusinginfected quarters with 20 ml of natural liveyogurt at 12–hourly intervals for 2 to 3 days.The objectives are to decrease the raised pHof mastitic milk and to eliminate residualmastitis organisms by the probiotic effect ofnatural lactobacilli in yogurt. The procedurehas apparently been used successfully intreating yeast and coliform infections.

Topical preparations

Products such as Cai-Pan Japanese pepper-mint oil (‘Uddermint’) have been recom-mended for topical application (that is, toareas of the udder skin). They certainlystimulate warmth in the skin, leading toincreased blood flow, but whether this canbe translated into increased blood flowthrough the udder is difficult to assess. Ifsuch products improve the feeling of well-being in the affected cow (udder massagecan be soothing) and lead to attention beingpaid to (and stripping of) the affected quar-ter, then they are worth using. As with somany mastitis preparations, clinical trialsare difficult to carry out because a propor-tion of cases self-cure.

Homoeopathy

Homoeopathic medicine states that a sub-stance that produces the symptoms of an ill-ness can also be used in the treatment of anyillness that causes similar symptoms.Homoeopathic remedies are all obtainedfrom natural sources. The system relies on aseries of dilutions being made, one part

mother tincture to 99 parts of water andalcohol mixture. The mother tincture is anextract of natural substances, e.g. of a cultureof the bacteria that originally caused thesymptoms. Dilutions are repeated, and it issaid that all impurities are filtered out, leav-ing only a more potent preparation withmore energy. It is apparently this ‘energy’and not the material dose of the initialpreparation that is critical and many ‘rem-edies’ have been diluted down to well belowsubmolecular levels.

The value of homoeopathic mastitistherapy remains questionable. At present ithas the attraction of offering treatment with-out a milk withdrawal period. Lay homoeo-pathic advisers stress the concurrent need toprevent infections and promote the basicprinciple of sealing the teat canal betweenlactations, which is also the principle onwhich mainstream dry cow preparations arebased.

Homeopathic nosodes (remedies) usedto ‘prevent’ mastitis are administered indrinking water, by drenching and evenspraying them into the vulva. Althoughthere are plenty of anecdotal reports show-ing a benefit, specific trial work is lacking.The one controlled trial carried out(Egan, 1995) showed no benefits. Perhaps, ifthe herdsman adds a ‘remedy’ to the drink-ing water each day, he ‘thinks’ mastitis eachday, and this also results in improvedcontrol.

Dry Cow Therapy

The physiology of the udder at drying offand the importance of new infections duringthe dry period were discussed in Chapter 4,which needs to be read in conjunction withthe following. This section deals with thecontrol options available.

Although opinions may vary concern-ing the value of treatment during lactation,there are few who would doubt the wisdomof dry cow therapy. Dry cow therapy consistsof two parts:

1. The administration of a long-actingantibiotic into each quarter at drying off


to remove existing infections and preventsome new infections.

2. The infusion of an internal wax sealantinto the canal and base of the teat to pre-vent new infections.

Long-acting antibiotics

The aim of using long acting antibiotics atdrying off is twofold, namely: (i) it reducesthe reservoir of contagious organisms thathave accumulated over the previous lacta-tion; and (ii) it reduces the number of newinfections likely to be contracted during theensuing dry period.

In Fig. 4.3, it was shown that most newinfections occur during the first and the last2 weeks of the dry period. Dry cow therapywill help to reduce the number of new infec-tions at drying off, but by the time of the nextcalving, antibiotic levels will be quite lowand probably ineffective (the exception tothis is a product containing the antibioticframycetin, which it is claimed, persists atbacteria-killing levels throughout).

In a comparison of treated and non-treated cows, Berry and Hillerton (2002)showed that cows given dry cow therapy:

� Produced 179 kg more milk during thefirst 120 days of the next lactation.

� Had a tenfold reduction in clinical mas-titis in the dry period.

� Showed a threefold reduction in infec-tions at calving.

� Had a threefold reduction in clinical casesin the first 21 days after calving.

The benefits of dry cow therapy are thereforeobvious:

� No milk is discarded.� Response to treatment is much more effec-

tive during the dry period than during lac-tation (Table 4.4). This is partly becausemuch higher doses of antibiotic can beinfused into the dry quarter without con-cerns over witholding milk. The differ-ence is particularly apparent for Staphy-lococcus aureus, where response to lacta-tion treatment may be especially poor.

� A concurrent ‘self-cure’ takes place duringthe dry period, which is why many quar-ters dried off early return to normal milkproduction in the next lactation.

� Longer-acting antibiotic preparations canbe used to improve the efficacy of action.Slow-release dry cow products are pre-pared by incorporating the antibiotics intowaxes, by using benzathine or aluminiumsalts, or by manufacturing a product witha much smaller particle size.

� It provides some protection against sum-mer mastitis (see Chapter 13).

Dry cow preparations should be effectiveagainst S. aureus (including beta-lactamaseproducers), as these are carried in the udderfrom one lactation to the next, and againstcoliforms and Streptococcus uberis, whichmay be contracted as new dry period infec-tions. Table 12.7 shows the results of a 1990sIrish survey of 294 cows (1176 quarters)found to be infected at drying off. It is likelythat Staphylococcus aureus levels would belower than this in most herds under currentUK conditions.

Table 12.7. Intramammary pathogen types andresponse to treatment in cows at drying off. (FromMeany, 1992.)

No. of % %Bacterium quarters of total response

Staphylococcus aureus 259 61 48Other staphylococci 27 6 78typesStreptococci 118 28 78Combined 12 3 42staphylococci andstreptococciE. coli 5 1 –Non-specific 4 1 –

Total 425 100

S. aureus was once by far the most com-mon organism isolated at drying off,although the incidence of Streptococcusuberis is now increasing in some countries.The drugs most commonly used in dry cowpreparations are therefore those that are

210 Chapter 12

most effective against Staphylococcusaureus. These are:

� Cloxacillin.� Cephalosporins.� Nafcillin.� Combination pencillin/streptomycin pro-

ducts.

Some people suggest that dry cow prepara-tions should be changed occasionally, toavoid the development of antibiotic resist-ance. As no strains of S. aureus have everbeen found resistant to cloxacillin orcephalosporins, no benefit is likely to beobtained from changing the antibiotic,although additional antibiotic cover to pre-vent new coliform infections during the dryperiod would be logical.

Frequently, failure of dry cow therapy isnot the fault of the drug, but rather of theway in which it is used and administered.Despite the fact that dry cow tubes containlarge amounts of antibiotic, they will notnecessarily eliminate bacteria accidentallyinfused into the udder at the time of admin-istration as a result of poor hygiene.

Treat all quarters

All quarters should be treated at drying off(blanket dry cow therapy) and not just thosewhich had clinical mastitis during the previ-ous lactation, or those with high cell counts(selective dry cow therapy). This is because:

� Many cows infected during lactationnever show clinical signs.

� Some cows may become infected but donot show a particularly high or consis-tently elevated cell count.

� Even in cows with quite low cell counts,e.g. 200,000, this may be the result of threequarters with a cell count of close to zero,but one quarter obviously infected with acell count of close to 800,000. Chronicforms of Streptococcus uberis are oneexample of this. Even Staphylococcusaureus does not consistently produce highcell counts (see Table 4.5).

� Every attempt should be made to preventthe establishment of chronic S. aureus

infections. Table 12.8 shows that responseto treatment declines with age. The prac-tical conclusion to be drawn from this isto ensure that even first lactation heifersare given dry cow therapy. The longertheir udders can be kept free of S. aureus,the better.

� Cows are 15–20 times more likely to con-tract new infections in the first 2 weeks(and last 2 weeks) of the dry period.Antibiotic cover of all cows during asmuch of the dry period as possible istherefore likely to be highly beneficial.Because of the risk of antibiotic contam-ination of the milk after calving, full pro-tection clearly cannot be given during thelast 2 weeks of the dry period.

In one NIRD trial, in which dry cow therapywas not used, it was shown that:

� 25% of all quarters were infected at dry-ing off.

� 5% of these quarters shed their infectionnaturally, i.e. underwent self-cure.

� Another 10% contracted new infectionsduring the dry period. Hence 30% of quar-ters were infected at the start of the nextlactation (25 – 5 + 10 = 30).

In another trial, carried out in theNetherlands (Schukken et al., 1993),68 cows had only two quarters infused withdry cow therapy at drying off, while theirother two quarters were left untreated.During the dry period, there were ten cases


Table 12.8. Response of Staphylococcusaureus infections to treatment during the dryperiod. First and second lactation animalsrespond much better than older cows. (FromMeany, 1992.)

Lactation No. of cows % response tonumber treated treatment

1–2 51 633–5 99 37>5 40 33

Total 190 Average 43

of clinical mastitis in the untreated quarters,seven of which occurred in the first 2 weeksafter drying off. Only one case of mastitisoccurred in the treated quarters. This is fur-ther evidence of the benefit obtained fromgiving dry cow therapy to all animals.

Some say that continued use of dry cowtherapy will produce such low cell countsthat cows become excessively prone toE. coli mastitis. This is unlikely to be correct.The reasons for this are given on page 31.

Teat sealants

One of the major advances in mastitis con-trol over the past 10 years is undoubtedlythe introduction of commercially availableinternal teat sealants. This has dramaticallyreduced the incidence of mastitis in earlylactation.

Two types of teat seal are available toreduce dry period infections: the externalfilm sealant, which provides a flexible bar-rier film over the teat end for up to 7 days,and the internal teat canal wax plug. Theexternal seal is no longer commonly usedand will not be discussed in detail, althoughit can be used in the late dry period if nointernal seal has been administered.

The internal seal is by far the mosteffective and the most commonly used. It isa bismuth salt in a wax base that is infusedinto the teat canal at drying off. It has noantibacterial properties and hence stricthygiene during administration, as describedabove, is essential. Whereas antibiotic ismassaged up into the teat and gland cistern,when administering a teat sealant the baseof the teat should be constricted between fin-ger and thumb so that the sealant is confinedto the teat itself and ‘sits’ in the base of theteat just above the canal. Failure to do thismay lead to prolonged excretion of sealantin the milk during the next lactation andpossibly the formation of ‘black spot’ incheese, small foci of bismuth leading toharmless discolorations.

Teat sealants are commonly used inaddition to dry cow antibiotic tubes, inwhich case the antibiotic should be admin-istered first. The effects of teat sealants and

dry cow antibiotics on the incidence of mas-titis in the next lactation are additive, i.e. itis not a question of dry cow therapy or teatsealant, but rather of dry cow therapy andteat sealant. In a New Zealand study of 1200cows in seven herds, all with bulk milk cellcounts of less than 200,000, Woolford et al.(1998) divided the cows into four groups.The first was a negative control, i.e. no treat-ment at drying off. The second and thirdwere treated with either dry cow antibiotic(cephalonium) or a teat seal, and the fourthgroup was given a combined antibiotic(cloxacillin) and teat seal. Results confirmedthat:

� All treatments reduced clinical mastitis inthe next lactation by 50% compared withthe untreated controls.

� Incidence of new intramammary infec-tions decreased by tenfold.

� The combination of antibiotic and teat sealgave the best protection.

A similar trial in the UK, comparing dry cowtherapy plus teat seal with teat seal alone,showed a 30% reduction in the incidence ofnew infections in the first week of the sub-sequent lactation.

Administration of dry cow tubes

Cows should be dried off abruptly andremoved from the milking herd immedi-ately, even if they are still giving 20–25 litresof milk a day. If they continue to go throughthe parlour, milk let-down will be stimu-lated, i.e. the alveoli will contract, expellingmilk and inhibitor protein (see page 18),thus synthesizing more milk. In addition, ifdry cows are left running with the mainherd, there is a risk that one of them will bemilked inadvertently, leading to antibioticcontamination of the bulk tank. It should notbe necessary (or advisable) to limit food andwater severely, although for higher-yieldinganimals it is logical to stop feeding concen-trates 4–5 days before drying off, and pos-sibly change groups.

Cows with lower yields at drying off aremore likely to produce an effective teat seal.

212 Chapter 12

Gradual drying off is contraindicated for tworeasons. Incomplete milking allows bacter-ial proliferation in the teat canal before ther-apy and hence predisposes to mastitis. Inaddition, cows left unmilked for 1–2 daysdevelop large increases in cell count. In onetrial (Meany, 1992), a group of late lactationcows, with an average cell count of 237,000cells per ml, were monitored. When theywere left unmilked for 2 days, the cell countincreased to 540,000. After they had beenunmilked for 6 days, the average cell countincreased to 5,600,000 and in one individ-ual cow it rose to almost 17 million. Abruptdrying off is therefore important to maintainlow cell counts. Similarly, if a damaged teatis left unmilked for 7–14 days and allowedto heal, the first few milkings should be dis-carded.

Infusion technique

Dry cow tubes should be administered gen-tly and hygienically. Ideally, drying offshould be carried out as a separate job, e.g.split off the cows during morning milkingand then bring them back into the parlourafter breakfast for tubing. If cows are tubedduring milking there is too great a risk that itwill be done rapidly or unhygienically, orperhaps, even worse, the wrong cow will betubed. This has happened on several occa-sions. Cows have been dried off, the bulktank fails the antibiotic test the next day, andno one knows which of the 100 or 200 milk-ing cows was treated in error.

The technique for inserting an intra-mammary tube was described earlier in thischapter. Points specific to the administrationof dry cow therapy and internal teat sealantare as follows:

� Dry off cows in batches, making it a spe-cific task carried out after milking. Cowsneed to be split off during milking andthen infused after milking has finished. Ifdone during milking, the herdsman can-not concentrate properly on what he isdoing and hygiene may be compromised.

� Dry cow therapy should not be adminis-tered at the same time as routine foot-trim-

ming, as the operator’s hands are likely tobe badly soiled and the teats will probablybe splashed with faeces. Administerantibiotic to the whole group first, andthen do the foot-trimming as a separate joblater.

� Strict hygiene is essential, especially ifteat sealant is being administered alone, asthis has no antibacterial properties. Therehave been several reports of sick anddying cows following the unhygienicadministration of dry cow preparations.

� Hands should be clean and ideally glovesworn. It is essential to scrub the teat endwith surgical spirit or commercial wipes(e.g. Mediwipes) before administration.One cause of failure of dry cow therapy isthat bacteria are introduced as it is beingadministered.

� Swab the two teats furthest from you firstand then the two near teats. When tubing,infuse the two near teats first and then thetwo far teats. In this way contamination ofteat ends will be reduced.

� An alternative is to swab the two far teatsand administer the tubes and then swaband tube the two near teats.

� Only insert the nozzle a very short wayinto the teat or, even better, use a tube witha small, short nozzle (see Fig. 12.1). Excessdilation of the teat canal produces cracksin its lipid and keratin layers, therebycompromising its defence mechanisms. Inaddition, by squeezing the antibioticthrough the teat canal, rather than fullyinserting the nozzle, bacteria colonizingthe canal may also be killed. This may notoccur if the nozzle is inserted directly intothe teat sinus.

� Infuse the dry cow antibiotic first andwork this up the teat and into the udder.When infusing the teat sealant, hold thebase of the teat between your finger andthumb so that all the sealant is retained inthe teat.

� Ensure that teats are dipped immediatelyafter tubing, thereby removing any bac-teria that might be able to colonize the teatend and produce a new infection. A fewfarmers regularly dip cows throughout thedry period, or at least for the final 3 weeks.This is excellent practice. Others suggest


dipping teats after cleaning and thenadministering dry cow therapy through afilm of teat dip.

� Record dates of drying off and details ofthe tubes used. In addition to being a legalrequirement, it is important to know when

a cow has calved early, as an extendedmilk-discarding period may be required.

� Cows should be particularly carefullychecked for mastitis in the 5 days afterdrying off and, if possible, teat-dippeddaily.

214 Chapter 12


13 Summer Mastitis

The Bacteria Involved 215Mode of Transmission 216Clinical Signs 216Treatment 217Control 218

Reduce exposure 218Fly control 218Dry cow management 218

Summer mastitis has a very different aetiol-ogy and epidemiology from other forms ofmastitis and does not fit either the conta-gious or environmental categories listed onpage 36. It is essentially a disease of drycows and heifers, although very occasionallysteers, or even bulls, may be affected. Thedisease is common in temperate areas of thenorthern hemisphere, although the inci-dence varies enormously from one year tothe next.

