salud e la ubre slu

7/29/2019 salud e la ubre SLU

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Udder health and milk composition, withspecial reference to beef cows

A literature review

Miguel Velazquez

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SLU Specialarbete 11

Institutionen fr husdjurens milj och hlsa

Swedish University of Agricultural SciencesSkara 2000

Faculty of Veterinary Medicine ISSN 1402-3342

Department of Animal Environment and Health ISBN 91-576-6004-2

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FOREWORD

This literature review was written by Miguel Velazquez, a recently qualifiedveterinarian from the University of Merida in Mexico. He was invited to participate intwo projects within FOOD21, and stayed in Sweden from April to November 2000.FOOD21 is a large research programme mainly working in the area of a sustainableenvironment and agriculture. The programme has been funded by MISTRA during1997-2000 and is expected to be funded for a second period during 2001-2004. As a

part of the synthesis work, a group called Tema Ko-kalv (theme: Cow-calf) has beenorganising meetings, seminars, research projects and collaboration with developingcountries, as for example Mexico and Colombia. The major interest of this group is toincrease the knowledge about systems where dairy cows and calves are kept together,

and to study the effects of these systems on behaviour, health and production.

One of the projects Miguel Velazquez was working with during his stay in Sweden wason the nursing behaviour, milk production, udder health and milk composition of beefheifers during their first lactation. There was a need in the project to have a goodliterature review on the udder health and milk composition related to beef cattle.

This review has been checked by us and approved for publication after some revision. Itis published as a joint publication between the Department of Animal Environment andHealth and FOOD21. It is our hope that this review will be of value both for students,and for other researchers going into this field.

The visit of Miguel Velazquez was funded by the International Foundation for Science(IFS).

Skara 2000-11-27

Lena Lidfors Charlotte Berg


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CONTENTS

SUMMARY 7

RESUMEN (ESPAOL) 8

INTRODUCTION 10

THE EFFECT OF MASTITIS ON PRODUCTION IN BEEF CATTLE 11

FACTORS INVOLVED IN INFECTION AND MASTITIS 12

COMMON TYPES OF INFECTIOUS MASTITIS 16

Staphylococcal mastitis 16Streptococcal mastitis 17Coliform mastitis 17

THE EPIDEMIOLOGY OF MASTITIS IN BEEF CATTLE 18

SOMATIC CELL COUNT 20FACTORS AFFECTING SOMATIC CELL COUNT 20

Infection status 20Season 21

Age 22Stage of lactation 22Diurnal variation 23Day to day variation 23Stress 24Technical aspects 24Effects of quarter 25Milk fraction 25

BOVINE MASTITIS BACTERIOLOGY 26

MILK CONSTITUENTS 27NUTRITIONAL FACTORS AFFECTING MILK CONSTITUENTS 28

Fat content 29Protein content 30Lactose content 30

NON-NUTRITIONAL FACTORS AFFECTING MILK CONSTITUENTS 31Breed 31Stage of lactation 31


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Mastitis and somatic cell count 33Milk fraction 33Other factors affecting milk constituents 33

ARE TEAT TRAITS IMPORTANT IN UDDER HEALTH AND

MILK COMPOSITION ASSESSMENTS? 35FACTORS AFFECTING TEAT LENGTH AND ITS IMPORTANCE ONMILK YIELD AND UDDER HEALTH 35TEAT INJURY AND TEAT PAPILLOMATOSIS 35

MILK UREA CONCENTRATION 37NUTRITIONAL FACTORS AFFECTING MILK UREACONCENTRATION

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Effect of protein 38Importance of balance between protein and energy 38Effect of rumen undegradable protein (RUP) 39

NON-NUTRITIONAL FACTORS AFFECTING MILK UREACONCENTRATION 40

Diurnal variation 40Season 41Stage of lactation 41Age 42Mastitis and somatic cell count (SCC) 42Body weight 43

Milk yield 43Technical aspects 43Other factors affecting milk urea concentration 44

EFFECTS OF NURSING ON UDDER HEALTH STATUS 45RESTRICTED SUCKLING VERSUS ARTIFICIAL REARING 45

CONCLUSION 49

CONCLUSION (ESPAOL) 49

ACKNOWLEDGEMENTS 50

REFERENCES 52


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SUMMARY

Mastitis is a significant disease in beef cattle production. However the prevalence ofmajor pathogens in beef cows is lower compared to dairy cows, S.aureus being themain major pathogen isolated. The reason for the lower prevalence may be the absenceof opportunity for infection at machine milking time, which is considered an importantfactor for mastitis in dairy cows. Immunoglobulins, cell-mediated immunity andanatomic teat traits play an important role in the protection against mastitis.

The most important factor affecting somatic cell count (SCC) is the infection status ofthe quarter, and the threshold for dividing quarters into uninfected and infected (with amajor pathogen) is usually set at 200 000 cells/ml or 300 000 cells/ml. However several

samplings, at least five during a lactation, must be done to achieve reliable results.Although several factors have a significant effect on SCC, some of them could beexplained by the dilution effect, related to the milk yield of the cow. Interpretation of

bacteriology and SCC in milk together is not straighforward, and possible reasons forunexpected results must be taken into account.

Milk fat percentage is the most variable component in milk. Despite of somecontradictory works, most of the literature have reported that in general high amountsof energy in the feed result in milk fat depression, and that the feed protein level haslittle or no effect on the milk fat content. Increased dietary energy will increase milk

protein percentage. Increased protein levels in the diet generally have no effect on milk

protein content. However fat supplements may decrease milk protein percentage.Lactose is the most constant component in milk. Milk constituents are also affected bynon-nutritional factors and mastitis is the most important such factor. Some non-nutritional factors that have influence on milk composition could be explained bydilution effects as well.

The most important nutritional factor affecting milk urea concentration is the balancebetween energy and protein. Milk urea concentration must be measured only in samplesfrom healthy quarters and preferably in fresh samples or after a short period ofconservation. Also, due to the diurnal variation, time sampling and feeding time must

be considered.

Teat traits have an important role in the development of intramammary infections,therefore this must be taken into consideration in mastitis risk factor assessment.Suckling has a beneficial effect on the incidence of mastitis. This could be due to themechanical effect of suckling, the better emptying of the udder and to the cleaningeffect of the calfs saliva.


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RESUMEN

Mastitis es una enfermedad significativa en la produccin de ganado de carne. Sinembargo la prevalencia de patgenos mayores en vacas de carne es menor comparadocon vacas de leche, siendo S. aureus el principal patgeno mayor aislado. La razn paraesta menor prevalencia puede ser la falta de oportunidad de infeccin al momento de laordea, lo cual es considerado un factor importante en mastitis en vacas lecheras.Inmunoglobulinas, inmunidad mediada por celulas y caractersticas anatmicas de lateta juegan un papel muy importante en la proteccin contra mastitis.

El factor ms importante afectando el conteo de celulas somticas es el estado deinfeccin del cuarto, y el lmite para dividir cuartos en infectados y no infectados es

usualmente fijado en 200 000 cels/ml o 300 000 cels/ml. Sin embargo varios muestreos,por lo menos cinco durante la lactation, deben ser hechos para conseguir reultadosfiables. Aunque varios factores tienen un efecto significante sobre el conteo de celulassomticas, algunos de ellos podran ser explicados por el efecto de dilucin,relacionado con la produccin de leche de la vaca. La interpretacin de examenes

bacteriolgicos y conteo de celulas somticas en leche, cuando se utilizan juntos, no essencillo, y posibles razones para resultados inesperados deben ser tomados en cuenta.

El porcentage de grasa en la leche es el componente ms variable en la leche. A pesarde algunos trabajos contradictorios, la mayora de la literatura ha reportado que engeneral altas cantidades de energa en el alimento resulta en una disminucin de la

grasa en leche, y que los niveles de proteina en el alimento tienen poco o ningn efectosobre el contenido de grasa en leche. Energa diettica incrementada incrementar el

porcentage de proteina en leche. Niveles de proteina incrementados en la dietageneralmente no tienen efecto sobre el contenido de proteina en leche. Sin embargo lossuplementos grasos pueden disminuir el porcentage de proteina en leche. Lactosa es elcomponente ms constante en la leche. Los constituyentes de la leche tambin sonafectados por factores no nutricionales y mastitis es el ms importante de ellos. Algunosfactores no nutricionales que tienen influencia sobre la composicin de la leche podranser explicados tambin por el efecto de dilucin.

El factor nutricional ms importante afectando la concentracin de urea es el balanceentre energa y proteina. La concentracin de urea en leche debe ser medida solo enmuestras provenientes de cuartos sanos y de preferencia en muestras frescas o despusde un perodo corto de conservacin. Tambin, debido a las variaciones diurnas, tiempode muestreo y tiempo de alimentacin deben ser considerados.


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Las caractersticas de las tetas tienen un papel importante en el desarrollo deinfecciones intramamarias, por lo tanto esto debe ser tomado en consideracin enevaluaciones de factores de riesgo de mastitis. El amamantamiento tiene un efecto

benfico sobre la incidencia de mastitis. Esto puede ser debido a el efecto mecnico del

amamantamiento, el mejor vaciado de la ubre y al efecto de limpieza proporcionado porla saliva del becerro.


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INTRODUCTION

The udder is one of the most important physiological and conformational characteristicsof the cow (White and Vinson, 1975) due to its importance for milk production. It isoften believed that milk production is only important in dairy cattle. However milk

production in beef cows is the greatest single factor influencing preweaning weightgains (Beal, et al., 1990).

