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Effect of Prepartum Administration of Monensin in a Controlled-Release Capsule on Milk Production and Milk Components in Early Lactation
PHYSIOLOGY AND MANAGEMENT Effect of Prepartum Administration of Monensin in a Controlled-Release Capsule on Milk Production and Milk Components in Early Lactation T. F. DUFFIELD,*,1 K. E. LESLIE,*,1 D. SANDALS,*,1 K. LISSEMORE,*,1 B. W. McBRIDE,*,2 J. H. LUMSDEN,*,3 P. DICK,† and R. BAGG† *University of Guelph, Guelph, ON, Canada N1G 2W1 a Division of Eli Lilly, Inc, Research Park Centre, Guelph, ON, Canada N1G 4T2
†Provel,
ABSTRACT
INTRODUCTION
Dry cows and pregnant heifers from 25 farms near Guelph, Ontario, Canada were enrolled in a large double-blind, randomized clinical trial that was designed to evaluate the impact of monensin on energy metabolism, health, and production. A total of 503 cows was given monensin in controlled-release capsules, and 507 were administered placebo capsules 3 wk prior to the expected calving date. The effects of treatment on milk production and milk components at the first three Dairy Herd Improvement (DHI) tests were evaluated using repeated measures analysis of variance. Treatment with monensin increased milk production, but this effect was dependent on body condition score prior to calving. Cows that were classified as thin (score of ≤3.0) did not have increased production in response to monensin treatment. Cows with fair body condition (score of 3.25 to 3.75) produced significantly more milk at the second DHI test (+0.85 kg), but cows that were fat (score of ≥4.0) produced significantly more milk than did controls for all three DHI tests (+1.25 kg) in early lactation. Monensin significantly increased projected 305-d milk production in cows from herds at increased risk of ketosis. Treatment with monensin had no significant effect on either milk fat percentage or milk protein percentage. ( Key words: monensin, dairy cows, milk production, milk components)
Ionophores have been available for use in food animals for over 20 yr (16); however, limited information is available about their effects in lactating dairy cows. There have been relatively few reports on the influence of monensin or lasalocid on milk production or milk components of North American dairies. Both Lynch et al. ( 1 1 ) and Lowe et al. ( 1 0 ) observed milk production increases between 6 to 8% in early lactation dairy cows treated with monensin in a controlled-release capsule ( CRC) . A New Zealand trial involving all the cows from three pasture-fed herds reported that monensin-treated cows produced 0.41 L more milk/d over a 4-mo period and 1.38 L more milk/d than untreated controls at the 2nd mo after treatment ( 4 ) . Two other trials involving a monensin CRC treatment reported conflicting results. In a small study using 16 cows ( 1 ) , no difference in milk production was found, but milk fat percentage was significantly lower in monensin-treated cows. A much larger Australian project ( 9 ) involving 1061 lactating cows from six different herds found that milk fat and milk protein production was not significantly influenced by monensin treatment. Milk production was significantly increased only for cows within one herd. Three North American studies have reported no significant effect of lasalocid on milk production for cows in early (6, 7, 12) or midlactation (18). However, lasalocid has been shown to reduce milk fat percentage (6, 7 ) and milk fat production ( 6 ) . Monensin in late lactation has been reported to reduce the persistency of milk production ( 2 ) but has significantly increased milk production and decreased milk fat percentage in a study of early lactation cows ( 8 ) . One of the few trials to evaluate the impact of monensin fed to prepartum cows and continuing through early lactation detected no effect on milk production or on milk composition in monensintreated cows (17). Monensin fed at 150, 300, or 450
Abbreviation key: BCS = body condition score, CRC = controlled-release capsule.
Received June 29, 1998. Accepted October 15, 1998. 1Department of Population Medicine, Ontario Veterinary College. 2Department of Animal and Poultry Science. 3Department of Pathobiology, Ontario Veterinary College. 1999 J Dairy Sci 82:272–279
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mg/d commencing during the 6th wk of lactation was associated with a significant increase in milk production of 2.8 and 2.5 kg/d for 150 and 300 mg of monensin, respectively (13). Both milk fat and milk protein production were reduced, and the effect seemed to increase with the higher concentrations of monensin in the feed. Seven of the last eight experiments cited were North American projects that included typical North American feedstuffs. Those trials are difficult to interpret because they were conducted using different dose levels, were applied at different stages of lactation, and were performed on farms with different management. Nevertheless, based on those results and those from Australia and New Zealand, it appears that early lactation may be the optimal time for inclusion of ionophores in the diet of dairy cows. The objective for this part of the study was to evaluate the impact of monensin treatment during the prepartum period on milk production and milk components in early lactation. MATERIALS AND METHODS A total of 1010 cows and heifers from 25 farms near Guelph, Ontario, Canada were enrolled in a doubleblind, randomized clinical trial designed to assess the efficacy of a monensin CRC (Rumensin CRC; Provel, a Division of Eli Lilly Canada, Guelph, ON, Canada) administered prepartum on the prevention of subclinical ketosis. Complete details of the study design and herd characteristics have been previously reported ( 3 ) . Within each farm, cows were randomized to receive either a monensin CRC or a placebo capsule at 3 wk prior to the expected calving date. The monensin CRC delivered approximately 335 mg of monensin sodium for an average of 95 d (R. Bagg and P. Dick, 1996, personal communications). The placebo was identical to the monensin CRC except that it did not contain monensin. All CRC were embossed with a four-digit number that was recorded for each cow. In the event of regurgitation, the capsule was readministered. Data Collection Individual test day data for milk production were collected for all cows on the trial through the Ontario DHI Corporation and were downloaded monthly via a bulletin board service. These data were then uploaded into a microcomputer database (FoxPro, Version 2.6 for Windows, 1989–1994; Microsoft Corp., Redmond, WA) and were crossreferenced with treatment assignments. Because the placebo and monensin capsules
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were both administered 3 wk prior to the expected calving date and monensin is released for an average of 95 d, only the data from the first three DHI tests of each cow were used to assess the effect of monensin on test day milk production and milk components. The 305-d milk production that was projected at the third DHI test was used to assess the impact of treatment on lactation milk production. Data Analysis The analysis of the milk production data was conducted using repeated measures ANOVA because there were up to three DHI tests for each cow. A separate model was built for test day milk weight, for test day milk fat percentage, and for test day milk protein percentage. Variables considered for each model included cow and herd level factors that were considered to be related to the DHI outcomes. The herd level variables were selected to help to refine possible herd effects and included nutrition data, herd size, and barn design. Nutrition data offered to the models included type of feeding system, combination of forages fed, frequency of grain feeding, type of grain mixture, and weeks of lead feeding prior to calving. Cow level variables included information on test day production, body condition data, health, parity, and season of calving. Analysis of variance using the mixed procedure in SAS ( 1 5 ) was utilized for analysis. Cow and herd were included as random variables to account for the correlation between observations from the same cow and the correlation between cows within the same herd. All variables were included and were tested in a backward stepwise elimination procedure using a probability value of ≤0.05. All possible two-way interactions with treatment were tested with the significant variables that were remaining. In any analysis for which the treatment by test number interaction was significant, the evaluation was stratified by DHI test number, and the probability value that was used to assess the significance of the treatment effect was adjusted using a Bonferroni correction. Analysis of variance was also used for evaluating the treatment effect on projected 305-d milk yield. The projected milk production was based on the first three DHI tests but was calculated at the third DHI test. Lactation milk production was assessed in this manner because the third DHI test was chosen as the end point of the study. This evaluation allowed the maximum number of cows with projected 305-d milk production for our analysis because two DHI tests are required for a projection, and some cows did not have a milk weight recorded at the first DHI test. The herd risk of ketosis Journal of Dairy Science Vol. 82, No. 2, 1999
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DUFFIELD ET AL. TABLE 1. Postpartum herd means of BHBA for cows in the group receiving the placebo to determine herd risk for ketosis. BHBA Herd
Log mean
1 2 3 4 5 6 7 8 9 10 11 12 13
6.68 6.94 6.62 7.081 6.62 6.57 6.35 6.53 6.87 6.96 6.72 6.35 7.111
Actual mean ( mmol/L) 796 1033 750 1188 750 713 572 685 963 1054 829 572 1224
BHBA Herd
Log mean
14 15 16 17 18 19 20 21 22 23 24 25 All
6.56 6.74 6.97 7.101 6.86 6.73 6.981 6.62 6.59 6.95 6.52 6.94 6.77
Actual mean ( mmol/L) 706 846 1064 1212 953 837 1075 750 728 1043 679 1033 871
1Mean of herd ≥1.0 standard deviations from the average of the herd means and, therefore, designated to be at increased risk for ketosis.
