the high-producing dairy cow and its reproductive performance

The High-producing Dairy Cow and its Reproductive Performance

H Dobson1,RF Smith1, MD Royal1, CH Knight2 and IM Sheldon3

1Faculty of Veterinary Science, University of Liverpool, Leahurst, Neston, Wirral, UK; 2Institute of Comparative Medicine, University of GlasgowVeterinary School, Glasgow, UK; 3Royal Veterinary College, University of London, London, UK

Contents

There is evidence that the reproductive performance of dairycows has declined as milk yields have increased over the last40 years. Identifying the precise cause(s) of this problem mayprovide focused solutions. Intensive genetic selection for veryhigh yields has reduced fertility, due mainly to an increase inpostpartum clinical problems, poor expression of oestrus,defective oocytes/embryos and uterine infections. It is a chal-lenge to solve the problem by getting enough food into thesecows to meet the high demands of peak milk yields in earlylactation, as well as providing the considerable veterinaryattention required in the early period after calving. Both theseaspects also pose welfare issues. A better solution would be tomake genetic and management changes to increase thepersistency of lactations to reduce the number and intensityof clinical risk periods throughout a cow’s life withoutcompromising milk output.

Introduction

The high-yielding dairy cow has doubled output overthe last 40 years with an associated decline in fertility.To provide focussed solution(s) to this problem, we needto understand the cause(s). The main emphasis for dairyfarmers is to sell as much milk as possible withmaximum efficiency, both financially and in terms ofanimal welfare. The number of calves produced is ofsecondary importance, and this should be rememberedby managerial/agricultural advisors and veterinarians.Of course, a cow must have a calf to begin lactating andthe need to create the next generation must not beforgotten. However, the prime commodity for the dairyindustry is milk of a quality appropriate for furtherprocessing to drink (the liquid market), or manufactureinto cheese, butter, cream, yoghurt, etc.

Why We are Where We are in 2007

What is ‘high’ milk production? This depends on thebreed of cow; for example Channel Island herds(Jerseys, Guernseys) have average 305-day lactationsof approximately 4000 l with substantial constituents ofapproximately 4.5% fat and approximately 4% protein;in comparison, Friesians have typical 305-day lactationsof approximately 7000 l at approximately 4% fat and3.5% protein; whereas, Holstein cows can achieveapproximately 10 000 l (approximately 3.5% fat and3% protein). Hence, the total lactation yields of fat are180, 280 and 350 kg for Channel Island, Friesian andHolstein cows respectively. However nowadays, mostmilk is divided into its constituents during the initialmanufacturing process (even drinking milk), and thenreconstituted with varying percentages of fat (and

protein to a lesser extent) depending on the nature ofthe final product – milk, cream, butter or cheese.

Cowsmust be fed appropriately to produce high yields.However, there is a maximum output that can besupportedmainly by forage, the natural diet of ruminants(approximately 6000 l per 305-day lactation). Herds thatdepend on grazing ± conserved forage for the majorityof the diet will be constrained by environmental oppor-tunities to grow herbage. Thus, their calving patterns aredictated by the need to maximize the efficiency of ‘milk-from-forage’. Nevertheless, these animals may suffer thesame problems as those herds housed all-year-roundproducing 10 000 l. Thus, the implications of ‘high-producing’ cannot be defined in finite litres of milk orkilogram fat; but must also take into account the breedand management systems involved.

Financial efficiency and welfare depend in large parton the correct feeding of the cow. When working outfeed-rations, there is a component for maintenance ofthe cow’s own body and a further requirement depend-ing on the amount of milk produced. For example, eachday a mature 666 kg Holstein requires 60 MJ each dayfor maintenance plus 5 MJ per litre of milk produced.Whatever the breed or size of cow, financial efficiencydepends on the amount of milk that can be producedper kilogram cow requiring maintenance. Table 1compares current financial aspects of producing milkfrom a typical cow from three different breeds in theUK; there may be variances between different countriesbut the nuances will not have major effects on thecomparison.