High correlations between milk yield and calf weight have been found by severalresearchers (Neville, 1962; Totuseket al., 1973; Stobbs and Brett, 1976; Boggs et al.,1980; Doornbos et al., 1981; Beal et al., 1990). Studies done by Neville (1962) andJeffery et al. (1971) determined that milk yield accounted for more than 60% of

variation in calf preweaning weight gain. Rutledge et al. (1971) suggested thatapproximately 60% of the variance in weaning weight could be attributed to the directinfluence of the dams milk yield. Jeffery and Berg (1971) and Boggs et al. (1980)reported that each additional kg of milk per day increased calf preweaning weights by 7to 14 kg. Therefore factors affecting milk production in beef cattle are certainlyimportant. However, research about factors that can influence the quality and quantityof bovine milk has hitherto mainly been carried out in dairy cows.

The effects of feeding and separation in cow-calf pairs on milk yield, cow body weight,calf growth, udder health, milk composition and behaviour have been studied in beefcows in a experimental studies carried out in Sweden recently. The investigation was

done with 7 Hereford, 3 Angus and 4 Angus x Hereford primiparous cows with an ageof 23-26 months and their calves. The study consisted of two phases, with the first onein the indoor season (5 days after calving) and the second one in the grazing season (3months after calving). In the first phase cows were fed with silage ad libitum and 1kg ofconcentrate which was a mixture of barley (35%) and oats (65%). In the second phase 6kg of concentrate were given. Milk yield was estimated by the calf weighing methodusing a scale. The cows body weight was recorded by scale (phase 1) and by tapemeasure (phase 2). Three milk samples were taken per day at a number of occasions,two (in the morning and in the afternoon) for analysis of fat, protein, lactose andsomatic cell count and one for bacteriology (only in the morning). The suckling

behaviour was recorded using a portable video camera. For each cow separate teat traitswere recorded in both phases. Analysis of the results is currently being undertaken.

More information is needed in order to interpret, in the best way possible, the results ofthis investigation and also for future investigations on the subject. The aim of thisreview is to present some basic knowledge about factors that influence udder healthand milk composition in beef cows, mainly by comparing data from dairy and beefcattle reported in the literature.


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THE EFFECT OF MASTITIS ON PRODUCTION IN BEEF CATTLE

The relationship between cow-calf performance and udder health status has beeninvestigated in beef cattle. Watts et al. (1986) found that intramammary infections with

pathogenic organisms were associated with increased somatic cell count (SCC) levelsand decreased weaning weights, reporting that calves from cows with one, two, threeand four quarters infected weighed 10.4, 22.7, 27.2 and 27.2 kg less (P


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FACTORS INVOLVED IN INFECTION AND MASTITIS

Mastitis (from the Greek word mastos meaning breast and the suffix itis meaninginflammation) classically is defined as inflammation of the mammary gland (Kehrli andShuster, 1994). Similarly, inflammation is defined simply as a reaction to injury. Hence,injury of any type to mammary tissue may be expected to induce an inflammatoryresponse or mastitis (Jain, 1979). However, the udder disease usually arises as a resultof microbial infection. The signs of mastitis vary according to factors in the host andthe invading pathogen (Leigh, 1999).

The characteristic features of an inflammatory response are swelling, heat, redness, painand disturbed function.Peracute mastitis exhibits all the signs of inflammation along

with systemic signs of fever, depression, shivering, loss of appetite, rapid weight lossand in some cases development of bacteraemia, septicaemia and death of the animal.Acute mastitis also is characterized by all gross signs of inflammation and some signsof systemic disturbance such as fever and mild depression. In Subacute mastitis, thecardinal signs of mastitis are less pronounced and there are no systemic signs. Theexistence of inflammation in the absence of gross signs is referred to assubclinicalmastitis. Mastitis is chronic when the inflammatory process persists for months. It mayremain subclinical indefinitely or, in some cases, may have temporary exacerbations ofsubacute or acute nature. The existence of a pathogen within the mammary glandwithout any evidence of mastitis is referred to as latentinfection (Jain, 1979)

The internal environment of a normal mammary gland is ideally sterile, but saprophyticbacteria may be found as commensals in some "normal mammary glands. However, toinduce mastitis, a pathogen must first gain entrance into the mammary gland, survivethe intramammary bacteriostatic and bactericidal agents, and then multiply insignificant numbers. Mastitis begins with penetration of pathogenic bacteria through theteat canal (streak canal) into the interior of the gland. If the internal environment of thegland is favorable to survival and multiplication of the invading bacteria, the productsof bacterial growth and metabolism may irritate the delicate mammary tissue andinduce an inflammatory reaction. The clinical signs of mastitis are, in reality, anexpression of the host defense intended to destroy the invader and to make way for

repair to regain normality (Jain, 1979).

The normal bovine mammary gland is divided by the medial susphensory ligament andsupplied by separate arteries, veins and nerves. The front and rear quarters are separatedfrom each other with regard to secretory tissue but share a common blood and nervesupply. Each quarter has a gland cistern, which serves as a collecting duct for thatquarter. The gland cistern continues distally to the teat cistern and is demarcated by adistinc fibrous tissue, which is called the annular ring. At the most distal aspect of theteat cistern is the teat canal canal (papillary duct), which communicates with the outsideof the teat (fig. 1) ( Weber, 1977; Trostle and OBrien, 1998).


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Figure 1. Diagram of the main structures of the bovine udder (adapted from Sisson, 1975 and

Willian, 1985).

The immune system of the mammary gland must serve a dual function: to providepassive immunity for the neonate and to protect the organ itself against pathogenic

insult (Opdebeeck, 1982). The first line of defence the organisms encounter is theepidermis of the teat (McDonald, 1979; Fox and Gay, 1993; Sordillo et al., 1997).

Resistence to bacterial invasion of a mammary quarter is determined, for the most part,by the structure and function of the teat canal. The normal teat canal has severalanatomic features that act as barriers to penetration of bacteria (Smith, 1983; Hibbitt,1983b). These features are most effective in the first lactation and tend to decrease withincreasing lactational age. The lining of the teat canal consists of a stratified squamous


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epithelium, like the skin of the teat, and its surface continually undergoes keratinizationto form sebum-like material which fills the lumen of the canal (Smith, 1983; Hibbitt,1983b). Teat canal keratin act as barrier to microorganisms involved in mastitis (Jacketal., 1992).This material is rich in long-chain fatty acids having a bacteriostatic affect on

certain bacteria (Mosdoel, 1978).

Partial removal of keratin from the teat canal has been reported to compromise theability of the teat to prevent passage of bacterial pathogens from the externalenvironment into the mammary gland (Bramley and Dodd, 1984; Capuco et al., 1992).The teat canal is surrounded by a true sphincter of smooth muscle fibers which functionin maintaining a tight closure of the canal (fig. 1). Quarters having patent teat canals(lack of tight closure) have a greater incidence of infection (Jain, 1979; Sordillo et al.,1997). McDonald (1968) reported that the teat canals lengthen and dilate with increasein lactational age of cows. Motomura et al. (1994) reported that cows with larger canal

diameters could make them more liable to contract mastitis. Other authors have foundsimilar results (Grega and Szarek, 1985; Jorstad et al., 1989; Hamana et al., 1994).However Kartashova et al. (1992) reported no significant correlation between teatdiameter and incidence of mastitis.

The neutrophile polymorphonuclear (PMN) leukocytes is the second line of defenseagainst mammary gland infection (McDonald, 1979). The PMN leukocytes make upmost of the leukocytes in circulating blood of many animal species. However, in the

bovine, PMN leukocytes make up only 25% of the total leukocyte count (Paape et al.,1979). These neutrophils are capable of phagocytosing a wide variety of particles.Phagocytosis is the process of recognition, ingestion and digestion of foreign particles.

In the bovine species there is a difference between the phagocytic ability of PMNleukocytes of milk and PMN leukocytes of blood (Paape et al., 1979). It has beenreported that the number of staphylococci killed by PMN leukocytes isolated from milkwas significantly less than the number killed by PMN leukocytes isolated from blood(Russell and Reiter, 1975). This inhibition of function in the milk has been attributed to

poor glycogen reserves within the cell and diversion of phagocytic effort into theingestion of milk fat globules and casein (Opdebeeck, 1982).

Immunoglobulins also have an important role in the pathogenesis of mastitis. These inmammary secretation are either humoral origin or are made locally by cells of the

lymphocyte plasma cell series located near the glandular epithelium. The most of theIgG in mammary secretation has a humoral derivation whereas IgA and IgM aresynthesized locally (Lascelles, 1979; Hibbitt, 1983a).

Gram-positive cocci account for more than 90% of infections in the bovine mammarygland. The opsonization of bacteria and neutralization of toxins constitute importanteffector functions in the protection of the gland and these functions are mainly ascribedto the IgG immunoglobulin (Opdebeeck, 1982).


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Some studies have investigated if there is a relationship between oestrus and incidenceof mastitis (Reece and Murphy, 1943; Berger and Francis, 1951; Frank and Pounden1961) as well as the influence on mastitis of forages containing legumes which haveestrogenic properties (Franket al., 1959; Pounden et al., 1960; Pounden and Frank,

1961; Frank and Pounden; 1961). The main results of these investigations were that anexcess of oestrogens might predispose to mastitis, mainly at oestrus when estrogenicactivity is considered to be highest. Also it was found that the incidence of mastitis wasrelated positively to feeding legume-grass forages in the fresh state or as silage.


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COMMON TYPES OF INFECTIOUS MASTITIS

A total of 137 microbial species, subspecies and serovars have been isolated from thebovine mammary gland (Watts, 1988). However, the most common causes of udderdisease include staphylococci (Staphylococcus aureus and Staphylococcusepidermidis), streptococci (Streptococcus agalactiae, Streptococcus dysgalactiae,Streptococcus uberis and Streptococcus bovis) and coliforms (mainlyEscherichia coliandKlebsiella pneumoniae). Other etiological agents less frequently encounteredinclude pseudomonads, nocardia, mycoplasmas and yeast (McDonald, 1979).Organisms colonizing the mammary gland can be divided as well into one group,referred to either as minor pathogens or commensals (e.g. corynebacterium bovis orcoagulase negative staphylococci) and a second group containing the major pathogens

(streptococci spp., S. aureus and coliforms) (Dohoo and Meek 1982).

