J. Dairy Sci. 2008. 91:1845-1851. doi:10.3168/jds.2007-0795
© 2008 American Dairy Science Association ®
Production and Health of Cows Given Monensin Prepartum and a High-Energy Diet Postpartum
A. Arieli*,1,
U. Dicken*,
I. Dagoni
,
Y. Spirer
and
S. Zamwel*
* The Hebrew University of Jerusalem, Faculty of Agricultural, Food and Environmental Quality Sciences, Rehovot 76100, Israel
Hachaklait, Veterinary Services, PO 3039, Caesarea 38900, Israel
Mifalei Granot M.P., Hefer 38100, Israel
1 Corresponding author: Arieli{at}agri.huji.ac.il
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ABSTRACT
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The object of this study was to evaluate the impact of monensin administration on the early lactation performance of cows maintained on a high-energy diet, and on health traits during the transition period. Cows (n = 168; parity 3.3 ± 1.4, initial body condition score 3.1 ± 0.08, and milk yield of 34.3 kg/d ± 0.9 for multiparous cows in the preceding lactation) were divided into control and monensin treatment groups. A controlled-release capsule supplying 335 mg of monensin/d for 95 d was inserted into the rumen of monensin-treated cows 30 d before the expected calving. Blood samples were obtained 2 h after feeding on d 14 prepartum and on d 7, 14, and 50 postpartum. Plasma glucose concentration was 3% higher (58 ± 0.5 vs. 56.4 ± 0.5 mg/dL) and β-hydroxybutyric acid was 17% (6.7 ± 0.3 vs. 8.0 ± 0.3 mg/dL) lower in monensin-treated than control cows. Plasma glucose was 10% higher (60.0 ± 0.6 vs. 54.5 ± 0.3 mg/dL) and β-hydroxybutyric acid was 16% lower (6.8 ± 0.3 vs. 7.9 ± 0.2 mg/dL) in primiparous than multiparous cows. Plasma nonesterified fatty acid concentration (measured only in primiparous cows) was 17% lower (287 ± 15 vs. 336 ± 17 µEq/L) in treated than in control cows. Rate of ketosis incidence was 60% lower (8 vs. 21%) in monensin-treated than in control cows, and the proportion of control cows that required a supply of glucogenic precursors was 3-fold higher than in monensin-treated cows. The body condition score was 3.1 ± 0.05, 2.7 ± 0.05, and 2.4 ± 0.05 on d 60 prepartum and d 7 and 50 postpartum, respectively, and was not affected by treatment. During the first 5 mo of lactation, milk yield was 7% higher (37.6 ± 0.6 vs. 35.2 ± 0.6 kg/d) in monensin-treated cows than in control cows. Our results showed that monensin administration, as a controlled-release capsule in prepartum cows, can be beneficial, even if these cows are maintained on a high-energy diet during the subsequent lactation.
Key Words: high-energy diet • monensin • parity
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INTRODUCTION
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Transition cows are exposed to considerable modifications in their nutrient metabolism because of the increased energy and protein demands of the developing fetus and the switch to lactation. Because the energetic demands during the transition period (from 3 wk before to 3 wk after parturition) are larger than the cow’s dietary energy intake, substantial adipose tissue mobilization must occur, with an inevitable increase in the rate of metabolic disorders (Overton and Waldron, 2004), leading to a subsequent decrease in productivity and profitability. Solutions for improving the energy balance have been aimed toward decreasing the energy deficit during this period. Nevertheless, specific feeding strategies, for example, those attempting to decrease body fat mobilization, prime for body fat mobilization, or prime the rumen for increased intake, have had only limited success (Friggens et al., 2004).
In contrast, supplying these cows with a gluconeogenic precursor, such as propylene glycol, has generally been effective in decreasing the rate of metabolic disorders (Nielsen and Ingvartsen, 2004). Improving the energy balance of transition cows can be accomplished by administering ionophores such as monensin (MON), which exert their effect by modifying rumen fermentation. The beneficial effect of MON might be attributed to several different mechanisms: an increased propionate:acetate ratio in the rumen, decreased energy loss through methane production, and decreased digestion of protein and starch in the rumen, with subsequent improved utilization of these nutrients in the small intestine (McGuffey et al., 2001). These effects lead to decreased blood NEFA and BHBA concentrations, an increase in glucose status, and a more positive energy balance (Duffield et al., 2003). When provided postpartum, MON may increase the milk yield of dairy cattle (Granzin and Dryden, 1999), although at that stage, its effect is less pronounced. According to Ipharraguerre and Clark (2003), significant effects of increased milk yield were reported in 50% of the surveyed experiments.