Defining the Problem with respect to Milk Yield

The financial comparisons in Table 1 emphasize whymany dairy farmers enthusiastically engaged in thegenetic transformation to breed high-producing cows –the comparison between breeds is stark but the sameprinciples apply even within a breed. But at what costhas this change occurred? There is now considerableevidence available suggesting that cattle fertility(expressed in terms of pregnancy rates to first insemin-ation) has declined over the last 50 years during therapid increase in yields (Royal et al. 2000). Thus, geneticcorrelations between fertility and production are gener-ally unfavourable, although there are also some breedexceptions, such as the Norwegian Red (Chang et al.2006). Nevertheless, are the majority of our moderncows trying to tell us something? Cows of high geneticmerit for milk yield mobilize more body tissue in earlylactation than cows of average genetic merit (Pryce et al.2003). Thus, there is a negative correlation between milk

Reprod Dom Anim 42 (Suppl.2), 17–23 (2007)

� 2007 The Authors. Journal compilation � 2007 Blackwell Verlag

yield and body condition score (BCS) in early lactationraising the question whether we are able to adequatelyfeed these high genetic merit cows. The critical limitingfactor is total dry matter intake (DMI) – bigger cows arecapable of higher milk yields but there is a limit to thesize of the rumen and appetite! Higher energy densityfeeds have been employed but eventually these interferewith efficient functioning of the rumen leading todigestive problems (Krajcarski-Hunt et al. 2002). Inspite of this, some high yielding herds continue tomaintain high reproductive performance avoiding theimpact of yield on fertility; however, close examinationof such herds reveals that very high veterinary attentionis required (Lopez-Gatius et al. 2006).

Indeed, from a welfare point-of-view, examining theincidence of (sub) clinical problems around calving isdisturbing, the vast majority of veterinary attention ispaid to cows from 1 week before to 10 weeks aftercalving (Zwald et al. 2004). Clearly, calving presentsa considerable welfare risk to a dairy cow – so why makeher calve so frequently? Taking an extreme example foremphasis, think of a 3-year period (this is the UKaverage cow life-span after first calving) during whicha cow calves at intervals of 1.5 years. She would only

experience two periods of high risk compared with threeif she calved once per year. Obviously, to be financiallyviable, the cow would need to continue to produceadequate amounts of milk until the necessary 6–8 weeksdry period prior to the next calving. Persistent lactationsare characterized by achieving lower and later peakyields but reasonable production is maintained forlonger (Fig. 1).

Persistency is flexible in that it can be enhanced bymore frequent milking, feeding more concentrate duringdeclining lactation, and by calving in the winter ratherthan the summer in the UK (Knight 2001). In part,persistence is also due to avoiding pregnancy soon aftercalving: pregnancy leads to depressed milk productionin the second and third trimester. In other words,farmers need to voluntarily delay the first postpartuminsemination – and there is evidence to show thatpregnancy rates per insemination in later lactation areequivalent or better than those soon after calving.Retnayake et al. (1998) found no significant differencesin pregnancy rates for cows managed to calve at 12-, 15-or 18-month intervals. Furthermore, high-yielding cowsdeliberately rebred at 11.5–13 months greatly improvedprofitability without any other deliberate action toimprove lactation persistency (Arbel et al. 2001).

Some people may be concerned that there will bea reduction in the number of calves born per year – but,dairy farmers are in business to sell milk, not surpluscalves. Others may be worried about an interruption inthe availability of replacement heifers. In a reasonablywell-managed stable herd, with an annual culling rate ofapproximately 20% (which could decrease with im-proved cow welfare due to lowered peri-parturientclinical risk), only approximately 20% replacementsare required. The increasing use of sexed semen will alsoovercome this problem, especially when genetic changesare required (Klinic et al. 2007).

To be financially acceptable, the milk yield from twocalvings over 3 years will have to be at least equal orgreater than that delivered by three annual calvings in

Milk

yie

ldM

ilk y

ield

Autumn Autumn AutumnAutumn

Autumn Autumn AutumnAutumn

Fig. 1. Diagram of milk yields incows that (a) calve every year,(b) calve every 1.5 years. Thehorizontal bars represent periodsof risk around calving. The dottedline in (b) represents yields in cowscalving every year

Table 1. Financial aspects of feeding a cow of different breedscompared with milk yield

Channel island Friesian Holstein

Average 305-day yield (l) 4000 6000 10 000

Average daily yield (l) 13 20 33

Mature weight (kg) 444 555 666

Feed costs £ (euro) £536 (788 €) £666 (979 €) £808 (1187)

Milk income £ (euro) £764 (1123 €) £1116 (1640 €) £1640 (2410 €)

‘Profit’ (milk minus feed) £228 (335 €) £450 (661 €) £832 (1223 €)

These calculations assume average costs of £125 (184 €) per tonne concentrates,and £25 (38 €) per tonne conserved forage, and income of 18p (0.26 €) perstandard litre (4% fat, 3.3% protein) with 2p (0.03 €) per litre adjustment per

1% above/below standard for fat and protein. Fixed costs and labour per cow

are the same irrespective of breed but have not been included in the ‘profit’

figure.

