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Concentrate feeding, dry-matter intake, and metabolic disorders

in Danish dairy cows

a ,

_*

¨

S. Østergaard

, Y.T. Grohn

Department of Animal Science and Animal Health, Royal Veterinary and Agricultural University, Bulowsvej 13, DK-1870 Frederiksberg C, Copenhagen, Denmark

Department of Population Medicine and Diagnostic Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA

Received 3 May 1999; received in revised form 26 October 1999; accepted 2 November 1999

Abstract

Data from 3676 lactations of 1856 cows recorded during 12 years in three Danish research herds was used to study the associations between postpartum feeding, diseases, and feed intake. The diseases included four clinical metabolic disorders diagnosed by veterinarians: decreased rumen motility, enteritis, ketosis, and left-displaced abomasum (LDA). Because the feeds offered to and refused by cows were weighed individually for each cow, the actual concentrate dry-matter intake (DMI) and roughage DMI were used. Weekly recordings of feed intake were available. Odds of metabolic disorders according to concentrate management in the early lactation were studied through three analyses. Effect of total concentrate DMI was analysed for cows fed their concentrates mainly separately from roughage. Effect of concentrate DMI to total DMI ratio was analysed for cows that predominately were fed a total mixed ration (TMR). Effect of percentage of the total concentrate DMI that was fed with roughage was analysed for cows that did not have access to summer pasture. From these analyses it seems to be the early-lactation feeding of concentrates separately from roughage and not the concentrate to roughage ratio within a TMR that is associated with increased odds of metabolic disorders. Through analyses of DMI in the weeks around the diagnoses, it was found that each disorder was associated with decreased total DMI, for at least the week before and 2 weeks after diagnosis. The effect persisted more than 4 weeks in cows with ketosis and in primiparous cows with LDA. LDA and ketosis was associated with more weeks of ‘pre-clinical’ decreased DMI.  2000 Elsevier Science B.V. All rights reserved.

Keywords: Concentrate to roughage ratio; Dry-matter intake; Metabolic disorders; Diseases; Dairy cows

1. Introduction

Important management decisions for dairy cows *Corresponding author. Present address: Danish Institute of _{concern the amount of concentrates to be fed and the} Agricultural Sciences, Research Centre Foulum, P.O. Box 50,

manner of their feeding. An important task in dairy DK-8830 Tjele, Denmark. Tel.: 145-89-991-304; fax: 1

45-89-herd management is to control the feed level or 991-500.

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roughage ratio in the feeds given to the cows. Energy complex into analyses of some underlying mecha-is the nutrient for which intake mecha-is most closely nisms. Within homogenous feeding management related to the level of milk production (Bath, 1985) types, various feeding measures may be defined and is, consequently, widely used in systems for independently of feed intake, such as the concentrate predicting milk production (Kaustell et al., 1997) to roughage ratio for cows fed a TMR. In this study, and in relation to profitability in dairy herds (Van- such measures were defined to be studied as potential dehaar, 1998). Decisions relating to concentrate risk factors for diseases. By supplementing such feeding also might affect metabolic and presumed analysis with an estimation of feed intake as a feeding-related disorders (Veenhuizen et al., 1991; disease specific function of day of diagnosis may Geishauser, 1995; Gustafsson et al., 1995; Shaver, explain some of the ‘feeding–health’ complex. Con-1997). Since, significant economic loss may be sequently, we addressed such analyses for decreased associated with incidence of metabolic disorders rumen motility, enteritis, ketosis, and left-displaced (Kossaibati and Esslemont, 1997), the relationship abomasum (LDA).

between feeding and diseases may be important for The purposes of this study were (1) to test the production in a dairy herd. Unfortunately, the whether odds of metabolic disorders varied accord-relationships between feeding of concentrates and ing to concentrate management in the early lactation, metabolic disorders are poorly quantified — pre- and (2) to test whether metabolic disorders were sumably because of the lack of detailed recording related to either DMI of concentrates fed separately from the individual cow (Østergaard and Sørensen, from roughages or total DMI, both, in the three

1998). weeks before and the 3 weeks after the clinical

Cows on the same diet including roughages ad diagnosis was made. libitum, may differ in concentrate DMI and in

concentrate to roughage ratio, due to variations in

feed preference, intake capacity, and presentation of 2. Materials and methods

concentrates such as separately or mixed with

roughage. Also, associations between concentrate 2.1. The herds and lactations DMI and roughage DMI and metabolic disorders,

might vary according to when the DMIs are mea- Data for this retrospective study originate from sured in relationship to the date of diagnosis. These three research herds of the Danish Institute of facts call for data with frequently recorded feed Agricultural Sciences, Denmark, between April 1985 intake for each individual cow, which is very costly and August 1997 (The breeds and parities are shown to fulfil simultaneously with the demand for many in Table 1). Except during the periods where cows observations on cows due to the relatively low had access to summer pasture (two herds), the incidence of feeding related diseases. However, these milking herds were kept in tie stalls. Feedstuffs demands have been fulfilled in the data available for offered and refused (except pasture) were measured this study. These data have been recorded during 12 daily for each cow. Because ration analyses were years in three Danish research herds. These herds available, it was possible to calculate weekly or had records on weekly or bi-weekly individual-cow bi-weekly, the total concentrate and roughage DMIs DMIs for all concentrates and most roughages for each cow for at least 168 days in milk (DIM). (exception: summer pasture in two herds), on the Throughout this study we used feed intake measures manner of feeding the concentrates (within a total (i.e. what the cows actually eat) as opposed to mixed ration (TMR), entirely separate from measures of what the cows were offered. Hay, straw roughage, or partly separate from roughage), and on and feedstuffs with dry matter ,70% was defined to diagnoses of clinical disorders. be roughages. Other feedstuffs were defined to be The fact that an analysis of the effect of feeding concentrates. It was also possible to identify the DMI on disease should control for feeding management of concentrates fed separately from roughages (rather and feed intake as a disease specific function of day than fed, e.g. within a TMR) and of roughages of diagnosis made us split-up the study of the (except pasture) fed separately from concentrates. If

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Table 1

Number of lactations by herd, breed, and parity (1856 total cows with 3676 total lactations, three Danish dairy-research herds, 1985 to 1997)

Breed Parity Number of lactations

Herd I Herd II Herd III Total

Danish black and white 1 224 762 184 1170

2 101 533 131 765

.2 54 623 158 835

Danish jersey 1 136 – – 136

2 46 – – 46

.2 23 – – 23

Danish red 1 232 50 – 282

2 81 39 – 120

.2 31 29 – 60

Danish red and white 1 14 – – 14

2 11 – – 11

Crossbreed dairy cows 1 – 95 1 96

2 – 71 – 71

.2 – 47 – 47

All breeds All 953 2249 474 3676

roughages and concentrates were only fed separately, The order in which the diagnoses are mentioned the general strategy was to feed roughages ad above indicates this ranking.

libitum, whereas concentrates were fed as a set We chose not to study milk fever because it occurs amount regardless of test-day milk yields of the so soon after parturition that post-parturient feeding

individual cow. (our interest) could not logically be a risk factor.