Treatment of transition cows with a MON controlled-release capsule (CRC), supplying MON for approximately 100 d (McGuffey et al., 2001), enabled producers to treat periparturient cows, with the advantage of manipulating metabolism during the prepartum and post-partum stages as well. Most studies relating to the application of an MON CRC in dairy cattle have been carried out in cows consuming low- to medium-energy diets (Ipharraguerre and Clark, 2003). Tedeschi et al. (2003) suggested that the potential effect of MON on increasing propionate production and reducing methane dissipation was limited in cows maintained on concentrated diets. Nevertheless, MON CRC administration can exert a positive effect on the energy metabolism of high-energy-fed dairy cows because of a reduced rate of metabolic disorders around parturition and a reduction in excessive ruminal fermentation. In the current study, we examined the impact of MON CRC administration to periparturient cows on health traits and subsequent milk production when the cows were fed a high-energy diet.
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MATERIALS AND METHODS
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Feeding and Management of Cows
The Hebrew University Animal Care Committee approved all experimental procedures involving animals. The trial was conducted at the dairy barn of the communal farm of Nir Galim, Israel, from March 2003 to March 2004. Nonlactating Israeli Holstein cows from first lactation (n = 40), second lactation (n = 39), and third and greater lactations (n = 89) were used. Once monthly, a list of milking cows expected to calve within the subsequent 2 mo was divided randomly into 2 equal sets based on lactation number, DIM, previous lactation milk yield, and BCS at drying off. These sets were randomly assigned to control and treatment groups. Primiparous cows were enrolled according to their BCS only. For both treatments, the initial BCS was 3.1 and 3.0 (SE = 0.08) in primiparous and multiparous cows, respectively. Milk yield of the preceding lactation in multiparous cows was 34.4 kg/d in control cows and 34.2 kg/d in MON-treated cows (SE = 0.9), and the lactation number in both treatments was 3.3 ± 1.4.
A CRC supplying 335 mg of MON/d for 95 d (CRC, Elanco, Guelph, Canada) was administered orally to MON-treated cows 30 d before the expected calving. Records of cows treated with MON were not accessible to the farm workers or observation staff, who were blinded to treatments throughout the study period.
Prepartum and postpartum cows of both experimental groups were maintained together in the same open sheds (2 sheds for prepartum cows and 4 sheds for lactating cows); fans were available in each shed to cool the cows in the summer. Daily feed was provided at approximately 0730, 1000, and at 1500 h, and cows had free access to feed (Table 1
) and water. Cows were milked 3 times daily at approximately 0600, 1400, and 2100 h, and individual milk yields were recorded. The BCS (Wildman et al., 1982) was evaluated on d 60 pre-partum and on d 7 and 50 postpartum.
Sample Collection, Measurements, and Analyses
Milk production was recorded for each milking by automatic meter (Afimilk, Zaham Afikim, Israel). Individual daily milk production was calculated and used to compute mean weekly milk yields. Milk yields for the first 18 wk of lactation are reported. Milk samples were collected every month during the experimental periods from each daily milking and composited by milk volume.
Blood samples for plasma composition analysis were collected via jugular venipuncture into evacuated tubes (BD Vacutainer, Belliver Industrial Estate, Plymouth, UK). Blood was sampled approximately 2 h after feeding at 14 d prepartum and at 7, 14, and 50 d (±1) post-partum. Plasma-collection tubes for glucose analysis contained sodium fluoride-K3EDTA, and plasma tubes for other analyses contained sodium heparin. Plasma tubes were placed on ice immediately after sampling, centrifuged at 4°C at 3,300 x g for 15 min within 1 h of collection, and stored at –20°C for later analysis.
Milk samples (20 mL) from 3 consecutive milking sessions were analyzed by the Israeli Cattle Breeders Association (Milk Recording Laboratory, Industrial Area, Caesarea, Israel) for fat, CP, lactose, urea N, and SCC by midinfrared spectrometry (MilkoScan FT 6000; Foss Electric, Hillerød, Denmark). Plasma was analyzed for urea N (PUN; Coulomb and Favereau, 1963), glucose (Raichem Kit 85188; Raichem, Columbia, MD), NEFA (NEFA-C kit; Wako, Richmond, VA), BHBA (Sigma kit 310-A; Sigma Chemical Co., St. Louis, MO), and aspartate aminotransferase (AST; AST kit; Raichem Diagnostics Co., San Diego, CA).
