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. Østergaard, Y.T. Grohn Livestock Production Science 65 2000 107 –118 115
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
a
Week relative to Study disease
date of diagnosis Decreased rumen
Enteritis Ketosis
LDA
b
motility n 584 n 5127
n 5208 n 522
b S.E.
b S.E.
b S.E.
b S.E.
2 4
2 0.6
0.3 2
0.1 0.3
2 0.7
0.3 2
1.1 0.9
2 3
2 0.5
0.4 0.0
0.3 2
0.8 0.2
2 1.5
0.8 2
2 2
0.9 0.4
2 0.1
0.3 2
0.9 0.2
2 2.4
0.7 2
1 2
3.8 0.4
2 2.0
0.3 2
2.8 0.2
2 6.6
0.7 1
1 2
2.9 0.4
2 1.9
0.3 2
2.1 0.2
2 6.6
0.7 1
2 2
1.9 0.3
2 0.9
0.3 2
1.4 0.2
2 4.2
0.6 1
3 2
0.8 0.3
2 0.4
0.2 2
1.0 0.2
2 1.2
0.6 1
4 2
0.2 0.3
0.0 0.2
2 0.7
0.2 2
0.1 0.4
a
Intercept based on the period between the 19th to 24th weeks in milk for multiparous not Jersey cows without the study disease.
b
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, ¨
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
¨ 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 ¨
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 accom-
¨ 116
S . Østergaard, Y.T. Grohn Livestock Production Science 65 2000 107 –118
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
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.
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. Østergaard, Y.T. Grohn Livestock Production Science 65 2000 107 –118 117
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