One survey estimated that 35–60% ofherds in the UK are likely to experience thecondition each year, with approximately20,000 animals (or 1.5% of the nationalherd) affected. In some other countries innorthern Europe, the incidence is evenhigher; for example, in Denmark, it is 5.0%.It is therefore a significant problem.

The Bacteria Involved

At least six organisms have been isolated.These are:

� Arcanobacter (Corynebacterium) pyo-genes: this is the most frequent isolateand is the organism responsible for thesevere necrosis and destruction of thequarter.

� Peptococcus indolicus: ferments milk anddamaged tissue into organic acids andindole and is responsible for the charac-teristic foul smell.

� Streptococcus dysgalactiae: this may bethe primary infection, allowing A. pyo-genes to enter and/or proliferate in themammary gland. It is commonly found onflies and on damaged teat skin.

� Microaerophilic cocci: sometimes knownas Stewart–Schwann cocci.

� Bacteroides melaninogenicus.� Fusobacterium necrophorum.

However, by no means are all six organismsisolated from every case of summer mastitis.Table 13.1 shows the percentage of occa-sions on which each organism is isolated.A. pyogenes and P. indolicus are the mostcommonly isolated in the UK, whereas in

Denmark the Stewart–Schwann coccus ismore common.

Table 13.1. The percentage of occasions on whichdifferent bacteria are isolated in summer mastitiscases, in the UK, Denmark and the Netherlands.(From Hillerton, 1988.)

% isolated

Bacterium UK Denmark Netherlands

A. pyogenes 85 72 37P. indolicus 62 87 33S. dysgalactiae 24 37 8Stewart–Schwann 22 83 –

coccusF. necrophorum 1 51 22B. melaninogenicus <1 35 8

Mode of Transmission

The major means of transmission of infec-tion in the UK is thought to be by the sheephead fly, Hydrotoea irritans, which lives bysucking the blood of cattle. The fly preferswoods, copses and damp ground that is shel-tered from the wind. Larvae overwinter inlight, sandy soils and emerge as adults inJuly. They are present primarily during July,August and September, and these are there-fore the most common months for summermastitis. Cases may also occur in June andOctober, if the weather is exceptionally hotand humid. Eggs are laid into the soil inOctober, and there is only one generation ofadults each year.

The flies live in bushes and trees andonly fly out to feed on cattle when windspeeds are low (less than 20 km per hour)and in the absence of rain. Their favouredlanding areas are the legs, abdomen andudder. The fore teats are more commonlyaffected than the rear teats, possibly becausethe swishing tail removes flies from the hindteats.

Although there is considerable evidencethat H. irritans is a vector for summer mas-titis (and hence fly control is a major part ofprevention), there are still doubts about itbeing the only factor involved. This isbecause:

� Hydrotoea flies are often found in associ-ation with cattle, but without causingsummer mastitis. Possibly some other fac-tor simultaneous with the presence of thefly is required to damage the teat end: forexample, thorns, nettles, thistles or longgrass, another type of fly, or even cattlelicking themselves excessively.

� Summer mastitis can occur in parts of theworld where H. irritans is not present.

� Disease can occur in winter (usually asso-ciated with teat-end damage), when thereare no flies.

� Although many of the bacteria causingsummer mastitis can be found in the intes-tine of the fly and are regurgitated duringfeeding, experiments that attempt to trans-mit summer mastitis from infected flies tocows have been unsuccessful.Experimentally, it is possible to inducesummer mastitis by infusing A. pyogenesand P. indolicus through the teat canal.

One theory, therefore, is that the first case ofsummer mastitis occurs spontaneously, pos-sibly by infection tracking in from infectedteat sores, and subsequent cases are causedby flies spreading the infection. Outbreaks ofdisease do occur and hence there must besome vector, perhaps in association with areduction in the immune status of the ani-mal.

Clinical Signs

The classic symptoms of summer mastitisare a hot, hard and swollen quarter, usuallywith a tense and enlarged teat, as inPlate 13.1. The quarter is painful and thesecretion is thick and clotted, with a charac-teristic foul smell. More severely affectedcows have a raised temperature, are oftenlame because of the painful quarter and maydevelop swollen hocks. Some animals mayabort (summer mastitis primarily affectspregnant cattle), and others give birth to afull-term but retarded and weakly calf.Neglected cases may die, especially if drycows and pregnant heifers do not receive asmuch attention as they should. Prompt treat-ment is certainly important.

216 Chapter 13

In some cows and heifers, the disease isvery mild and is not seen during the dryperiod. It is only after calving, when a blind(i.e. non-functional) quarter is detected, thatprevious infection becomes apparent. Theseanimals have a thickened teat, with a fibrouscore running down the centre, replacing theteat cistern. This can be detected by rollingthe teat between your finger and thumb. It isworth comparing the feel with an adjacentnon-affected teat to emphasize the differ-ence. Attempts to infuse antibiotics oftendemonstrate how small the cistern hasbecome – much of the antibiotic will runback out under pressure.

A further syndrome, which hasincreased in frequency over the past fewyears, is seen in cows calving down withwhat appears to be a low-grade mastitis,with just a few clots at each milking. On cul-ture, this proves to be summer mastitiscaused by A. pyogenes. Presumably only avery small part of the mammary gland isaffected and it is only when the glandbecomes active, as at calving, that clinicalsigns appear. However, these cows often donot recover, even with high and prolongeddoses of antibiotic.

Treatment

The two main organisms causing summermastitis (A. pyogenes and S. dysgalactiae)

are both highly sensitive to penicillin, andhence penicillin and its derivatives are theantibiotics of choice for treatment. Even so,very few quarters ever recover. Intra-mammary tubes are of very doubtful value,but prompt parenteral (injectable) antibiotictherapy is essential, and can be combinedwith anti-inflammatory agents such as flu-nixin if the cow is sick. This will reduce thechances of abortion and death. Antibioticsneed to be continued for 4 to 5 days, or untilthe animal’s temperature has returned tonormal. If at all possible, the infected teatshould be stripped very regularly, especiallyduring the first 2 to 3 days. This may thenreduce the chances of an abscess burstingthrough the side of the udder, as seen inPlate 13.2. Pus discharge through the side ofthe udder is a normal part of the healingprocess in many cows, however. If it doesoccur, simply flush the affected area with anantiseptic solution, keeping the wound asopen as possible to allow it to drain. Mostcases will eventually heal and the animal isnot adversely affected. Once the temperaturehas returned to normal, further antibiotictherapy is likely to be of limited benefit.Some animals resent manual stripping andan alternative is to drain the udder by mak-ing a longitudinal cut through the teat, as inPlate 13.3 (anaesthetic is required and thevenous plexus at the base of the teat must beavoided.). Infection and pus then dischargefrom the teat. The environment is already

Summer Mastitis 217

Plate 13.1. A teat and quarter swollen with summermastitis. Sometimes the legs also swell.

Plate 3.2. Summer mastitis. When it is neitherpractical nor possible to strip the teat, the uddermay burst and discharge.

highly contaminated with A. pyogenes(which is a normal environmental organism)and so, provided the cow is removed fromthe group, to avoid fly-borne transmission,the risk is minimal. Even if the teat is notopened, the affected animal should alwaysbe removed from the rest of the group toavoid spreading infection to other cows.

Control

Prevention of summer mastitis is primarilybased on fly control, long-acting intra-mammary antibiotics and internal teatsealants. The most common measures are asfollows.

Reduce exposure

Keep susceptible cattle away from knownsummer mastitis pastures. Open fields onhigh ground exposed to wind and with aclay soil are ideal, as the sheep head fly dis-likes these conditions. Avoiding high-riskareas is probably the best controlmeasure.

Fly control

There are a variety of methods available, butmost rely on the flow of sebum over the bodysurface. However, the udder has no seba-ceous glands and so there is no flow ofsebum over teat skin.

� Pour-on preparations are applied along theanimal’s back, but also give poor teat pro-tection. In addition, during wet periods,when flies are most active, their persist-ence is reduced.

� Fly tags give good protection of the headand back, particularly if two are used, onein each ear. The abdomen and udder arestill not well protected, however, andthese are the favourite landing places forH. irritans.

� Sprays: one needs to be very conscientiousto achieve a thorough covering of eachanimal, including the udder.

� Micropore tape. Sealing the teat ends withtape has been used successfully on thecontinent, particularly in Denmark, but isnot popular in the UK. The tape is not easyto apply and has to be replaced every3 weeks.

� By far the best approach is to apply flyrepellent directly on to the udder and teatsevery week in high-risk areas. Althoughthis incurs a huge labour cost, only oneanimal has to be saved to make the effortworthwhile. In very high-risk areas, somefarms successfully use weekly applica-tions of a mixture of pour-on fly repellentand Stockholm tar, although such prepa-rations are, of course, unlicensed.Stockholm tar alone, regularly applied toteats, is also effective. Chlorhexidine teatdips combined with a fly repellent areavailable, although to be effective theymust be applied daily.

� Segregate and house affected animals; thisremoves an important source of infection.

Dry cow management

Dry cow antibiotic therapy undoubtedlyhelps, as most cases of summer mastitis

218 Chapter 13

Plate 13.3. When manual stripping is not possible,the teat can be drained by making a longitudinalslit. However, the cow will still be discharginginfection and needs to be removed from other drycows.

occur 4 or more weeks after drying off, inother words, when the antibiotic concentra-tions are declining. Measures include thefollowing:

� A combination of long-acting intra-mammary antibiotic and internal teatsealant would be ideal.

� In high-risk areas, some farmers repeatinfusions of dry cow antibiotic every 3 to4 weeks. However, this breaks the teat sealand hence may not be ideal. Careful atten-tion to expected calving dates is alsoneeded to avoid antibiotic contaminationof milk after calving.

� Heifers can be tubed, but the tip of thetube must be abutted against the teat ori-fice and the antibiotic squeezed throughthe teat canal under pressure, rather thaninserting the tube into the teat canal itself.Some farms have used internal teat sealanton heifers, with a New Zealand trial show-ing a 50% reduction in postcalving

mastitis. Care is needed to avoid teat canaldamage.

� House the late pregnant dry cows: H. iri-tans will not enter buildings and thereforethere is less irritation and nuisance inside.The cows can go out later at night, i.e. afterdark, when the fly is not active.

� Move the calving pattern to earlier in thesummer, so that there are fewer dry cowsin July, August and September.

� On some small farms the dry cows are runwith the milkers so that they can be teat-dipped and a watchful eye kept on theudder. Provided the dry cows are clearlyidentified (to avoid being milked), this formof control can prove to be very effective.

As approximately 20,000 animals areaffected in the UK each year, summer masti-tis continues to represent a major cost to thedairy industry. It seems extraordinary thatthere is no adequate technology to controlflies.

Summer Mastitis 219


14 Disorders of the Udder and Teats

Disorders Caused by Metabolic and Toxic Conditions 221Blood in milk 221Anterior udder sore/intertrigo/UMD 221‘Pea’ in teat 222Photosensitization 222Teat sunburn 223Udder oedema 223Single-quarter oedema 224Wet eczema/necrotic dermatitis/udder skin slough 224Ischaemic necrosis of the teat 224Single-quarter agalactia 226Chemical teat damage 226

Diseases with Infectious Causes 226Bacterial eczema 226Bovine herpes mammillitis 227Pseudocowpox 227Staphylococcal impetigo 228Summer sores (licking eczema) 228Teat warts 228Black spot 229

Disorders Caused by Physical Trauma 230Injuries from crushing of teats 231Cut teats 231Cuts penetrating the canal 232Total amputation 232

Teat Damage from Machine Milking 232Hyperkeratosis 232Teat scoring 233A parlour audit 234Teat oedema and teat-end wedging 235Teat ringing 236Teat chaps 236Teat-end haemorrhage and pressure necrosis 237

Machine Milking Factors Associated with Teat Damage 237Machine factors 237Milker factors 238

Mastitis is clearly the most common disor-der of the udder and teats, but the herdsmanwill encounter a wide range of other condi-tions. These may or may not be directlyrelated to mastitis, but any problem involv-ing the mammary gland has the potential ofincreasing susceptibility to mastitis. In addi-tion, a few of these disorders may be con-fused with mastitis. Some of the morecommon conditions are described in the fol-lowing section.

Disorders Caused by Metabolic andToxic Conditions

Blood in Milk

This is seen in freshly calved cows and canvary from a few clots of blood in the milkfrom one quarter (Plate 14.1) to almost pureblood coming from all four quarters(Plate 14.2). Some herds may experience avery high incidence of this problem infreshly calved cows, resulting in large quan-tities of milk being discarded. Althoughextensively investigated, often no cause isfound. In individual animals, blood in milkmay be the result of trauma at calving (thelegs bruising the udder during abdominalcontractions), excessive udder oedema, cowswith unusual gaits, or pendulous udders thatare knocked by the legs when walking. Inoccasional cases, rupture of the anterior

udder ligaments (see pages 8–9 and Plate2.3) can produce severe blood in the milk,and the blood may even discharge throughthe ruptured skin at the front of the udder.For treatment, most people recommend onlylight milking (sufficient to flush bacteriafrom the teat canal), thus producingincreased pressure within the udder, in anattempt to stop the bleeding.

Anterior udder sore/intertrigo/UMD

This condition, also referred to as ulcerativemammary disease (UMD), is often firstnoticed because of its purulent smell. A foul,moist, discharging area is seen at the front ofthe udder (Plate 14.3). The condition occurs

Disorders of the Udder and Teats 221

Plate 14.1. Blood in the milk: a mild case.

Plate 14.2. Blood in the milk: a severe case, withalmost neat blood drawn from the udder.

Plate 14.3. Necrotic dermatitis, also known asintertrigo and ulcerative mammary disease, UMD, isoften first noticed as a foul-smelling sore at the frontof the udder.

primarily in freshly calved cows, especiallyolder animals, with large deep folds of skinaround the front of the udder. The conditionis thought to be caused by an ischaemicnecrosis (death of tissue due to lack of blood)of the skin, resulting from severe congestionof the udder around the time of calving.Outbreaks have been seen in herds with dig-ital dermatitis, with typical spirochaetesseen on microscopic examination, but digi-tal dermatitis is not the only cause. No treat-ment is particularly effective, but thoroughlywashing the area with antiseptic, removingdead tissue and applying glycerine and anantiseptic or antibiotic ointment will help.

‘Pea’ in teat

The first sign of a ‘pea’ in the teat will bewhen one quarter is found to be full of milkafter the cluster has been removed. Hand-stripping will initially produce a few gooddraws, but flow suddenly stops. At thisstage, the ‘pea’, a thick pad of fibrousmaterial, has become lodged in the teat canal(Plate 14.4). A variety of shapes, sizes andcolours of ‘pea’ are seen (Plate 14.5). Theyoccur most commonly in freshly calvedcows, usually up to peak yield, and, fromtheir red colour, must originate from bloodclots.

If possible, the ‘pea’ should be extrudedfrom the teat under pressure. Local anaes-thetic, infused into the teat canal, may be

needed. One method of extruding the ‘pea’is to pull two 30 ml syringes down over theteat under pressure. Lubricate the teat welland then, with a syringe on each side of theteat barrel, hold the two syringes together atthe base of the teat and slowly draw themdown to the sphincter. This will build upconsiderable pressure within the teat, whichis often enough to express the ‘pea’. If not,then dilate the canal with a semicircularMcClean’s teat knife and try again. Somevets prefer to use a spiral metal coil insertedthrough the teat canal. If the ‘pea’ is attachedto the side of the teat wall, then it may haveto be removed by using crocodile forceps tocut the tissue away from the inner teat wall.

Photosensitization

Occasionally, photoreactive chemicals accu-mulate under the skin of individual cows.These are chemicals that react with sunlightand ultraviolet rays. When exposed to ultra-violet light, the chemicals produce thermalenergy, which in turn causes intense inflam-mation, very similar to a burn. Only whiteor lightly pigmented skin is affected, sinceblack skin prevents absorption of ultravioletlight.

The initial photoreactive agents mayhave been eaten (e.g. St John’s wort in theUK, or lantana poisoning in New Zealand),or may be produced as a result of liver dam-age. The teat skin is initially thickened andoften very painful. It later becomes dry andpeels off, leaving a raw surface beneath(Plate 14.6), before eventually healing.

222 Chapter 14

Plate 14.5. ‘Peas’ are found in a variety of shapesand colours.

Plate 14.4. ‘Pea’ protruding from teat.