A uniform procedure of making a diagnosis was Only four right-displaced abomasa were recorded, used in all of the three herds. All diseases were consequently, we could not investigate that disorder. diagnosed and treated by a veterinarian. The cows Cows were typically being used in various trials were not routinely vetted. If the stockmen noted while the data we used was being recorded. If cows something wrong, then a veterinarian was sent for. were assigned to trials unlikely to affect feeding and At each disease case, a single diagnosis was made metabolic disorders, we did not take it into account and recorded by the veterinarian, according to a (e.g. trials of milking management or of animal standard protocol of disease diagnoses. handling). Most cows were only on a single herd The LDA diagnosis was entrapment of the en- trial between parturition and 168 DIM. In all cases larged fluid- or gas-filled abomasum high in the left we only accounted for the initially-assigned trial in abdominal cavity. Ketosis was diagnosed by using any lactation in our study. If a cow was not assigned clinical signs combined with a test on a milk sample. to a trial before 168 DIM, a dummy value specific Enteritis was diagnosed primarily by the presence of for the herd-year was used. In total, the lactations we diarrhoea, which in some cases could be bloody. used and trials which we accounted for included 71 Cows with enteritis were typically feverish. De- trials and 230 treatment groups.

creased rumen motility was diagnosed if rumen

contractions were considered significantly reduced. 2.2. Data exclusions and subsets of the data Cows with decreased rumen motility were typically

not feverish. Data from fistulated, intensively managed cows

Some of the clinical signs related to these diag- were excluded. Data from weeks where cows had noses could be related to more than a single diag- access to summer pasture were excluded from any nosis. Generally, those relatively less well-defined analyses that required measures of roughage DMI. diagnoses were made only if a better-defined diag- Data were used only from the first 168 DIM, for nosis could not be made, based on the clinical signs. three reasons. Firstly, as stated above, most

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lacta-tions were involved in only a single trial before 168 all of the total DMI was fed between parturition and DIM. Secondly, the disorders we studied were 42 DIM as a TMR and in which the cow did not diagnosed primarily in early or mid-lactation. Third- have access to summer pasture early on in that ly, when concentrates and roughages were fed separ- lactation. This subset of the data was used to study ately, the feeding plan for concentrates tended not to whether the odds of metabolic disorders varied be based on milk yield until at least 168 DIM had according to concentrate DMI to total DMI ratio. been reached. Diagnoses made earlier than 14 DIM The third subset of the data included the lactations in were excluded from analyses in which the aspects of which the cow did not have access to summer feeding were risk factors, as opposed to outcomes, pasture between parturition and 42 DIM. This subset because we felt that post-partum feeding was unlike- of the data was used to study whether the odds of ly to be a major risk factor for disorders occurring so metabolic disorders varied according to the per-soon after calving. Finally, lactations were excluded centage of the total concentrate DMI that was fed if the data were not available for most of the weeks with roughages [(concentrate DMI fed with between parturition and 168 DIM. The 3676 lacta- roughages)4(total concentrate DMI)3100%]. In tions remaining after these exclusions are described this way, it was possible to compare cows fed TMR in Table 1 and the disease diagnoses are described in with those fed some or all concentrates separately

Table 2. from the roughages.

To study whether the odds of disease varied In addition, a fourth and a fifth subset of the data, according to post-partum feeding, three subsets of based on feeding management, was created to ex-the data were created, based on feeding management. plore the effects of each metabolic disorder on week-The first subset of the data included only lactations specific feed intake. The fourth subset of the data in which all of the concentrates fed between parturi- included only lactations in which .90% of concen-tion and 42 DIM were fed separately from trates fed between parturition and 168 DIM were fed roughages. This subset of the data was used to study separately from roughages. This subset of the data whether the odds of metabolic disorders varied was used to explore the effects of each metabolic according to total DMI of concentrates. The second disorder on week-specific concentrate DMI fed subset of the data included only lactations in which separately from roughages. The fifth subset of the Table 2

Frequency, lactational incidence and DIM for the first diagnoses of each study disease: data include 1698, 1013, and 965 lactations (,168 DIM) from parities 1, 2, and.2, respectively (3 Danish dairy-research herds, 1985 to 1997)

Study diseases

Decreased Enteritis Ketosis LDA

rumen motility Frequency

Parity 1 40 72 39 6

Parity 2 24 54 80 10

Parity.2 60 73 128 12

Total 124 199 247 28

Lactational incidence (%)

Parity 1 2.4 4.2 2.3 0.4

Parity 2 2.4 5.3 7.9 1.0

Parity.2 6.2 7.6 13.3 1.2

Total 3.4 5.4 6.7 0.8

DIM at diagnosis

Median 25 22 25 17

SIR 10 31 10 8

LDA, left-displaced abomasum.