was forced into the final analysis to allow testing of the treatment by ketosis risk interaction. Herd risk of ketosis was determined by calculating the herd means of the loge of BHBA concentrations from blood samples taken from the placebo group postcalving. In accordance with a method suggested by Herdt et al. ( 5 ) , if a herd mean exceeded the average herd mean by one or more standard deviations, that herd was considered to be at risk of ketosis. This method identified four herds with increased risk of ketosis (Table 1). Differences between treatments for test day and projected 305-d milk production adjusted for all other factors in the model were compared using adjusted least squares means. RESULTS Data on a total of 952 cows were available for the analysis of the treatment effect on test day milk production and milk components. All test day data with zero values were recorded as missing for the analysis of milk production and milk component outcomes. Milk production and milk components were not recorded by DHI for cows that were <5 DIM or that were designated as sick by the herd manager. There were no significant differences between monensin and placebo cows for this censoring (Table 2). The final model for test day milk production included parity, DHI test number, season of calving, season of DHI test, DIM, SCC linear score, body condition score ( BCS) at treatment administration, change in BCS between treatment and wk 9 postcalving, multiple illness (cows having more than one illness postcalving), days from capsule administration to calving, Journal of Dairy Science Vol. 82, No. 2, 1999
and the interaction terms treatment with DHI test number and treatment with BCS. The random effects of cow and herd were significant in this model. No treatment by farm interaction was detected. Because the interaction term of treatment and BCS was significant ( P = 0.006), the same model was used to analyze the data stratified by the three levels of body condition. The effect of treatment was not significant for cows classified as being thin (BCS <3.25). The model for cows of fair condition (BCS 3.25 to 3.75) indicated that a significant treatment by DHI test number interaction existed, and, thus, the analysis was further stratified by test number for these cows. A Bonferroni correction was necessary because there were three DHI tests per cow and the critical probability value became 0.0167. Treatment with monensin had a positive effect on milk production at the second
TABLE 2. Number of cows available for milk production analysis. Description
Monensin
Placebo
Cows treated Sold by 94 DIM Died by 94 DIM First DHI Recorded milk Not tested Second DHI Recorded milk Not tested Third DHI Recorded milk Not tested
503 43 11
507 59 16
418 62
393 79
451 22
435 29
440 18
424 16
(no.)
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DHI test in cows of fair condition ( P = 0.014). There was no significant treatment by test number interaction ( P = 0.51) for the analysis in fat cows (BCS ≥4.0). Monensin treatment increased milk production for all three DHI tests ( P = 0.03) in cows classified as fat. Graphs of mean milk production by treatment and DHI test number for each body condition class are illustrated in Figures 1, 2, and 3. The least
squares means for milk production, adjusted for all the model variables and stratified by body condition class, are illustrated in Table 3. A model was developed for assessing the effect of treatment on test day milk fat percentage and milk protein percentage. In the final models, the random effects of both farm and cow were significant for protein percentage, but only cow was a significant ( P = 0.001) random variable for fat percentage. Again, there were no treatment by farm interactions detected. No treatment effect was found for milk fat percentage ( P = 0.44) or milk protein percentage. There was a significant ( P = 0.001) interaction of DHI test number with treatment for milk protein percentage; however, when the analysis was stratified by DHI test number and the Bonferroni-adjusted probability value was used, there was no significant effect ( P > 0.15) of treatment detected for milk protein percentage at any of the first three DHI tests. Graphs of mean values for milk fat percentage and milk protein percentage by treatment and DHI test number are given in Figures 4 and 5. The effects of treatment on lactation milk production were assessed using ANOVA on the 305-d milk production projected at third DHI test. The treatment by farm interaction term was significant ( P = 0.02). Because the effect of treatment on lactation milk production depended on the farm, the herd risk of ketosis was forced into this model to help to explain the treatment by herd interaction. The final model
Figure 2. Mean ( ±SE) DHI test day milk production by treatment for cows categorized as fair (body condition score of 3.25 to 3.75) at treatment administration 3 wk prior to calving. Milk production was different ( P < 0.05) at the second DHI test.
Figure 3. Mean ( ±SE) DHI test day milk production by treatment for cows categorized as fat (body condition score >3.75) at the time of treatment administration 3 wk prior to calving. Milk production was different ( P < 0.05) for the entire period.
Figure 1. Mean ( ±SE) DHI test day milk production by treatment for cows categorized as thin (body condition score of <3.25) at treatment administration 3 wk prior to calving. No differences ( P ≤ 0.05) in milk production were observed between treatments.
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TABLE 3. Least squares means1 of DHI test day milk production by treatment and body condition class. Body condition class Treatment
Thin (BCS 2 < 3.25)
Monensin Placebo
79 96
Monensin Placebo
32.9a 34.5a
Fair (BCS 3.25 to 3.75)
Fat (BCS > 3.75)
(n) 331 318 Milk production ( k g ) DHI DHI Test 1 Test 2
DHI Test 3
34.4a 34.0a
33.6a 33.4a
36.8a 35.6b
70 58
36.1a 33.6b
a,bMeans within the same column followed by different superscript letters differ ( P ≤ 0.05). 1Adjusted for parity, DHI test number (except for cows in fair body condition for which there was a treatment by test number interaction), season of calving, season of DHI test, DIM at DHI test, test day linear score, loss in body condition, multiple illness, days from treatment administration to calving, and the random effects of both cow (except for cows in fair body condition) and farm. 2Body condition score (where 1 = thin to 5 = fat).
contained a significant ( P < 0.05) interaction of treatment with herd ketosis risk, and the model was then reanalyzed after being stratified by herd risk for ketosis. Initial BCS and its interaction with treatment were not significant in these models. There was a positive effect ( P = 0.01) of treatment on projected 305-d milk production for herds that were at increased risk of ketosis; however, treatment had no effect on 305-d milk production for herds with normal risk for ketosis. Adjusted least squares means for projected lactation milk production by herd risk for ketosis and body condition class are in Table 4.