Teat sunburn

Occasionally, cows with non-pigmentedteats and large udders develop sunburnalong one side of the teat (Plate 14.7). Thiscan be an irritant and, if flies are attracted,may develop into a summer sore. The use ofemollients and fly repellents is effective.

Udder oedema

‘Oedema’ is the name given to an accumula-tion of fluid in and under the skin. The clas-sic test for oedema is to press the surface ofthe udder with your finger for 4 to 5 seconds:a pit remaining at the point where youapplied pressure (Plate 14.8) is characteristicof oedema. It can also occur on the lowerabdomen, running from the front of theudder towards the forelegs (Plate 14.9). Notehow in the heifer shown the teat skin is dryand cracking, again due to poor circulation.This is the early stage of necrotic dermatitis.

Excess udder oedema can become aproblem, particularly in heifers. In its mostsevere form it can lead to such extensivenecrotic dermatitis that the teat and udderskin is eventually sloughed (i.e. falls off).These animals are impossible to milk andhave to be culled. Many develop mastitis.Even in those which can be milked, milkingis such a painful process that let-downis poor and yields suffer. Because of theturgidity of the teats, there is an increased


Plate 14.6. Photosensitization: the udder skinthickens, becomes dry and, in the later stages, peelsoff.

Plate 14.7. Teat sunburn: note that it affects one sideof the teat only.

Plate 14.8. Udder oedema characteristically leavesa ‘pit’ after finger pressure.

Plate 14.9. Oedema under the belly (A). Note alsothe dry, cracked teat skin (teat necrosis/necroticdermatitis).

⎫ ⎬ ⎭A

incidence of liner slip and teat-end impacts,which will increase the risk of mastitis.Finally, gross congestion of the udder putsan enormous strain on the suspensory liga-ments, which may then rupture (seepages 8–9), seriously reducing the longevityof the heifer.

Possible causes of excess udder oedemaat calving include:

� Excessively old and/or overfat heifers.� Excessive feeding immediately prior to

calving.� Overzealous precalving mineral supple-

mentation, leading to fluid retention.There are anectodal reports that udderoedema problems have resolved coinci-dent with the removal of ad lib mineralsupplementation. Feeding caustic-treatedstraw or wheat has also been suggested asa causal factor, because it leads to exces-sive sodium intakes.

� Inadequate exercise. Natural flow of fluidfrom the udder is via the lymphatics (thebody fluid drainage system), movingupwards towards the pelvis. The flow oflymphatic fluid is promoted by limbmovement during exercise. Lack of exer-cise at calving increases fluid stasis, lead-ing to oedema.

� Rupture of udder ligaments can also dis-rupt flow into the lymphatic ducts, andthis may result in a fluid accumulationand oedema.

Single-quarter oedema

Over the past few years a new form ofudder oedema has begun to increase inincidence. This is sudden in onset, mayaffect one or perhaps two quarters only andis most commonly seen in cows in mid-lac-tation, well after the periparturient oedema(close to calving) has disappeared. Skinsloughing does not occur. The cause isunknown. Affected animals respond onlyvery slowly to diuretics, i.e. drugs thatremove excess fluid from the body. Cowsmay be difficult to milk while the conditionis present. This is because the teat mayalmost disappear into the hard, swollen and

oedematous quarter. At first sight, the herds-man is highly likely to suspect mastitis, butthere are no changes in the milk, there is noincrease in body temperature and the cow isnot off-colour in any way. The finger-pres-sure test shows that the swelling is a typicaloedema.

Wet eczema/necrotic dermatitis/udder skinslough

This is thought to be a degeneration of skin,often in association with excessive udderoedema, and is most commonly seen inheifers between the legs and udder (Plate14.10). More advanced cases may developinto a necrotic dermatitis affecting the wholeudder (Plate 14.11). The skin is initiallyswollen and thickened, later becoming drywith a flaking surface. Occasionally heifersare so badly affected that they becomeimpossible to milk. In other cases, damageto the teat end leads to mastitis. Insome cows, it is only the udder skin thatis affected, and the teats remain softand pliable, as in Plate 14.12. A heavygrowth of Streptococcus uberis was iso-lated from beneath the scab in this cow, sotopical antibiotics were applied to theaffected area and a successful resolutionresulted.

Ischaemic necrosis of the teat

This condition starts as a small, insignifi-cant-looking area of dry skin (A) at the baseof the teat (Plate 14.13) and, if identified andtreated at this stage, the disorder may notprogress. Almost always on the medialaspect, the area of dry skin commonlyerodes more deeply into the base of the teat,and may eventually spread over the wholeteat barrel. It can become intensely irritant,leading to extensive licking, and self-inflicted injury may totally remove the teat,as in Plate 14.14. It has been proposed thatthe intense irritation may be caused by a‘pins and needles’ effect as the lesion pene-trates the erectile venous plexus (Fig. 2.7) atthe base of the teat.

224 Chapter 14

In the early stages of the condition, useof emollients and anti-inflammatory agentssuch as flunixin will help, and vasodilatorshave also been suggested. It may be prefer-able to discontinue milking. The cause of thecondition is unknown, but suggestionsinclude reaction to rubber liners (but whyonly at one site?), the liner pulling on theteat, e.g. due to poor cluster alignment, or aninherent poor blood flow within the erectileplexus at the teat base.


Plate 14.10. Wet eczema between the legs andudder, seen mainly in heifers.

Plate 14.11. Advanced wet eczema, which hasdeveloped into necrotic dermatitis: some heifers areso badly affected that they are impossible to milk.

Plate 14.12. Udder skin slough. In this cow theteats were only slightly affected.

Plate 14.13. The early stage of ischaemic teatnecrosis is seen as an area of dry skin (A) at the baseof the teat.

Plate 14.14. Severe ischaemic teat necrosis. Thisheifer eventually removed her teats by excesslicking due to the intense irritation.

A

Single-quarter agalactia

This condition occurs primarily in heifersduring the first 4 months of lactation. Onequarter starts to become ‘light’, i.e. milk out-put is reduced, and this progresses until thequarter is completely non-functional. Thereare no visible changes in the milk, noincrease in cell count and no significantorganisms are obtained on culture. Affectedanimals are non-pyrexic and continue to eatand to produce milk in the remaining threequarters. If retained, the majority of heifersreturn to production in the next lactation,although in occasional animals the quarterbecomes agalactic (= no milk) for a secondtime. The cause is unknown.

Chemical teat damage

The most common mistake is to accidentallyuse an iodophor/phosphoric acid bulk tankcleaner as a teat dip. Others have used per-acetic acid, which is used for cluster flush-ing when diluted. This has happened onnumerous occasions and can lead to severeproblems, with chapped teats, sores, skinslough and subsequent mastitis. A typicalexample is shown in Plate 14.15. Note howboth the teat and udder skin are affected.The teat ends are raw, which will predisposeto mastitis. These chemicals can also affectthe milker’s skin. Drums of chemicals mustbe carefully labelled.

Diseases with Infectious Causes

Bacterial eczema

A relatively uncommon form of teat eczemais shown in Plate 14.16. Note how only oneside of the teats is affected. This was causedby an open sore on the lower lip of this beefsuckler cow (Plate 14.17) and hence the teatswere only affected on the side of the sore. Agood response was obtained to parenteral(injectable) antibiotics and topical antisep-tic teat ointment. The most probable causeof the lesion was Fusobacterium necropho-rum, although a culture was not carried out

226 Chapter 14

Plate 14.15. Chemical teat and udder burn. Thesecows became almost impossible to milk.

Plate 14.16. Bacterial eczema: this case was causedby contact with an infected sore on the cow’s lowerlip. Note that eczema appears only on one side ofthe teats.

Plate 14.17. Open sore suckler on cow’s lip, actingas the source of infection for the teat lesion in Plate14.16.

to confirm this. The same organism is asso-ciated with ‘black spot’ on the teat end (seepage 229), and is indicated in summer mas-titis (see page 215).

Bovine herpes mammillitis

This is a much more serious viral infectionof the teats than pseudocowpox (see nextsection), and in some cases can lead to suchsevere and painful teat skin damage that theanimal becomes impossible to milk. Inappearance it is very similar to necrotic der-matitis (seen in Plate 14.11), but usuallywith the teats more affected than the udder.Treatment with emollient dips helps, butteats are slow to heal. In painful cases,predipping with glycerine (which shouldbe wiped off prior to the application of thecluster) will soften the teats and assist milk-ing. During the active phase of the disease,the vesicles (fluid blisters) that appear on theteat skin contain large numbers of virus par-ticles. Affected cows should therefore eitherbe milked last or the milking unit shouldbe thoroughly cleaned and disinfectedbetween cows. Fortunately, once a cow hasbeen infected and recovered, she is left withlifelong immunity. The condition is virtuallynever seen in dry cows and some peopleconsider that the herpes mammillitis virusmay remain dormant on carrier dry cowsto become active and cause disease aftercalving.

Pseudocowpox

This is a viral infection of teat skin and pro-duces characteristic horseshoe-shapedlesions. The teat shown in Plate 14.18 isquite extensively affected. More commonly,a smaller area of teat skin with a smaller andless well-defined lesion is seen, as inPlate 14.19. In the initial stages, there iscommonly redness of the skin, which devel-ops into pustules and finally forms scabbyareas, which when removed expose thehorseshoe-shaped lesions. The condition isnot particularly painful and milking cancontinue. Most animals heal in 3–4 weeks,

resolution being assisted by the use of teatdips containing an emollient. Provided thatthe weather conditions are mild, hypochlo-rite dips are thought to be particularly effec-tive. Iodine dips may also be used. Dips areprobably better than sprays, as they achievea more thorough cover. They also reduce thegrowth of mastitis bacteria, such asStaphylococcus aureus and Streptococcusdysgalactiae, which could otherwise prolif-erate in the pseudocowpox scars. Greasy


Plate 14.19. Pseudocowpox: single circular lesion –this is the most commonly seen form.

Plate 14.18. Pseudocowpox: characteristicspreading area of superficial, non-painfulhaemorrhage.

ointments are not recommended, as theyattract dirt, may spread bacteria and do notkill viruses.

Immunity to pseudocowpox is short-lived and further infections can occur6–12 months later. The same virus may alsoproduce small warts, sometimes calledmilker’s nodules, on the herdsman’s hands.It has been suggested that pseudocowpox isrelated to orf, because it is often seen inherds that have contact with sheep.However, the milker’s nodules seen in manare very different from human orf lesions.

Staphylococcal impetigo

Not a common condition in dairy cattle butfrequently seen in lactating goats, staphylo-coccal impetigo is a red, raw rash, appearingon the surface of the udder (Plate 14.20). Thelesions are not particularly painful, but theyproduce moist, pimply areas on the udderskin and could represent a reservoir of mas-titic bacteria. Washing the skin and treat-ment with topical antiseptics are usuallyeffective.

Summer sores (licking eczema)

This is thought to be caused by fly irritation.Some cows lick their teats and abdomenexcessively, causing surface erosions andsores. A typical example is seen inPlate 14.21. Much worse cases can occur andmay lead to summer mastitis. Treatmentwith fly repellents allows rapid healing. Teatdips may also help.

Teat warts

Warts are caused by papovaviruses. Thereare five different strains of virus, whichpossibly explains the big variation in thetype of wart seen. The most commonare fleshy nodules (Plate 14.22) andfeathery warts (Plate 14.23). The latter canbe pulled off quite easily, as their roots read-ily detach. Nodular warts are more difficultto remove.

Vaccines have been prepared by grind-ing up the wart to release the virus, inacti-vating it with formalin and then injecting thefiltrate back into affected animals. A licencemay be required to do this. Such vaccinesseem to be of only limited value as there isoften a poor response to treatment. Most ani-mals eventually undergo self-cure and by thesecond or third lactation the warts have gone.

When present on the teats, these wartscan cause considerable disturbance tomilking:

� They may lead to poor liner attachment,air leakage and therefore teat-end impacts.

228 Chapter 14

Plate14.20. Staphylococcal impetigo. Note the redrash on the udder.

Plate 14.21. Summer sores: fly irritation andsubsequent excess licking are the probable cause ofthese belly and teat sores.

In some heifers the warts may be soextensive that the animal is impossible tomilk.

� Warts may be painful, thereby inhibitingmilk let-down, increasing residual milkand decreasing overall yields.

� Warts around the teat canal can predis-pose to mastitis.

� Skin damage from warts could predisposeto secondary infections withStaphylococcus aureus and Streptococcusdysgalactiae.

The virus causing warts is thought to betransmitted by flies and certainly warts areseen more commonly in heifers reared nearrivers and streams (an ideal habitat for flies).Fly control is therefore an important pre-ventive measure. This is discussed onpage 218.

However, flies are not the only vector fortransmission, since warts may also be seenin housed heifers, especially when stockingdensities are high. Similar warts may be seenon the genitalia of young bulls, especially ifthey are group-housed.

Black spot

This is the term given to a necrosis of the teatsphincter, often with a secondary bacterialinfection with organisms such asF. necrophorum. A typical example is shownin Plate 14.24. Because of the extensive teat-end damage, the risk of mastitis is enormous.Affected cows are best not milked or justhand-stripped for 1 or 2 weeks and allowedto heal. The use of a chemical debridingointment improves the rate of healing.

Black spot may initially be the result ofmachine damage to the teat end, followed byexposure of the teat to an adverse environ-ment, e.g. dirty conditions. Low-emollientteat dips may exacerbate this, although thereis some anecdotal evidence that hypochlo-rite dips are beneficial, in that they promotehealing by removing dead tissue from theteat end. With infection already at the teatend, use of a cannula (Plate 14.26) carries ahigh degree of risk.


Plate 14.22. ‘Fleshy’ teat warts.

Plate 14.23. ‘Feathery’ teat warts.

Plate 14.24. Black spot, an infected erosion of theteat end.

Disorders Caused by Physical Trauma

Trauma to teats will be the result of eitherexternal crushing or damage caused bymachine milking. Factors associated withexternal crushing are considered first.

Injuries from crushing of teats

Some herds seem to suffer almost epidemicsof teat crushing and teat injury. Factors toconsider as possible causes when a highincidence of physical injuries is encounteredinclude:

� High stocking densities and inadequateloafing areas: cows are simply too tightlypacked together.

� Slippery floors and passageways.Dramatic improvements are often seen fol-lowing grooving of the concrete, to pro-vide a surface with a better grip. (Heatdetection may also improve.)

� Excessively narrow cubicle passages:cows either reverse clumsily into the cub-icle opposite or may fall when pushingpast one another.

� Very narrow cubicles: large cows maypush their legs through into the adjacentcubicle and damage the teats of theirneighbours.

� Poor cubicle comfort, for whatever reason,could lead to an increased number of cowslying outside on slippery surfaces andhence increase teat injuries. Cubicledesign and dimensions are discussed inChapter 8.

� Slippery cubicle beds, for example, rubbermats with inadequate bedding: if the bedsurface is too smooth, a cow may falland injure her teats while attempting tostand.

� Loose housing, particularly in long, nar-row and poorly designed yards and wherecows are heavily stocked; although cub-icle systems can produce teat injuries,they are probably more common in poorloose yard systems.

� Rough handling, such as rushing the cowsalong passageways and around corners,excessive use of the backing gate, excess

use of dogs, etc., so that the cows are liableto fall.

� Continually changing groups: once cowshave settled into a group of 50–100 ani-mals, they are best left as such. Movinganimals from one group to another leadsto aggression and fighting and could pro-duce teat injuries.

� Inadequate fly protection: cows grazingoutside, irritated by flies, may chasearound fields and through fences, injuringtheir teats. Dogs could conceivably pro-duce a similar effect. However, most teatinjuries occur in housed cattle.

� Increased lameness: cows feeling uncom-fortable on their feet are stiff and cumber-some when rising and are likely to have anincreased incidence of self-inflictedinjuries.

� Poorly maintained buildings: jaggededges, especially on cubicle beds, couldincrease the incidence of teat damage.

Plate 14.25 is a typical example of a cowwhose teat has been crushed, rendering herextremely difficult to milk. This photographwas taken immediately after milking anddemonstrates that the affected quarter hasnot milked out properly. The preferredcourse of action by many herdsmen is tosimply stop milking the teat until it hashealed. Within a few days the pressure ofmilk within the udder declines and, by notapplying the milking machine, healing

230 Chapter 14

Plate 14.25. Crushed teat engorged with milkbecause the cow could not be milked.

occurs much more rapidly. Admittedly thereis a risk of mastitis, although this is nogreater (and is probably less) than if a teatcannula (Plate 14.26) is inserted and left inposition for 1 or 2 weeks. If the cow will per-mit it, the risk can be minimised by a fewhand-strippings at each milking.