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data included only data from weeks in which they and for the clustering of lactations by trial and by did not have access to summer pasture. This subset treatment group within trial.

of the data was used to explore the effect of each Because there were four disorders and three metabolic disorder on week-specific total DMI. ‘types’ of feeding management, defining the first, The definition of the created subsets of the data second, and third subset of the data (Table 3), the are summarised in Table 3, along with a clarification model was used for 12 different analyses. Within of the specific analyses that the data were applied to. each of the three subsets of the data, each lactation’s According to the criteria for each subset of the data, mean value, between parturition and 42 DIM for the each lactation may be included in one or more subset’s defining feeding characteristic, was

calcu-subsets. lated. These mean values were then used to define

the lactation as being within the lowest, middle, or highest tercile for the feeding characteristic. The 2.3. Statistical analyses: odds of disorders _{specific comparisons were lowest to middle tercile,} lowest to highest, and middle to highest. Odds ratios The odds of disorders (diagnosed between 14 and _{(OR) and 95% confidence intervals were calculated} 168 DIM) according to feeding characteristics were _{from the models.}

explored using this generalised linear mixed-model _{The specific fixed effects (}_b_{) offered to each} (GLMM) analysis for binomial data: _{model, in addition to tercile of the feeding} charac-teristic, were herd (three categories; not random logit( p)5Xb 1Zg 1e (Model 1) _because _there _were _only _three), _breed _(two categories; Jersey and not Jersey), calving season Where, p is a vector representing the response on a (four categories, each of three months; winter5

logit scale ‘ln( p /(12p))’ of the expected chance to December–February), parity (three categories ac-contract the metabolic disorder under study. b is a cording to parity 1, 2, and .2), and interaction vector of fixed effects being analyses as risk factors. between parity and tercile of the feeding

characteris-g is an unknown vector of random effects distributed tic (nine categories). Also, depending on the specific

2 2

N(0, I(s) ), in which (s) was the variance of the disorder being modelled, other ‘risk-factor’ disorders

effects of treatment group nested within trial. In this (yes / no for each such risk factor) were offered to the way, we accounted for the effects of the trials in model as fixed effects; these decisions were based

¨ which lactations were used in these research herds mainly on the findings of Østergaard and Grohn

Table 3

Definition of the created subsets of the data and for which analyses each of them is used

Subset Criterion for including records Number of Number of Analysis

number lactations weekly recordings

1 All of the concentrates fed 0 to 498 Aggregated measure Effect of total concentrate 42 DIM were fed separately per lactation used DMI on disease

from roughages

2 All of the total DMI was fed as 1282 (as above) Effect of concentrate

a TMR and no access to summer DMI to total DMI

pasture, both 0 to 42 DIM ratio on disease

3 No access to summer pasture 2864 (as above) Effect on disease of percentage

0 to 42 DIM of the total concentrate DMI

that was fed with roughages 4 .90% of concentrates fed 0 to 664 16 459 Effects of each disease on

168 DIM were fed separately week-specific concentrate DMI

from roughages fed separately from roughages

5 No access to summer pasture 3673 73 422 Effect of each disease on

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(1999) regarding disease interrelationships within neous. The variation in repeated measures within these same 12 years of data. cows was accounted for by multiplying the error

We used the PQL procedure (Breslow and variance (se) by the covariance matrix R, which was Clayton, 1992) implemented in the SAS macro assumed to have first-order autoregressive covar-GLIMMIX (Littell et al., 1998) (version GLMM iance.

6.12 last updated 5th December 1997) to fit the Each model included several fixed effects, includ-models. Model selection was based on a backwards- ing those for herd, breed, and season as in model 1. elimination strategy, using the F-statistic as the Parity was only in the multiparous cow models of criterion at P,0.05 (two-tailed). Because we total DMI (two categories according to parity 2 and thought that parity would be a significant effector of .2) and the models of total concentrate DMI (two disease incidence, parity was forced to remain within categories according to parity 1, 2, and .2). Stage

all models. of lactation included nine categories according to

week of lactation (0, 1, 2, 3–4, 5–6, 7–9, 10–13, 14–18, and 19–24). The indicator variable to de-2.4. Statistical analyses: effects of disorders on

scribe week of lactation, relative to the week of

DMI

diagnosis of the disorder also had nine categories. Category 0 represented cows free of the disorder. The analyses of the effects of disorders on total

The other eight categories were for cows with the DMI were carried out separately for primiparous and

metabolic disorder, and indicated whether that week multiparous cows, because of differences in shapes

of data was from before ($ 24, 23, 22, 21) or of the feed intake capacity curves and because there

after (11,12,13,$4) the week of diagnosis. The were parity-specific differences in median DIM at

day of diagnosis was the first day of week11 in this ¨

diagnosis (Østergaard and Grohn, 1999). However,

coding. the analyses of the effect of disorders on total

To fit model 2 we used the SAS MIXED pro-concentrate DMI were not carried out separately for

cedure from SAS Institute (1996) with the restricted primiparous and multiparous cows. This was because

maximum-likelihood method. Model selection pro-of concentrates being fed restrictively and separately,

cedures were as already presented for the modelling consequently, smaller parity-specific differences

of the odds of disorders (model 1). occurred in total concentrate DMI. Separate analyses

of separately fed concentrate DMI, primiparous total DMI and multiparous total DMI for each of the four

3. Results

metabolic disorders, resulted in 12 analyses. The ‘effects’ of disorders on weekly DMI were tested in

The first diagnoses of each of the four disorders these analyses by this repeated-measures ANOVA

are summarised in Table 2; overall, at least one of model:

the four disorders was recorded for 23% of the cows

y5Xb 1Zg 1e (Model 2)

and 14% of the lactations. For results of disease Where y is a vector representing the response interrelationships, reference is made to the study of

variable of DMI.b is a vector of fixed effects. As in Østergaard and Grohn (1999) on the same data. model 1,g is an unknown vector of random effects

2 2

distributed N(0, I(sg) ). The (sg) is the variance of 3.1. Odds of disorders the effects of treatment group nested within trial. In

this way, we accounted for the effects of the trials, in The numbers of lactations in the three data subsets which lactations were used in these research herds were 498, 1282, and 2861 for concentrates mainly and for the clustering of lactations by trial and by fed separately, concentrate DMI to total DMI ratio in treatment group within trial. e is an unknown random the TMR, and percent of all concentrates fed with

error vector distributed N(0, R(se) ), whose elements roughages, respectively (Table 3). The exclusion of are not required to be independent and homoge- lactations with the study disease before 14 DIM

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caused minor reductions in these numbers, in some not related significantly to tercile of percentage of analyses with model 1. The number of metabolic total concentrate DMI fed with roughages (Table 5). disorder incidents were so low (,8) for three

analyses with model 1, that we excluded them. These 3.2. Effects of disorders on DMI analyses were the analysis of decreased rumen

motility based on subset 1 and the two analyses of The fixed effects of herd and season were removed LDA based on subset 1 and 2, respectively. from the models to solve convergence problems. The estimated effects of total concentrate DMI, Furthermore, the covariance parameters in some analysed for cows fed all concentrates separately models were estimated using minimum-variance (subset 1), are shown in Table 4. The risk of enteritis quadratic unbiased estimation (MIVQUE0) (SAS was increased significantly (i.e. where the confidence Institute, 1996).

interval did not included 1.0) by lower tercile of total Decreased rumen motility (11 cases), enteritis (38 concentrate DMI fed separately (Table 4). The odds cases) and LDA (five cases) had no effects on the of ketosis were not related significantly to total DMI of concentrates fed separately from roughages concentrate DMI fed separately (Table 4). (subset 4) within the weeks before and after diag-The concentrate DMI to total DMI terciles for nosis. Ketosis (82 cases) had a significant effect on cows fed TMR (subset 2) were not related sig- the DMI of concentrates (20.4 kg / day; S.E.50.2) nificantly to the odds of any disease studied. The only for the week immediately preceding the diag-thresholds dividing the terciles of the concentrate nosis (the week coded as 21).