Staphylococcal mastitis

This type of mastitis is usually associated with udder infection by S. aureus. Thisbacteria mainly produces subclinical and chronic mastitis, but it also may causeperacute mastitis and lead to gangrene of the quarters. Bacterial toxins and toxicproducts are thought to be involved in the causation of mastitis and gangrene. The alfatoxin is potentially the most damaging, because it causes vasoconstriction leading toischemic necrosis of affected tissues and gangrene (Schalm, 1977). Gangrenous mastitis

is most often found in young cows and after calving. Coagulase and other bacterialproducts are thought to enhance infection, allowing bacterial growth in the face of hostdefense mechanisms like phagocytosis (Jain, 1979). Delayed type hypersensitivity isconsidered an important part of the pathogenesis of staphylococcal mastitis and isrelated to peptidoglycan fraction of the cell wall (Woolcock, 1979).

The principal reservoirs ofS. aureus are the udder and teat skin and the milk of infectedglands (McDonald, 1977). As few as 10 colony forming units (CFU) ofS. aureus caninfect the udder. The organisms have the capacity to penetrate tissues producing deepseated foci; hence, intramammary antibiotic therapy is not completely successful in

eradication of staphylococcal mastitis. Leukocytosis in milk is not successful indisposing of virulent S. aureus because a) certain bacterial products like alfa toxin andleucocidin are damaging to neutrophils, b) protein A is antiphagocytic, and c) certain

bacterial products protect them from intracellular killing. Intramammary infections withS. epidermidis are being increasingly recognized, but it is still not considered a seriousmammary pathogen since most infections are eliminated spontaneously (Jain, 1979).


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Streptococcal mastitis

In this case species frequently reported to cause mastitis are Str. agalactiae, Str.dysgalactiae and Str. uberis, with the first one being most prevalent (McDonald, 1977).

Str. agalactiae multiplies in the milk and on the mammary epithelial surfaces, generallycausing a subacute or chronic inflammatory reaction with periodic acute flareups.

The affected tissue eventually is destroyed resulting in reduced milk production oragalactia. Str. agalactiae is an obligate parasite of the udder and, unlike coliformorganisms, it does not survive in the environment of the cow; hence, it is relatively easyto eradicate. Str. uberis and Str. dysgalactiae are not obligate udder pathogens.

They can survive for long periods in the environment of the cow and may be culturedfrom skin and other parts of the cow; hence these organisms are difficult to eradicate

(Jain, 1979). These infections are not contagious as is Str. agalactiae. These organismsinvade the udder when conditions become favorable and may cause acute or chronicmastitis but more commonly a subclinical reaction. Although udder and teat surfacesseem to be the most common reservoirs ofStr. uberis, mastitis due to this organism isless frequent (Jain, 1979).

Coliform mastitis

The coliforms organisms commonly involved in mastitis areEscherichia coli,Klebsiellasp., andEnterobacter aerogenes, the first one being most prevalent

(Eberhart, 1977). Their pathogenic effect is an attribute of endotoxin contained inbacterial cell wall. Coliform bacteria are ubiquitous in the environment of the cow.Coliform mastitis is typically acute or peracute, but chronic and subclinical infectionsaccompanied with periodic acute flareups also occur. Cows suffering from peracutemastitis may die within a few days due to endotoxemia but usually overcome acutemastitis. Coliform mastitis is generally self-limiting and does not cause extensivedamage to the mammary parenchyma; hence milk production does not decreasesignificantly following recovery (Jain 1979).

Infections usually are acquired from the environment via the teat canal and are not

transmitted directly from cow to cow, as is the case with most streptococcal andstaphylococcal infections. Although coliforms are widespread in the environment of thecow and frequently are isolated from teat skin, coliform mastitis is relativelyuncommon. This is perhaps due to relative susceptibility of most coliform bacteria tohumoral and cellular factors in milk. Natural antibodies to coliform organisms in milkand leukocytosis in the udder generally prevent establishment of udder infection withmost of these organisms.

Hence, glands infected with more common udder pathogens and experiencing mildleukocytosis generally remain free of coliform infection. Therefore, coliform mastitis isconsidered to be a disease of the gland uninfected with other pathogens (Jain, 1979).


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THE EPIDEMIOLOGY OF MASTITIS IN BEEF CATTLE

Mastitis can be an important factor in preventing beef cows from achieving their truegenetic potential for milk production (Kasari and Gleason, 1996). Two epidemiologicaltools used in order to quantify udder health are prevalence and incidence. Prevalencemeasures the amount of mastitis prevailing at a given point in time, and incidencemeasures the rate of new cases of mastitis over a period of time (Thurmond, 1993).

Newman et al. (1991), working with purebred and crossbred beef cows reported thatthe numbers of new intramammary infections (IMI) with S. aureus at each samplingtime (early, mid and late lactation) tended to be about equal to the number of infectionslost (infected quarter recovered), so their prevalence did not greatly increase duringlactation. Incidence measures are of particular interest because they provide estimates

of risk (Thurmond, 1993).

Figures on prevalence of mastitis has been reported in a number of studies in beefcattle. In a two-year study made in two beef suckler herds; in which the cow not onlyraised her own calf but several other calves were frequently purchased and were raisedto weaning on the same cow, 2400 quarter milk samples were examined. Theresearchers found that 18% of all quarters were infected and 67% of all infections weredue to staphylococci and 20% to streptococci (Hunter and Jeffrey, 1975). Sobari et al.(1976) reported a prevalence of 42.3% in beef cows from various parts of NorthernQueensland. Kirkbride (1977) reported that of 20 beef cows, 8 were infected (40%)with coagulase-positive staphylococci. These cows were 2 to 6 years old and had been

lactating 1 to 8 months.

Haggard et al. (1983) reported in two different beef herds, a prevalence of 13% (12 of92) in confined Angus cows and heifers; and 10.7% (8 of 75) in Hereford and Hereford-cross-bred females that were in a range-pasture operation. The total prevalence (bothgroups) was 11.9%. In the confined group the agents identified were S. aureus (n=9),streptococcus spp other than agalactiae (n=1), and klebsiella spp (n=2). For the range-

pasture herd S. aureus was the only agent identified. This test was done 30 days aftercalving.

In 1600 Charolais cows 24 (1.5) cases of clinical mastitis were detected, mostappearing during the calving period, also infected quarters rarely recovered andfrequently dried up, sometimes temporarily but often permanently (Boucomont, 1985).Watts et al. (1986) identified IMI in 37% of Hereford, Hereford x Brahman, andHereford x Brown Swiss cows and in 18% of the quarters. Coagulase-positivestaphylococci and coagulase-negative staphylococci were isolated in 17.9% and 16.1%of the cows respectively. For coagulase-positive staphylococci, S. aureus accounted for39.9% of these infections. Samples from quarters in this study were collected at

parturition and at weaning.


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Timms et al. (1989) working with 80 beef cattle reported high levels of infection atcalving (41% of cows, 17.5% of quarters), throughout lactation (33%, 13%) and atweaning (28%, 12%).

Predominant organisms in this study were coagulase-negative staphylococci (67% ofinfections), S. aureus (28%) and environmental streptococci (5%). In 213 quarter milksamples taken at random from 7 beef herds, it was found that 36% of cows and 14% ofquarters had subclinical mastitis, mostly associated with coagulase-negativestaphylococci (Hoyeret al., 1991).

Newman et al. (1991) reported 25.8, 29.2 and 54.4% of the cows being infected withmastitis pathogens in early (2 to 4 weeks postcalving), mid (100 days postcalving) anslate lactation (200 days postcalving) respectively. The corresponding prevalence ofinfection in quarters in that study was 13.1, 14.9 and 27.5% respectively. S.aureus was

isolated from 2.9, 2.7 and 3.2% of quarters in early, mid and late lactation. Simpson etal. (1995) found that in 25 primiparous Simmental cows, 32% of the cows and 18% ofthe quarters were infected with mastitis organisms at least once during their initiallactation. The sampling on these cows was done on day 34, 49, 80, 108, 147 and 189+/-3 postpartum. Nickerson et al. (2000) working with beef heifers observed that the

prevalence of infection in quaters was 10% in early lactation and the mainmicroorganisms isolated were coagulase-negative staphylococci, followed by S. ureus.Ridgway et al. (1999) also reported have isolated these two microorganisms fromAngus x Hereford cows.

As we can see the prevalence of IMI in beef cows in these works ranged from 10% to

54% and the prevalence of infected quarters ranged from 10% to 27%. These data alsoshow that the predominant microorganisms isolated were coagulase-negativestaphylococci and S.aureus and that most of the IMI occurred soon after calving (earlylactation). In dairy cows it has been found that most of the IMI that ultimately developinto clinical mastitis do so during the first few weeks of lactation, which correlates wellwith immunosuppression observed during this period (Kehrli and Shuster, 1994)

Compared to data from dairy cows the prevalence of infection by major pathogens inbeef cows is low. Prevalence of major pathogens within a dairy herd is influenced bymastitis control practices, especially teat dipping and dry cow therapy, and therefore,

varies considerably from herd to herd. The usual method of transmitting majorpathogens in a dairy herd is from cow to cow during milking. In beef cows, with thecalf as a vector, the organism can be spread from one quarter to another in the samecow, but spread from cow to cow seems unlikely because cross-suckling is believed tooccur only rarely in beef cows (Hoyeret al., 1991; Newman etal., 1991). Hence it is

possible that in beef cows, the prevalence of major pathogens remains relatively lowbecause of the absence of opportunity for infection at milking time (Newman et al.,1991).