When milking is resumed, thequarter returns to production surprisinglyquickly, even if it has not been milked for3 or 4 weeks. However, the first few milkingsshould be discarded, as this milk will have avery high cell count.

Cut teats

Teats are subjected to a wide variety of cutsand lacerations, one of the most commonbeing a horizontal cut on the lower third andtowards the teat end, as seen in Plate 14.27.Although this cut has not penetratedthrough to the canal, the cow will be diffi-cult to milk because the flap of skin will bepulled down each time the unit is pulled off.It is unlikely that the skin flap will be thickenough for successful suturing.

The most effective treatment is toremove the flap under local anaesthetic (asin Plate 14.28) and perhaps leave the teat toheal for a few days before starting to milk itagain. Most of these cuts heal extremelywell. During the early stages, the wound canbe protected from dirt and flies withMicropore tape, a thin bandage that allowsthe wound to ‘breathe’, thereby promotinghealing.

Cuts penetrating the canal

If the canal has been penetrated, then theteat needs to be sutured. This is best done ina crush, especially where the side of thecrush can be removed. The hind leg of thecow should be lifted and fixed, as if for foottrimming, thus giving greater access to the


Plate 14.26. A teat cannula avoids the need to milka cow following teat-end injury, but there is highrisk of mastitis, especially when the cannula isremoved.

Plate 14.27. Typical cut teat before removal of skinflap.

Plate 14.28. Amputation of skin flap promoteshealing.

site and greater security for the operator.Local anaesthetic is infiltrated around thebase of the teat as a ring block; the wound iscleaned and then sutured. Some suture thelining of the teat cistern, followed by theskin, but in many wounds a single layer isadequate, especially if the cistern lining canbe pulled together using the external suture.Either stop milking the teat for 1 to 2 weeksor, if milking is continued, remove themachine very quickly.

Total amputation

It is surprising how many cows arrive formilking having totally amputated one oftheir teats at its base, as in Plate 14.29. Manyof these cows continue to produce milk inall four quarters, the affected gland simplydischarging onto the parlour floor when let-down occurs. Unfortunately the cow inPlate 14.29 developed a severe mastitis andhad to be culled.

Teat Damage from Machine Milking

Teats are commonly damaged by the milk-ing machine, and an assessment of teat con-dition at unit take-off is an extremelyimportant part of assessing overall machinefunction. The fault is invariably related to

machine milking, but the cause may be:

� in the design or function of the machine(e.g. poor pulsation or excess plant vac-uum); or

� the way in which the machine is used bythe milker. Examples include clustersreapplied to extract the final few milli-litres of milk, or poor udder preparationleading to reduced and biphasic milk let-down and longer unit on times.

Any physical damage to the teat end reducesthe effectiveness of the various defencemechanisms described in Chapter 3 andconsequently increases the risk of mastitis.The extent of the increase in mastitis willclearly depend on a range of factors, such asthe severity of the teat damage, the length oftime that the damage has been present, andother factors influencing mastitis, such asthe efficiency of postmilking teat disinfec-tion and the cleanliness of the environment.

The following section describes some ofthe conditions seen, such as hyperkeratosis,oedema, wedging and haemorrhage, and themethod of ‘teat scoring’ by which they aremonitored. Teat scoring (see Plates14.30–14.33) is an invaluable method ofassessing the efficiency of machine milking.

Hyperkeratosis

Hyperkeratosis of the teat canal orifice is oneof the most common teat lesions associatedwith machine milking. It is seen as a protru-sion of dry, creamy brown or white tissuesurrounding the teat sphincter. It has alsobeen known as sphincter eversion, althoughthis term is now rarely used. A typical exam-ple is seen in Plate 14.31, and a more severecase in Plate 14.33.

A degree of hyperkeratosis may be anormal feature of high-yielding cows, as it isseen particularly at, or soon after, peak lac-tation. If the herd scores are grouped intofresh calvers, high yielders and late lactationcows, then often fresh calvers have a lowscore, ‘highs’ a medium score and ‘lows’ thehighest score, because they have had thelongest exposure to adverse machine func-tion. Even quite severely affected teats

232 Chapter 14

Plate 14.29. Teat accidentally amputated at its base– this is a surprisingly frequent occurrence.

recover during the dry period, althoughdamage may be cumulative, i.e. cowsaffected in one lactation are likely to getworse in the next lactation.

It is thought that hyperkeratosis lesionsare most likely to occur at the end of milkingwhen milk flow is minimal. Pointed teats areworse than flat ends (which may develop‘blisters’), and older cows are more affectedthan heifers because they have less elastic-ity in their teats.

Teat scoring

Attempts have been made to devise a teatscoring system based on the appearance ofthe teat orifice (Shearn and Hillerton, 1996).The examination is best done as soon as themilking units are removed. It is essential touse a head lamp to fully view teats, and sur-gical gloves should be worn. Ideally, theteats also need to be handled: first, to assessthe degree of oedema (i.e. hardness) of theteats and, second, tipping the teat end intoview allows the operator to fully visualize


Plate 14.30. Teat score zero – a perfect teat end.

Plate 14.31. Moderate hyperkeratosis and ‘raised’teat orifice: teat score two.

Plate 14.32. Teat score 3 – note the protrusion of theteat canal and the keratin fronds.

Plate 14.33. Severe teat-end hyperkeratosis: teatscore 4.

changes to the teat end. In some herds, thecows resent teats being handled, and inthese circumstances the operator may haveto just examine the teats visually and thenassess a score per cow – rather than a scoreper teat, as is described below.

Much of the scoring is based on theseverity of hyperkeratosis of the teat canal.On a 0–4 basis, this is approximately as fol-lows:

0. The perfect teat end. Although there maybe a slightly thickened ring visible (theteat sphincter), there is no roughening(Plate 14.30).

1. The orifice appears slightly too ‘open’and has lost its normal smooth, circularappearance. The canal ring has a slightlyraised appearance, and there may beearly keratin fronds.

2. Moderate hyperkeratosis: a few small,rough fronds of keratin are protruding1–2 mm from the raised teat orifice (Plate14.31).

3. Orifice very rough, with keratin protrud-ing all the way round the teat sphincter(Plate 14.32).

4. Advanced protrusion of keratin, 2–4 mmlong, and the sphincter has the appear-ance of having turned almost inside out(Plate 14.33).

Every herd will have a proportion of cowswith a degree of teat-end damage. Targetherd values are a mean score of between 0.5and 1.0 per teat. Herds with a mean score of1.0 and above should be investigated. In theinvestigation, there may be value in subdi-viding the scores, for example, the meanscore of front versus hind teats, or meanscores of high- versus low-yielding cows orof cows versus heifers.

As shown in Fig. 5.9 only higher scoresare likely to lead to an increased incidenceof subclinical mastitis in an individual cow.The cell count and clinical mastitis inci-dence of cows with high scores can be com-pared with those that have low scores toassess whether teat-end damage is indeed acause of the clinical problems on a particu-lar farm.

Other systems score teats 0–5, where

score 5 is an advanced stage of score 4. Mostscoring systems involve handling individualteats, but where this is not practical, forexample the cows resent being handled,then a mean score per cow from a solelyvisual examination can also be used, asalready mentioned.

Teat club international scoring

In this system, teats are scored as:

� Normal. The teat end is smooth (score 0).� Smooth ring. The teat sphincter is raised

and visible (score 1 above).� Rough rings (scores 2 and 3 above).� Very rough rings (score 4 above).

Target values are no more than 20% roughand very rough rings and no more than 10%very rough rings. Values above this requireinvestigation.

A parlour audit

In addition to scoring teat-end changes, theobserver might also find it useful to recordother factors that might have an influence onteat condition and overall mastitis inci-dence. Some examples follow (furtherdetails can be found in the Appendices):

� The number of biphasic let-downs, i.e.where there is initial milk flow, followedby a 30- to 90-second period of slow orzero flow and then a build-up to full flow.This is best recorded by the Lactocorder(on page 106), but simple visual observa-tion of milk flow into the claw bowl isquite useful. More than 5% biphasic let-downs indicate a problem with udderpreparation and milk let-down, and thiscan produce teat-end damage.

� The number of audible liner slips (on page80). There should be no more than 5% ofcows with liner slip, and any liner slipshould be attended to by the milker as amatter of urgency.

� Teat skin condition, e.g. dry or crackedskin (Plate 14.34) will predispose to mas-titis and lengthen unit on times.

234 Chapter 14

� Teat oedema and wedging (see next sec-tion).

� Presence of haemorrhages (Plates 14.35and 14.36).

� Faecal soiling of teats at unit removal. Theauthors classify a cow as ‘dirty’ if one ormore teats have an area of soiling greaterthan the size of a fingernail. Ideally, nocows should be affected, and if more than10% of cows score ‘dirty’ then this repre-sents a problem.

� Is ACR (automatic cluster removal) func-tion rough or gentle, i.e. does the cow kickor does she remain quiet at unit removal?If more than 20% of cows kick or defae-cate, this indicates a problem.

� Is there milk present in the cluster bowl atunit removal, or is it empty? A totallyempty claw at unit removal is a sign ofovermilking, which in turn leads to teat-end damage.

� The number of cows where one or moreteats are less than 50% covered with post-dip. This figure should be less than 5%(see pages 123–125).

Teat oedema and teat-end wedging

Oedema is one of the earliest changes likelyto be detected with adverse machine milk-ing. It is often more easily detected by pal-pation of the teats rather than visualexamination. Teats should be soft and pli-able at unit removal. In affected cows theyare firm, almost hard to the touch, slightlydiscoloured, and may be painful. If signifi-cant oedema is found in more than 10% ofcows, corrective action should be taken.

The small amount of swelling andoedema of the teat end seen immediatelyafter unit removal (Plate 14.37) is an accept-able change, and is particularly common inheifers and freshly calved cows. Theswelling and line of flattening of the teat willfollow the plane of collapse of the liner,since liners always open and close in thesame lateral plane. Hence, if the teat inPlate 14.37 were viewed from the side, itwould in fact appear thinner, rather than fat-ter. In more advanced cases, compression ofthe teat may be so severe that a wedge forms


Plate 14.34. Dry and cracked teat skin predisposesto mastitis, especially contagious infections.

Plate 14.36. Severe teat-end haemorrhage.

Plate 14.35. Mild teat-end haemorrhage.

across the teat end, and in some cases thismay crack and produce chaps. Triangularliners will produce a triangular compressionof the teat end (Plate 14.38). Some triangularliners have an air vent inserted into themouth piece of the liner (the air bleed in theclaw is then closed off). Vented liners areclaimed to provide better milk flow awayfrom the teat and less teat end damage.

Teat ringing

In some cows, ‘rings’ will be visible at thebase of the teat on unit removal, as shown inPlate 14.39.

If seen in a few freshly calved cows, it isof no major significance and is probablyassociated with a temporary periparturientoedema. However, if present in a greaternumber of cows, it indicates a problem withthe liners or liner shell, or perhaps, plantvacuum. If the teat is constricted at the base,then this will compromise the rate of milkflow from the udder cistern into the teat cis-tern and, in so doing, it will decrease milkflow rates, increase unit on time and predis-pose to further teat-end damage.

Teat chaps

‘Chaps’ are cracks in teat skin. They occurparticularly when cows are exposed to wet,cold and windy weather or to damp anddirty environmental conditions. Teat dip-ping in severe cold, for example, in sub-zeroconditions, can produce chaps, especially ifdamp teats are exposed to a wind chill fac-tor. The development of chaps may be aggra-vated by poor unit alignment, leading totwisting of the teats (and hence opening ofskin cracks) when the cluster is removed.Postmilking disinfection with high-emol-lient dips, or even neat glycerine, promotesrapid healing. Not only are chaps painful,but they can also harbour mastitic bacteria,particularly Staphylococcus aureus andStreptococcus dysgalactiae.

236 Chapter 14

Plate 14.37. Teat-end oedema: note the swelling atthe end of the teat, best seen immediately afterremoval of the milking machine.

Plate 14.39. Note the ‘ringing’ at the base of the teatfollowing unit removal. This excess pressure fromthe liner mouthpiece reduces milk flow rates,prolongs milking times and predisposes to teat end-damage.

Plate 14.38. A wedge across the teat end is causedby the liner, in this case triangular, closing.

Teat-end haemorrhage and pressure necrosis

Small haemorrhages, as seen in Plate 14.35,result from poor machine function and sub-optimal pulsation, leading to inadequate teatmassage during milking. This is discussedin Chapter 5. Plate 14.36 shows a moreadvanced case; note the extensive haemor-rhage around the teat end, the protrusion ofthe sphincter and the haemorrhage at thebase of the teat, adjacent to the udder, causedby the liner crawling up the teat and pinch-ing it closed. In advanced cases, there maybe a slough of teat-end skin, such as inPlate 14.40.

In liners with shields (see page 73) theeffective length may be reduced so muchthat, in cows with long teats, the liner fails tofully compress the teat end during the restphase of the pulsation cycle (see pages68–70). This leads to poor blood circulationat the end of the teat and can sometimes bea cause of teat-end haemorrhage.

Machine Milking Factors Associated withTeat Damage

As mentioned earlier, teat damage will bethe result of either the way in which themachine is set up, or the way in which theequipment is used by the milker. This is alsodiscussed in Chapter 5.

Machine factors

A very wide range of potential factors areinvolved, and in any one farm, there may bemore than one cause. As yields haveincreased, unit on times are longer, and thishas increased the risk of teat damage. Someof the more important factors are as follows.

Overmilking

The greatest adverse effect of the milkingmachine occurs when vacuum is applied to ateat in the absence of milk flow. This isbecause there is then nothing to dissipate thevacuum, and teat-end vacuum rises to plantvacuum (teat-end vacuum would normally be3–5 kPa lower than plant vacuum during milkflow). Overmilking can occur at unit attach-ment if udder stimulation was insufficient, orat the end of milking if the cluster is notremoved before milk flow ceases. Wheneverthe unit is attached to the cow, there shouldalways be milk present in the cluster bowl.

Excess plant vacuum

Excessively high or fluctuating vacuum canlead to teat damage. The correct vacuumlevel for the plant will depend on whetherit is a high-line or low-line plant, and a num-ber of other factors, such as cluster weight.

Poor pulsation

The most common pulsation defect leadingto teat damage would be an inadequate mas-sage phase (‘d’ phase), perhaps arising froman excessively wide pulsation ratio,e.g. 65:35 or less, or a ‘d’ phase less than200 ms. An incomplete or slow opening ofthe liner (namely the ‘a’ phase of the pulsa-tion cycle) might occur if milk flow startswhile the liner is still partially closed, whenmilk is effectively being ‘squeezed’ outthrough the teat end. This may happen withold liners that open more slowly due to par-tial collapse of the rubber.

Cluster weights

There is some evidence that heavy cluster


Plate 14.40. Pressure necrosis of the teat end,resulting in a total slough of the superficial skin.

weights lead to more teat end damage. It iscertainly not advisable to put a brick or otherweight on to the clawpiece. However, verylightweight clusters might increase the inci-dence of liner slip.

ACR settings

The setting of the ACR can certainly affectteat condition, and plants where cows kickand/or defaecate excessively at unit take-offprobably need correction. The main settingsinfluencing ACR function are: (i) the milkflow rate that triggers vacuum shut off; (ii)the delay interval between reaching thisminimum flow rate and vacuum shut-off;and (iii) the delay between vacuum shut-offand the ACR cord pull.

The two most commonly incorrectsettings are that the milk flow rate is toolow, and the delay between vacuum shut-off and ACR pull is too short. A low flowrate trigger (e.g. less than 500 ml/min – seepage 68) leads to excess unit on timeand teat-end damage. If the ACR cordpulls before the vacuum in the claw has hadtime to vent (i.e. the delay is too short), thenthe cluster is pulled off with the teats undervacuum, a bit like pulling a cork from a

bottle. This can cause significant discomfortto the cows, leading to kicking, excess muckin the parlour and teat-end damage.

Milker factors

The major milker factors that might influ-ence the degree of teat damage are brieflylisted below, and are discussed more fully inChapter 6.

1. Inadequate udder stimulation beforeapplying the unit, such that there is aperiod of unit on time with no milk flow.This is often referred to as a biphasic let-down.