DMI to total DMI ratio for cows fed TMR (subset 2) In contrast, the four metabolic disorders had many were 0.44 and 0.51. There were 14, 10 and 19 effects on total DMI (subset 5) both before and after incidents of decreased rumen motility, enteritis, and diagnosis and in both primiparous (Table 6) and ketosis for these analyses. multiparous (Table 7) cows. Only enteritis in The estimated effects of percentage of concentrate primiparous cows and ketosis in multiparous cows DMI fed with roughages (subset 3) are shown in had ‘effects’ (decreases in DMI) evident earlier than Table 5. The odds of enteritis and ketosis were 3 weeks before diagnosis, although all disorders was significantly higher for lower terciles of percentage associated with decreased DMI at least once in of concentrate DMI fed with roughages (Table 5). weeks 23,22, or21. All disorders had detrimental The odds of decreased rumen motility and LDA were effects (lower DMI) in weeks 11 and 12, and all

Table 4

Effect of total concentrate DMI on adjusted odds ratios of metabolic disorders

Metabolic Number of Tercile of total Odds ratio

disorder concentrate DMI and 95% confidence interval

Lactations Disorders

OR 95% CI (OR)

Enteritis 495 22 Lowest vs. middle 1.7 [0.8; 3.6]

Lowest vs. highest 10.0 [2.9; 35.2] Middle vs. highest 5.8 [1.8; 18.8]

c,d

Ketosis 494 48 Lowest vs. middle 1.5 [0.7; 3.2]

Lowest vs. highest 1.0 [0.4; 2.2] Middle vs. highest 0.7 [0.3; 1.5]

Estimated by model 1 on data subset 1, which includes cows fed concentrates separately from roughages. Only diseases with significant effect are included.

Lowest, middle and highest terciles (kg / day): lowest: ,5.2; middle:$5.2 and,6.6; highest:$6.6.

Herd retained in the final model.

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Table 5

Effect of percentage of total concentrate DMI fed with roughages on adjusted odds ratios of metabolic disorders Metabolic Number of Tercile of percentage of total Odds ratio

disorder concentrate DMI fed with and 95% confidence interval

Lactations Disorders b

roughages

OR 95% CI (OR)

Decreased rumen 2840 52 Lowest vs. middle 1.8 [1.1; 2.9]

motility Lowest vs. highest 1.2 [0.6; 2.4]

Middle vs. highest 0.7 [0.3; 1.4]

Enteritis 2822 96 Lowest vs. middle 1.2 [0.8; 1.7]

Lowest vs. highest 4.5 [2.3; 8.7] Middle vs. highest 3.9 [2.0; 7.7]

Ketosis 2832 126 Lowest vs. middle 2.1 [1.4; 3.2]

Lowest vs. highest 3.9 [2.2; 3.7] Middle vs. highest 1.8 [1.0; 3.3]

Left displaced 2861 12 Lowest vs. middle 0.7 [0.2; 2.7]

abomasum Lowest vs. highest 1.3 [0.3; 5.4]

Middle vs. highest 2.0 [0.5; 8.1]

Estimated by model 1 on data subset 3, which includes cows that did not have access to summer pasture. Only diseases with significant effect are included.

Lowest, middle and highest terciles (ratio): lowest: ,0.32; middle:$0.32 and,1.0; highest:$1.0.

Milk fever retained in the final model.

Acute clinical mastitis and clinical mastitis evident only as flakes in the milk retained in the final model.

Due to few disease incidents, parity was excluded from this model.

Table 6

Effects of study diseases on kg total DMI in weeks around the day of diagnosis in primiparous cows (final mixed models) (34679 observations from 1698 lactations in three Danish dairy-research herds, 1985 to 1997)

Week relative to Study disease

date of diagnosis b

Decreased rumen Enteritis Ketosis LDA

motility (n540) (n572) (n539) (n56)

b S.E. b S.E. b S.E. b S.E.

# 24 20.1 0.3 20.5* 0.2 20.5 0.3 0.3 1.0

23 0.1 0.4 20.5 0.3 20.5 0.3 0.4 0.9

22 0.0 0.4 20.4 0.3 20.7* 0.3 23.1*** 0.8

21 22.0*** 0.3 22.0*** 0.3 22.7*** 0.3 25.5*** 0.8

11 21.8*** 0.3 21.6*** 0.3 21.5*** 0.3 23.4*** 0.8

12 21.1*** 0.3 20.5* 0.2 21.0*** 0.3 22.4** 0.7

13 20.7* 0.3 0.5* 0.2 20.7** 0.3 22.3*** 0.7

$ 14 20.4 0.2 0.5 0.2 20.6** 0.2 21.6** 0.6

Intercept based on the period between the 19th to 24th weeks in milk for primiparous not Jersey cows without the study disease.

Covariance parameters were estimated using minimum variance quadratic unbiased estimation (MIVQUE0) as explained in the text. * P,0.05, ** P,0.01, *** P,0.001.

disorders (except enteritis in multiparous cows) also lactation was 13.5 kg / day (S.E.50.2) for primipar-‘caused’ decreased DMI in week 13. The losses ous Jersey cows without ketosis; the effect on DMI continued for more than 3 weeks after diagnosis in of other breeds (same circumstances) was 13.3 kg / cow with ketosis and in primiparous cows with LDA. day (S.E.50.1). Analogous values for multiparous The estimated total DMI during weeks 19–24 of cows were 15.6 kg / day (S.E.50.3) and 14.5 kg /

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Table 7

Effects of study diseases on kg total DMI in weeks around the day of diagnosis in multiparous cows (final mixed models) (38743 observations from 1975 lactations in three Danish dairy-research herds, 1985 to 1997)

Week relative to Study disease date of diagnosis

Decreased rumen Enteritis Ketosis LDA

motility (n584) (n5127) (n5208) (n522)

b S.E. b S.E. b S.E. b S.E.