Animal Health
A veterinarian recorded disease and health conditions throughout the experiment. The following health disorders were recorded for all cows: ketosis (a high level of ketones detected in the urine by KetoStrips, Bayer Co., Dublin, Ireland), retained placenta (a placenta that was retained for >12 h, verified by vaginal exploration), and metritis (diagnosed by vaginal exploration). Animals suspected of displaced abomasum were subjected to veterinary examination for verification and surgery. Traits used to evaluate health status included general demeanor, rectal temperature, and milk production. Sick cows were treated with antibiotics. Cows from both groups that were diagnosed as ketotic were injected with 50% dextrose (500 mL, i.v.) and drenched with 300 g of propylene glycol for 3 consecutive days.
Statistical Analysis
Statistical analysis was performed by a repeated measures method using the PROC MIXED procedure of SAS (v. 9.1; SAS Inst. Inc., Cary, NC). The model analyzed concentration of metabolites in the blood plasma:
where Yij is the dependent variable, µ is the overall mean, Ti is the effect of treatment (i = 1, 2), Pj is the effect of parity (primiparous or multiparous cows), Cijk is the effect of cow k in treatment i and parity j, Dl is the effect of sampling date (l = 1, 2, 3, or 4), TP is the effect of a treatment x parity interaction, TD is the effect of a treatment x sampling date interaction, TPD is the effect of a treatment x parity x sampling date interaction, and 
ijkl is the within-cow residual error.
A similar model was used to analyze monthly milk yield and the percentage and yield of milk constituents. The variable D was the effect of milk sampling month (l = 1, 2, . . ., or 5) for analyzing the weekly milk yield (averaged of daily milk data; l = 1, 2, . . ., or 18), and BCS (l = 1, 2, 3).
The comparisons for the main effects were performed on the least squares means. For most traits, the interaction terms were not significant (P > 0.05), in which case only the main effects are reported. When the TP, TD, or TPD effect was significant, least squares means were compared at each time point by contrast t-tests.
Incidence of health problems and incidence of glucogenic precursor application were analyzed for treatment effects by using the FREQ procedure of SAS with 
2 or Fisher’s exact tests.
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RESULTS AND DISCUSSION
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Plasma Metabolites
Concentrations of blood metabolites were measured concurrently with MON CRC application; hence, the differences between MON-treated and control cows represent a direct effect of MON. The effects of the interactions were not significant. Concentrations of plasma glucose, BHBA, NEFA, and AST activity revealed a clear temporal pattern (Figures 1 and 2).
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Figure 1. Least squares means of plasma concentrations of glucose (A), BHBA (B), and NEFA (only in multiparous cows; C) in control cows (CON) and cows treated with a monensin (MON) controlled-release capsule 1 mo before parturition. Standard error values in CON and MON-treated cows were 2.8 and 2.7 for glucose, 0.4 and 0.4 for BHBA, and 18 and 17 for NEFA, respectively.
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Figure 2. Least squares means of plasma concentrations of plasma urea nitrogen (PUN; A) and aspartate aminotransferase activity (AST; B) in control cows (CON) and cows treated with a monensin (MON) controlled-release capsule 1 mo before parturition. Standard error values in CON and MON-treated cows were 0.4 and 0.4 for PUN, and 2.8 and 2.7 for AST, respectively.
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Glucose
Plasma glucose was 3% higher in MON-treated (58.0 ± 0.5 mg/dL) than in control cows (56.4 ± 0.5 mg/dL, P < 0.02) and 10% higher in primiparous (60.0 ± 0.6 mg/dL) than in multiparous cows (54.4 ± 0.4 mg/dL, P < 0.001). Plasma glucose concentration was 60.5 ± 0.5, 51.5 ± 0.6, 53.2 ± 0.5, and 57.7 ± 0.5 mg/dL at –14, 7, 14, and 50 d, respectively (P < 0.001). Our data support previous studies in which MON treatment did not affect prepartum glucose concentration (Duffield et al., 1998, 2003; Vallimont et al., 2001). The postpartum diet (Table 1
) was formulated according to NRC (2001) recommendations.