2. Aggressive handling of cows, thusinhibiting milk let-down. Examplesinclude, the use of dogs or of electrifiedbacking gates, and the milker chasing thecows into the parlour.

3. Poor teat skin condition, leading toslower milk flow rates and longer unit ontimes.

4. Over riding the ACR and/or reapplyingunits, for example, to get the final 250 mlof milk out of a cow or to milk nervous orstressed heifers.

238 Chapter 14

Medicine residues in milk are a major foodsafety issue. They pose a potential humanhealth hazard as some people are hypersen-sitive to antibiotics and they can causeantibiotic resistance. Also, they can interferewith product manufacturing processes byinhibiting yogurt and cheese starter cultures.

There has been a great drive to reducethe number of bulk tank failures, but thelevel of failures in the UK has been increas-ing slightly over the past years, despite thereduction in the number of dairy farmers.

The majority of failures are due to humanerror, with most farmers knowing why thefailure has occurred. Part of this increasemay be due to larger farms and fewer staff,and therefore a greater risk of human error. Itmay also be compounded by the increase inforeign milkers, where there may be lan-guage difficulties and a lack of adequatetraining.

In the event of an unexpected failure inwhich a tanker or silo is contaminated, thefinancial implications for dairy farmers are


15 Residue Avoidance in Milk

Reasons for Antibiotic Failures 240‘Off Label’ Treatment 240Steps to Avoid Residues 241

Cow identification 241Identify all treated dairy cows 241Record all treatments 242All milk from treated cows must be discarded 242Milk all treated cows last or separately 242Withdrawal periods 243Antibiotic screening tests 243Use only licensed medicines 243Store all drugs correctly 243Medicine labelling 244Purchased cows 244Cows that calve early 244Training 244Recorder jars 244Communication 244Written treatment protocols 245

Antibiotic Screening Tests 245Natural Inhibitors 246Study Herd 246

very great. They may have to pay for themilk lost and any consequential costs fordisposal. Some farmers may be complacentas some dairy companies have an insurancescheme that allows up to two failures eachyear without penalty, provided the farmernotifies the dairy company in advance. Thecosts of disposal of contaminated milk underthe new EU Animal By-products Regulationswill be significant. An unexpected residuefailure presents a major problem to any dairycompany.

Some dairy farmers consider that theonly residues of significance are antibiotics.It must be remembered that other medicines,such as anthelmintics, hormones, steroids,etc., can also be responsible for causingresidues in milk. Throughout the EU, ran-dom milk samples are collected from farmsfor extensive testing for these substances.

Reasons for Antibiotic Failures

The suggested reasons for bulk tank antibi-otic test failures, taken from a UK survey byBooth in 1982, are shown in Table 15.1. Thereasons suggested for test failures add up tomore than 100%, as many farmers gave morethan one possible reason. Poor or non-exis-tent records of treatment for clinical mastitisand not withholding milk for the whole ofthe recommended period stand out as themajor reasons for test failures. Cows calvingearly where the full withdrawal period has

not been observed, along with accidentaltransfer of milk from recorder jars, wereother significant contributors to failures. Atthe time of this survey, herd sizes were sig-nificantly lower than they are at present and‘off label’ medicine use was relativelyunknown.

The Northwest Illinois DairyAssociation carried out a similar survey in2000 on the most common causes of bulktank antibiotic residues, and the results areshown in Table 15.2. Farmers did not knowwhy the failure occurred in 20% of cases.However, the use of ‘off label’ drug medi-cines accounted for 17% of failures. Poorcow identification, human error and milkinga dry cow by mistake made up the majorityof the rest of the failures.

Table 15.2. A US survey of suggested reasons forbulk tank antibiotic test failures. (From NorthwestIllinois Dairy Association, 2000.)

Employee error 25%Unknown/insufficient data 20%ʻOff labelʼ drug use 17%Poor cow identification 16%Milking a dry cow 13%Poor communication 4%Treated cows not separated 3%Other 2%

Both of these surveys support the factthat the majority of failures are down tohuman error. But there can be other moreunusual reasons for antibiotic failure, whichinclude cows drinking from a medicatedfootbath or accidentally mixing medicatedfeed into the lactating cow ration. There areno known problems where residue failuresoccur if medicines have been used accord-ing to data sheet recommendations.

‘Off Label’ Treatment

The use of medicines ‘off label’ is increasingsignificantly. ‘Off label’ use is defined as anydeviation from the manufacturers’ data sheetrecommendations. ‘Off label’ treatmentincludes:

240 Chapter 15

Table 15.1. A UK survey of suggested reasons forbulk tank antibiotic test failures. (From Booth,1982.)

Poor/no records 32%Not withholding milk for full period 32%Calving early/short dry period 15%Accidental transfer of milk 14%Prolonged excretion 12%Contamination of recorder jars 9%Withholding milk from treated quarter only 8%Lack of advice on withholding period 6%Mechanical failure 6%Recently purchased cows 3%Milking through jars 1%Use of dry cow preparation during lactation 1%

� Increasing the dose rate (usually increaseddose level, such as infusing two tubes ofintramammary antibiotic at the sametime).

� Changes to frequency of treatment, e.g.cows treated three times a day rather thantwice (if that is the data sheet recommen-dation).

� Extending the duration of therapy.� Unlicensed combination treatments (com-

bination refers to the use of intramammaryand injectable antibiotics).

� Changing treatments to another productbefore the milk withdrawal period of theinitial treatment has lapsed.

� Using a product intended for a non-lactating animal in a lactating animal.

A typical example of ‘off label’ use would bean intramammary preparation combined withparenteral injections of penicillin as there isno licensed combination therapy with peni-cillin injections (see Plate 15.1). Anotherexample would be treating a cow with antibi-otics twice daily instead of the data sheet rec-ommendation of daily treatment.

There are some combination mastitistreatments (intramammary and injectableantibiotics) that are licensed as such andhave a milk withdrawal period for the com-bination. The number of licensed combina-tion treatments for dairy animals is verysmall.

In the EU, the minimum milk with-drawal period for any medicine used ‘offlabel’ is not less than 7 days. It may be longerdepending on the products and how they areused. The onus is on the veterinary surgeonto caution the farmer to ensure the milk issafe from any treated cows prior to it enter-ing the bulk supply. Ultimately, the finalresponsibility is with the farmer to ensurethat all milk sold off farm is safe and freefrom residues. Bulk tank milk must passwhatever inhibitory tests are used by themilk purchaser.

Steps to Avoid Residues

The risk of residue violations will be negli-gible if the following steps are taken. A sum-mary of these key points is shown in the‘Best Practice Guides’ (Chapter 16).

Cow identification

There are still some farmers who fail to haveany recognizable form of cow identificationother than an official ear tag number. It isessential that all treated dairy cows areclearly identifiable so that the milker is ableto identify individual cows from the milkingpit. Herds with poor cow identification prac-tices are more likely to have a higher risk offailures.

Identify all treated dairy cows

It is essential that all treated cows are iden-tified as such by using leg or tail tape orspraying of the udder (see Plate 15.2), or, ifpossible, entering their details in the milk-ing parlour’s computerized system. Thereare still some farmers who rely on theirmemories to identify all cows receivingtreatment. Problems may occur if someoneelse comes in to carry out the milking, or ifthe farmer simply forgets which cowreceived what treatment and when.

It is best practice to mark cows for treat-ment before any medicine is administered toensure that the farmer knows which cow is

Residue Avoidance in Milk 241

Plate 15.1. ‘Off label’ treatment includes use ofunlicensed combination therapy.

being treated. Some farmers have treated acow in the parlour but marked a differentanimal in error, which has resulted in a bulktank failure.

Record all treatments

It is a legal obligation to record all treatmentsgiven to food-producing animals. These datamust include the identity of the animalstreated, date of treatment, name of productand amount dispensed, together with thebatch number and the milk and meat with-drawal periods. This is not only importantfor all lactating treatments but also for drycow therapy, where farmers can checkrecords if cows calve early. In the event ofan unexpected bulk tank failure, theserecords are essential as part of an investiga-tion (Plate 15.3).

All milk from treated cows must be discarded

All milk from the treated cow must be dis-carded. Some farmers think it necessary todiscard only milk from an individual quarterthat is treated with an intramammary prepar-ation, and the milk from the untreated quar-ters still enters the bulk supply. The udderis a very vascular organ, with 500 litres ofblood flowing through the udder for everylitre of milk produced. Antibiotics arepicked up from the treated quarter and are

transferred to the other quarters via thebloodstream and then excreted from all fourquarters (see Plate 15.4).

Milk all treated cows last or separately

It is advisable to milk any treated cows lastto avoid any accidental transfer of milk tothe bulk supply. This is easy in large herdswhere there can be a treatment group orholding facilities for small groups of animals

242 Chapter 15

Plate 15.2. All cows should be identified before anytreatment is administered.

Plate 15.3. Record all treatments in the medicinebook.

Plate 15.4. All milk from treated cows must bediscarded, not just the milk from a treated quarter.Quarter milkers should not be used.

(see Plate 15.5). If this is not possible, it isadvised that treated cows are milkedthrough a dump bucket, which avoids acci-dental transfer of milk. Many new parloursare fitted with a dump line, which avoidsaccidents provided that milkers rememberto identify treated cows and milk them intothe dump line.

Some farmers still milk treated cowsthrough a recorder jar in the parlour andthen discard this milk. There are occasionswhere this milk may accidentally be trans-ferred or, if the valves at the bottom of thejar leak, milk with residues can contaminatethe bulk tank.

Withdrawal periods

It is important that farmers clearly under-stand and follow the withdrawal periods forall medicines. ‘Off label’ treatments must beclearly understood, the longer milk with-drawal periods observed and the milk testedbefore it is returned to the bulk tank.

Antibiotic screening tests

Screening tests are very useful in identifyingwhether the milk is safe to be returned to thebulk tank or not. The UK industry standard is

the Delvo SP and many farmers have on-farmtest kits. However, many tankers are initiallyscreened with the BetaStar test, a rapid testtaking about 10 minutes, before the tank isunloaded at the dairy. In other countries, awide range of tests are used. In the US, spe-cific tests are commonly used to detect tracesof antibiotics used to treat the cow.

There is no need to screen milk before itgoes back into the bulk tank where a medi-cine has been used following data sheet rec-ommendations. Indeed, such screening isinadvisable as false positive or negativeresults may occur. If a product is used ‘offlabel’, milk must be screened 7 days after theend of treatment, and when it passes the testit can then be included in the bulk supply.

Use only licensed medicines

All medicines used in food-producing ani-mals must be licensed with the regulatoryauthority of that country. These medicineswill have a product licence printed clearlyon the medicine. Foreign medicines of anidentical brand name may have a differentformulation and withdrawal period, whichcould result in a residue failure (seePlate 15.6).

Store all drugs correctly

Medicines must be stored in the correctmanner according to the data sheet. Some


Plate 15.5. Ideally milk all treated cows last. Notethat these cows are also colour marked to showthey are under treatment.

Plate 15.6. Use only licensed veterinary medicines.

medicines will have to be refrigerated; oth-ers may need to be stored away from sun-light, etc. It is a legal requirement in the UKthat all medicines are kept under lock andkey. Any products that have passed theirexpiry date must be discarded appropriatelyand not used. In the USA, there is a require-ment to keep medicines for dairy cows andnon-lactating animals separately to avoidaccidental use.

Medicine labelling

Medicine labels must include the milk with-drawal period. The dispensing veterinarian,pharmacist or wholesaler must give adviceon drug administration for all dispensedmedicines. This will include the dose rate,frequency of treatment and route of admin-istration (oral, intramuscular, intra-mammary, topical, intravenous, intrauterineor subcutaneous). Remember, if there is anydeviation from any of this, then the medi-cine is being used ‘off label’ and the mini-mum milk withdrawal period must beapplied.

Purchased cows

Farmers buy cows on trust and presume,unless told otherwise, that these animals arefree from residues. It is possible that cowsmay have been treated prior to purchase ormay have calved early and still have residuesfrom dry cow therapy. It is advisable toscreen all purchased cows before their milkenters the bulk tank (see Plate 15.7).

Cows that calve early

Check the dry-off date against the calvingdate. If the withdrawal period has expired,then this milk can be included in the bulktank. Remember that it is a legal requirementnot to sell milk from cows calved less than96 hours in the EU, irrespective of any milkwithdrawal period.

If the withdrawal period still has notexpired, then this must be observed. If in

doubt, test the milk. Dry cow therapy con-tains high levels of antibiotic that is con-tained in a slow-release base and thewithdrawal period for some products can beas much as 54 days after drying off. Some ofthe cloxacillin dry cow preparations in theUK also have a requirement to withholdmilk for up to 81⁄2 days postcalving.

Training

All individuals in the medicine chain mustbe trained to ensure that they play their partfully in minimizing error. This includes vet-erinary surgeons, agricultural merchants,herdsmen and farm managers. All need to beaware of their part in ensuring that milk pro-duced is free from any residues.

Recorder jars

Ideally, treated cows should not be milkedinto recorder jars. However, if treated cowsare milked through recorder jars, they mustbe rinsed out as antibiotics concentrate inthe fat and traces could pose a risk of a bulktank failure (Plate 15.8).

Communication

In herds where there is more than onemilker, good communication is essential to

244 Chapter 15

Plate 15.7. Be aware that purchased cows may haveresidues. Test before putting milk in the bulk tank.

avoid treated cows being milked into bulktank. A simple board system works well(Plate 15.9).

Written treatment protocols

Written treatment protocols should clearlyexplain treatments commonly administeredby the farmer, along with any milkwithdrawal periods. There should be aclear definition of ‘off label’ treatments.Written treatment protocols form best prac-tice and will help to ensure that all cows aretreated correctly and to avoid any risk ofresidues.

Antibiotic Screening Tests

Withdrawal periods are set by regulatoryauthorities and are based on the maximumresidue limit (MRL). An MRL is the maxi-mum concentration of residue followingadministration of a veterinary medicine thatis legally permitted or acceptable in foodunder the laws of any regulatory authoritysuch as the EU or, in the USA the FDA (Foodand Drugs Administration). At the end of thewithdrawal period milk will below the MRLlevel and is safe for human consumption.

There are a variety of antibiotic screen-ing tests that are available for use, includingthe Delvo SP, which is the test most fre-quently used by the EU dairy industry. Themajority of screening tests used in the EU aredesigned for testing bulk milk rather thanindividual cows.

The Delvo SP tests to variable levels ofantibiotic. These levels do not necessarilymatch the MRL. For example, the MRL forcloxacillin is 30 p.p.b. but the Delvo SP willdetect levels as low as 15 p.p.b., half theMRL or legal limit. On the other hand, theMRL of oxytetracycline is 100 p.p.b. but theDelvo SP test detects levels at 400 p.p.b.,four times the MRL.

This means that a farmer who uses acloxacillin preparation and tests the milkwith the Delvo SP test at the end of the milk


Plate 15.9. A board at the front of the parlour showseveryone which cows’ milk needs to be kept out ofthe tank.

Plate 15.8. Milking cows into recorder jars is notrecommended. If they are, ensure that the fatresidues are rinsed before milking the next cow.

withdrawal period can have a positive resulteven though the correct withdrawal periodhas been observed. This is one of the limita-tions of individual cow screening tests.

There is no single test that detects allantibiotics at the MRL. This is the reasonwhy it is not recommended to test cows thathave been treated according to data sheetinstructions, as many positive results mayappear even though this milk is perfectly fitfor consumption and gets diluted out in thebulk tank.

Some farmers dilute milk from individ-ual cows to be tested one part in four withmilk from the bulk tank. If the milk passes itis then returned to the bulk tank. This helpsto overcome the oversensitivity of some ofthe tests.

There are also differences betweenscreening tests. The BetaStar test is a rapidscreening test that is commonly used toscreen milk tankers before milk is offloadedinto silos at the dairy. The BetaStar test candetect cloxacillin residues as low as 5 p.p.b.(the MRL is 30 p.p.b.) but does not detecttylosin, streptomycin or oxytetracycline. Acomparison of the MRLs of the Delvo SP,BetaStar and Charm MRL tests is shown inTable 15.3.

There are other tests that can be used,and some test only for a specific antibiotic.However, it must be remembered that mostdairy contracts require producers to ensurethat all milk sold off farm passes any residuetests that the milk buyers choose to use andso this is the important criterion for farmers.