# 24 20.6 0.3 20.1 0.3 20.7*** 0.3 21.1 0.9

23 20.5 0.4 0.0 0.3 20.8*** 0.2 21.5 0.8

22 20.9* 0.4 20.1 0.3 20.9*** 0.2 22.4** 0.7

21 23.8*** 0.4 22.0*** 0.3 22.8*** 0.2 26.6*** 0.7

11 22.9*** 0.4 21.9*** 0.3 22.1*** 0.2 26.6*** 0.7

12 21.9*** 0.3 20.9** 0.3 21.4*** 0.2 24.2*** 0.6

13 20.8** 0.3 20.4 0.2 21.0*** 0.2 21.2* 0.6

$ 14 20.2 0.3 0.0 0.2 20.7*** 0.2 20.1 0.4

Intercept based on the period between the 19th to 24th weeks in milk for multiparous not Jersey cows without the study disease.

Covariance parameters were estimated using minimum variance quadratic unbiased estimation (MIVQUE0) as explained in the text. * P,0.05, ** P,0.01, *** P,0.001.

three disorders. TMR (subset 2) — that is associated with increased

odds of metabolic disorders. The results from the analyses of the effect of concentrate DMI for cows

4. Discussion fed all concentrates separately (subset 1) are ex-cluded from this general implication from model 1. As we discussed in a previous paper Østergaard This is due to the fact that increased risk of enteritis,

and Grohn (1999), the incidences and dates of caused by a low level of concentrate DMI for cows diagnoses of the diseases in our data set (in par- fed all concentrates separately (subset 1), needs ticular, of ketosis and LDA) seemed consistent with further verification. This is because we nor believe

Shaver, 1997). 22. The results of no significant effect of the

Herd effects on disease can be important (Morris, concentrate to roughage ratio within a TMR (subset ¨

1988; Enevoldsen and Grohn, 1994). However, the 2), were also based on relatively few incidents of herd effects in this study were only minor (data not each disease. However, non-significance was found shown) — which is not surprising, because the for any analysed outcome disease. The implication of intention of the Institute was for the herds to be feeding of concentrates separately from roughages similar to one another (and to commercial herds) being a risk factor for metabolic disorders, is based except for the trials taking place. We accounted for on the odds of enteritis and ketosis being signifi-trials in all models, and we feel that between our cantly higher for lower terciles of percentage of design and analyses, we have to a reasonable extent concentrate DMI fed with roughages (Table 5). accounted for potential confounding. With regard to the validity of the analyses with

model 1, we have made different efforts to ensure 4.1. Odds of disorders causality. First, the risk factors were created based on feed intake as opposed to feed offered, which The general implication from the analyses with addresses how to ensure no influence of the outcome model 1, is that it is the early-lactation feeding of disease on the created risk factor. That was

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accom-plished for the analyses based on subset 1 and 2 this analysis, so failure to identify ‘concentrate through the creation of the respective subsets and the terciles’ as risk factors, might have been due to poor findings from model 2, of no significant effect of the power (OR and 95% CI for low vs. high level was metabolic disorders on concentrate DMI for cows fed 1.4 [0.3, 5.4]). No effect on LDA may also be concentrates separately. Excluding cows fed concen- because of the mixing process, causing a more finely trates mixed up with roughages in subset 1, ensured chopped feed, which increases the risk of accumulat-that decreased DMI caused by the outcome disease, ing gas in the abomasum and ultimately displace-did not significantly affect the concentrate DMI. ment (Geishauser, 1995).

Including only those cows eating concentrates and In contrast with our study (Table 4), Gustafsson et roughages mixed together (TMR) in subset 2, en- al. (1995) found increased risk of hyperketonemia sured that decreased DMI caused by the outcome from higher amounts of concentrates fed early in disease did not significantly affect concentrate DMI lactation. We must acknowledge, though, that our to total DMI ratio. By excluding only cows with herds typically were fed lower total amounts of access to summer pasture did not ensured causality concentrates than those in studies by Gustafsson et for the analyses with subset 3. However, by defining al. (1995). The 67th percentile in our herds was 7.8 the highest tercile in subset 3 to be cows fed entirely kg / day (absolute concentrate DMI) whereas their TMR, this specific tercile could not be affected by herds often were fed .12 kg / day even to primipar-decreased DMI caused by the outcome disease. ous cows. However, the general conclusion from the Consequently, differences between the highest tercile study of Gustafsson et al. (1995), that high feeding and the other terciles do reflect causality according to frequency and a cautious strategy of concentrates odds of disease. feeding early in lactation, are important factors in the Another problem of causality with regard to model prevention of subclinical or clinical ketosis, is sup-1, relates to the timing of risk factor and the outcome ported by our results specifically suggesting that the diseases. However, we believe that our exclusion of increased risk stems from concentrates fed separately diagnoses made before 14 DIM together with the from roughages (Table 5). In another study it was findings from model 2, of no significant effect of the found that feed restriction of 20% did not increase metabolic disorders on concentrate DMI for cows fed the risk of ketosis or fatty liver (Drackley et al., concentrates separately, partially addressed this prob- 1991). This supports the indication that feed level by

lem. itself is not of major importance for the incidence of

The terms of concentrate and roughage may also ketosis. be a problem because of the fact that in some cases a

feed component may be classified as either concen- 4.2. Effects of disorders on DMI trate or roughage depending on its treatment before

general-roughages. ly accepted (Forbes, 1996) — but we could find no

Finally, grouping the data into three broad direct estimations of magnitudes or patterns to categories according to the feeding related risk compare to ours. The persistence (for $3 week) of factors should have eliminated some misclassifica- the decreased intake (especially in primiparous cows) tion bias. In addition, we took the average of several might be due to influences of additional or recurrent measurements in an attempt to increase precision. diseases occurring within that time frame. Neverthe-LDA was not affected by the percentage of total less, the metabolic disorder in each model remains concentrate DMI fed with roughages early on in the interpretable as a risk indicator for decreased DMI lactation (Table 5). We had only 12 cases of LDA for for multiple weeks.