18 H Dobson, RF Smith, MD Royal, CH Knight and IM Sheldon


the extreme example used above; but currently thisextreme is not achievable. However, the heritability forpersistent lactation has been estimated at 0.09–0.18;compared with 0.03–0.19 for fertility (Dekkers et al.1998; Haile-Mariam et al. 2003; Muir et al. 2004). Thisis in comparison to the heritability for 305-day milkyield of 0.45 that has increased average UK productionfrom 3000 l in 1960 to 7000 l in 2000. So, it should bepossible with the widespread use of AI in dairy cattle tomake quite considerable advances in persistency so thatfarmers can effectively manage voluntarily extendedcalving-to-calving intervals. Predictions are encouraging– the economic value of persistency almost triples whenthe calving interval increases from 12 to 13 months(Dekkers et al. 1998). However, caution has been urgedas cows with high mean somatic cell counts havereduced yield persistency but this can be overcome byattention to udder health (Haile-Mariam et al. 2003).

Understanding the Causes behind theConstraints to Reproductive Performance

Until the full genetic delivery of persistent lactations, itis instructive to reflect on exactly how reproductiveperformance is being limited in high-producing cows.Knowing the precise nature and extent of the constraintswill enable melioration of the effects.

Clinical conditions

Some infectious diseases do have indirect effects due tocompromised immune status in high-producing cows oreven direct effects on pregnancy rates (for example,‘Leptospirosis’: Dhaliwal et al. 1996; ‘BVDv’: Frayet al. 2002). Other infections, such as Brucella orNeospora cause abortions and hence reduce the milkoutput of herds and sometimes fertility (Bartels et al.2006). However, even though infectious diseases aredamaging in individual herds, on a larger scale theimpact of infectious diseases can be overcome byeradication schemes (e.g. Brucella) or by vaccinationprogrammes (e.g. Leptospirosis, BVDv, IBR).

More insidious are the ‘management/production’diseases, such as undernutrition (poor BCS or loss ofBCS), hypocalcaemia, mastitis and lameness that all

lead to reduced reproductive performance comparedwith unaffected contemporaneous herd-mates. Cowswith high milk yields and low BCS in the earlypostpartum period, take >10 days longer to conceive(Lopez-Gatius et al. 2003; Garnsworthy 2007), andthose succumbing to hypocalcaemia can take onaverage 13 extra days to get pregnant (Parker 1992).Indeed, there is evidence that the calving-to-pregnancyinterval is extended for at least 7, 8, 26 and 31 days incows treated for mastitis, retained fetal membranes,hypocalcaemia or endometritis, respectively, comparedwith healthy herd-mates (Borsberry and Dobson 1989;Schrick et al. 2001). Lameness is associated with evenworse reproduction performance, as up to 40 days canbe lost to get lame cows in-calf again even though thelameness has been treated (Collick et al. 1989; Melen-dez et al. 2003; Hernandez et al. 2005; Fig. 2). In part,these poor fertility data may be related to delayedresumption of ovarian cyclicity after calving. Forexample, if cows have mastitis soon after calving,luteal activity starts approximately 7 days later thanhealthy animals (Huszenicza et al. 2005). Similarly,lame cows begin postpartum luteal activity later thanunaffected herd-mates (50 days vs 33 days in onestudy; Petersson et al. 2006) However, delayed cyclic-ity is not the whole cause of lowered fertility as thisonly accounts for approximately half the delay ingetting lame cows pregnant again; the ability toexpress oestrus is also important (see later).

Obviously, prevention of all the above clinical condi-tions by the implementation of good managementpractices will be rewarding, both financially but perhapsmore importantly with respect to animal welfare.Prevention may be partially achieved via selectivebreeding as genetic correlations for production diseasesare typically between +0.10 and +0.40 (Weigel 2006).

With an ironic downwards twist in the tail, whilehigh milk yields make dairy cows more susceptible toproduction diseases (including lowered fertility), theconverse is also true – several production diseasesreduce milk yield. For example, systemic or localmastitis, lameness, ketosis or hypocalcaemia are asso-ciated with respective losses of around 160, 75, 75–100,90 or 45 kg milk over the first 140 days of lactation(Bareille et al. 2003).