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SOMATIC CELL COUNT

The alveolar epithelial cells of the mammary gland are highly active secretory cells that

are normally subjected to continuous high turnover and therefore must be replacedcontinually with new cells. These displaced cells are discharged into the milk as anormal process. In response to irritation, whether physical or microbial, white bloodcells enter the milk from the blood and perialveolar interstitium. The displaced alveolarepithelial cells, phagocytes and white blood cells comprise the somatic cells of the milk(Kirk, 1984; Concha, 1986; Sordillo et al., 1997). The measurement of the number ofsomatic cells in milk is known as a somatic cell count (ORourke, 1999). Somatic cellcount (SCC) of milk samples, is one of the techniques used to monitor the level oroccurrence of subclinical mastitis in herds or individual cows or quarters (Dohoo andMeek, 1982). The prevalence of subclinical infection is difficult to ascertain, as this can

only be determined by the isolation of bacteria from the gland; however, SCC is oftenused as an indirect estimation (Leigh, 1999).

FACTORS AFFECTING SOMATIC CELL COUNT

The ability to correctly interpret SCC depends on an understanding of the factors whichmay affect them. These factors may exert their influence at the quarter, cow or herdlevel (Dohoo and Meek, 1982). The following factors have been identified; infectionstatus, season, age, stage of lactation, diurnal variation, day to day variation, stress,

technical aspects, effects of quarter and milk fraction.

Infection status

The most important factor affecting the SCC of the milk from an individual quarter, andconsequently the cow and the herd, is the infection status of the quarter (Dohoo andMeek, 1982; Kirk, 1984; Senderet al., 1987; Schepers et al., 1997). The normalsomatic cell count in milk in various parts of the same udder varies widely from nearzero in uninfected areas to something in the order of three hundred million cells per

litre in the worst infected areas (ORourke, 1999).

It is difficult to nominate appropiate cell count thresholds above which the udder istermed diseased (Francis, 1993). The main problem has been determining acorrelation between a given somatic cell count and the corresponding probability thatinfection might be present (Kirk, 1984). In dairy cattle both 400 000 and 500 000cells/ml have been evaluated as possible thresholds, for classifying a quarter as beinginfected, but both resulted in a high false negative rate (i.e. too many cases ofsubclinical mastitis were missed) (Dohoo and Meek, 1982). On a quarter basis, Poutreland Rainard (1982) found that 93% of samples from uninfected quarters had cell countsof less than 500 000 cells/ml, but 45% of quarters infected with major pathogens also

had counts of less than 500 000 cells/ml. However in beef cattle it has been reported


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that staphylococcal infections were associated with cell counts over 500 000 cells/ml(Hunter and Jeffrey, 1975; Nickerson et al., 2000).

It has been recommended that the threshold be set at 200 000 cells/ml for firts lactation

(Senderet al., 1987; Dohoo and Leslie, 1991; Schepers et al., 1997) at 300 000 cells/mlfor all lactations (Dohoo and Meek, 1982; Senderet al., 1987). aureus However Neave(1975) found that 11% of quarters with long lasting Staphylococcus aureus had, at oneor more samplings, cell counts of less than 100 000 cells/ml, and 19 % of these quartershad at some time a count of less than 300 000 cells/ml.

Also secretory disturbances including declining milk yield, have been reported to startonce cell counts exceed 100-150 000 cells/ml, and the probability of isolating a major

pathogen is increased with counts above 200 000 cells/ml (Dohoo and Meek, 1982).

Hence no matter what threshold is used, a proportion of quarters or udders will beincorrectly classified (Francis, 1993). Therefore the evaluation of several successivecounts is preferable to the interpretation of an individual count (Dohoo and Meek,1982). Sampling at least five times during a lactation has been recommended(Clarkson, 1975).

Season

The season appears to affect the SCC of dairy herds in various locations and is notentirely related to ambient temperature or stressful seasonal conditions (Dohoo and

Meek, 1982). In general, SCC are lowest during winter and highest during the summer.Data from Wisconsin shows a peak SCC from July through August and a low count inMarch; marked differences also existed between months during different years (Bodohet al., 1976). Data from Quebec, Canada, indicates a low count in May, with a steadyincrease beginning in June and registering the highest count in December. The increase,which began when the cows went to the pasture and peaked when they returned tohousing is possibly attributable to environmental stress and renewed challenges from

bacteria (Kennedy et al., 1982). During the summer in Scandinavia, cows on pasture(cooler temperatures) have had higher cell counts than cows confined to the barn(warmer temperatures), and the increase in cows on pasture was primarily seen in

noninfected quarters (Simensen, 1976).

In a recent study Pomies et al. (2000) concluded that the increase in SCC observed insummer is not due to the environmental change when cows are turned out to pasture,and alternative explanations were suggested, such as physiological, health or climaticfactors which may be exacerbated by the period at pasture. No studies on seasonal


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effects on SCC in beef cattle were found. In temperate climates, such as in Scandinavia,beef calves are generally born in the spring or early summer. It is therefore difficult toanalyse any seasonal diference in SCC, as any seasonal change will always beconfounded by the lactational stage.

Age

An increase in the cellular content of milk with increasing age has been reported in beefcattle (Duenas et al., 1994) and in dairy cattle (Daniel et al., 1966; Schultz, 1977; Gilland Holmes, 1978; Syrstad et al., 1979; Taralik, 1998; Choi et al., 1999). However,Wilson et al. (1971), working with Angus-Holstein F1 cows (dual-purpose cattle), withan age from 2 to 7 years found that number of lactations did not significantly affectSCC. Laevens et al. (1997) found similar results in dairy cattle.The increase in SCC

with the age is primarily due to an increased prevalence of infection in older cows andis not due to any large increase due to the age per se, being a pathological rather than aphysiological change (Kirkbride, 1977; Dohoo and Meek, 1982).

It has been found that older cows have a greater cellular response to both minor andmajor pathogens, and therefore older cows usually have high cellular readings (Dohooand Meek, 1982; Kirk, 1984). This has been attributed to a number of factors, includingmore quarters being infected, more extensive tissue damage in long lasting infections,and a greater cellular response in quarters that have been previously infected (Dohooand Meek, 1982).

Stage of lactation

In dairy cattle SCC has been found to be high in the first week after calving, with thelowest count occurring at the peak level of production, and tend to rise slightly in thelast few weeks of lactation (Kennedy et al., 1982; Kirk, 1984; ORourke, 1999).stensson (1993b), working with dairy cattle, reported that SCC did not changesignificantly but tended to increase as lactation proceeded. Wilson et al. (1971) in dual-

purpose cows found the SCC was significantly influenced by lactation stage, reporting,as in dairy cattle, that SCC tended to be the highest early in lactation, declined, and then

increased appreciably at the end of lactation. Another study in beef cows also foundthat early and late lactation animals were more frequently associated with high cellcounts than animals in mid-lactation (Hunter and Jeffrey, 1975). However Laevens etal. (1997) reported no effect of stage of lactation on SCC in dairy cows.

A partial explanation for this variation could be the milk yield of the cow duringlactation, as Emanuelson and Funke (1991) and Milleret al. (1993) found a dilutioneffect due to an inverse relationship between milk yield and milk SCC. In these worksit was assumed that a dilution effect caused the regression of milk yield on milk SCC.Milleret al. (1993) suggested that the observed negative relationship between milkyield and SCC may partly reflect both the true biological effects of udder inflamation

and a dilution effect. stensson (1993b) mentioned that the milk somatic cell counts


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increases towards the end of lactation, because of the higher prevalence of mastitis,normal involution of the udder and decreased milk production which causes lessdilution of the milk leucocytes.

Diurnal variation

Diurnal variation in SCC has been reported in dairy cattle; Smith and Schultze (1967)reported that cell counts are lowest just prior to milking and are highest immediatelyafter milking with these levels persisting for up to four hours, then decreasing

progressively to a minimum value near the end of the intermilking period. Theseauthors suggested that most normal quarters have a rather high leucocyte concentrationfor as long as 8 hours after each milking. Syrstad and Ron (1978) found that samplesfrom morning milkings had about 20% lower cell counts than samples from afternoon

milkings. White and Rattray (1965) reported similar results. These differences havebeen attributed to a dilution effect, where SCC decrease as volume of milk increase(Emanuelson and Funke, 1991; Milleret al., 1993).

The dilution effect probably result from the cyclic pressure changes in the alveoli,where for the first few hours after milking, the pressure within the alveolus is lowest;this tends to cause a release of polymorphonuclear leucocytes and squamous epithelialcells into the milk. Therefore, the samples taken at this time have the highest dailySCC, whereas samples taken just before milking have the lowest SCC, because increasein alveolar pressure prevents cells from being released into milk while milk synthesisand release of milk into the lumen continues, thereby diluting concentration of somatic

cells in milk (Donovan et al., 1992). Newman et al. (1991) working with beef cowssuggested that the low levels of SCC found in their study could be a result of allsamples being collected about 16 hours after the cows had last been nursed. Thus, cells

present may have been diluted by relatively high milk volume.

Day to day variation

In dairy cattle it has been reported that cell counts of cows also vary from day-to-day byup to 25% of the baseline count. The variation is small in uninfected cows but may be

much greater in cows with active infections (Kirk, 1984).

It has been reported that fluctuations in individual quarter samples from uninfectedcows have run in parallel, suggesting physiological factors acting at the cow level(Dohoo and Meek, 1982). Donovan et al. (1992) mentioned that day-to-day variation inmilk SCC, could be due to other factors affecting SCC like age, stage of lactation,environmental temperature and stress. However, Simpson et al. (1995) reported thatday of sampling did not influence SCC in beef cattle.