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Of course, decreased DMI was by definition and in primiparous cows with LDA. There were associated with ketosis — but only for the date of ‘pre-clinical’ effects of each disorder on total DMI diagnosis (and perhaps a few days prior to diag- for the week preceding diagnosis. LDA and ketosis nosis). However, the decreased DMI seems to have was associated with decreased DMI for more weeks been present for weeks — not merely days — for prior to clinical diagnosis. Except for the first week multiparous cows that eventually were diagnosed preceding the diagnosis of ketosis, there were effects with ketosis (Table 7). We speculate that the reduc- of the clinical metabolic disorders on total concen-tions of ,1 kg / day were not recognisable in the trate DMI for cows fed concentrates separately from current management scheme; if attendants could be roughages.

trained to recognise such small decreases, it might be interesting to test whether treatment at that ‘pre-clinical’ stage (Veenhuizen et al., 1991) might

6. Notation

prevent the clinical episode of ketosis. The decreased total DMI before diagnosis, combined with the

DIM, day in milk results from model 1, supports suggestions of

dis-DMI, dry matter intake eases, such as ketosis, predominantly being caused

LDA, left displaced abomasum by a reduction in feed intake caused by other

TMR, total mixed ration ¨

diseases (Grohn et al., 1989; Goff and Horst, 1997). Milk fever has not been studied specifically, but it may still play an important role in such complexes

(Goff and Horst, 1997). We also suggest that cows of Acknowledgements

any parity that decrease DMI .2 kg / day in early

lactation should be monitored carefully for LDA Data for this study were available from the Danish

(Tables 6 and 7). Institute of Agricultural Sciences, Department of

Breeding and Genetics, and Department of Livestock Management, Research Centre Foulum. The authors

5. Conclusions would like to thank Erik Luc Decker, Connie Harbo Middelhede, and Uffe Thorøe Christensen for assis-The initial purpose of this study was to establish tance with databases, and Hollis N. Erb for assis-whether odds of metabolic disorders varied accord- tance with drafting the manuscript.

ing to concentrate management in the early lactation. The concentrate DMI to total DMI ratio for cows fed a TMR early in lactation, was not related to odds of

References

metabolic disorders. Increased odds of ketosis and enteritis, which accounted for the majority of

meta-Bath, D.L., 1985. Biological requirements for economics of bolic disorders cases under study, were associated _{lowering feed costs. J. Dairy Sci. 68, 1579–1584.}

with lower terciles of percentage of concentrate DMI Breslow, N.E., Clayton, D.G., 1992. Approximate inference in fed with roughages. The overall finding from this generalized linear mixed models. J. Am. Stat. Assoc. 88, 9–25.

Detilleux, J.C., Grohn, Y.T., Quaas, R.L., 1994. Effects of clinical study of the concentrate-management characteristics

ketosis on test day milk yields in Finnish Ayrshire cattle. J. as risk factor for metabolic disorders, is that it seems

Dairy Sci. 77, 3316–3323.

to be the early-lactation feeding of concentrates _{Dohoo, I.R., Martin, S.W., Meek, A.H., Sandals, W.C.D., 1983.}

separately from roughages and not the concentrate to Disease, production and culling in Holstein-Friesian cows. I. roughage ratio within a TMR — that is associated The data. Prev. Vet. Med. 1, 321–334.

Drackley, J.K., Veenhuizen, J.J., Richard, M.J., Young, J.W., 1991. with increased odds of metabolic disorders.

Metabolic changes in blood and liver of dairy cows during According to the second purpose of this study,

either feed restriction or administration of 1,3-butanediol. J. each disorder was associated with decreased total _{Dairy Sci. 74, 4254–4264.}

DMI for at least 2 weeks after diagnosis. The effect Enevoldsen, C., Grohn, Y.T., 1994. Disease effects on milk yield¨ persisted more than 4 weeks in cows with ketosis in dairy cows: Development and reliability assessment of a

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simplified within herd and within test day approach for Kossaibati, M.A., Esslemont, R.J., 1997. The costs of production estimation. Kenya Vet. 18, 418–420. diseases in dairy herds in England. Vet. J. 154, 41–51. Forbes, J.M., 1996. Integration of regulatory signals controlling Littell, R.C., Milliken, G.A., Stroup, W.W., Wolfinger, R.D. (Eds.),

forage intake in ruminants. J. Anim. Sci. 74, 3029–3035. 1998. SAS Systems for Mixed Models, SAS Institute Inc, Geishauser, T., 1995. Abomasal displacement in the bovine — a Cary, NC.

review on character, occurrence, aetiology and pathogenesis. J. Morris, R.S., 1988. The effects of disease on productivity and Vet. Med., Ser. A 42, 229–251. profitability of livestock: How should it be assessed? Proc. NZ Goff, J.P., Horst, R.L., 1997. Physiological changes at parturition Soc. Anim. Prod. 48, 117–125.

and their relationship to metabolic disorders. J. Dairy Sci. 80, Østergaard, S., Sørensen, J.T., 1998. A review of the feeding– 1260–1268. health–production complex in a dairy herd. Prev. Vet. Med 36, ¨

Grohn, Y.T., Thompson, J.R., Bruss, M.L., 1984. Epidemiology 109–129. ¨

and genetic basis of ketosis in Finish Ayrshire cattle. Prev. Vet. Østergaard, S., Grohn, Y.T., 1999. Effects of diseases on test day Med. 3, 65–77. milk yield and body weight of dairy cows from Danish ¨

Grohn, Y.T., Erb, H.N., McCulloch, C.E., Saloniemi, H.S., 1989. research herds. J. Dairy Sci. 82, 1188–1201.

Epidemiology of metabolic disorders in dairy cattle: Associa- SAS Institute Inc., 1996. SAS / STAT Software: Changes and tion among host characteristics, disease, and production. J. Enhancements through Release 6.11, SAS Institute Inc, Cary,

Dairy Sci. 72, 1876–1885. NC.

Gustafsson, A.H., Anderson, L., Emanuelson, U., 1995. Influence Shaver, R.D., 1997. Nutritional risk factors in the etiology of left of feeding management, concentrate intake and energy intake displaced abomasum in dairy cows: a review. J. Dairy Sci. 80, on the risk of hyperketonaemia in Swedish dairy herds. Prev. 2449–2453.