Figure 4. Mean ( ±SE) DHI test day milk fat percentage by DHI test number for cow treated with monensin in a controlled-release capsule or a placebo 3 wk prior to expected calving. No difference ( P = 0.44) in milk fat percentage between treatments was observed.
peak milk production. It has been estimated that, for every 1 kg increase in peak milk production, about 200 kg more milk is produced during a lactation (14). Although there were no statistically significant ( P = 0.34) differences in projected 305-d milk production, the cows treated with monensin had a projected milk production of 106 kg per lactation more than that of cows receiving the placebo (using least squares means). Milk production of cows in fair condition at
DISCUSSION Monensin treatment exerted a positive influence on milk production; however, the response depended on the initial BCS prior to calving. The DHI test day milk production was not significantly influenced by treatment in cows categorized as being thin at the time of treatment administration. Cows in fair body condition that were given monensin produced significantly ( P = 0.014) more milk at the second DHI test compared with that of placebo cows. This increase amounted to a difference of 0.85 kg more milk/d at the second DHI test using arithmetic means and an adjusted difference of 1.2 kg/d using least squares means. The second DHI test occurred at an average of 60 d postpartum and was the measurement closest to Journal of Dairy Science Vol. 82, No. 2, 1999
Figure 5. Mean ( ± SE) DHI test day milk protein percentage ( ±SE) by DHI test number for cow treated with monensin in a controlled-release capsule or a placebo 3 wk prior to expected calving. No difference ( P = 0.27) in milk protein percentage between treatments was observed.
MONENSIN, MILK PRODUCTION, AND MILK COMPONENTS TABLE 4. Least squares means of projected 305-d milk production by treatment, herd risk for ketosis,1 and initial body condition class.2 Variable Herd ketosis risk Increased Normal BCS3 Thin (<3.25) Fair (3.25 to 3.75) Fat (>3.75)
Monensin
Placebo
Difference
8766a 8463
8187b 8452
+579 +11
8413 8611 9132
8485 8505 8665
–72 +106 +467
a,bMeans within a row with different superscript letters differ ( P ≤ 0.05). 1Adjusted for the effects of parity, DIM at third DHI test, season of calving, change in body condition class, disease (cow having one or more diseases postcalving), and the random effects of farm. 2Adjusted for the same variables as for ketosis except that herd risk of ketosis was ignored. 3Body condition score (where 1 = thin to 5 = fat).
both first and third DHI test was not significantly different between treatments. Because the average time from treatment to calving was 21 d and the capsule was empty at approximately 95 d, the daily release of monensin would have ceased at about 74 d postpartum, half way between the second and third DHI test. It is possible that a second monensin capsule, administered at d 75 postcalving, might have continued to improve milk production. Few studies to date have evaluated the effects of monensin for the exact period investigated in the current project. Thomas et al. ( 1 7 ) found no effect of monensin treatment on milk production or milk components when fed from 2 to 4 wk prepartum until 84 d of lactation. However, that study involved only 47 Holsteins that were divided among a placebo group and three monensin groups (150, 300, and 450 mg/d). The small sample size and the use of only one herd might account for the lack of an observed effect. Absolute milk production was not reported, and BCS were not measured. An effect of monensin was detected in the lowering of both NEFA and BHBA concentrations, suggesting that an improvement occurred in energy metabolism. In the study by Lynch et al. (11), capsule administration commenced near peak lactation at 46 DIM, and the CRC would not have ceased delivering monensin until 141 d postpartum. Lean et al. ( 9 ) started capsule treatment during the 1st wk of lactation, causing daily monensin release to end near 100 DIM, which is still well beyond the 75 d of our trial. Cows that were treated with monensin and classified as fat prior to capsule administration produced more ( P = 0.03) milk than did fat cows receiving the
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placebo. The difference amounted to an additional 1.2 kg/d unadjusted and 2.5 kg/d using least squares means to control for other factors in the model. The response in unadjusted milk production observed in this study was a 3.4% increase at peak lactation for cows in fair condition and was 7.4% for fat cows during all three DHI tests. This response is comparable with the 7 to 8% increase found by Lynch et al. ( 1 1 ) and the 6% increase reported by Lowe et al. (10). The absolute increase of 0.85 kg/d for fair cows at peak lactation and 1.25 kg/d for fat cows during the first 94 DIM is very similar to the 1.1-kg/d increase observed by Lowe et al. ( 1 0 ) and the 1.0-kg/d increase reported by Lynch et al. (11). Other studies have not identified the monensin treatment by BCS interaction that was observed in this trial. This interaction could possibly help explain the observed treatment with herd interactions found by Lean et al. ( 9 ) in a study in which one herd out of six showed increased milk production for monensintreated cows. It is unclear why there appears to be a dose-response effect with monensin and BCS prior to calving. Heavier body condition prior to calving appeared to favor a greater production response to monensin. From the BHBA data previously reported ( 3 ) , concentrations of BHBA were shown to increase postcalving with increasing initial BCS class. Although monensin consistently reduced BHBA concentrations for all BCS classes, perhaps heavier BCS classes have concentrations of BHBA approaching a subclinical ketosis threshold. The observed increase in milk production may simply be the result of an improved energy supply that alleviates the negative impact of subclinical ketosis on milk production. It is possible that the cows in the trials of both Lynch et al. ( 1 1 ) and Lowe et al. ( 1 0 ) were hyperketonemic, because they were fed pasture in early lactation without additional grain supplementation. Metabolic parameters were not measured in those trials. Hayes et al. ( 4 ) evaluated cows from three herds fed pasture and reported 0.41 L more milk/d for monensin-treated cows. However, no difference in the levels of BHBA or glucose were detected. These seasonally calving cows were treated 1 mo prior to the start of artificial insemination, which would have been later in lactation than the current study. Both control and treated cows were likely to have been in a positive energy balance during that trial as indicated by the findings of high glucose and low ketone bodies. Therefore, the positive milk production response was probably not related to the antiketogenic effects of monensin. In the current study, the treatment-related improvement in concentrations of BHBA, glucose, and asparJournal of Dairy Science Vol. 82, No. 2, 1999