Stress


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It has been reported in dairy cattle, that stress can affect the SCC. In a study in whichthe cows were stressed by corticotropin injection, confinement in a heat-humiditychamber, or environmental heat stress by exposure during the hot summer months ofJune through November in southern Arizona; a modest increase in SCC was found in

cows treated with corticotropin injection and exposed to environmental heat stress, butno significant changes occurred during the chamber heat stress period (Wegneret al.,1976). However Convey et al. (1971) reported that corticoid-induced leucocytosis of

blood is not reflected by increases in somatic cell numbers in milk.

In another trial with a heat-humidity chamber, Roussel et al. (1969) reported that therewas no evidence that increased thermal stress significantly caused an elevation in theSCC. Nelson et al. (1969) working in environmental heat stress, reported that sampleshaving somatic cell counts in excess of 500 000/ml were greatest during periods ofmaximum temperature, and that individual quarters responded independently during the

period of high atmospheric temperatures. This indicates that, while stress of the entireanimal undoubtedly is a factor, manifestation of the stress condition is determined byfactors operative in the individual quarters of the animal.

It has been reported that there is no increase in SCC associated with cows being inoestrous. In a study involving 14 cows; it was found that the oestrous did not affectSCC, milk production or occurrence of clinical mastitis (Guidry et al., 1975). stensson(1993b) neither found differences in SCC between oestrous and dioestrous in variousmilk fractions.

Technical aspects

The method of transportation and storage of milk samples, as well as the method usedto count the somatic cells, all have an influence on the resultant counts (Dohoo andMeek, 1982; Coleman and Moss,1989). Fresh, nonpreserved samples becomeunacceptable for use 16 hours following collection. Refrigerated, nonpreserved samplesremain acceptable for up to three days (Kirk, 1984).

Differences among preservatives were not found in studies comparing bronopol,potassium dichromatic, sodium azide, boric acid and milkofix ( Hamann, et al., 1991,

Hanus et al., 1992; Bertrand, 1996). However some differences can be found, whichwill depend of the amount of preservative used in the milk sample, temperature andtime of storage (Heeschen etal., 1993; Gencurova et al., 1994). SCC are lower afterfreezing than before freezing and the decrease is greater when the freezing period islonger , but when thresholds of 200 000, 250 000 and 500 000 cells/ ml are used to

predict infection, freezing appear to have a little impact on the sensitive and specifity ofdiagnostic parameters (Barkema et al., 1997).

Effects of quarter

Wilson et al. (1971) reported that in dual-purpose cows means for log SCC were lower

for front than for rear quarters, although differences between left front and left rear


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quarters were not significant. These authors suggested that a partial explanation for this,could be the sucking preferences of the calves, because in their trial they found thatthere was a preference for calves to nurse the fore quarters more frequently than the rearquarters .

Failure to partially or completely empty a quarter would tend to increase the cell countof the milk (Wilson et al., 1971). Natzke et al. (1965) reported increased milk cellcontent from the omission of a milking.

Milk fraction

In dairy cattle SCC may vary considerably among different fractions of milk obtained ata single milking (Paape and Tucker, 1966, stensson and strm, 1994). Berning et al.(1986) reported that SCC was higher in residual milk than in foremilk. Berning et al.(1987) found that SCC (log thousand cells/ml) in foremilk was 2.52 and in residualmilk 5.53. stensson (1993a) reported that in healthy udder quarters there weresignificant differences in SCC between foremilk and residual milk, with the highervalues for residual milk. Similar results have been found by other authors (Woolford etal., 1998; Hamann and Gyodi 1999; Waldmann et al., 1999). stensson (1993a) alsoreported that during the course of inflammation there were no consistently significantdifferences between foremilk and residual milk in the SCC .

The higher values for SCC in residual milk, compared with foremilk may suggestedthat cell counts in residual milk is a more sensitive measure of the inflammatory

condition in the udder tissues. Differences between foremilk and residual milk may beattributable to that cells, because of their close contact with the epithelium, are retainedin the alveoli and ducts until residual milk is collected (stensson, 1993b). stenssonet al. (1988) suggested that for research purposes it may be adequate to analyse 2 milksamples, for instance foremilk and residual milk, in order to get a more precisecharacterization of the condition of the udder.

Although there are no data in beef cattle on some factors reviewed above (that areaffecting SCC), it is important to consider them during udder health assessment in beefcows.


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BOVINE MASTITIS BACTERIOLOGY

The prevalence of subclinical infection is difficult to ascertain, as this can only bedetermined by isolation of bacteria from the gland (Leigh, 1999). Many organisms

present in the cows environment can cause mastitis. When one of these organisms isisolated from mastitic milk the question arises as to whether it is the cause of themastitis, or a contaminant (Jones, 1994).

Bacteriology and cell counting are sometimes used together to determine the infectionstatus of the mammary gland (Barkema et al., 1997). However the interpretation ofthese combined results is not straightforward (Francis 1993; Shoshani et al., 2000).Francis (1993) present some of the possible reasons for contradictory results (Tab. 1).

Table 1-Possible reasons for inconsistent results using bacteriology and somatic cell counts

Together (Francis, 1993).

High cell count and NEGATIVE

Bacteriology

Low cell count and POSITIVE

Bacteriology

Small numbers of bacteria not beingdetected in the 10 ul aliquot cultured

Teat canal infections

Culture medium unsuitable for the causal

agent

Sample contaminated during collection

Milk sample is bactericidal (death in thepost)

Long-standing subclinical infection

Physical or chemical damage to the udder Contaminated sample bottle

Teat canal infections producing endotoxinwhich raises the cell count


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MILK CONSTITUENTS

Milk is a biological fluid containing a large number of different constituents (Davies etal., 1983; Kennelly, 1996). However most of the research carried out on milkcomposition has been done investigating the major constituents, which are fat, proteinand lactose.

The composition of milk in dairy cows generally ranges between 3.0-5.3% fat, 2.8-4.5% protein and 4.2-5.1% lactose. Some works have reported either only fat (Morgan,1991; Griinary et al., 1997), or fat and protein (Oldenbroek, 1984; Higginbotham et al.,1988; Jones-Ensley et al., 1997; Pirlo et al., 1997, Wu et al., 1997; Bremeret al.,1997). However other studies have reported the all three constituents (Tab. 2).

Table 2. Percentage of fat, protein and lactose in milk from different dairy breeds.

Breed type Milk fat

(%)

Milk

protein

(%)

Milk lactose

(%)

Reference

Holstein 3.5 3.0 4.6 Jennes 1985

Holstein 3.3 3.7 4.5 Sharaby 1988

Holstein 3.9 2.8 4.9 Nagel and Broderick 1992

Holstein 3.6 3.0 4.9 Rodriguez et al. 1997a

Holstein 3.8 2.9 5.1 Rodriguez et al. 1997b

Jersey 4.9 3.6 4.7 Jenness 1985

Jersey 4.3 4.5 4.2 Sharaby 1988

Jersey 5.0 3.7 5.0 Rodriguez et al. 1997a

Jersey 4.3 4.5 4.2 Rodriguez et al. 1997b

Dairy* 3.2 3.2 3.8 Mondragon et al. 1983

Guernsey 4.6 3.5 4.8 Jenness 1985

Ayrshire 4.0 3.3 4.6 Jenness 1985

Brown Swiss 3.8 3.2 4.8 Jenness 1985*=Brown Swiss and Holstein and their crosses

In beef cows a variation of 2.5-6.5%, 3.0-4.0% and 3.8-5.3% for fat, protein and lactoserespectively has been found. Some researchers have reported 3 major constituents ofmilk from beef cows (Tab. 3). However some investigations have worked only with fat(Danilevskaya et al., 1972; Carwright et al., 1976; Belcher and Frahm, 1979; Frankeand Martin, 1983; Morgan, 1991; Kovacks, 1997), fat and protein (Rahnefeld, et al.,1990; Lalman et al., 2000), or protein and lactose (Mollet et al., 1989).Table 3. Percentage of fat, protein and lactose in milk from different beef breeds.


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Breed type Milk fat

(%)

Milk protein

(%)

Milk lactose

(%)

Reference

Angus 4.1 3.3 4.7 Beal et al. 1990Hereford 4.9 3.5 5.5 Butson and Berg 1984

Hereford 6.3 3.3 5.0 Daley et al. 1986

Chianina 4.3 3.8 5.1 Meregalli et al. 1983

Red Poll 5.8 3.0 5.2 Daley et al. 1986

Hungarian Grey 4.9 3.5 5.1 Kovacs et al. 1999

Charolais 3.4 3.5 5.2 Mondragon et al. 1983

Angus x Hereford 5.8 3.0 5.0 Daley et al. 1986

Hereford x Red Poll 5.7 3.1 5.1 Daley et al. 1986

Red Poll x Hereford 5.9 3.2 5.1 Daley et al. 1986

Angus x Charolais 5.7 3.1 5.1 Daley et al. 1986

Brahman x Hereford 6.5 3.3 5.1 Daley et al. 1986

Brahman x Angus 5.7 3.2 5.0 Daley et al. 1986

British1 2.8 3.3 5.3 Mondragon etal. 1983

Dairy2 x British 3.1 3.2 5.1 Mondragon etal. 1983

Charolais x British 3.6 3.3 5.2 Mondragon etal. 1983

Burwash x British 3.1 3.5 5.2 Mondragon etal. 1983

Dairy x Burwash 3.1 3.3 5.0 Mondragon etal. 1983

Jersey x British 3.9 3.5 5.2 Mondragon etal. 1983

Exotic3 x Dairy 3.3 3.5 5.1 Mondragon etal. 1983

Beef-Synthetic4 4.9 3.5 5.5 Butson and Berg 1984

Dairy-Beef5 4.8 3.5 5.2 Butson and Berg 1984

Dairy-Synthetic6 4.8 3.5 5.3 Butson and Berg 1984

1=Angus, Hereford, Shorthorn and their crosses 2=Brown Swiss, Holstein and their crosses 3= Chianina,

Limousin, Charolais and Maine Anjou 4=crosses of Charolais, Angus and Galloway 5=crosses of dairy sires with

Hereford or beef-synthetic dams 6=crosses of Holstein or Brown Swiss with beef breeds

NUTRITIONAL FACTORS AFFECTING MILK CONSTITUENTS

When discussing milk constituents, one must be careful to distinguish between yield(quantity) and content (percentage) (DePeters and Cant, 1992). The chemicalcomposition of milk depends on factors related to the animal and to its environment(Hoden and Coulon, 1991).