Here, in both treatments, plasma glucose was higher in primiparous than in multiparous cows by 8% (63.0 ± 0.7 vs. 60.0 ± 0.6 mg/dL), 12% (56.3 ± 1.3 vs. 50.3 ± 0.6 mg/dL), 16% (59.8 ± 0.8 vs. 51.5 ± 0.5 mg/dL), and 5% (59.8 ± 1.0 vs. 57.1 ± 0.6 mg/dL) on d 14 prepartum and d 7, 14, and 50 postpartum, respectively. This finding probably reflects the lower demand of primiparous cows as compared with multiparous cows for milk lactose synthesis.
BHBA and NEFA
Plasma BHBA concentration was 16% lower in MON-treated cows than in control cows (6.7 ± 0.3 vs. 8.0 ± 0.3 mg/dL, P < 0.001) and in multiparous cows (7.9 ± 0.2 mg/dL) than in primiparous cows (6.8 ± 0.3 mg/dL, P < 0.01). Plasma BHBA concentration was 5.0 ± 0.1, 9.1 ± 0.4, 8.1 ± 0.3, and 8.4 ± 0.2 g/dL on d –14, 7, 14, and 50, respectively (P < 0.001). The effect of MON is in agreement with the reports of Stephenson et al. (1997), Duffield et al. (1998), and Melendez et al. (2004). Plasma NEFA concentration (measured only in multiparous cows) was 17% lower in MON-treated cows (287 ± 16 µEq/L) relative to control cows (336 ± 17 µEq/L, P < 0.04). Plasma NEFA concentration was 277 ± 28, 497 ± 27, 339 ± 28, and 231 ± 29 µEq/L on d –14, 7, 14, and 50, respectively (P < 0.001).
Our data support a study in which MON administration did not affect NEFA concentration, whereas plasma BHBA concentration was reduced consistently (Ipharraguerre and Clark, 2003). Increased hepatic conversion of NEFA to ketone bodies during the transition period was considered a strategy to compensate for insufficient intake of glucose precursors (Drackley et al., 2001). In our study, there was a negative correlation between plasma BHBA and glucose concentrations (r = –0.53, –0.47, and –0.54 for d 7, 14, and 50 postpartum, respectively; n = 130, P < 0.001). These correlations are compatible with the potential of MON to increase the supply of glucose precursors.
Urea
Concentration of PUN tended to be affected by treatment (13.9 ± 0.3 mg/dL in control cows vs. 14.7 ± 0.3 mg/dL in MON-treated cows, P = 0.09), but not by parity (P > 0.1). Concentration of PUN was 15.7 ± 0.3, 13.5 ± 0.3, 13.7 ± 0.2, and 14.9 ± 0.3 mg/dL on d –14, 7, 14, and 50, respectively (P < 0.001).
AST Activity
Aspartate aminotransferase activity was 66.1 ± 1.0, 100.2 ± 2.6, 94.2 ± 1.6, and 81.5 ± 1.4 units/mL on d –14, 7, 14, and 50, respectively (P < 0.001). Activity of AST was not affected by treatment or by parity. In contrast, a large-scale study using approximately 1,000 cows found a significant, albeit subtle, effect of MON, lowering AST activity during the first 2 wk postcalving (Duffield et al., 1998). Others (Ramanzin et al., 1997; Juchem et al., 2004) did not observe any effect of MON on AST in postcalving cows. Thus, AST activity appears to be a weak indicator for transition in the energy state of the cow.
Health Conditions and BCS
Frequency of health disorders and rates of propylene glycol application are shown in Table 2. Rate of ketosis incidence was 60% lower in MON-treated than in control cows. Likewise, the rate of cows treated with propylene glycol supplementation was 62% lower in MON-treated than in control cows. In previous studies, MON decreased the prevalence of ketosis and improved rumen health in the early-lactating dairy cow (Duffield et al., 1998, 2002; Green et al., 1999). Indeed, compared with MON-treated cows, the proportion of control cows that required a supply of glucogenic precursors was 3-fold higher. Metabolic disorders (i.e., milk fever and ketosis) usually occurred during the first 2 wk postpartum and were caused by low DMI and negative energy balance (Goff and Horst, 1997), yet there was no significant effect of MON on the incidence rate of retained placentas or uterine infections.