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tate aminotransferase previously reported ( 3 ) support the hypothesis that the observed increase in milk production stemmed from an improvement in the energy status of the cow. The 305-d milk production projected at the third DHI test was used to identify treatment effects for the entire lactation. Season of the DHI test, multiple illness, days from bolus administration to calving, test day linear score (at third DHI test), and the BCS by treatment interaction term were not significant compared with the primary model for test day milk production. There was an interaction detected between farm and treatment for this analysis. To help to explain this interaction, herd risk of ketosis was forced into the model and was found to have a significant interaction ( P = 0.025) with treatment. Within the four herds identified with increased risk of ketosis, based on elevated BHBA concentration in the cows administered the placebo, monensin-treated cows had higher ( P = 0.01) projected lactation milk production (+580-kg difference in least squares means) than did cows given the placebo treatment. Cows within the remaining 21 herds did not have lactation milk production that varied with treatment. This result further supports the theory of improved milk production being associated with a reduction in the level of subclinical ketosis. The lack of an observed interaction of treatment with initial BCS for lactation milk production could be a function of a high variance combined with an inadequate sample size to test this effect. Stratification of the analysis by BCS and ignoring ketosis risk and ketosis risk by treatment interaction revealed differences in least squares means of –72, +107, and +466 kg for the treatment effect on projected lactation milk production in thin, fair, and fat cows, respectively. None of these differences was different at P ≤ 0.05. The treatment effect on test day milk fat percentage and test day milk protein percentage in the current study differs from the findings of other studies (1, 4, 10, 11) that indicated that monensin lowered milk fat percentage. Those studies involved pasturefed cattle, but the cows in the current project were fed a mix of concentrate and dry or ensiled forage (which is more representative of North American rations for lactating cows). Phipps et al. ( 1 3 ) found a dose relationship between monensin concentrations and milk fat: higher monensin concentrations cause greater fat depression. The constant dose of monensin delivered by the CRC results in a decreasing concentration as DMI increases in early lactation. The observed numerical decrease in milk fat percentage of 0.1% at the first DHI test and virtually identical milk fat percentJournal of Dairy Science Vol. 82, No. 2, 1999
ages at second and third DHI test could be related to less monensin being delivered per kilogram of DMI. Lean et al. ( 9 ) found that monensin treatment increased milk production in only one of six study herds, which may help to explain the lack of an observed effect on milk components. The herd with the positive milk production response was found to have no significant increase in milk protein production or milk fat production. Although percentages were not reported, this finding implied a decrease in both milk fat and milk protein percentages associated with monensin for this particular herd. The reverse would be true for the present study. A lack of treatment effect for either milk fat percentage or milk protein percentage in the presence of increased total test day milk production suggests an absolute increase in both milk fat and milk protein production. CONCLUSIONS Administration of a monensin CRC 3 wk prior to calving improved milk production of lactating Holstein cows and first parity heifers. The influence of monensin on DHI test day milk production was dependent on initial BCS at the time of treatment administration; a higher production response was observed with greater BCS. Monensin significantly increased projected 305-d milk production projected at the third DHI test for cows within herds at increased risk of ketosis. No effect of monensin on milk fat percentage or milk protein percentage was found. ACKNOWLEDGMENTS We thank Eleanor McNaughton and Shelley James for technical assistance and Provel, a Division of Eli Lilly, Ontario, Canada, for financial support. REFERENCES 1 Abe, N., I. J. Lean, A. Rabiee, J. Porter, and C. Graham. 1994. Effects of sodium monensin on reproductive performance of dairy cattle. II. Effects on metabolites in plasma, resumption of ovarian cyclicity and oestrus in lactating cows. Aust. Vet. J. 71: 277–282. 2 Coutinho, L. L., P. F. Machado, and R. M. Cook. 1987. Effect of isoacids and monensin on lactating cows. J. Dairy Sci. 70(Suppl. 1):217.(Abstr.) 3 Duffield, T. F., D. Sandals, K. E. Leslie, K. Lissemore, B. W. McBride, J. H. Lumsden, P. Dick, and R. Bagg. 1998. Effect of prepartum administration of monensin in a controlled release capsule on postpartum energy indicators in lactating dairy cattle. J. Dairy Sci. 81:2354–2361. 4 Hayes, D. P., D. U. Pfeiffer, and N. B. Williamson. 1996. Effect of intraruminal monensin capsules on reproductive performance and milk production of dairy cows fed pasture. J. Dairy Sci. 79:1000–1008.
MONENSIN, MILK PRODUCTION, AND MILK COMPONENTS 5 Herdt, T. H., J. B. Stevens, W. G. Olson, and V. Larson. 1981. Blood concentrations of b-hydroxybutyrate in clinically normal Holstein-Friesian herds and in those with a high prevalence of clinical ketosis. Am. J. Vet. Res. 12:503–506. 6 Johnson, J. C., P. R. Utley, B. G. Mullinex, Jr., and A. Merrill. 1988. Effects of adding fat and lasalocid to diets of dairy cows. J. Dairy Sci. 71:2151–2165. 7 Knowlton, K. F., M. S. Allen, and P. S. Erickson. 1993. Effect of lasalocid and corn grain particle size on performance, feed digestibility, and rumen parameters in early lactation dairy cattle. J. Dairy Sci. 76(Suppl. 1):280.(Abstr.) 8 Kube, J. C., J. E. Shirley, T. D. Smith, and R. A. Frey. 1988. Effect of monensin supplementation on lactating dairy cows. J. Dairy Sci. 71(Suppl. 1):218.(Abstr.) 9 Lean, I. J., M. Curtis, R. Dyson, and B. Lowe. 1994. Effects of sodium monensin on reproductive performance of dairy cattle. I. Effects on conception rates, calving-to-conception intervals, calving-to-heat and milk production in dairy cows. Aust. Vet. J. 71:273–277. 10 Lowe, L. B., G. J. Ball, V. R. Carruthers, R. C. Dobos, G. A. Lynch, P. J. Moate, P. R. Poole, and S. C. Valentine. 1991. Monensin controlled-release intraruminal capsule for control of bloat in pastured dairy cows. Aust. Vet. J. 68:17–20. 11 Lynch, G. A., M. E. Hunt, and S. N. McCutcheon. 1990. A note of the effect of monensin sodium administered by intraruminal
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controlled-release devices on productivity of dairy cows at pasture. Anim. Prod. 51:418–421. 12 Murphy, M. R., J. M. Campbell, S. W. Nombekela, and P. S. Erickson. 1993. Effect of lasalocid on dairy cows in early lactation. J. Dairy Sci. 76(Suppl. 1):279.(Abstr.) 13 Phipps, R. H., B. A. Jones, J.I.D. Wilkinson, and M. E. Tarrant. 1995. Effect of monensin on milk production of Friesian dairy cows in the United Kingdom. J. Dairy Sci. 78(Suppl. 1): 268.(Abstr.) 14 Radostits, O. M., K. E. Leslie, and J. Fetrow. 1994. Dairy health and production management program. Pages 97–140 in Herd Health: Food Animal Production Medicine. 2nd ed. W. B. Saunders Co., Philadelphia, PA. 15 SAS/STAT Software: Changes and Enhancements, Release 6.07. 1992. SAS Tech. Rep. P 229. SAS Inst., Inc., Cary, NC. 16 Schelling, G. T. 1984. Monensin mode of action in the rumen. J. Anim. Sci. 58:1518–1527. 17 Thomas, E. E., S. E. Poe, R. K. McGuffey, D. H. Mowrey, and R. D. Allrich. 1993. Effect of feeding monensin to dairy cows on milk production and serum metabolites during early lactation. J. Dairy Sci. 76(Suppl. 1):280.(Abstr.) 18 Weiss, W. P., and B. A. Amiet. 1990. Effect of lasalocid on performance of lactating dairy cows. J. Dairy Sci. 73:153–162.