Natural Inhibitors

Natural inhibitors can cause problems thatresult in failure of a residue test in individ-ual cows. For example, mastitic milk fromindividual untreated cases of coliform mas-titis may fail the antibiotic residue test forup to 21 days after infection. This is due tohigh levels of the enzyme lysozyme, the pro-tein lactoferrin, and complement. High tem-peratures kill off these natural inhibitors.

In a Japanese study, 24 milk samplesfailed the Delvo SP test after the milk with-drawal period had expired. These sampleswere then heated at 82°C for 5 minutes andthe samples were retested. After this heattreatment, 21 of the 24 samples passed theDelvo SP test. Heating samples destroys nat-ural inhibitors but has no effect on anyantibiotic that may be present. Naturalinhibitors are unlikely to be responsible fora bulk tank failing a residue test.

Study Herd

The owner of a herd of 150 dairy cows hadbeen advised by his dairy company to testall cows after calving to ensure that theywere free of residues before the milk enteredthe bulk tank. This was designed to improvefood safety and reduce the risk of residuesentering the bulk tank. This farm had neverhad any bulk tank failures in the past10 years.

The farmer had been using a dry cowpreparation containing cephalonium for sev-eral years and always observed the correctmilk withdrawal period. The dairy company

246 Chapter 15

Table 15.3. Comparison of MRL (maximum residue limit) with sensitivities of different antibiotic test kits.

Antibiotic MRL Delvo SP BetaStar Charm MRL

Penicillin 4 2 2–4 4Cloxacillin 30 15 5–10 30Ceftiofur 100 50 75–150 100Tylosin 50 50 Not detected Not detectedStreptomycin 200 300–500 Not detected Not detectedOxytetracycline 100 100 Not detected Not detectedCephalonium 20 5–10 7.5–15 3–5

tested individual cow samples in its ownlaboratory, using either the Delvo SP or theCharm MRL.

The farmer found that cows kept failingthe Charm MRL test for up to 21 days afterthe manufacturer’s withdrawal period. As aresult he was discarding up to 1000 litres ofmilk per day, as instructed by his dairy com-pany, which said that the milk from thesecows was unfit for human consumption.

On one particular day, 21 milk samplesfrom cows where the milk withdrawalperiod had expired were tested with both theCharm MRL and the Delvo SP test. Sixteensamples tested positive with the Charm MRLtest but only three tested positive with theDelvo SP test. On the basis of these results,milk from the 18 cows that passed the DelvoSP test were included in the bulk tank at thenext milking. The bulk tank passed all futureresidue tests.

The three samples that failed the DelvoSP test were sent off for antibiotic assaywhere individual antibiotics are measured.Two samples had no traces of cephaloniumpresent, suggesting that this failure musthave been due to natural inhibitors. Theother sample had traces of cephalonium butthese were well below the MRL. On further

questioning, the farmer realized that he hadsampled this cow at 48 hours after calvingand not at 96 hours, and so a trace of anti-biotic would not have been surprising, as themilk withdrawal period had not yet expired.

The farmer had lost all faith in individ-ual cow testing. He no longer tested indi-vidual cows after calving provided thewithdrawal period had been observed, afterwhich time all milk was put into the bulktank. Any cows treated ‘off label’ had theirmilk diluted one part in five with milk fromthe bulk tank to overcome the sensitivity ofthese tests. If the milk passed, this was thenincluded in the bulk tank.

What can we learn from this herdexample?

1. There is a variation in sensitivity betweendifferent antibiotic residue test kits.

2. Some test kits are oversensitive to levelsof antibiotics and detect levels below theMRL.

3. There is no benefit in testing cows aftercalving provided the correct milk with-drawal period has been observed.

4. Natural inhibitors can cause failures withresidue test kits on individual cowsamples.


Top Tips to Reduce Cell Counts

These are general recommendations for anydairy herd. Other control measures willapply depending on the herd managementand mastitis problems present in the herd.

1. Carry out regular individual cow cellcounts. Use the data to identify the per-sistently high cell count cows. Havethese cows tested to identify the mas-titis bacteria that are causing the highcell count on your farm.

2. Postdip every cow after every milkingthroughout the year. Postdipping killsbacteria that have been transferred ontothe teats during milking. This happensall year round.

3. Use antibiotic dry cow therapy on allcows at the end of lactation.

4. Change the liners of the milkingmachine every 2500 milkings or every6 months, whichever is the shorterperiod.

5. All milkers to wear clean gloves during

milking to reduce the risk of cross-contamination. Rinse the gloves regu-larly in disinfectant solution duringmilking. Do not use common uddercloths.

6. Detect clinical mastitis early and treatall clinical cases with antibiotics.

7. Have the milking machine servicedtwice a year and follow the recommen-dations made in the test report.

8. Disinfect the milking cluster after milk-ing any cow with clinical mastitis orhigh cell count to avoid the spread ofinfection.

9. Cull persistently high cellStaphylococcus aureus cows in lacta-tion four and above. Other high cellcount cows may need to be culled, sodiscuss this with your vet or adviser.

10. Ensure that you buy low cell count ani-mals and not cows infected withStaphylococcus aureus or Streptococcusagalactiae. Check the herd and individ-ual cell count history before purchasinganimals.


16 Best Practice Guides

Top Tips to Reduce Cell Counts 248Top Tips to Minimise Environmental Mastitis 249Milking Routine Best Practice 249Best Practice to Avoid Residues 249Best Practice: How to Administer Dry Cow Antibiotic Therapy 250and an Internal Teat SealBest Practice for Circulation Cleaning 250Sterile Milk Sample Collection for Bacteriology 251

Top Tips to Minimise EnvironmentalMastitis

These are general recommendations for anydairy herd. Other control measures willapply depending on the herd managementand mastitis problems present in the herd.

1. Teats and udders should be clean. Keepcows on clean, dry beds. If udders andteats are dirty, the beds are not cleanenough.

2. Predip cows to disinfect teats prior tomilking. Teats must be dried. If the milksock is dirty after milking, teat prepara-tion must be reviewed.

3. Encourage cows to remain standing for30 minutes after every milking so thatthe teat canal closes. The best way is tooffer fresh feed. Lame and sick cowsmust be allowed to lie down.

4. Always use clean, dry bedding; thisabsorbs maximum moisture and doesnot get mouldy or damp. Scrape pas-sageways twice daily.

5. Pay particular attention to the calvingpens. These must be kept as clean aspossible, as freshly calved cows aremost prone to toxic mastitis.

6. Have a minimum of one cubicle per cow(ideally 5% more cubicles than cows). Ifon straw yards, allow at least 6.5 sq. mof lying space, bed up daily with clean,dry straw and clean out every 2 to 4weeks.

7. Make sure you have stable vacuum lev-els throughout milking. You should nothave liner slip and the regulator mustalways be letting in air.

8. Check teat-end conditions. If the teatsare damaged, then there is an increasedrisk of mastitis as the teat end is the bar-rier that keeps infection out of theudder.

9. Use an internal teat seal with dry cowtherapy, ensuring excellent hygieneprior to infusion. Pinch the teat halfwayup and infuse the internal teat sealso that it remains at the bottom of theteat.

10. Monitor progress. Check on your masti-tis incidence and timings of infection.

Use bacteriology tests to identify thecause of clinical mastitis on your farm.

Milking Routine Best Practice

Goal: milk clean, dry teats with minimal riskto udder health.

1. Wear gloves and keep them cleanthroughout milking.

2. Detect mastitis promptly and accuratelyby foremilking.

3. Prepare your cows in batches of five toeight.

4. Predip and strip the batch. Then go backand wipe and attach each cow. Units tobe attached within 1 to 2 minutes ofpreparation.

5. Ensure the unit is alligned so it sitssquarely on the udder.

6. Remove the unit to avoid overmilking.ACRs should be set to come off at a flowrate of 400–500 ml/min for twice-dailymilking and 600–800 ml/min for 3 timesa day milking.

7. After milking, thoroughly coat the entiresurface of each teat with a postdip.

8. Mastitis management:� Milk mastitis cows last or through a

separate cluster.� Disinfect the cluster after milking

every mastitic cow.9. Allow cow to exit from the parlour and

encourage standing for 30 minutes byoffering fresh feed during the housedperiod.

10. Remember that the milking parlour is afood factory and must be kept cleanthroughout milking.

Best Practice to Avoid Residues

1. Use only licensed veterinary medicines.2. Store all drugs correctly. Ideally medi-

cines for lactating and non-lactating ani-mals are kept separately.

3. Ensure medicines are clearly labelledwith the milk withdrawal period.

4. Ensure all treated cows are clearly iden-tified.

Best Practice Guides 249

5. Record all treatments in the medicinebook.

6. Treat cows only after carrying outstep 4.

7. Have a separate treatment group wheretreated animals are milked last or, if thisis not possible, milk separately intodump buckets.

8. Observe the correct withdrawal periods.9. Discard all milk from treated cows

where there is a withdrawal period, notjust from a treated quarter.

10. Keep milking and dry cows separately ifat all possible, or ensure that dry cowsare clearly identified.

11. Use antibiotic screening tests to test anycows treated ‘off label’ or which calveearly.

12. If in doubt, test milk from purchasedcows to ensure they are clear of residuesbefore putting the milk in the bulktank.

13. Check treatment dates and withdrawalperiods of cows that calve early andensure that milk is discarded until thewithdrawal period has expired.

14. Ensure that all milkers are trained inresidue avoidance measures.

15. Have written treatment protocols andmedicine withdrawal period data.

16. If in doubt, keep the milk out. Test toensure the milk is safe.

Best Practice:How to Administer Dry Cow Antibiotic

Therapy and an Internal Teat Seal

No internal teat sealant contains antibioticsand so scrupulous hygiene during adminis-tration is essential.

Preparation is everything and a smallamount of extra time will pay dividends. It isrecommended that cows to be dried off arekept separately and brought into the parlourat the end of milking. This will allow plentyof time to administer treatments without thepressure of milking.

Best practice is as follows:

1. Identify the cows to be treated with ared spray or other marking method. This

is especially important if these treat-ments are carried out as and when thesecows come into the parlour to bemilked.

2. Strip out all quarters.3. Wear clean gloves during the drying off

procedure.4. Teat-dip the furthest two teats.5. Wipe off this solution with clean dry

paper towel.6. Scrub the teat end with cotton wool and

surgical spirit until no more dirt appearson the cotton wool.

7. Infuse dry cow therapy and massage upthe teat.

8. Infuse the internal teat sealant, pinchingat the teat and udder junction to ensureit remains at the bottom of the teat. Donot massage up into the teat.

9. Repeat the above procedures for the twonearest teats.

10. Teat-dip all four teats.11. Record the treatments in the medicine

book.

Best Practice for Circulation Cleaning

Goal: clean parlour to maximize milk qualityand extend parlour life. Remember:

� Too much dairy chemical is corrosive andexpensive.

� Too little is ineffective and the plant willnot be properly cleaned.

� Work out the wash volumes used and thecorrect concentration of dairy chemicalsand write these clearly on the dairy wallor a noticeboard.

1. Wash the plant as soon as possible aftermilking so that milk does not solidify inthe plant.

2. Clean off the clusters and jetters andattach. Remove the line into the bulktank. Turn off the plate cooler water sup-ply. Set up the plant for the cleaningcycle.

3. Remove the milk sock and replace witha clean sock.

4. Rinse warm water (body temperature)through the plant to waste. This

250 Chapter 16

removes 95% of milk soil and keeps theplant warm.

5. If you are using a hot detergent solution,circulate the hot wash solution aroundthe plant. Hot water should be enteringthe system at about 85°C. If using a coldsolution, circulate it around the plant.

6. As the wash solution returns to thewash trough, add in the correct amountof dairy chemicals for the volume ofwater used.

7. Hot washes should circulate at between60–70°C. All solutions should only cir-culate for between 5 and 8 minutes.

8. The parlour has now been cleaned.Discard the used wash solution.

9. Circulate cold water and hypochlorite todisinfect the plant.

10. Drain from the plant either after wash-up or before the next milking.

11. Hang the units to drain.

Sterile Milk Sample Collection forBacteriology

It is essential that sterile milk samples arecollected to identify the cause of clinicalmastitis or high cell counts. If this procedure

is not followed, then the outcome will resultin contaminated samples and will be of nobenefit.

You must use sterile sample pots.

1. If the teat is dirty, wash and dry. If it isvisibly clean, then dry-wipe with papertowel.

2. Discard three squirts of foremilk fromeach quarter to be sampled.

3. Coat the teat with a pre- or postdip,allow a contact time of 30 seconds andwipe dry with paper towel.

4. Put on a clean pair of gloves.5. Scrub the end of the teats with cotton

wool soaked in surgical spirit so that theend of the teat is spotless.

6. Take the top off the sample bottle, holdit at a 45° angle and squirt one stream ofmilk into the bottle, making sure thatyou do not touch the end of the teat.

7. Replace the top on the bottle.8. Label with cow number, quarter/s, farm

and date.9. If there is any doubt about the sterility

of the sample, repeat the entireprocedure.

10. Freeze the sample or send directly to thelab keeping it cool if possible.

Best Practice Guides 251

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Appendix: Liner Life Charts

Table A.1. Liner life in days according to herd and parlour size and assuming a liner life of 2500 milkings:three times a day milking.

Number of milking units

Herd size 6 8 10 12 14 16 18 20 24 28 30 32

50 100 133 167 16760 83 111 139 16770 71 95 119 143 16780 62 83 104 125 146 167 18290 56 74 93 112 130 148 167 182

100 50 67 84 100 117 133 150 167110 45 61 76 90 106 122 136 152120 42 56 70 84 98 112 125 139130 38 51 64 76 89 102 114 128140 36 48 60a 72 84 96 108 120150 33 44 55 66 77 88 99 110 133160 31 42 53 62 74 84 93 105 125170 29 39 49 58 68 78 87 98 116 137180 28 37 46 56 65 74 84 93 112 130 139190 26 35 44 52 61 70 78 88 104 123 131200 25 33 41 50 58 66 75 83 100 116 125210 24 32 40 48 56 64 72 80 96 112 119 127220 45 53 61 68 76 90 106 114 122240 42 49 55 62 69 84 98 165 110260 45 51 58 64 77 90 145 102280 42 48 54 60 71 84 89 96300 39 44 50 56 67 78 83 88320 36 42 47 52 62 72 78 84340 34 39 44 49 59 68 73 78360 32 37 42 46 55 64 69 74380 30 35 39 43 52 61 65 70400 29 33 37 41 50 58 62 66450 26 30 33 37 44 52 55 59500 23 26 30 33 40 46 50 53

aFor example, a herd of 140 cows milking twice daily with 10 milking units needs to have its liners changed every 60 days, or2 months.

254 Appendix: Liner Life Charts

Table A.2. Liner life in days according to herd and parlour size and assuming a liner life of 2500 milkings:two times a day milking.

Number of milking units

Herd size 6 8 10 12 14 16 18 20 24 28 30 32

50 150 183 183 18360 125 167 183 18370 107 143 179 18380 94 125 156 183 18390 83 111 139 166 183 183

100 75 100 125 150 175 183110 68 91 114 136 159 182 183120 82 83 104 164 145 166 183 183130 58 77 96 116 135 154 174 183140 54 71 89 108 124 142 162 178150 50 67 84 100 117 134 150 168 183160 47 62 78 94 109 124 141 155 183170 44 59 74 88 103 118 132 148 176 183180 42 56 70 84 98 112 126 140 168 183 183190 39 53 66 78 93 106 117 133 156 183 183200 38 50 63 76 88 100 114 125 152 175 183210 48 60 71 84 96 107 120 142 168 180 183220 68 79 91 102 114 136 158 170 182240 62 73 83 94 104 124 146 165 166260 67 77 86 96 115 134 145 154280 62 71 80 89 107 124 134 142300 58 67 75 83 100 116 125 134320 55 62 70 78 94 110 117 124340 51 59 66 73 88 102 110 118360 49 55 62 69 83 98 104 110380 46 53 59 66 79 92 99 106400 44 50 56 62 75 88 94 100450 39 44 50 55 66 78 83 88500 35 40 45 50 60 70 75 80

Appendix: Parlour Audit 255

Appendix: Parlour Audit

References and Further Reading

References

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Berry, E.A. and Hillerton, J.E. (2002) The effect of selective dry cow treatment on new intramammary infectionS.Journal of Dairy Science 85, 112–121.