Vet. Med. 22, 237–248. Vandehaar, M.J., 1998. Efficiency of nutrient use and relationship Kaustell, K., Tuori, M., Huhtanen, P., 1997. Comparison of energy to profitability on dairy farms. J. Dairy. Sci. 81, 272–282.

evaluation systems for dairy cows feeds. Livest. Prod. Sci. 51, Veenhuizen, J.J., Drackley, J.K., Richard, M.J., Sanderson, T.P., 255–266. Miller, L.D., Young, J.W., 1991. Metabolic changes in blood Klerx, H.J., Smolders, E.A.A., 1997. Herd and cow random and liver during development and early treatment of ex-variation in models of interrelationships between metabolic and perimental fatty liver and ketosis in cows. J. Dairy Sci. 74, reproductive disorders in high yielding multiparous Holstein 4238–4253.

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analyses with model 1, that we excluded them. These 3.2. Effects of disorders on DMI analyses were the analysis of decreased rumen

Table 4

Effect of total concentrate DMI on adjusted odds ratios of metabolic disorders

Metabolic Number of Tercile of total Odds ratio

disorder concentrate DMI and 95% confidence interval

Lactations Disorders

OR 95% CI (OR)

Enteritis 495 22 Lowest vs. middle 1.7 [0.8; 3.6]

Lowest vs. highest 10.0 [2.9; 35.2]

Middle vs. highest 5.8 [1.8; 18.8]

c,d

Ketosis 494 48 Lowest vs. middle 1.5 [0.7; 3.2]

Lowest vs. highest 1.0 [0.4; 2.2]

Middle vs. highest 0.7 [0.3; 1.5]

Estimated by model 1 on data subset 1, which includes cows fed concentrates separately from roughages. Only diseases with significant effect are included.

Lowest, middle and highest terciles (kg / day): lowest: ,5.2; middle:$5.2 and,6.6; highest:$6.6.

Herd retained in the final model.

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Table 5

Effect of percentage of total concentrate DMI fed with roughages on adjusted odds ratios of metabolic disorders

Metabolic Number of Tercile of percentage of total Odds ratio

disorder concentrate DMI fed with and 95% confidence interval

Lactations Disorders b

roughages

OR 95% CI (OR)

Decreased rumen 2840 52 Lowest vs. middle 1.8 [1.1; 2.9]

motility Lowest vs. highest 1.2 [0.6; 2.4]

Middle vs. highest 0.7 [0.3; 1.4]

Enteritis 2822 96 Lowest vs. middle 1.2 [0.8; 1.7]

Lowest vs. highest 4.5 [2.3; 8.7]

Middle vs. highest 3.9 [2.0; 7.7]

Ketosis 2832 126 Lowest vs. middle 2.1 [1.4; 3.2]

Lowest vs. highest 3.9 [2.2; 3.7]

Middle vs. highest 1.8 [1.0; 3.3]

Left displaced 2861 12 Lowest vs. middle 0.7 [0.2; 2.7]

abomasum Lowest vs. highest 1.3 [0.3; 5.4]

Middle vs. highest 2.0 [0.5; 8.1]

Estimated by model 1 on data subset 3, which includes cows that did not have access to summer pasture. Only diseases with significant effect are included.

Lowest, middle and highest terciles (ratio): lowest: ,0.32; middle:$0.32 and,1.0; highest:$1.0.

Milk fever retained in the final model.

Acute clinical mastitis and clinical mastitis evident only as flakes in the milk retained in the final model.

Due to few disease incidents, parity was excluded from this model.

Table 6

Week relative to Study disease

date of diagnosis b

Decreased rumen Enteritis Ketosis LDA

motility (n540) (n572) (n539) (n56)

b S.E. b S.E. b S.E. b S.E.

# 24 20.1 0.3 20.5* 0.2 20.5 0.3 0.3 1.0

23 0.1 0.4 20.5 0.3 20.5 0.3 0.4 0.9

22 0.0 0.4 20.4 0.3 20.7* 0.3 23.1*** 0.8

21 22.0*** 0.3 22.0*** 0.3 22.7*** 0.3 25.5*** 0.8

11 21.8*** 0.3 21.6*** 0.3 21.5*** 0.3 23.4*** 0.8

12 21.1*** 0.3 20.5* 0.2 21.0*** 0.3 22.4** 0.7

13 20.7* 0.3 0.5* 0.2 20.7** 0.3 22.3*** 0.7

$ 14 20.4 0.2 0.5 0.2 20.6** 0.2 21.6** 0.6

Intercept based on the period between the 19th to 24th weeks in milk for primiparous not Jersey cows without the study disease.

Covariance parameters were estimated using minimum variance quadratic unbiased estimation (MIVQUE0) as explained in the text. * P,0.05, ** P,0.01, *** P,0.001.

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Table 7

Week relative to Study disease date of diagnosis

Decreased rumen Enteritis Ketosis LDA

motility (n584) (n5127) (n5208) (n522)

b S.E. b S.E. b S.E. b S.E.

# 24 20.6 0.3 20.1 0.3 20.7*** 0.3 21.1 0.9

23 20.5 0.4 0.0 0.3 20.8*** 0.2 21.5 0.8

22 20.9* 0.4 20.1 0.3 20.9*** 0.2 22.4** 0.7

21 23.8*** 0.4 22.0*** 0.3 22.8*** 0.2 26.6*** 0.7

11 22.9*** 0.4 21.9*** 0.3 22.1*** 0.2 26.6*** 0.7

12 21.9*** 0.3 20.9** 0.3 21.4*** 0.2 24.2*** 0.6

13 20.8** 0.3 20.4 0.2 21.0*** 0.2 21.2* 0.6

$ 14 20.2 0.3 0.0 0.2 20.7*** 0.2 20.1 0.4

Intercept based on the period between the 19th to 24th weeks in milk for multiparous not Jersey cows without the study disease.