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†Provel,
ABSTRACT
INTRODUCTION
Dry cows and pregnant heifers from 25 farms near Guelph, Ontario, Canada were enrolled in a large double-blind, randomized clinical trial that was designed to evaluate the impact of monensin on energy metabolism, health, and production. A total of 503 cows was given monensin in controlled-release capsules, and 507 were administered placebo capsules 3 wk prior to the expected calving date. The effects of treatment on milk production and milk components at the first three Dairy Herd Improvement (DHI) tests were evaluated using repeated measures analysis of variance. Treatment with monensin increased milk production, but this effect was dependent on body condition score prior to calving. Cows that were classified as thin (score of ≤3.0) did not have increased production in response to monensin treatment. Cows with fair body condition (score of 3.25 to 3.75) produced significantly more milk at the second DHI test (+0.85 kg), but cows that were fat (score of ≥4.0) produced significantly more milk than did controls for all three DHI tests (+1.25 kg) in early lactation. Monensin significantly increased projected 305-d milk production in cows from herds at increased risk of ketosis. Treatment with monensin had no significant effect on either milk fat percentage or milk protein percentage. ( Key words: monensin, dairy cows, milk production, milk components)
Ionophores have been available for use in food animals for over 20 yr (16); however, limited information is available about their effects in lactating dairy cows. There have been relatively few reports on the influence of monensin or lasalocid on milk production or milk components of North American dairies. Both Lynch et al. ( 1 1 ) and Lowe et al. ( 1 0 ) observed milk production increases between 6 to 8% in early lactation dairy cows treated with monensin in a controlled-release capsule ( CRC) . A New Zealand trial involving all the cows from three pasture-fed herds reported that monensin-treated cows produced 0.41 L more milk/d over a 4-mo period and 1.38 L more milk/d than untreated controls at the 2nd mo after treatment ( 4 ) . Two other trials involving a monensin CRC treatment reported conflicting results. In a small study using 16 cows ( 1 ) , no difference in milk production was found, but milk fat percentage was significantly lower in monensin-treated cows. A much larger Australian project ( 9 ) involving 1061 lactating cows from six different herds found that milk fat and milk protein production was not significantly influenced by monensin treatment. Milk production was significantly increased only for cows within one herd. Three North American studies have reported no significant effect of lasalocid on milk production for cows in early (6, 7, 12) or midlactation (18). However, lasalocid has been shown to reduce milk fat percentage (6, 7 ) and milk fat production ( 6 ) . Monensin in late lactation has been reported to reduce the persistency of milk production ( 2 ) but has significantly increased milk production and decreased milk fat percentage in a study of early lactation cows ( 8 ) . One of the few trials to evaluate the impact of monensin fed to prepartum cows and continuing through early lactation detected no effect on milk production or on milk composition in monensintreated cows (17). Monensin fed at 150, 300, or 450
Abbreviation key: BCS = body condition score, CRC = controlled-release capsule.
Received June 29, 1998. Accepted October 15, 1998. 1Department of Population Medicine, Ontario Veterinary College. 2Department of Animal and Poultry Science. 3Department of Pathobiology, Ontario Veterinary College. 1999 J Dairy Sci 82:272–279
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mg/d commencing during the 6th wk of lactation was associated with a significant increase in milk production of 2.8 and 2.5 kg/d for 150 and 300 mg of monensin, respectively (13). Both milk fat and milk protein production were reduced, and the effect seemed to increase with the higher concentrations of monensin in the feed. Seven of the last eight experiments cited were North American projects that included typical North American feedstuffs. Those trials are difficult to interpret because they were conducted using different dose levels, were applied at different stages of lactation, and were performed on farms with different management. Nevertheless, based on those results and those from Australia and New Zealand, it appears that early lactation may be the optimal time for inclusion of ionophores in the diet of dairy cows. The objective for this part of the study was to evaluate the impact of monensin treatment during the prepartum period on milk production and milk components in early lactation. MATERIALS AND METHODS A total of 1010 cows and heifers from 25 farms near Guelph, Ontario, Canada were enrolled in a doubleblind, randomized clinical trial designed to assess the efficacy of a monensin CRC (Rumensin CRC; Provel, a Division of Eli Lilly Canada, Guelph, ON, Canada) administered prepartum on the prevention of subclinical ketosis. Complete details of the study design and herd characteristics have been previously reported ( 3 ) . Within each farm, cows were randomized to receive either a monensin CRC or a placebo capsule at 3 wk prior to the expected calving date. The monensin CRC delivered approximately 335 mg of monensin sodium for an average of 95 d (R. Bagg and P. Dick, 1996, personal communications). The placebo was identical to the monensin CRC except that it did not contain monensin. All CRC were embossed with a four-digit number that was recorded for each cow. In the event of regurgitation, the capsule was readministered. Data Collection Individual test day data for milk production were collected for all cows on the trial through the Ontario DHI Corporation and were downloaded monthly via a bulletin board service. These data were then uploaded into a microcomputer database (FoxPro, Version 2.6 for Windows, 1989–1994; Microsoft Corp., Redmond, WA) and were crossreferenced with treatment assignments. Because the placebo and monensin capsules
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were both administered 3 wk prior to the expected calving date and monensin is released for an average of 95 d, only the data from the first three DHI tests of each cow were used to assess the effect of monensin on test day milk production and milk components. The 305-d milk production that was projected at the third DHI test was used to assess the impact of treatment on lactation milk production. Data Analysis The analysis of the milk production data was conducted using repeated measures ANOVA because there were up to three DHI tests for each cow. A separate model was built for test day milk weight, for test day milk fat percentage, and for test day milk protein percentage. Variables considered for each model included cow and herd level factors that were considered to be related to the DHI outcomes. The herd level variables were selected to help to refine possible herd effects and included nutrition data, herd size, and barn design. Nutrition data offered to the models included type of feeding system, combination of forages fed, frequency of grain feeding, type of grain mixture, and weeks of lead feeding prior to calving. Cow level variables included information on test day production, body condition data, health, parity, and season of calving. Analysis of variance using the mixed procedure in SAS ( 1 5 ) was utilized for analysis. Cow and herd were included as random variables to account for the correlation between observations from the same cow and the correlation between cows within the same herd. All variables were included and were tested in a backward stepwise elimination procedure using a probability value of ≤0.05. All possible two-way interactions with treatment were tested with the significant variables that were remaining. In any analysis for which the treatment by test number interaction was significant, the evaluation was stratified by DHI test number, and the probability value that was used to assess the significance of the treatment effect was adjusted using a Bonferroni correction. Analysis of variance was also used for evaluating the treatment effect on projected 305-d milk yield. The projected milk production was based on the first three DHI tests but was calculated at the third DHI test. Lactation milk production was assessed in this manner because the third DHI test was chosen as the end point of the study. This evaluation allowed the maximum number of cows with projected 305-d milk production for our analysis because two DHI tests are required for a projection, and some cows did not have a milk weight recorded at the first DHI test. The herd risk of ketosis Journal of Dairy Science Vol. 82, No. 2, 1999
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DUFFIELD ET AL. TABLE 1. Postpartum herd means of BHBA for cows in the group receiving the placebo to determine herd risk for ketosis. BHBA Herd
Log mean
1 2 3 4 5 6 7 8 9 10 11 12 13
6.68 6.94 6.62 7.081 6.62 6.57 6.35 6.53 6.87 6.96 6.72 6.35 7.111
Actual mean ( mmol/L) 796 1033 750 1188 750 713 572 685 963 1054 829 572 1224
BHBA Herd
Log mean
14 15 16 17 18 19 20 21 22 23 24 25 All
6.56 6.74 6.97 7.101 6.86 6.73 6.981 6.62 6.59 6.95 6.52 6.94 6.77
Actual mean ( mmol/L) 706 846 1064 1212 953 837 1075 750 728 1043 679 1033 871
1Mean of herd ≥1.0 standard deviations from the average of the herd means and, therefore, designated to be at increased risk for ketosis.