Fat content


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The percentage of milk fat is influenced by a number of interacting dietary factors(Ashes et al., 1997). It has been proposed that the percentage of milk fat is affected by

plasma insulin concentrations. The glucogenic-insulin theory proposes that increasedinsulin release which occurs when high starchy concentrate diets are fed, preferentially

channels nutrients to adipose tissue, resulting in a shortage of nutrients at the mammarygland and thus milk fat depression (Brockman and Laarveld, 1986; Sutton et al., 1988;Griinari et al., 1997a). This theory has been questioned because injections of insulin insome cases did not result in a lower milk fat content (Mcguire et al., 1995; Griinari etal., 1997a). It is therefore possible that other hormones are also involved in theregulation of milk fat synthesis (Samuelsson, 1996). Samuelsson et al. (1998) found a

positive relation between somatostatin and milk fat content. They hypothesised that oneway for somatostatin to stimulate milk fat synthesis was through a modulation of theaction of insulin in which high levels of somatostatin promotes deposition of fat in themilk through an inhibition of lipogenesis in adipose tissue, i.e. the milk synthesis in the

udder is given priority before the deposition of fat in the body.

Samuelsson (1996) mentioned that cows on a high plane of nutrition generally have areduced fat content in the milk whereas cows with low energy intake have an increasedfat content. It has been reported a depresion in milk fat content in diets contain highamounts of grain (fermentable starch)(Palmquist et al., 1993; Jenkins, 1993). In

primiparous beef heifers Lalman et al. (2000) comparing four treatments with low (L),maintenance (M), maintenance high (MH) and high dietary energy concentration (H),found that increasing dietary energy it was increased milk fat percentage, however thiseffect apparently was seen only in the L, M and MH treatments, as the lowest milk fat

percentage was found in the H treatment (3.5, 3.8, 3.7% vs. 3.3%). Lowman et al.

(1979) working with beef cows reported that increasing the energy allowancesignificantly increased milk yield but did not affect milk composition.

The effect of dietary energy on milk composition vary depending of the source(ingredients) of energy used in the cows diet and other dietary factors like effectivefiber (chewing time), particle size and additives (buffers) (Schultz, 1974; Emery, 1988;Jelec, 1990; Hoden and Coulon, 1991).

The role of protein in milk fat was investigated by Jones-Enslay et al. (1997) whoreported that the percentage of milk fat produced by grazing dairy cows was unaffected

by crude protein in the supplement or by the amount of supplement offered. Emery(1988) mentioned that amount of protein have a little or no effect on content of milk fat.Emery (1991) mentioned that increasing crude protein from 10% to about 18% of thediet in lactating dairy cows, milk fat percentage may decrease due to dilution byincreased milk yield. In studies investigating the effect of ruminally undegradable

protein (RUP) milk fat percentage was reported to be affected by RUP (Christense etal., 1992a; Christensen et al., 1992b; Wiley et al., 1991) whereas others reported noeffect (Wu et al., 1997).

Also is important to take into consideration the intake of water. In a study done inIsrael, it was reported that dairy herds given insufficient drinking water produced milk

with significantly increased water content and significantly reduced fat content. It was


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suggested that these changes are physiological adaptations to enable sucking young tosurvive (Yagil et al., 1986).

Protein content

Protein percentage in milk is also influenced by nutritional factors. The amino acidswhich are taken up by the mammary gland for milk protein synthesis arise from dietaryundegraded protein which reaches the duodenum and rumen microbial protein (Murphyand OMara, 1993). According to this higher values of percentage of milk protein have

been observed in abomasal infusion of casein (Griinari et al., 1997b) and in diets withhigh RUP (Komaragiri and Erdman, 1992; Bremmeret al., 1997; Wu et al., 1997).However Rodriguez et al. (1997a) reported that milk protein content was reduced indiets with high amounts of RUP. It has been found that increasing dietary energy

concentration resulted in an increase in milk protein percentage (Murphy and OMara,1993; Lalman et al., 2000) and vice versa (Wiley et al., 1991). However Pirlo et al.(1997) reported that milk protein percentage was positively influenced by diets withlow energy.

In some investigations it has been found that fat supplements often have decreased milkprotein percentage (Coppock and Wilks, 1991; DePeters and Cant, 1992; Wu andHuber, 1994; Rodriguez et al, 1997a). The mechanism for this decrease in milk proteinis not understood. Current theories include ruminal effects; such as toxic effects of faton ruminal microbes, decreased microbial protein synthesis when fat is substituted forruminally available carbohydrates, or absorption of certain fatty acids that may directly

or indirectly alter uptake of amino acids by the mammary gland (Chow et al., 1990).Grummer (1991) suggested that protein percentage decrease maybe due to a dilutioneffect when milk yield increases as a result of fat supplementation.

It has been reported that increasing the protein level in the diet had no effect on themilk protein concentration (Emery, 1991; Christensen et al., 1992a; Murphy andOMara, 1993; Jones-Endsley et al., 1997). However Pirlo et al. (1997) reported highermilk protein percentages in high protein diets.

Lactose content

Milk lactose is the main osmotic component in milk and therefore the lactose content israther constant (Schultz, 1974; Samuelsson, 1996). Wiley et al. (1991) evaluated theeffect of diets made to induce or prevent weight loss before parturition and diets aftercalving with ruminally undegradable or degradable protein supplement. They found no


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effect of either of these four treatments on lactose content of milk from primiparousbeef cows. However Rodriguez et al. (1997a) found that the lactose content of milkincreased 1.4% with added fat and increased 1.6% with diets having high RUP contentin dairy cows.

NON-NUTRITIONAL FACTORS AFFECTING MILK CONSTITUENTS

There are several factors which are non-nutriotional and can have an affect on theconstituents in milk, they are mainly breed, stage of lactation, udder health, milkfraction and some other factors.

Breed

The effect of breed has been reported in some studies with beef cattle. Cartwright et al.(1976) compared Aberdeen-Angus x Jersey cows with Hereford cows and reporteddifferences in milk fat percentages. Belcheret al. (1979) found no significantdifferences for milk fat percentage, but milk protein percentages had differences

between breeds. Daley et al. (1986) found that milk fat percentage differed significantlyamong breed types. Breed effects for other milk traits were reported nonsignificant inthat study. Rahnefeld et al. (1990) reported breed effects on milk fat percentage and onmilk protein percentage. Sharaby (1988) found breed differences for fat, protein andlactose content in milk in Jersey and Holstein cows. Butson and Berg (1984) working

with beef and dairy-beef cows reported that all milk constituents percentages werehigher than those reported for commercial dairy cattle.

Stage of lactation

The stage of lactation has been reported to have an effect on milk composition as well.In dairy cows in general tha fat (Dash et al., 1978; Yadav and Sharma, 1984;Chaudhary et al., 1998), protein (Ettala, 1976; Taralik, 1998) and lactose (Sharma etal., 1990; Holdaway et al., 1996) are high in early lactation, increase in mid lactation

(peak milk yield) and decrease during mid- to late-lactation. However in some studies ithas been reported that lactation stage had no significant effect on milk constituentpercentages (Sharaby, 1988; Ibeawuchi and Dangut, 1996). In beef cattle milk fatpercentage was found to be highest in early lactation, while milk protein percentageincreased during lactation, and milk lactose percentage remained constant (Mondragonet al., 1983). Morgan (1991) reported the lowest values for milk fat percentage duringthe peak milk yield (middle of lactation) for Hereford cows. Butson and Berg (1984)working with beef and dairy-beef cows observed that all recorded milk constituent

percentages increased significantly from June to September at about 130 days oflactation. Other authors have found similar results (Yanagita et al., 1978; Daley et al.,1986).


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These data suggest that maybe this effect can partly be explained by the lactation curveof the cow, resulting in a dilution effect (fig.2). Dilution effect is the inverserelationship between milk yield and percentage of milk constituents. This is supported

by Pitcheret al. (1992) who reported that the dilution effect was responsible for the

changes in milk composition in dairy cows and by Ibeawuchi and Dangut (1996) whofound a significant inverse correlation between milk yield and milk fat in Zebu cattle.

Rahnefeld et al. (1990) found that the percentage of fat and protein decreased as milkyield increased in beef cows. Also Butson and Berg (1984) found that in beef cows,correlations between milk yields and constituent percentages were significant andnegative. According to the previously mentioned Ettala (1976) observed that when theeffect of milk yield was eliminated in the analysis, stage of lactation had only a slighteffect on milk constituents.

Owing to that changes in milk yield result in a dilution effect, the changes in percentageof milk constituents will automatically be more significant in dairy cattle than in beefcattle, as dairy cows have a higher milk production. This is belived to be a result ofdairy cows having a greater number of secretory cells and greater activity per cell (Keyset al., 1989).

Fig. 2. Lactation curves 0 to 25 weeks for mature crossbred cows ( Angus x Hereford or Hereford

x Angus; Charolais x Angus or Hereford; Jersey x Angus or Hereford;

Simmental x Angus or Hereford). (From Jenkins and Ferrel, 1984).