Blowey, R. and K. Collis (1992) Effect of premilking teat disinfection on mastitis incidence, total bacterialcount, cell count and milk yield in three dairy herds. Veterinary Record 130, 175–178.

Blowey, R. and Deyes, E. (2005) The effectiveness of drying off individual quarters as a treatment of mastitis.Cattle Practice 13, 99–102.

Booth, J.M. (1982) Antibiotic residues in milk. In Practice 4, 100–109.Booth, J.M. (1993) Proceedings of the British Cattle Veterinary Association. In: Cattle Practice 1, 125–131.Bradley, A.J. and Green, M.J. (1998) A prospective investigation of intramammary infections due to

Enterobacteriacae during the dry period: a presentation of preliminary findings. Cattle Practice 6, 95–101.Bradley, A.J., Leach, K.A., Breen, J.E., Green, L.E. and Green, M.J. (2007) Survey of the incidence and

aetiology of mastitis on dairy farms in England and Wales. Veterinary Record 160, 253–258.Bramley, A.J. (1981a) The role of hygiene in preventing intramammary infection. In: Mastitis Control and Herd

Management, Technical Bulletin No. 4, National Institute for Research in Dairying, Reading, UK,pp. 53–66.

Bramley, A.J. (1981b) Infection of the Udder with Streptococcus uberis, E. coli and minor pathogens. In: Mastitiscontrol and Herd Management. Technical Bulletin No. 4, National Institute for Research in Dairying,Reading, UK, pp. 70–80.

Bramley, A.J., Dodd, F.H. and Griffin, T.K. (1981) Mastitis Control and Herd Management. Technical BulletinNo. 4, National Institute for Research in Dairying, Reading, UK.

Bramley, A.J. (1992) Mastitis. In: Andrews, A.H., Blowey, R.W., Boyd, H. and Eddy, R.G. (eds) Bovine Medicine:Diseases and Husbandry of Cattle Blackwell Scientific Publications, Oxford, pp. 289–300.

Bramley, A.J., Godinho, K.S. and Grindal, R.J. (1981) Evidence of penetration of the bovine teat duct byEscherichia coli in the interval between milkings. Journal of Dairy Research 48, 379–386.

Dingwell, R.T., Leslie, K.E., Schukken, Y.H., Sargeant, J.M., Timms, L.L., Duffield, T.F., Keefe, G.P.,Kelton, D.F., Lissemore, K.D. and Conklin, J. (2004) Association of cow and quarter-level factors atdrying-off with new intramammary infections during the dry period. Preventive VeterinaryMedicine 63, 75–89.

Egan, J. (1995) Evaluation of a homeopathic treatment for subclinical mastitis. MRCVS Thesis, The VeterinaryResearch Laboratory, Abbotstown, Dublin, Ireland.

Galton, D.M., Petersson, L.G., Merrill, W.G., Bandler, D.K. and Shuster, D.E. (1984) Effects of premilking udderpreparation on bacterial population, sediment, and iodine residue in milk. Journal of Dairy Science 67,2580–2589.

Galton, D.M., Peterson, L.G. and Merrill, W.G. (1988) Evaluation of udder preparations on intrammary infec-tions. Journal of Dairy Science 71, 1417–1421.


Green, M.J., Green, L.E. and Cripps, P.J. (1996) Low bulk milk somatic cell counts and endotoxin-associated(toxic) mastitis. Veterinary Records 138, 305–306.

Green, M.J., Huxley, J. and Bradley, A. (2002) A rational approach to dry cow therapy 1. Udder health priori-ties during the dry period. In Practice 24, 582–587.

Grindal, R.J., Walton, A.W. and Hillerton, J.E. (1991) Influence of milk flow rate and streak canal length on newintramammary infection in dairy cows. Journal of Dairy Research 58, 383–388.

Harrison, R.D., Reynolds, I.P. and Little, W. (1983) A quantitative analysis of mammary glands of dairy heifersreared at dirrerent rates of live weight gain. Journal of Dairy Research 50, 405–412.

Hill, A.W. (1981) Factors influencing the outcome of Escherichia coli mastitis in the dairy cow. Research inVeterinary Science, 31, 107–112.

Hill, A.W. (1990) Proceedings of the British Mastitis Conference, p. 49.Hill, A.W. (1992a) Proceedings of the British Cattle Veterinary Association 1991–1992, p. 279.Hill, A.W. (1992b) Proceedings of the Mastitis Conference, Frampton, UK, p. 281.Hillerton, J.E. (1988) Summer mastitis – the current position. In Practice 10, 131–137.Lee, C.S., Wooding, F.B.P. and Kemp, P. (1980) Identification, properties, and differential counts of cell popu-

lations using electron microscopy of dry cows secretions, colostrum and milk from normal cows. Journalof Dairy Research 47, 39–50.

Leigh, J.A. (2000) Streptococcus uberis: current and future prospects for a vaccine. Cattle Practice 8,pp. 265–268.

Lewis, S., Cockraft, P.D., Bramley, R.A. and Jackson, P.G. (2000) The likelihood of clinical mastitis in quarterswith different types of teat lesions in the dairy cow. Cattle Practice 8, 293–299.

Logan, E.F., Meneely, D.J. and Mackie, D.P. (1982) Enzyme-linked immunosorbent assay for Streptococcusagalctiae antibodies in bovine milk. Veterinary Record 110, 247–249.

MacKellar, Q.A. (1991) Intramammary treatment of mastitis in cows. In Practice 13, 244–249.Mackie, D.P., Pollock, D.A., Meneely, D.J. and Logan, E.F. (1983) Clinical features of consecutive intramam-

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Meany, W.J. (1992) In: Mastitis and Milk Quality. Handbook for Veterinary Practitioners, Irish Vet Associationand Irish Veterinary Union, Teagasc Research Centre, Moorepark, Ireland.

Menzies, F.D., Gordon, A.W. and McBride, S.H. (2003) An epidemiological study of bovine toxic mastitis.Proceedings of the British Mastitis Conference, Garstang, pp. 1–13.

Milner, P., Page, K.L. and Hillerton, J.E. (1997) The effects of early antibiotic treatment following diagnosis ofmastitis detected by a change in the electric conductivity or milk. Journal of Dairy Science 80, 859–863.

Neave, F.K., Dodd, F.H., Kingwill, R.G. and Westgarth, D.R. (1969) Control of mastitis in the dairy herd byhygiene and management. Journal of Dairy Science 52, 696–707.

Northwest Illinois Dairy Association (2000). [Details unknown.]Owens, W.E., Watts, J.L., Boddie, R.L. and Nickerson, S.C. (1988) Antibiotic treatment of mastitis: comparison

of intramammary and intramammary plus intramuscular therapies. Journal of Dairy Science 71,3143–3147.

Pankey, J.W., Wildman, E.E., Drechsler. and Hogan, J.S. (1987) Field trial evaluation or premilking test disin-fection. Journal of Dairy Science 70, 867–872.

Peeler, E.J., Green, M.J., Fitzpatrick, J.L. and Green, L.E. (2002) Study of clinical mastitis in British dairy herdswith bulk milk somatic cell counts less than 150,000 cells/ml. Veterinary Record 151, 170–176.

Philpot, W.N. (1984) Economics of mastitis control. Veterinary Clinics of North America: Large Animal Practice6, 233–245.

Philpot, W.N. and Nickerson, S.C. (1991) Mastitis: Counter Attack. Babson Bros. (Westfalia-Surge), Naperville,Illinois.

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Schukken, Y.H., Vanvliet, J., Vandegeer, D. and Grommers, F.J. (1993) A randomized blind trial on dry cowantibiotic infustion in a low somatic cell count herd. Journal of Dairy Science 76, 2925–2930.

Shearn, M.F.H. and Hillerton, J.E. (1996) Hyperkeratosis of the teat duct orifice in the dairy cow. Journal of DairyResearch 63, 525–532.

Sol, J., Sampimon, O.C. and Snoep, J. (1995) Proceedings of the 3rd International Mastitis Seminar, Israel, pp.5–68.

Spencer, S.B. (1990) The basics of vaccum in milking systems and milking management. Proceedings of theNational Milking Center Design Conference, Harrisburg, Pennsylvania.

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Tyler, J.W. and Baggot, J.D. (1992) Antimicrobial therapy of mastitis. In: Andrews, A.H., Blowey, R.W., Boyd,H. and Eddy, R.G. (eds) Bovine Medicine: Diseases and Husbandry. Blackwell Scientific Publications,Oxford, pp. 836–842.

Williamson, J.H., Woolford, M.W. and Day, A.M. (1995) The prophylactic effect of a dry-cow antibiotic againstStreptococcus uberis. New Zealand Veterinary Journal 43, 228–234.

Woolford, M.W., Williamson, J.H., Day, A.M. and Copeman, P.J.A. (1998) The prophylactic effect of a teatsealer on bovine mastitis during the dry period and the following lactation. New Zealand VeterinaryJournal 46, 12–19.

Further Reading

Andrews, A.H., Blowey, R.W., Boyd, H. and Eddy, R.G. (2004) Bovine Medicine: Diseases and Husbandry ofCattle, 2nd edn. Wiley-Blackwell, Chichester, UK.

Biggs, A. (2009) Mastitis in Cattle. The Crowood Press, Marlborough, UK.Blowey, R.W. (1999) A Veterinary Handbook for Dairy Farmers, 3rd edn. Old Pond Publishing, Ipswich, UK.Bramley, A.J., Dodd, F.H. and Griffin, T.K. (1981) Mastitis Control and Herd Management. Technical Bulletin

No. 4, National Institute for Research in Dairying, Reading, UK.Bramley, A.J., Bramley, J.A., Dodd, F.H. and Mein, G.A. (1992) Machine Milking and Lactation. Insight Books,

Newbury, Berkshire, UK.Countdown Downunder see http:www.countdown.org.au (accessed December 2009).International Dairy Federation. http:www.fil-idf.org

258 References and Further Reading

http://www.countdown.org.au

http://www.fil-idf.org

Acid boiling wash (ABW) 90Acidified sodium chlorite 121ACRs see Automatic cluster removersActinomyces pyogenes see Arcanobacter

pyogenesAcute mastitis 34ADF (automated dipping and flushing) 125Aesculin 47Aggressive therapy 203–204Air bleed hole 66, 83Air injectors 84–85, 88Alveoli (in mammary gland) 5, 50Aminoglycosides 200–201Amputation (of teats) 232Antibiotics

acidity and liquid solubility 202aggressive therapy 203–204bactericidal and bacteriostatic 201–202coliforms responses 201intracellular effects 202residues 3, 111, 245sensitivity 57–58therapy

benefits 199combination 203–204Streptococci and Staphylococcus

aureus cure rates 198versus self-cure rates 198–199

udder penetration 199–201withdrawal period 202

Antibiotic screening tests, residue avoidanceBetaStar and Charm MRL 246Delvo SP 245–246MRL level 245

Arcanobacterium pyogenes 55Ash (as cubicle bedding) 133–134Aspergillus mastitis 55Automatic cluster removers (ACRs) 63, 68, 111,

238Automatic milking system (AMS) see Robotic

milkingAutomatic teat disinfection 124–125

Back-flushing units 109–110

Bacillus 36, 41, 44, 54–55, 57, 58, 148, 173, 177Bacillus species, mastitis

B. cereus 54B. licheniformis 54–55

Bacterial eczema 226–227Bacterial sources, milk

dirty milking equipment 174environmental contamination

coliform count 173TBC versus coliform count 173winter bedding 174

mastitis organismsStreptococcus agalactiae and Streptococcus

uberis 172–173Streptococcus agalactiae infection 173

Bacteriology of milk 42, 167, 182, 251Bacteriostatic 201–202Bacteriocidal 201–202Bacteroides melaninogenicus 215, 216Bactoscan and TBC

BTA see Bulk tank analysiscomparison 172refrigeration failure

milk quality 174–175pasteurized milk, shelf life 176plate and tube coolers 175

Balance tank 63–64Barrier dips 122–123Bedding see CubiclesBetaStar antibiotic test 243, 246Beta-lactamase producing bacteria 200–201,

204, 205Biphasic let down 81, 84, 234, 238Black spot 25, 121, 212, 227, 229Blitz therapy 206Blood in milk 221BMSCC see Bulk milk; Somatic cell countBovine herpes mammillitis 227Bovine somatotrophin (BST) 17Brisket boards see CubiclesBulk tank analysis (BTA)

applications 178–179methodology 59sample interpretation 179

259

Index

Bulk tank analysis (BTA) (continued)study herds 180–183tests

bacteria individual significance176–177

Bactoscan problems 177coliform count 176Pseudomonas count 176psychotrophics bacteria 177sample collection 177–178target levels 177thermoduric count (TD) 176

Bulk milk 160–161, 176Bulk tank, cleaning 86Butterfat 85

Cai-Pan peppermint oil 209Calcium 3, 15, 17, 85, 154, 208California mastitis test (CMT)

benefits 155cow cell count 163–164disadvantages 155method 155–156

Candida 55Casein 2, 3, 15, 16, 17, 32, 47, 48, 154

see also Milk proteinCell counts

action for high cell count cowsearly dry cow therapy 163–164lactation, treatment 164–165milking order 165milk withholding 165quarter drying off 164treatment efficacy 166

effect on milkconsumption 154production 153–154

factors affecting 157–159financial penalties 153individual cow cell count 166–170legal compliance 153low cell counts 153measurement 154–155milk yield reduction 153–154

Cefquinome 200Cephalosporins 201, 211Chaps (on teats) 236Charm test 246–247Chemical teat damage 226Chemotaxins 27, 29Chlorhexidine 120Chlorine (in plant washing) 86–87Chronic mastitis 34Circulation cleaning 86–89Citrobacter 36, 46Claw piece 66, 68, 79–81Cloxacillin 199, 200, 211, 246Clusters see Milking machineClusters – flushing between cows 44, 109,

110Cluster removal see ACRCMT see California mastitis testCoagulase-negative staphylococci (CNS) 42Coagulase test 42–44

Coliform counts (CC) 58, 59, 104, 127, 173–174,182

Coliforms including E. coli 44–46Colony forming units, CFU 171, 172Colostrum 15 Complement 26Contagious organisms, mastitis

CNS 42Mycoplasma species 44overall incidence, clinical 36–37Staphylococcus aureus 38–41, 59Streptococcus agalactiae 42–43Streptococcus dysgalactiae 43–44

Contaminated samples 251Corynebacterium bovis 55, 125, 177, 180, 181Corynebacterium pyogenes see Arcanobacter

pyogenesCorynebacterium ulcerans 56Costs of mastitis 191Cow mattresses 134Crushed teats 230Cubicle/free-stall systems

basesconcrete pyramid 142–143floor slope 143–144

bedding types 145–146brisket boards 141–142discomfort 139division height 140features 138length 140management

cleaning and renewing 144, 145semi-automated system 144

neck rails 141rejection 141–142single and double row facing 139size 138–139

Cut teats 231

DCC (DeLaval cell counter) 155Defences, teat

canalflow rate and mastitis incidence

relationship 24Furstenberg rosette 22milk lakes 22short teat versus open teat 23

closureimportance, sphincter closure 22–23required pressure, force fluid back up

23keratin

flush 22plug 22

mastitis susceptibility and milkingfrequency 24–25skin

average teat condition and averagemilkout 21intact surface 21

teat-end damageblack spot, milking machine damage

and excessive dilatation 25

260 Index

hyperkeratosis and physical trauma25

DelvoSP test 245–247Diapedesis 29Dipping see Teat disinfectionDisinfection, teat

assessment 118–119dipping

anti-spill teat dip cups 117chemicals 120–123dips versus spraying 117, 119pots 118preparation and storage 119

iodine residues 128postmilking

automatic system 124–125limitations 125mastitis bacteria removal 123–124postdip products 127skin quality, dip additives 124sore, bacteria removal 124

premilking (predipping)advantage 127dry wiping 126ineffectiveness, predip 128

Dodecyl benzene sulfonic acid (DDBSA) 121Dry cow therapy

blanket versus selective 211failure 211infusion technique 213–214intramammary pathogen types 210long-acting antibiotics

benefits 210Staphylococcus aureus 210–211

quarter treatdrying off 211Staphylococcus aureus infection

response 211teat sealant

tube administration 212–213Drying off quarters 164, 204Dry matter intake (DMI)

metabolic disorder 54rumination rate 53

Dry period infectionsdescription 50host immune response 53phases

IMIs incidence 50–51keratin plug formation 52versus lactation infections 50, 51

short dry periods 54Dry wipe 101–102, 128Drying off quarters 164, 168, 204Dump line 195, 196Dump bucket 91, 110, 111, 195Dynamic testing (of milking plant) 76–78