0 20 40 60 80 100 120 140

Normal

Mastitis

RFM

Hypocalcaemia

Endometritis

Lameness

Calving to pregnancy interval (days)

Fig. 2. Calving to pregnancyintervals for cows treated forvarious clinical conditions (datafrom Borsberry and Dobson 1989;Collick et al. 1989)

The High-producing Dairy Cow and its Reproductive Performance 19


Expression of oestrous behaviour and return to ovariancyclicity

Establishing a pregnancy involves high risk for animalsbecause, in the later stages, the foetus makes hugedemands on the dam (mainly nutritional). So followingthe survival instinct, animals will choose to not showsigns of oestrus to avoid conception. Indeed, a higherincidence of ‘silent’ ovulations (no oestrus) in Holsteinshas been associated with increasing levels of milkproduction (averages of 1.6 vs 0.7 silent oestruses; for36 and 28 kg/day respectively; Harrison et al. 1990).Furthermore, cows loosing most weight (BCS) in theearly postpartum period, take approximately 30 dayslonger to display the first postpartum oestrus (Butler2003), and once resumed, periods of oestrus are shorterin higher producing Holstein cows (Table 2). Otheraspects of oestrus are also affected by high milkproduction (Table 2).

If cows have mastitis around the time of the first‘silent’ oestrus (15–28 days postpartum), luteal activityresumed in one study on average 39 days vs 32 dayspostpartum; but the onset of oestrous behaviour did notoccur until 91 days vs 84 days, in mastitic and healthycows respectively (Huszenicza et al. 2005).

Concerning the mechanisms involved behind theseobservations, we have provided considerable evidence toshow that both acute and chronic stressors (includingsome of the production diseases cited above) areassociated with interactions between the hypothala-mus-pituitary-adrenal gland and hypothalamus-pituit-ary-ovarian axis (Dobson and Smith 2000; Dobsonet al. 2001, 2003). For example, acute stressors reduceGnRH and hence LH pulse frequency, leading to short-term decreases in follicular oestradiol production, aswell as delaying and reducing the magnitude of the LHsurge.

However, there do appear to be different conse-quences of chronic stressors as revealed by our moredetailed behavioural studies in high-producing lamecows. While lame cows displayed the same incidenceof oestrus in one herd (56% of low milk progesteroneperiods associated with at least one sign of oestrusbehaviour), the duration and intensities of behaviourare decreased mainly in terms of reduced sniffing ofthe vulva and less mounting activity (Table 2). Fur-thermore, although milk oestradiol profiles wereunexpectedly the same in chronically lame and non-lame cows, progesterone concentrations (especiallyover a period 6 days before oestrus) were lower in

lame cows and this may have consequences forpheromone production and/or detection mechanisms(Walker et al. 2006).

Oocyte and embryo quality

In the real world, reproductive performance is notdependant on one factor: there are many facets. Even ifsufficient oestrus signs are exhibited and inseminationdoes take place, the fertility of high-producing cows isstill compromised.

Reproductive performance can be affected by changesduring the breeding period; for example, heat stressseverely reduces fertility in cows with pregnancy ratesdecreasing to as low as 10% in environmental temper-atures of 33�C (Hansen and Arechiga 1999). On theother hand, some events have more long-lasting effects;for example, the signs of dystocia, or immediatepostpartum hypocalcaemia, endometritis or mastitiscan be ‘cured’ within days by clinical treatment butthe cows are subfertile many weeks later during thebreeding period (Borsberry and Dobson 1989; Hus-zenicza et al. 2005). Detailed data reveal that heat stressalso has long-lasting consequences, and fertility is stilllower when environmental temperatures have decreasedin the autumn (September, October and November).Furthermore, these effects are exacerbated by increasingmilk yields (Fig. 3). Clearly, high-producing postpartumcows are surviving on a knife-edge and in the long termare more susceptible to stressful challenges.

The growth of follicles destined to ovulate takes placeover 3–4 months (Webb et al. 2004) and involves severalcritical stages that can be disrupted during environmen-tal or physiological insult leading to development ofdefective oocytes, and subsequent poor embryo quality.Acute heat stress during early stages of antral folliculardevelopment in high-yielding cows reduces steroidproduction in pre-ovulatory follicles several weeks later,and oocyte quality improves slowly and gradually onlytowards the end of the cooler period in hot countries

Table 2. Effects of milk yield or lameness on aspects of oestrus

Milk yielda Lameness statusb

Average High Not lame Lame

Duration of mounting (h) 11 6* 11.0 7.5*

Incidence of vulval sniffing – – 13 6*

Incidence of standing in oestrus 8.8 6.3* 9.5 5.6*

Duration of standing (s) 28.2 21.7* – –

*p < 0.05 within a study.aLopez et al. 2004 (33 kg/day vs 46 kg/day).bWalker et al. 2005 (yield 43 kg/day).