was forced into the final analysis to allow testing of the treatment by ketosis risk interaction. Herd risk of ketosis was determined by calculating the herd means of the loge of BHBA concentrations from blood samples taken from the placebo group postcalving. In accordance with a method suggested by Herdt et al. ( 5 ) , if a herd mean exceeded the average herd mean by one or more standard deviations, that herd was considered to be at risk of ketosis. This method identified four herds with increased risk of ketosis (Table 1). Differences between treatments for test day and projected 305-d milk production adjusted for all other factors in the model were compared using adjusted least squares means. RESULTS Data on a total of 952 cows were available for the analysis of the treatment effect on test day milk production and milk components. All test day data with zero values were recorded as missing for the analysis of milk production and milk component outcomes. Milk production and milk components were not recorded by DHI for cows that were <5 DIM or that were designated as sick by the herd manager. There were no significant differences between monensin and placebo cows for this censoring (Table 2). The final model for test day milk production included parity, DHI test number, season of calving, season of DHI test, DIM, SCC linear score, body condition score ( BCS) at treatment administration, change in BCS between treatment and wk 9 postcalving, multiple illness (cows having more than one illness postcalving), days from capsule administration to calving, Journal of Dairy Science Vol. 82, No. 2, 1999
and the interaction terms treatment with DHI test number and treatment with BCS. The random effects of cow and herd were significant in this model. No treatment by farm interaction was detected. Because the interaction term of treatment and BCS was significant ( P = 0.006), the same model was used to analyze the data stratified by the three levels of body condition. The effect of treatment was not significant for cows classified as being thin (BCS <3.25). The model for cows of fair condition (BCS 3.25 to 3.75) indicated that a significant treatment by DHI test number interaction existed, and, thus, the analysis was further stratified by test number for these cows. A Bonferroni correction was necessary because there were three DHI tests per cow and the critical probability value became 0.0167. Treatment with monensin had a positive effect on milk production at the second
TABLE 2. Number of cows available for milk production analysis. Description
Monensin
Placebo
Cows treated Sold by 94 DIM Died by 94 DIM First DHI Recorded milk Not tested Second DHI Recorded milk Not tested Third DHI Recorded milk Not tested
503 43 11
507 59 16
418 62
393 79
451 22
435 29
440 18
424 16
(no.)
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DHI test in cows of fair condition ( P = 0.014). There was no significant treatment by test number interaction ( P = 0.51) for the analysis in fat cows (BCS ≥4.0). Monensin treatment increased milk production for all three DHI tests ( P = 0.03) in cows classified as fat. Graphs of mean milk production by treatment and DHI test number for each body condition class are illustrated in Figures 1, 2, and 3. The least
squares means for milk production, adjusted for all the model variables and stratified by body condition class, are illustrated in Table 3. A model was developed for assessing the effect of treatment on test day milk fat percentage and milk protein percentage. In the final models, the random effects of both farm and cow were significant for protein percentage, but only cow was a significant ( P = 0.001) random variable for fat percentage. Again, there were no treatment by farm interactions detected. No treatment effect was found for milk fat percentage ( P = 0.44) or milk protein percentage. There was a significant ( P = 0.001) interaction of DHI test number with treatment for milk protein percentage; however, when the analysis was stratified by DHI test number and the Bonferroni-adjusted probability value was used, there was no significant effect ( P > 0.15) of treatment detected for milk protein percentage at any of the first three DHI tests. Graphs of mean values for milk fat percentage and milk protein percentage by treatment and DHI test number are given in Figures 4 and 5. The effects of treatment on lactation milk production were assessed using ANOVA on the 305-d milk production projected at third DHI test. The treatment by farm interaction term was significant ( P = 0.02). Because the effect of treatment on lactation milk production depended on the farm, the herd risk of ketosis was forced into this model to help to explain the treatment by herd interaction. The final model
Figure 2. Mean ( ±SE) DHI test day milk production by treatment for cows categorized as fair (body condition score of 3.25 to 3.75) at treatment administration 3 wk prior to calving. Milk production was different ( P < 0.05) at the second DHI test.
Figure 3. Mean ( ±SE) DHI test day milk production by treatment for cows categorized as fat (body condition score >3.75) at the time of treatment administration 3 wk prior to calving. Milk production was different ( P < 0.05) for the entire period.
Figure 1. Mean ( ±SE) DHI test day milk production by treatment for cows categorized as thin (body condition score of <3.25) at treatment administration 3 wk prior to calving. No differences ( P ≤ 0.05) in milk production were observed between treatments.
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TABLE 3. Least squares means1 of DHI test day milk production by treatment and body condition class. Body condition class Treatment
Thin (BCS 2 < 3.25)
Monensin Placebo
79 96
Monensin Placebo
32.9a 34.5a
Fair (BCS 3.25 to 3.75)
Fat (BCS > 3.75)
(n) 331 318 Milk production ( k g ) DHI DHI Test 1 Test 2
DHI Test 3
34.4a 34.0a
33.6a 33.4a
36.8a 35.6b
70 58
36.1a 33.6b
a,bMeans within the same column followed by different superscript letters differ ( P ≤ 0.05). 1Adjusted for parity, DHI test number (except for cows in fair body condition for which there was a treatment by test number interaction), season of calving, season of DHI test, DIM at DHI test, test day linear score, loss in body condition, multiple illness, days from treatment administration to calving, and the random effects of both cow (except for cows in fair body condition) and farm. 2Body condition score (where 1 = thin to 5 = fat).
contained a significant ( P < 0.05) interaction of treatment with herd ketosis risk, and the model was then reanalyzed after being stratified by herd risk for ketosis. Initial BCS and its interaction with treatment were not significant in these models. There was a positive effect ( P = 0.01) of treatment on projected 305-d milk production for herds that were at increased risk of ketosis; however, treatment had no effect on 305-d milk production for herds with normal risk for ketosis. Adjusted least squares means for projected lactation milk production by herd risk for ketosis and body condition class are in Table 4.