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Mastitis and somatic cell count (SCC)

In a study done withBos taurus andBos indicus xBos taurus breed types, Daley et al.(1986) found that mastitis had an effect on milk constituent percentages, reporting that

cows that had mastitis in the tested quarter had a higher percentage of fat and protein intheir milk, but a decreased percentage of lactose. Watts et al. (1986) working with beefcows reported reductions in fat and protein in milk from udders with intramammaryinfection caused by Staphylococcus aureus. Simpson et al. (1995) in Simmental cowsreported an increase in fat and protein in milk with high SCC. These authors suggestedthat maybe inflammatory proteins and antibodies present in response to intramammaryinfections could have contributed to the higher percentage of protein in high SCC.However casein is the primary compound detected in the milk protein analysis.

In dairy cattle, high cell count milk has lower fat and lactose levels than low cell count

milk (Dohoo and Meek, 1982). Milleret al. (1983) reported low percentage of lactosein high SCC, but high percentages of fat and protein. Roussel et al. (1969) found asignificant positive correlation between milk fat and SCC in dairy cattle. HoweverEicheret al. (1999b) found that SCC did not influence protein in milk from dairycows..

Milk fraction

In dairy cattle an effect of milk fraction on some milk constituents has been found.Moore et al. (1981) reported that milk fat percentage was significantly higher at

evening than at morning milking for foremilk, but significantly higher at morning thanat evening milking for residual milk. Protein content was significantly higher at eveningthan at morning milking for machine milk and residual milk. Carlsson and Bergstrm(1994) reported that fat percentage was higher in residual milk than in foremilk.

Ugarte (1977; 1991) comparing normal milk (machine milking) and residual milk,reported that fat percentage was higher in residual milk, but protein percentage waslower in this fraction of milk. Waldmann et al. (1999) reported similars results.

Other factors affecting milk constituents

In beef cattle has been found that parity had no effect on milk composition (Mondragonetal., 1983; Meregalli et al., 1983). In beef cattle it has been observed that dams with

bull calves produced more fat and less protein than cows with heifer calves, and the calfage had a positive effect upon percentage of lactose, and as calf age increased the

percentage of protein increased significantly (Daley et al., 1986). However Meregalli etal. (1983) have not found effect sex of calf on milk composition in beef cows.

It has been found that estimates for all milk traits decrease as the length of time ofseparation (from their calves) increased in beef cows (Chenette and Frahm, 1981).

However Belcheret al. (1979) reported that milk fat percentage decreased as time of


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cow-calf separation increased in beef cattle but milk protein percentage was notaffected.

In dairy cows it was reported that udder shape had significant effects on milk fat and on

milk protein, but not on lactose (Barbary et al., 1999). However Baruah et al. (1991)found that milk composition of dairy cows was not significantly correlated with anyudder measurements. The effect of photoperiod and heat load on milk composition has

been studied in dairy cows, and protein as found to be affected by photoperiod, fat wasaffected by head load and lactose was affected by both environmental factors (Aharoni,et al., 1999).


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ARE TEAT TRAITS IMPORTANT IN UDDER HEALTH AND MILK

COMPOSITION ASSESSMENTS?

FACTORS AFFECTING TEAT LENGTH AND ITS IMPORTANCE ON MILKYIELD AND UDDER HEALTH

The importance of teat length has been studied in beef cattle, and it has been found thatcalves born from cows with large teats had higher pre-weaning growth rates than those

born from cows with smaller teats (Makarechian and Paputungan, 1998). In dairy cattlecorrelation values of 0.15 to 0.88 between teat length and mastitis have been reported(Janicki, 1977; Soldatov and Kholodkov, 1990). Lund et al. (1994) reported a

correlation between clinical mastitis and teat length in Danish Holsteins cows; andconcluded that their results indicated predisposition to mastitis with long teats. Similarresults were found by Roy et al. (1993) in crossbred cows. On the contrary Shukla et al.(1997) reported that small teats were a risk factor for mastitis in dairy cattle andMurrah buffaloes. An increase in teat length has been found in beef cows withincreasing age (Logan and Gibson, 1975; Olson et al., 1989; Prajapati et al., 1995).

In dairy cattle fore teats have been reported to be longer than rear teats (Naidu, 1972;Oldenbroek, 1984; Gupta et al., 1991; Singh and Gupta, 1995). In dairy cows it has also

been observed that the length of all teats increased with lactation number (Tomar, 1973,Sharma and Sidhu, 1980; Baruah et al., 1991). It has been reported that teat dimensions

(including teat length) does not affect milk yield in dairy cattle (Naidu, 1972; Panderand Chopra, 1986; Ghosh and Prasad, 1998; Ozbeyaz et al., 1998) or in beef cattle(Prajapati et al., 1998). However, Tomar (1973) reported that milk yield in dairy cattlewas significantly correlated with the length of both fore and rear teats. Baruah etal.(1991) working with Jersey cows reported a significant correlation between milk yieldand rear teat length in the 1st and 3rd lactation of 0.36 and 0.65 respectively. Similarresults were found in Gir cows by others (Tripathi et al. 1982; Qureshi et al. 1984)

In Zebu, European and crossbreed cattle teat length has been reported to be affected bygenetic group and lactation number, but not by stage of lactation (Sharma and Sidhu,

1980). However, Baruah et al. (1991) reported that udder measurements (including teatlength) were greater in early-lactation than in mid-lactation and late lactation in dairycows.

TEAT INJURY AND TEAT PAPILLOMATOSIS

The highly vascular and vulnerable mammary tissue is protected by the skin of theudder. In young animals it is thin and closely attached to the udder. Specialised flexibleand elastic skin is covering the teats, the epidermis of which is thicker than in other


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areas of the body and is tightly attached to the underlying dermis. The teat is normallycapable of withstanding minor trauma including suckling by the calf and milking byhand or machine (Jackson, 1996).

Any injury or infection involving the skin of the teat is a potential threat to its efficientfunction and to the welfare of the animal. The sources of injury may be barbed wire,sharp objects and damaged or inadequate fencing (Jackson, 1996).

In dairy cows tramped teats are a common source of teat injury (Oltenacu et al., 1990).However, beef cows generally have smaller udders and shorter teats, which decreasesthe risk of teat trampling. Multiple lacerations of varying depth and length may be seenin the skin of the udder and teats. Deep horizontal cracks may occur as a result ofexcessive sucking or biting by older calves or even older animals (Jackson, 1996).

The likelihood of cows developing mastitis is 50% higher in injured than in non-injuredcows (Modransky and Welker, 1993). Similar results were found by Pyorala et al.(1992) and Geishauseret al. (1999). Teat injury has been associated with high SCC indairy cattle (Jorstad, et al., 1989), and numerous studies have indicated a positiverelationship between milk SCC and udder disease (Coffey et al., 1986a; Coffey et al.,1986b; Emanuelson, 1988; Emanuelson etal., 1988; Shook, 1989; Welleret al., 1992).

Single or multiple papillomas caused by bovine papilloma viruses can be found on theteats of heifers and cows (Meischke, 1979; Olson et al., 1982). Lindholm et al. (1984)found that Hereford cows and their crosses had a high incidence of papillomas andshowed the highest numbers of warts, but it was not possible to make a realistic

comparison with other breeds because of the small numbers of animals involved in thestudy. This study was done with seven breeds and their crosses. Pobric et al. (1990)working with cows of various breeds found a prevalence of papillomatosis of 8% (91 of1124). William et al. (1992) reported that of 171 animals examined, 43 (25%) had

papillomatosis, of which 56% were cows, 28% heifers and 12% calves, and the highestincidence of papillomatosis was on the udder and navel. Wadhwa et al. (1996) reporteda prevalence of 83% (19 of 23). Nooruddin et al. (1997) reported a prevalence of 16%(73 of 459) for crossbred and pure bred dairy cows; they also found a significant higher

prevalence of papillomatosis in small herds compared to large herds.

These data show that teat traits have an influence on mastitis, but the effect on milkyield is apparently not as significant as for intramammary infections.


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MILK UREA CONCENTRATION

Milk urea reflects the balance between dietary carbohydrate and protein and thereforeserve as a feed efficiency indicator (Kirchgessneret al., 1986; Spohr and Wiesner,1991; Roth et al., 1996; Lyatuu and Eastridge, 1998). The main theory behind thisconcept is that urea concentrations in blood and milk can provide information onnitrogen losses following absorption of ammonia from the gut, particularly the rumen(Oltneret al., 1985).

The urea in milk arises primarily from massive transfer of urea from the blood (Roseleret al., 1993). Several authors have reported in dairy cattle a close correlation (0.77-0.98) between concentrations of urea in blood and milk (Bakanov et al., 1976; Oltner

and Wiktorsson, 1983; Refsdal, 1983; Gajdosik and Szaboova, 1984; DePeters andFerguson, 1992; Sato et al., 1992). The equilibration between blood urea and milk ureais relatively rapid; urea is equilibrated with serum with a time lag of 1 to 2 hours(Gustafsson and Palmquist, 1993). Due to its rapid and passive diffusion through cellmembranes (DePeterson and Cant, 1992), equilibration may be explained by diffusionof urea along the mammary ducts and through the mucosa in the alveoli (Gustafssonand Palmquist, 1993). Milk has the advantage of being easy to obtain from the lactatingcow and the stress of blood sampling is avoided (Oltner and Wiktorsson, 1983).