Fig. 3. Seasonal variation in 90-d nonreturn rate to first service asaffected by mature equivalent milk yield. Results represent leastsquares means ± SEM adjusted for interval to first service when cowswere grouped according to milk yield ((d) <4536 kg; (s) 4536 to 9072kg; ( ) >9072 kg). Reprinted from Al-Katannani et al. 1999 withpermission.



(Roth et al. 2001a,b). In addition, there is an interactionbetween high milk production and BCS as oocytescollected from high-producing cows with poor BCS havelower in vitro rates of cleavage than those derived fromhigh BCS animals (Snijders et al. 2000). Later, during invivo development, Leroy et al. (2005) recovered only13% excellent embryos on day 6 after oestrus from high-yielding first lactation cows in comparison to 62.5%from non-lactating heifers.

Uterine infection

With increasing milk yields from 1980 to 1998, there hasbeen an increase from 7% to 17% in the incidence ofpersistent corpora lutea as determined by milk prog-esterone profiles (Royal et al. 2000; Lucy 2001). Thisincrease in atypical progesterone profiles is also associ-ated with a greater incidence of uterine infection (onaverage, approximately 20% vs 11.5%) and longercalving intervals (averages around 400 days vs 380 days)compared with animals with normal progesterone pro-files. Indeed, one of the major risk factors for prolongedluteal phases in high-yielding dairy cows is uterineinfection (endometritis; Opsomer et al. 2000).

If cows are seen in oestrus and inseminated, theuterus must be fit to receive sperm and then thefertilized zygote. Unfortunately, a considerable decreasein fertility is associated with contamination of theuterus after calving, with approximately 40% animalsdeveloping uterine infection that persists for more than3 weeks in approximately 15% high-yielding cows(Sheldon et al. 2002; Sheldon and Dobson 2004).Escherichia coli is one of the most common isolatesfrom the uterus; and lipopolysaccharide (LPS), themain pathogenic product from E. coli, occurs in plasmaof cows with postpartum uterine infection (Sheldonet al. 2002; Mateus et al. 2003). Cells of the endome-trium express the specific receptor-complex for detec-tion of LPS, and LPS switches the main production ofprostaglandin (PG) secretion from PGF2a to PGE2,with the potential to disrupt luteolysis (Herath et al.2006). These infections are not only associated withuterine damage but also with disruption of ovariancycle control mechanisms resulting in subfertility. Eitheruterine disease associated with E. coli or infusions ofLPS suppress follicular growth, decrease oestradiolproduction and delay the LH surge and ovulation(Suzuki et al. 2001; Sheldon et al. 2002). Althoughplasma FSH concentrations in vivo are not affected,LPS treatment in vitro down-regulates the expression ofaromatase mRNA in granulosa cells, however, expres-sion of LH receptors remains unaffected (EJ Williams,unpublished data). Thus, folliculogenesis appears to bedirectly perturbed by the inability of ovarian granulosacells to aromatize androstenedione to oestradiol inresponse to FSH. Furthermore, plasma progesteroneconcentrations are lower after ovulation of dominantfollicles in cows with uterine infection, or those infusedwith LPS (EJ Williams, unpublished data). Takentogether, it appears that uterine disease not only causesendometrial pathology that would perturb fertility butalso interferes with endocrine function within andbetween both the uterus and ovary.

Conclusion – Providing the Solutions

Exploitation of genetics and advances in cow manage-ment have led to very high milk yields; however, we arestarting to pay the cost in terms of reduced reproduc-tive performance. Attempts to avoid the specific‘production diseases’ detailed above is undoubtedlybeing undertaken at farm level but the solution withthe greatest welfare and financial impact will bethrough genetic enhancement of persistent lactations.This should lead to a reduction in the number ofcalvings and hence avoidance of postpartum energydeficits, stress-induced disruption of follicular develop-ment and oestrus behaviour, production of defectiveoocytes and embryos and a reduction in the impact ofuterine infections.

Acknowledgements

The authors’ work was supported by grants from BBSRC, DEFRA,SEERAD and the Wellcome Trust. We are grateful to all the technicalstaff involved at the different institutes and all postgraduate students,postdocs and collaborators without whose interaction the above dataand ideas would not have emerged.

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Submitted: 02.02.2007

Author’s address (for correspondence): H Dobson, Faculty of Veter-inary Science, University of Liverpool, Leahurst, Neston, Wirral CH647TE, UK. E-mail: [email protected]



the high-producing dairy cow and its reproductive performance

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