Figure 4. Mean ( ±SE) DHI test day milk fat percentage by DHI test number for cow treated with monensin in a controlled-release capsule or a placebo 3 wk prior to expected calving. No difference ( P = 0.44) in milk fat percentage between treatments was observed.
peak milk production. It has been estimated that, for every 1 kg increase in peak milk production, about 200 kg more milk is produced during a lactation (14). Although there were no statistically significant ( P = 0.34) differences in projected 305-d milk production, the cows treated with monensin had a projected milk production of 106 kg per lactation more than that of cows receiving the placebo (using least squares means). Milk production of cows in fair condition at
DISCUSSION Monensin treatment exerted a positive influence on milk production; however, the response depended on the initial BCS prior to calving. The DHI test day milk production was not significantly influenced by treatment in cows categorized as being thin at the time of treatment administration. Cows in fair body condition that were given monensin produced significantly ( P = 0.014) more milk at the second DHI test compared with that of placebo cows. This increase amounted to a difference of 0.85 kg more milk/d at the second DHI test using arithmetic means and an adjusted difference of 1.2 kg/d using least squares means. The second DHI test occurred at an average of 60 d postpartum and was the measurement closest to Journal of Dairy Science Vol. 82, No. 2, 1999
Figure 5. Mean ( ± SE) DHI test day milk protein percentage ( ±SE) by DHI test number for cow treated with monensin in a controlled-release capsule or a placebo 3 wk prior to expected calving. No difference ( P = 0.27) in milk protein percentage between treatments was observed.
MONENSIN, MILK PRODUCTION, AND MILK COMPONENTS TABLE 4. Least squares means of projected 305-d milk production by treatment, herd risk for ketosis,1 and initial body condition class.2 Variable Herd ketosis risk Increased Normal BCS3 Thin (<3.25) Fair (3.25 to 3.75) Fat (>3.75)
Monensin
Placebo
Difference
8766a 8463
8187b 8452
+579 +11
8413 8611 9132
8485 8505 8665
–72 +106 +467
a,bMeans within a row with different superscript letters differ ( P ≤ 0.05). 1Adjusted for the effects of parity, DIM at third DHI test, season of calving, change in body condition class, disease (cow having one or more diseases postcalving), and the random effects of farm. 2Adjusted for the same variables as for ketosis except that herd risk of ketosis was ignored. 3Body condition score (where 1 = thin to 5 = fat).
both first and third DHI test was not significantly different between treatments. Because the average time from treatment to calving was 21 d and the capsule was empty at approximately 95 d, the daily release of monensin would have ceased at about 74 d postpartum, half way between the second and third DHI test. It is possible that a second monensin capsule, administered at d 75 postcalving, might have continued to improve milk production. Few studies to date have evaluated the effects of monensin for the exact period investigated in the current project. Thomas et al. ( 1 7 ) found no effect of monensin treatment on milk production or milk components when fed from 2 to 4 wk prepartum until 84 d of lactation. However, that study involved only 47 Holsteins that were divided among a placebo group and three monensin groups (150, 300, and 450 mg/d). The small sample size and the use of only one herd might account for the lack of an observed effect. Absolute milk production was not reported, and BCS were not measured. An effect of monensin was detected in the lowering of both NEFA and BHBA concentrations, suggesting that an improvement occurred in energy metabolism. In the study by Lynch et al. (11), capsule administration commenced near peak lactation at 46 DIM, and the CRC would not have ceased delivering monensin until 141 d postpartum. Lean et al. ( 9 ) started capsule treatment during the 1st wk of lactation, causing daily monensin release to end near 100 DIM, which is still well beyond the 75 d of our trial. Cows that were treated with monensin and classified as fat prior to capsule administration produced more ( P = 0.03) milk than did fat cows receiving the
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placebo. The difference amounted to an additional 1.2 kg/d unadjusted and 2.5 kg/d using least squares means to control for other factors in the model. The response in unadjusted milk production observed in this study was a 3.4% increase at peak lactation for cows in fair condition and was 7.4% for fat cows during all three DHI tests. This response is comparable with the 7 to 8% increase found by Lynch et al. ( 1 1 ) and the 6% increase reported by Lowe et al. (10). The absolute increase of 0.85 kg/d for fair cows at peak lactation and 1.25 kg/d for fat cows during the first 94 DIM is very similar to the 1.1-kg/d increase observed by Lowe et al. ( 1 0 ) and the 1.0-kg/d increase reported by Lynch et al. (11). Other studies have not identified the monensin treatment by BCS interaction that was observed in this trial. This interaction could possibly help explain the observed treatment with herd interactions found by Lean et al. ( 9 ) in a study in which one herd out of six showed increased milk production for monensintreated cows. It is unclear why there appears to be a dose-response effect with monensin and BCS prior to calving. Heavier body condition prior to calving appeared to favor a greater production response to monensin. From the BHBA data previously reported ( 3 ) , concentrations of BHBA were shown to increase postcalving with increasing initial BCS class. Although monensin consistently reduced BHBA concentrations for all BCS classes, perhaps heavier BCS classes have concentrations of BHBA approaching a subclinical ketosis threshold. The observed increase in milk production may simply be the result of an improved energy supply that alleviates the negative impact of subclinical ketosis on milk production. It is possible that the cows in the trials of both Lynch et al. ( 1 1 ) and Lowe et al. ( 1 0 ) were hyperketonemic, because they were fed pasture in early lactation without additional grain supplementation. Metabolic parameters were not measured in those trials. Hayes et al. ( 4 ) evaluated cows from three herds fed pasture and reported 0.41 L more milk/d for monensin-treated cows. However, no difference in the levels of BHBA or glucose were detected. These seasonally calving cows were treated 1 mo prior to the start of artificial insemination, which would have been later in lactation than the current study. Both control and treated cows were likely to have been in a positive energy balance during that trial as indicated by the findings of high glucose and low ketone bodies. Therefore, the positive milk production response was probably not related to the antiketogenic effects of monensin. In the current study, the treatment-related improvement in concentrations of BHBA, glucose, and asparJournal of Dairy Science Vol. 82, No. 2, 1999