Covariance parameters were estimated using minimum variance quadratic unbiased estimation (MIVQUE0) as explained in the text. * P,0.05, ** P,0.01, *** P,0.001.

day (S.E.50.2), respectively. These values differed concentrates separately from roughages (subset 3) only slightly in the models of the effects of the other and not the concentrate to roughage ratio within a three disorders. TMR (subset 2) — that is associated with increased odds of metabolic disorders. The results from the analyses of the effect of concentrate DMI for cows

4. Discussion fed all concentrates separately (subset 1) are

ex-cluded from this general implication from model 1. As we discussed in a previous paper Østergaard This is due to the fact that increased risk of enteritis,

the literature (Dohoo et al., 1983; Grohn et al., 1984; that there is an obvious explanation for the result and Detilleux et al., 1994; Klerx and Smolders, 1997; because the number of enteritis incidents was only Shaver, 1997). 22. The results of no significant effect of the Herd effects on disease can be important (Morris, concentrate to roughage ratio within a TMR (subset

(4)

The terms of concentrate and roughage may also ketosis. be a problem because of the fact that in some cases a

feed component may be classified as either concen- 4.2. Effects of disorders on DMI trate or roughage depending on its treatment before

feeding. By modelling a random term to control for The detrimental effects of disorders on total DMI different trials and subtrials, we partially addressed in the weeks immediately following diagnosis were this problem, because cows were typically fed simi- significant for all four disorders — and we believe larly within a subtrial. However, for application of that the magnitudes of some of these effects are the results from model 1, one should be aware of likely to be of practical importance (Tables 6 and 7). problems related to the definition of concentrates and That disease ‘causes’ reduced feed intake is general-roughages. ly accepted (Forbes, 1996) — but we could find no Finally, grouping the data into three broad direct estimations of magnitudes or patterns to categories according to the feeding related risk compare to ours. The persistence (for $3 week) of factors should have eliminated some misclassifica- the decreased intake (especially in primiparous cows) tion bias. In addition, we took the average of several might be due to influences of additional or recurrent measurements in an attempt to increase precision. diseases occurring within that time frame. Neverthe-LDA was not affected by the percentage of total less, the metabolic disorder in each model remains concentrate DMI fed with roughages early on in the interpretable as a risk indicator for decreased DMI lactation (Table 5). We had only 12 cases of LDA for for multiple weeks.

(5)

trained to recognise such small decreases, it might be interesting to test whether treatment at that ‘pre-clinical’ stage (Veenhuizen et al., 1991) might

6. Notation prevent the clinical episode of ketosis. The decreased

total DMI before diagnosis, combined with the

DIM, day in milk results from model 1, supports suggestions of

dis-DMI, dry matter intake eases, such as ketosis, predominantly being caused

LDA, left displaced abomasum by a reduction in feed intake caused by other

TMR, total mixed ration ¨

diseases (Grohn et al., 1989; Goff and Horst, 1997). Milk fever has not been studied specifically, but it may still play an important role in such complexes

(Goff and Horst, 1997). We also suggest that cows of Acknowledgements any parity that decrease DMI .2 kg / day in early

lactation should be monitored carefully for LDA Data for this study were available from the Danish (Tables 6 and 7). Institute of Agricultural Sciences, Department of Breeding and Genetics, and Department of Livestock Management, Research Centre Foulum. The authors

5. Conclusions would like to thank Erik Luc Decker, Connie Harbo

Middelhede, and Uffe Thorøe Christensen for assis-The initial purpose of this study was to establish tance with databases, and Hollis N. Erb for assis-whether odds of metabolic disorders varied accord- tance with drafting the manuscript.

ing to concentrate management in the early lactation. The concentrate DMI to total DMI ratio for cows fed a TMR early in lactation, was not related to odds of

References metabolic disorders. Increased odds of ketosis and

enteritis, which accounted for the majority of

meta-Bath, D.L., 1985. Biological requirements for economics of bolic disorders cases under study, were associated _{lowering feed costs. J. Dairy Sci. 68, 1579–1584.}

Detilleux, J.C., Grohn, Y.T., Quaas, R.L., 1994. Effects of clinical study of the concentrate-management characteristics

ketosis on test day milk yields in Finnish Ayrshire cattle. J. as risk factor for metabolic disorders, is that it seems

Dairy Sci. 77, 3316–3323.

to be the early-lactation feeding of concentrates _{Dohoo, I.R., Martin, S.W., Meek, A.H., Sandals, W.C.D., 1983.}

Drackley, J.K., Veenhuizen, J.J., Richard, M.J., Young, J.W., 1991. with increased odds of metabolic disorders.

Metabolic changes in blood and liver of dairy cows during According to the second purpose of this study,

either feed restriction or administration of 1,3-butanediol. J. each disorder was associated with decreased total _{Dairy Sci. 74, 4254–4264.}

(6)

forage intake in ruminants. J. Anim. Sci. 74, 3029–3035. 1998. SAS Systems for Mixed Models, SAS Institute Inc, Geishauser, T., 1995. Abomasal displacement in the bovine — a Cary, NC.

and their relationship to metabolic disorders. J. Dairy Sci. 80, Østergaard, S., Sørensen, J.T., 1998. A review of the feeding–

1260–1268. health–production complex in a dairy herd. Prev. Vet. Med 36,

Grohn, Y.T., Thompson, J.R., Bruss, M.L., 1984. Epidemiology 109–129. ¨

and genetic basis of ketosis in Finish Ayrshire cattle. Prev. Vet. Østergaard, S., Grohn, Y.T., 1999. Effects of diseases on test day

Med. 3, 65–77. milk yield and body weight of dairy cows from Danish

Grohn, Y.T., Erb, H.N., McCulloch, C.E., Saloniemi, H.S., 1989. research herds. J. Dairy Sci. 82, 1188–1201.

Dairy Sci. 72, 1876–1885. NC.

evaluation systems for dairy cows feeds. Livest. Prod. Sci. 51, Veenhuizen, J.J., Drackley, J.K., Richard, M.J., Sanderson, T.P.,

255–266. Miller, L.D., Young, J.W., 1991. Metabolic changes in blood

Klerx, H.J., Smolders, E.A.A., 1997. Herd and cow random and liver during development and early treatment of ex-variation in models of interrelationships between metabolic and perimental fatty liver and ketosis in cows. J. Dairy Sci. 74, reproductive disorders in high yielding multiparous Holstein 4238–4253.

Directory UMM :Data Elmu:jurnal:L:Livestock Production Science:Vol65.Issue1-2.Jul2000:

Concentrate feeding, dry-matter intake, and metabolic disorders

in Danish dairy cows

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