In experimental studies a variation of 2.1 to 9.1 mmol/l in urea concentration has beenreported in dairy cattle (Oltneret al., 1985; Refstal et al., 1985; Gustafsson and

Carlsson 1993; Carlsson and Pehrson, 1994; Eicheret al., 1999a;). In beef cattle it hasbeen reported a variation of 0.8 to 10.1 mmol/l (Sinclair, et al., 1994; Ponteret al.,1997; Knaus et al., 1999; Ponsart, et al., 1999). Carlsson and Perhson (1994) suggestedthat a milk urea concentration of 4.0-5.5 mmol/l could be considered as normal. This issupported by Gustafsson and Carlsson (1993) who observed a range from 4.5 to 5.0mmol/l in milk urea concentration from cows with optimal reproductive efficiency. Ithas been reported that either low or high milk urea concentrations are associated withlow reproductive efficiency (Ropstad and Refsdal, 1987; Ferguson et al., 1988;Canfield et al., 1990; Pehrson et al, 1992).

Other authors have reported milk urea values in mg/dl and they have found a variationof 5.6 to 34 mg/dl in dairy cattle (Kirchgessneret al., 1988; Pestevseket al., 1990;Roseleret al., 1993; Kroberet al., 1999; Ikuta et al., 2000b) and a variation of 3.7 to31.3 mg/dl in beef cows (Mathison et al., 1981; Kushibiki et al., 1991; Hess et al.,1998; Huston, et al., 1999; Lima et al., 1999). A range from 18 to 23 mg/dl has beenreported as normal (Kirchgessneret al., 1988). Paulicks (1992) suggested that when

protein and energy supply of dairy cows is balanced with requirements, milk ureaconcentrations are between 15 and 25 mg/dl.

This variation in milk urea concentration is due to the influence of nutritional and non-nutritional factors (Carlsson, 1994).

NUTRITIONAL FACTORS AFFECTING MILK UREA CONCENTRATION


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Effect of protein

Voluntary dry-matter intake and composition of the forages of the ration can beconsidered responsible for the base level of milk urea concentration. In dairy cattle theconcentrates are usually distributed according to the daily milk yield and are mostlyresponsible for the individual variations of milk urea (Eicheret al., 1999b).

Urea concentration in blood and milk are positively correlated with the intake of dietaryprotein; when protein intake exceeds requirements, the levels of ammonia will increasein the rumen and therefore in blood and milk, whereas a deficiency in protein shouldresult in low urea concentration (Carlsson, 1994). This relationship has been found in

beef cattle (Fishwicket al., 1974; Weisenburger and Mathison, 1977; Hennessy et al.,

1995; Lima et al., 1999) and in dairy cows ( Kreuzeret al., 1991; Homolka and Vencl,1993; Mackle et al., 1996; Sutton et al., 1997; Ikuta et al., 2000b).

Importance of balance between protein and energy

Although protein intake affect urea level in blood and milk; urea concentrations areparticularly affected by the balance between energy and protein in the diet (Ide et al.,1966; Payne et al., 1970; Oltner and Wiktorsson, 1983; Klein et al., 1987; Hofet al.,1997). The relation between protein and energy in the diet has a greater influence onmilk urea concentration than has the absolute amount of feed of a certain composition

that is consumed by the cow (Oltner and Wiktorsson, 1983; Oltneret al., 1985;Kirchgessner and Windisch, 1989; Ropstad et al., 1989).

Some recent studies have shown that if protein is according to or over the requerimentsof the cow and the energy is low, the urea concentrations are high, but if the protein isaccording to the requirements and there is a surplus of energy, decreases in ureaconcentration will be found (Carlsson and Pehrson, 1994; Kampl and Martincic, 1995;Carlsson et al., 1995; Steinwidderet al., 1998; Riha and Hanus, 1999). The reason forthese changes is that the rumen microorganisms require energy to synthesise proteinfrom ammonia; too little energy allows more ammonia to be converted into urea and

excess energy allows the microorganisms to synthesise more protein and deplete therumen of ammonia (Farries, 1982; Carlsson, 1994) In support of this a positivecorrelation between rumen ammonia and blood and milk urea concentrations have beenreported (Foldager and Huber, 1979; Folman et al., 1981; Hammond , 1983; Ha andKennelly, 1984; Kaim et al., 1987).

Hoffman and Steinhfel (1990) found that dairy cows being fed more than theirrequirement of both energy and protein had urea concentrations lower than cows beingfed according to their requirements of both energy and protein, they attributed thisdecrease to the more efficient utilisation of the dietary protein for the synthesis ofmicrobial protein. However Carlsson and Pershon (1994) found conflicting results,

reporting that when cows fed with a diet balanced according to their requeriments for


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energy and protein were fed with extra energy and protein, urea concentrations wereincreased.

Carlsson and Pershon (1994) suggested that 1 possible reason for this discrepancy

might be the much higher milk yields of the cows used in their experiment, as it ispossible that ruminal flora of intensively fed cows are less able to use aditional energyfor the synthesis of microbial protein.

Effect of rumen undegradable protein (RUP)

Carlsson (1994) suggested that a diet containing a high proportion of ruminallyundegradable protein (RUP) should result in lower concentrations of ammonia in therumen and, as a result, lower concentrations of urea in blood and milk and vice versa.

The same author mentioned that in his opinion, Ropstad et al. (1989) are in accordancewith this supposition, because they found a strong positive correlation between theprotein balance in rumen (the balance in the rumen between degraded feed protein andnitrogen used in the microbial protein synthesis) and milk urea concentration. However,Ropstad et al. (1989) in their study used two mixes (low and high protein) that weremade to provide similar amounts of RUP. Therefore, with the same levels of RUP inthe diet, it is not possible to measure the effect of RUP on urea concentration.

Studies done in beef cattle (Hess et al., 1998) and in dairy cattle (Higginbotham et al.,1989) have reported that urea concentrations were increased in cows receivingadditional protein, but no differences due to degradability were detected. Roseleret al.

(1993) found that the intake of undegradable protein elevated plasma and milk ureaconcentrations to a similar extend as intake of degradable protein. Similar results have

been found also in dairy cows by other authors (Roseleret al., 1990; Rodriguez et al.,1997b; Wu et al., 1997). In this aspect Roseleret al. (1993) suggested that the ability todetect subtle imbalances in degradable intake protein or undegradable intake protein bymilk urea probably is masked by the intake of dietary crude protein and the balance

between protein and energy, and that ruminal and postruminal excesses of nitrogen areeliminated from the body in the same process of hepatic urea synthesis; therefore excess

protein, whether degradable or undegradable will elevate urea concentrations. Howeverit has been reported that milk urea concentration was increased by effect of RUP in the

diet in beef (Wiley et al., 1991) and in dairy cows (Figueroa et al., 1992; Rodriguez etal., 1997a).


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NON-NUTRITIONAL FACTORS AFFECTING MILK UREA CONCENTRATION

Non-nutriotional factors sometimes can affect significantly the urea concentration,

therefore is important to consider them in milk urea assessments. Diurnal variation,season, stage of lactation, age, udder health, body weight, milk yield, technical aspectsand others factors play an important role in the milk urea concentration.

Diurnal variation

Diurnal variations of milk urea are influenced by feeding strategy (Miettinen andJuvonen, 1990; Gustafsson and Palmquist, 1993, Hess et al., 1998; Eicheret al.,1999a), time of sampling (Miettinen and Juvonen, 1990; Gustafsson and Palmquist,

1993; Eicheret al., 1999a) and the quality of protein (Miettinen and Juvonen, 1990).

Carlsson and Bergstrm (1994) reported that there was a significant diurnal variation inmilk urea and the highest values were found 3-5 hours after the beginning of morningfeeding and the lowest values during late night in dairy cattle.. These authors observedthat within 1 hour after the start of morning feeding the urea values had increasedsignificantly. Ikuta et al. (2000a) reported also that milk urea concentrations increasedafter feed intake and reached a peak from about 3 to 5 hours after feeding.

Ponsart et al. (1999) working with beef cattle observed the highest values of ureaconcentration 3-4 hours after the morning feeding. Similar results have been reported in

other investigations in dairy cows (Tomas and Kelly, 1976; Gustafsson and Palmquist,1993).

Some researchers have found that milk urea concentrations were highest in the morning(Gustafsson et al., 1993; Eicheret al., 1997a; Eicheret al., 1999a) while others havereported that milk urea is higher in the evening samplig (Miettinen and Juvonen, 1990;Broderick and Clayton, 1997). Miettinen and Juvonen (1990) attributed their results tothe time sampling and feeding, because milk were taken 1-3 hours after the onset offeeding when urea concentrations are still increasing and the feeding seem to influencethe urea level in the morning but not in the evening; this may due to the long fasting

period (12 hours) during the preceding night. Coggins and Fileld (1976) working withbeef cows also found diurnal variations in urea concentration. They suggested that thisvariation was due to feeding time.

However Oltner and Wiktorsson (1983) found no significant differences in milk urealevels between morning and afternoon sampling and the day-to-day variations weresmall.

Since urea is mostly excreted by the kidneys, the blood urea and consequently milkurea, is increased in renal failure. However in healthy animals the urea levels is

primarily affected by their feeding regime (Miettinen and Juvonen, 1990). Eicheret al.

(1999a) suggested that the difference of the diurnal patterns could be the result of the


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different feeding practices, possibly the concentrate feeding frequency. Miettinen andJuvonen (1990) observed that the circadian rhythm of milk urea was closely related tothe rhythmic feeding and fasting. According to that they mentioned a peak of ureaappearing 2-4 hours after feeding in twice daily feeding (Tomas and Kelly, 1976;

Gustafsson and Palmquist, 1993), whereas at higher feeding frequencies, a diurnalpattern is absent (Tomas and Kelly, 1976; Roth et al., 1996).

In some studies it has been concluded that under comparable feeding practices, a milksample taken 2 to 4 hours after first concentrate feeding, adequately reflects themaximum urea levels; also

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