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tate aminotransferase previously reported ( 3 ) support the hypothesis that the observed increase in milk production stemmed from an improvement in the energy status of the cow. The 305-d milk production projected at the third DHI test was used to identify treatment effects for the entire lactation. Season of the DHI test, multiple illness, days from bolus administration to calving, test day linear score (at third DHI test), and the BCS by treatment interaction term were not significant compared with the primary model for test day milk production. There was an interaction detected between farm and treatment for this analysis. To help to explain this interaction, herd risk of ketosis was forced into the model and was found to have a significant interaction ( P = 0.025) with treatment. Within the four herds identified with increased risk of ketosis, based on elevated BHBA concentration in the cows administered the placebo, monensin-treated cows had higher ( P = 0.01) projected lactation milk production (+580-kg difference in least squares means) than did cows given the placebo treatment. Cows within the remaining 21 herds did not have lactation milk production that varied with treatment. This result further supports the theory of improved milk production being associated with a reduction in the level of subclinical ketosis. The lack of an observed interaction of treatment with initial BCS for lactation milk production could be a function of a high variance combined with an inadequate sample size to test this effect. Stratification of the analysis by BCS and ignoring ketosis risk and ketosis risk by treatment interaction revealed differences in least squares means of –72, +107, and +466 kg for the treatment effect on projected lactation milk production in thin, fair, and fat cows, respectively. None of these differences was different at P ≤ 0.05. The treatment effect on test day milk fat percentage and test day milk protein percentage in the current study differs from the findings of other studies (1, 4, 10, 11) that indicated that monensin lowered milk fat percentage. Those studies involved pasturefed cattle, but the cows in the current project were fed a mix of concentrate and dry or ensiled forage (which is more representative of North American rations for lactating cows). Phipps et al. ( 1 3 ) found a dose relationship between monensin concentrations and milk fat: higher monensin concentrations cause greater fat depression. The constant dose of monensin delivered by the CRC results in a decreasing concentration as DMI increases in early lactation. The observed numerical decrease in milk fat percentage of 0.1% at the first DHI test and virtually identical milk fat percentJournal of Dairy Science Vol. 82, No. 2, 1999
ages at second and third DHI test could be related to less monensin being delivered per kilogram of DMI. Lean et al. ( 9 ) found that monensin treatment increased milk production in only one of six study herds, which may help to explain the lack of an observed effect on milk components. The herd with the positive milk production response was found to have no significant increase in milk protein production or milk fat production. Although percentages were not reported, this finding implied a decrease in both milk fat and milk protein percentages associated with monensin for this particular herd. The reverse would be true for the present study. A lack of treatment effect for either milk fat percentage or milk protein percentage in the presence of increased total test day milk production suggests an absolute increase in both milk fat and milk protein production. CONCLUSIONS Administration of a monensin CRC 3 wk prior to calving improved milk production of lactating Holstein cows and first parity heifers. The influence of monensin on DHI test day milk production was dependent on initial BCS at the time of treatment administration; a higher production response was observed with greater BCS. Monensin significantly increased projected 305-d milk production projected at the third DHI test for cows within herds at increased risk of ketosis. No effect of monensin on milk fat percentage or milk protein percentage was found. ACKNOWLEDGMENTS We thank Eleanor McNaughton and Shelley James for technical assistance and Provel, a Division of Eli Lilly, Ontario, Canada, for financial support. REFERENCES 1 Abe, N., I. J. Lean, A. Rabiee, J. Porter, and C. Graham. 1994. Effects of sodium monensin on reproductive performance of dairy cattle. II. Effects on metabolites in plasma, resumption of ovarian cyclicity and oestrus in lactating cows. Aust. Vet. J. 71: 277–282. 2 Coutinho, L. L., P. F. Machado, and R. M. Cook. 1987. Effect of isoacids and monensin on lactating cows. J. Dairy Sci. 70(Suppl. 1):217.(Abstr.) 3 Duffield, T. F., D. Sandals, K. E. Leslie, K. Lissemore, B. W. McBride, J. H. Lumsden, P. Dick, and R. Bagg. 1998. Effect of prepartum administration of monensin in a controlled release capsule on postpartum energy indicators in lactating dairy cattle. J. Dairy Sci. 81:2354–2361. 4 Hayes, D. P., D. U. Pfeiffer, and N. B. Williamson. 1996. Effect of intraruminal monensin capsules on reproductive performance and milk production of dairy cows fed pasture. J. Dairy Sci. 79:1000–1008.
MONENSIN, MILK PRODUCTION, AND MILK COMPONENTS 5 Herdt, T. H., J. B. Stevens, W. G. Olson, and V. Larson. 1981. Blood concentrations of b-hydroxybutyrate in clinically normal Holstein-Friesian herds and in those with a high prevalence of clinical ketosis. Am. J. Vet. Res. 12:503–506. 6 Johnson, J. C., P. R. Utley, B. G. Mullinex, Jr., and A. Merrill. 1988. Effects of adding fat and lasalocid to diets of dairy cows. J. Dairy Sci. 71:2151–2165. 7 Knowlton, K. F., M. S. Allen, and P. S. Erickson. 1993. Effect of lasalocid and corn grain particle size on performance, feed digestibility, and rumen parameters in early lactation dairy cattle. J. Dairy Sci. 76(Suppl. 1):280.(Abstr.) 8 Kube, J. C., J. E. Shirley, T. D. Smith, and R. A. Frey. 1988. Effect of monensin supplementation on lactating dairy cows. J. Dairy Sci. 71(Suppl. 1):218.(Abstr.) 9 Lean, I. J., M. Curtis, R. Dyson, and B. Lowe. 1994. Effects of sodium monensin on reproductive performance of dairy cattle. I. Effects on conception rates, calving-to-conception intervals, calving-to-heat and milk production in dairy cows. Aust. Vet. J. 71:273–277. 10 Lowe, L. B., G. J. Ball, V. R. Carruthers, R. C. Dobos, G. A. Lynch, P. J. Moate, P. R. Poole, and S. C. Valentine. 1991. Monensin controlled-release intraruminal capsule for control of bloat in pastured dairy cows. Aust. Vet. J. 68:17–20. 11 Lynch, G. A., M. E. Hunt, and S. N. McCutcheon. 1990. A note of the effect of monensin sodium administered by intraruminal
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controlled-release devices on productivity of dairy cows at pasture. Anim. Prod. 51:418–421. 12 Murphy, M. R., J. M. Campbell, S. W. Nombekela, and P. S. Erickson. 1993. Effect of lasalocid on dairy cows in early lactation. J. Dairy Sci. 76(Suppl. 1):279.(Abstr.) 13 Phipps, R. H., B. A. Jones, J.I.D. Wilkinson, and M. E. Tarrant. 1995. Effect of monensin on milk production of Friesian dairy cows in the United Kingdom. J. Dairy Sci. 78(Suppl. 1): 268.(Abstr.) 14 Radostits, O. M., K. E. Leslie, and J. Fetrow. 1994. Dairy health and production management program. Pages 97–140 in Herd Health: Food Animal Production Medicine. 2nd ed. W. B. Saunders Co., Philadelphia, PA. 15 SAS/STAT Software: Changes and Enhancements, Release 6.07. 1992. SAS Tech. Rep. P 229. SAS Inst., Inc., Cary, NC. 16 Schelling, G. T. 1984. Monensin mode of action in the rumen. J. Anim. Sci. 58:1518–1527. 17 Thomas, E. E., S. E. Poe, R. K. McGuffey, D. H. Mowrey, and R. D. Allrich. 1993. Effect of feeding monensin to dairy cows on milk production and serum metabolites during early lactation. J. Dairy Sci. 76(Suppl. 1):280.(Abstr.) 18 Weiss, W. P., and B. A. Amiet. 1990. Effect of lasalocid on performance of lactating dairy cows. J. Dairy Sci. 73:153–162.
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