Eczema 224–226, 228Edwards media 42, 43, 47, 57Effective reserve 82Electric current see Stray voltageEmollients 124Endotoxins 30, 45

Enterobacter 36Environmental organisms, mastitis

E. coli (Escherichia coli)chronic recurrent coliforms 46culture in milk 22–23dry period infections 45strain variation 45–46total bacterial count 58–59toxic effects 45

Klebsiella pneumoniae 46–47NLFs (non-lactose fermenters) 47Pseudomonas aeruginosa 47Streptococcus uberis 47–50, 59

Environmentbacterial contamination factors 131bedding types

ash 133–134bacteria growth 131–132coliform level 132cubicle sanitizer 135mats and mattresses 134–135sand 133sawdust and shaving 133shredded paper 134space allowances 135–136straw 132–133

cow handling 149cubicle/free-stall systemsdraughts 149–150dry cow hygiene 151heat stress 150open sand yard 131postcalving group 150–151rubber parlour floor surface 149sand yards 147–148stocking densities 148straw yard

bedding 145–146design 146–147stocking density 145

ventilationconventional roofing cowls 137heat and humidity 136–137multiple-span buildings 138roofing sheets 137straw yards 137wooden cubicle house 138

waste food 148Erythromycin 16, 200, 201, 202

Fast milkers 22, 24, 52Fat in milk see ButterfatFatty acids 17Five-point plan (NIRD) 1Flaming udders 98, 99Flooding (of claw piece) 66Fluid therapy

intravenous administration 207oral administration 207–208

Fly control 218Foot-and-mouth disease 34Foremilking

advantages and disadvantages 97internal teat sealants 97

Index 261

Foremilking (continued)risk, infection transfer 97–98

Forestripping see ForemilkingFossomatic counter 154–155Framycetin 53, 200, 210Free fatty acids 17Free stalls see CubiclesFrequency of milking

effect on mastitis 114effect on yield 18, 114

Fresh calved cow – immune response 30Frozen samples 177, 178Fungi 36, 55Fusobacter necrophorum 25, 215, 226Furstenburg’s rosette see Rosette of Furstenburg

Galactose 16Gangrenous mastitis 40, 41Gland cistern 9, 13, 14, 18, 106, 212Gloves 40, 50, 56, 85, 96, 97, 103, 123, 196, 213,

233, 248, 249, 250, 251Glucose 15–16, 208Glycerine (added to teat dips) 124Gram negative 26, 44, 57, 199–201Gram positive 57Gram stain 57

Hard milkers 24Heat stress 137, 147, 150Heifers – poor milk let down 14–15Hock sores (from cubicles) 134Humectants 124Hyperkeratosis

causes 78high-yielding cows 232–233occurrence 233teat scoring 234

immunoglobulins 26

Immunoglobulins (antibodies) 26Immunosupression (in fresh calved cow) 150Impact forces 73, 76, 79–81, 84, 102, 107, 111,

113Impetigo (staphylococcal) 228Incidence of mastitis 1–4, 36Individual cow somatic cell counts (ICSCCs)

162Inducible mechanisms, udder defences

chemotaxin alarminterleukin 8 and TNF 27phagocytosis process 27

inflammatory responsealarm signals 28diapedesis and epithelial cells damage

29endothelial cell junction 27, 29increased blood flow and margination

27PMN response, mid-lactation 29serum ooze and phagocytosis 29

Indurated quarter 53Infection – reservoirs of

host response to 35–36penetration of teat canal 34–35

Inhibitory protein 18Interceptor vessel 63Internal teat seal 97, 204, 212, 249, 250Intertrigo see Ulcerative mammary disease

(UMD)Intramammary infections (IMIs) 50–51Intrinsic mechanisms, udder defence

cellular responsecell types, milk and colostrum 26PMNs 27SCC 26

complement 26immunoglobulins 26lactoferrin

bacteriostatic effects 26E. coli infection, lactating and dry

cows 25lactoperoxidase 26

Involution 138–140Iodophor dips 127Iodine

in milk 128in teat disinfectants 118

Ischaemic teat necrosis 224–225

Keratin 12Keratin flush 22Klebsiella pneumoniae 46–47

Laboratory pasteurized count (LPC) 59, 174Lactation, control of 167–170Lactoferrin 25–26Lactose 15–16Lactoperoxidase 26Lanolin 124Lateral suspensory ligaments 7–9Leptospira hardjo 55Licking eczema 228Ligaments (of udder)

udder suspension 9rupture of 8–9

Lime (as cubicle bedding) 135Liner life charts

three times a day milking 253two times a day milking 254

Liners 71–73Liner slip 76, 79–81, 108, 127, 223–224Lipase (in mastitic milk) 2, 17Lipopolysaccharide 30, 45Listeria monocytogenes 56LPC see Laboratory pasteurized countLysozymes 246

Machine stripping 112, 113Macrophages 27, 31, 208‘Magic water’ 102Macrophages, function 27Margination 27Mastitis

categories 34clinical incidence, UK 1, 3, 37detection 98–100detectors 98–100economics 191

262 Index

effects, milk components 2, 3epidemiology 37–38financial penalties 3infection, development of 34–36lactation stage 192and milking frequency rate 24–25 overall incidence, clinical 36–37

Maximum residue limit (MRL) 245, 246Milk

blood in 7components effect of mastitis 2–3composition 15culturing

antibiotic sensitivity testing 57–58bulk tank analysis 58–59laboratory plating and incubation 56–

57methodology 59

mastitic milk appearance 1, 98–99pH 16

Milk let-downin heifers 14–15phases

erectile tissue engorgement 14myoepithelial contraction 13teat canal relaxation 14

reflexes and speed of milking 105–107Milking routine

best practice 249clusters disinfection 111–112drying teats 102–104effect on mastitis 95frequency 114hygiene regimes 95–96infection transfer, sources

gloves 97hands 96–97liners 96

mastitic infected cows 109–111mastitis detection 98–100order 113–114teat preparation 101–103

assessment 104–105unit attachment 108unit removal 111

Milk synthesisBST 17causes, poor quality 17colostrum 15dry period length 18–19environmental temperature 18fat 17lactose 15–16milking frequency 18minerals 17protein

casein 16plasmin 16

Milk yield reduction and cell count 153–154Milker’s nodules 228Milking cow tube usage 188Milking frequency

effect on cell count 159effect on mastitis 24

Milking machinesACRs (automatic cluster removers) 68air admission during milking 63air bleed hole 83balance tank 63–64cluster 66common faults 91–94direct to line 68, 84dynamic test 76–78effects on mastitis 78–81function 61–62high line/low line 67–68interceptor vessel 63maintenance 74–76pipelines 65–66pulsation 68–71pulsation rate and ratio 70pulsation ~ single and dual 70receiver vessel 67–68recorder jar 68regulator 64–65sanitary trap 65simple checks without testing equipment

82–83static test 75–76test report 76, 78vacuum gauge 65vacuum levels and reserve, plant 75vacuum pump 62–63vacuum reserve 82wash up routines 84–86

Milkstone removal 85Moulds causing mastitis see YeastsMycoplasma 44, 78, 109–110

Necrotic dermatitis/interigo 221, 223–225, 227Neutrophil see Polymorphonuclear leucocytesNitric acid 90Nocardia asteroides 55Non-lactose-fermenting (NLF) coliforms 47

Oedema, teat-end 235–236Oedema, udder 223–224Off label treatment 240–241Open sore suckler 226Overmilking 81Oxytocin

continual stripping 208–209level 105–106

Parlour audit report 255Parravaccinia, see PseudocowpoxPartial insertion technique 197Pasteurella/Mannheimia 55, 57Pasteurised milk, effect of temperature on shelf

life 176Pea in teat 222Penicillins, sensitivity and udder penetration

199–200Peppermint oil as topical treatment 209Peptococcus indolicus in summer mastitis 215Phagocytosis 27, 29Photosensitization 222Phosphoric acid 90

Index 263

Plasmin content of mastitic milk 2–3, 16, 17Plate cooler 175Polymorphonuclear leucocytes

(PMNs)(neutrophils) in milk 26Post calving group, establishment of 150–151Post milking teat disinfection

application 116–117automatic sprayers 117–119chemicals

barrier dips 122–123dodecyl benzene sulfonic acid

(DDBSA) 121foam dips 121hypochlorite and acidified sodium

chlorite 121lodophors and chlorhexidine 120quaternary ammonium compounds

(QACs) 120viscosity and surfactant 122

dipping 117dipping and spraying equipment 117–119effect on teat skin condition 127iodine residues 128–129limitations 125post and pre dipping comparison 127, 128rate of chemical use 125removal of bacteria from teat sores 124removal of mastitis bacteria 123–124seasonal use of post dips 126versus predipping 128

Predippingapplication 117chemicals used

foam dips 121hypochlorite and acidified sodium

chlorite 121lodine products 120

free iodine 120reasons for 126, 127speed of kill 101, 117versus postdipping 128

Prolactin in control of milk synthesis 17Protein

inhibitor, influence on yield 18removal during machine washing 85synthesis in milk 16

Proteus, culturing in milk 58Prototheca mastitis 55Pseudocowpox 227–228Pseudomonas aeruginosa 47

cause of environmental infection 47causing mastitis 177dry cow therapy 47, 102

Pseudomonad count 59Psychotrophs 177Pulsation

chamber 68–70checks during milking 69cycle 70massage phase 68, 69milkout phase 68, 70pulsator device 70–71rate and ratio 70single and dual 70

Quaternary ammonium compounds (QACs) 120

Receiver vessel 67–68Record keeping for mastitis 185Recorder jar 68Recurrence rate 187, 190–192Refrigeration failure, milk 174–176Regulator of the milking machine

clean air system 64effect of dirt 64function 75–76maintenance 64multiple weight controlled 93, 94servo 64spring 64testing 82–83

Residual milk 112–113Residue avoidance, milk

antibiotic screening testsBetaStar and Charm MRL 246Delvo SP 245–246MRL level 245

bulk tank antibiotic test failures reasons239, 240

natural inhibitors 246‘off label’ treatment

data sheet recommendations 240–241unlicensed combination therapy 241written treatment protocols 245

Rinse cycle in circulation cleaning 86Robotic milking (VMS) 74, 114–115Rosette of Furstenburg 22Rubber mats for bedding 132Rupture of the suspensory apparatus 8–9

Salmonella 56Sample collection

bulk tank 155high cell count cows 162sterile 251

Sand yards 147–148Sanitary trap of the milking machine 65Sawdust bedding 133Self cure 198–199Selenium and vitamin E effects 31–32Serratia 55Shavings, bedding 133Shredded paper bedding 134Single quarter agalactiae 226Size of cubicles 138–140Slow milkers, speeding up 108, 109Somatic cell counts, see Cell countSphincter eversion of teat-end 25Staphylococcal impetigo 228Staphylococcus aureus 38–42

acute gangrenous mastitis 40–42adhesive properties 35cause of contagious infection 37cell count variation 39culturing for in milk 56dry cow therapy 163mechanism of attack 35resistance to treatment 205response to antibiotics 198

264 Index

spontaneous cure 198–199subclinical, treatment during lactation

164–165teat contamination 40transfer from cow to cow 37treatment 38–39

Staphylococcus epidermis 42Staphylococcus hyicus 42Staphylococcus intermedius 42Staphylococcus xylosus 42Staphycocci, coagulsae negative 42Static test of the milking machine 75–76Stewart-Schwann cocci in summer mastitis

215–216Stocking density in housing systems 145Straw yards

advantages/disadvantages 144–145bedding

anaerobic fermentation 145–146design 146–147hard-core base 146

Streptococcus uberis infections 47–49Stray voltage 81–82Streak canal 57Streptococcus agalactiae 42–43

adhesive properties 35blitz therapy 43cause of contagious infection 37cell count 43culture 43mechanism of attack 35response to treatment 206spread of infection 97total bacteria count 176undermilking 43, 81

Streptococcus bovis 47Streptococcus dysgalactiae 43–44

cause of contagious infection 43in summer mastitis 215response to treatment 198

Streptococcus faecalis 55, 58, 180, 181Streptococcus uberis 47, 49, 50, 58, 59, 102,

173, 176, 200, 203, 210, 224association with straw bedding 176cell count 97clinical mastitis 36–37culture 58dry period infections 35, 49effect of lactoperoxidase 26outbreaks at pasture 49–50prevalence 50response to treatment 47strain variation 45–46total bacterial count 176vaccination 50variation in strains 45–46

Streptococcus zooepidemicus 55Stress

effect on cell count 158effect on cows 149

Subclinical infectiondefinition 43herd cell counts 167total bacterial count 59

Summer mastitisbacteria 215–216control 218–219Hydrotoea/sheep head fly 216treatment 217–218

Summer sores see Licking eczemaSunburn 223Supernumerary teats 9–11Supportive therapy 206–207Suspensory ligaments 8–9

Targets for mastitisBactoscan 186cell count 188mastitis rate 185milking cow tubes per cow per year 188percent of herd affected 185–187recurrence rate 187seasonal variations 188stage of lactation 188

TBC see Total bacterial countTeat canal 14, 22–24, 34–35, 78–79Teat club international scoring 234Teat congestion and oedema 92–94, 235–236Teat defences against mastitis see Defences, teatTeat diseases 226–229Teats, supernumerary/accessory 11Teat length and shape during milking 11Teat wall and structure 13–14Teat damage 232–237Teat disinfection see Predipping; Post milking

teat disinfectionTeat preparation

automatic washing in hot climates 103dry wiping 101–102drying teats before milking 103–104‘magic water’ 102pre-dipping 101–103robotic milking 114

Tetracyclines 201Total bacterial count (TBC) 3, 58–59

Bulk tank analysis 178dirty milking equipment 174effect of foremilking 97environmental contamination 173–174failure of refrigeration 174–176methodology 59

Toxins 27, 29, 207 see also EndotoxinsTreatment, mastitis

antibioticacidity and lipid solubility 202bactericidal and bacteriostatic 201–

202coliform response 201intracellular effects 202sensitivity and udder penetration

199–201tube withdrawal period 202

antibiotic therapycombination 203–204cure rates 198self-cure rates versus antibiotics

198–199Staphylococcus aureus 197–198

Index 265

Treatment, mastitis (continued)blitz therapy and Streptococcus agalactiae

206intramammary antibiotics 196–197mastitic cow separation 195–196Staphylococcus aureus resistance 205supportive therapy

anti-inflammatory drugs 208calcium and glucose 208continual stripping and oxytocin

208–209fluids 207–208homoeopathy 209non-antibiotic intramammary

infusions 209topical preparations 209

Treatment, poor response reasons 39Tube usage 188Tylosin 200, 202, 246

Udderblood supply 7bruising 42developmental phases 6–7rupture 8–10structure 5, 6suspension 7–8

Udder and teats disordersanterior udder sore/intertrigo/UMD

see Ulcerative mammary disease(UMD)

chemical damage 226machine milking 232oedema 223–224wet eczema/necrotic dermatitis/udder skin

slough 224Udder defences see Inducible mechanisms;

Intrinsic mechanismsindividual cow variation 31inducible mechanisms

chemotaxin alarm 27inflammatory response 27–29

intrinsic mechanisms 26–27PMN activity reduction 32poor response 30–31

Ulcerative mammary disease (UMD) 221–222Undermilking 81Uneven quarters 9

Vaccine 46, 228Vacuum fluctuations 76, 77Vacuum gauge 65Vacuum level 75, 82Vacuum pump 62–63Vacuum recovery time 82Vacuum reserve 62, 75, 82Ventilation

conventional roofing cowls 137heat and humidity 136–137multiple-span buildings 138roofing sheets 137straw yards 137wooden cubicle house 138

Vitamin E 31–32VMS (voluntary milking systems) see Robotic

milking

Wet eczema 224Warts 228–229Wash-up routine

ABW 90air injectors 84–85air lines 86best practice 250–251bulk tanks 86circulation cleaning 86–88efficiency evaluation 91

Wedging 235–236

Yeasts 55, 177cause of environmental mastitis 55culture 55treatment 55

Yersinia pseudotuberculosis 56

266 Index

mastitis control in dairy herds

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