The BCS was not affected by treatment or parity. The BCS was 3.1 ± 0.04, 2.6 ± 0.05, and 2.5 ± 0.04 on d 60 prepartum and d 7 and 50 postpartum, respectively.
Milk Yield and Composition
Weekly milk yield tended to be higher in MON-treated than in control cows (35.6 ± 0.6 vs. 34.2 ± 0.6 kg/d, P < 0.09), and it was higher in multiparous (41.1 ± 0.4 kg/d) than in primiparous (28.8 ± 0.7 kg/d) cows (P < 0.001). Effects of parity, week, and a treatment x parity x week interaction were significant (P < 0.001).
Weekly milk production during wk 1 to 18 in primiparous and multiparous cows is shown in Figure 3. Multiparous MON-treated cows produced 1.7 kg more milk on wk 3 and 5 than did their counterparts. In multiparous cows during the other weeks, and in primiparous cows throughout the entire experimental period, milk yield was similar among treatments. In primiparous cows, peak yield was attained in wk 17 in control cows compared with wk 10 in MON-treated cows, with respective milk production of 30.2 ± 1.4 and 31.7 ± 1.3 kg/d. In multiparous cows, peak yield was attained at wk 6, with milk yields of 43.9 and 45.0 kg/d in control and MON-treated cows, respectively. Analysis of Figure 3 revealed that MON increased milk yield during wk 3 and 5 of lactation for multiparous cows. The effect of MON on the milk yield of multiparous cows diminished after 5 wk, which suggests that MON had no carryover effect beyond the period of its application. A similar conclusion was reached by Melendez et al. (2004), based on a time course of MON effect on blood metabolite concentration.
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Figure 3. Least squares means of weekly milk yield in control cows (CON) and cows treated with a monensin (MON) controlled-release capsule 1 mo before parturition. Pooled SEM values were 0.7 and 0.4 for primiparous (PP) and multiparous (MP) cows, respectively. **P < 0.01, *P < 0.05.
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Ipharraguerre and Clark (2003) reviewed the effects of ionophore administration on milk production under various diets (concentrate-to-forage ratios) and physiological stages (starting either before or after parturition). Ionophore administration to dairy cows either did not affect (18 experiments) or increased (14 experiments) milk production. Of those studies that resulted in a positive response, the effect of MON on milk yield in the current study was within the range of 1.5 kg/d.
Daily milk yield based on monthly milk yield was affected by treatment (P < 0.001), parity, and month (37.6 ± 0.7, 41.6 ± 0.7, 41.2 ± 0.7, 39.5 ± 0.6, and 37.9 ± 0.6 kg/d in 1 to 5 mo, respectively, P < 0.0001). During the first 5 mo of lactation, milk yield was 7% higher in MON-treated than in control cows (Table 3). The treatment x parity interaction was not significant.
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Table 3. Least squares means of milk yield and composition for the first 5 mo of lactation of control cows and cows treated with a monensin controlled-release capsule 1 mo before parturition
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Compositions of fat, protein, lactose, MUN, and SCC were similar in both treatments. Nevertheless, yields of milk components (fat, 6%; protein, 6%; lactose, 7%) were higher in MON-treated cows. The increased yield of milk constituents in these cows simply reflected the increase in milk yield. Ipharraguerre and Clark (2003) reported that milk fat concentration was reduced by 4.5% in MON-treated cows, apparently via changes mediated by biohydrogenation intermediates. Nevertheless, analysis of the data set presented by Ipharraguerre and Clark (2003) suggests that the effect of MON on the decrease in milk fat percentage was proportional to the concentration of the control, and MON-induced reduction was minimized when the control cow milk fat concentration was approximately 3%, as was the case in the present study.
The concentration of MUN was 28% higher in multiparous than in primiparous cows (Table 3). This finding disagrees with earlier reports in which no parity effect on MUN was observed (Davidson et al., 2003; Johnson and Young, 2003). The apparent between-study variation in parity effect might be explained by the dependence of MUN on various factors (e.g., milk yield, season, lactation stage; Wattiaux et al., 2005).
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CONCLUSIONS
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This is the first study to examine the impact of prepartum MON CRC administration to dairy cows fed a high-energy diet postpartum. With this diet, the advantage of MON CRC was demonstrated at both the prepartum and postpartum stages. The higher production of milk, protein, fat, and lactose during the first 7 wk of lactation and the better health and energy status of treated cows indicate that, under conditions of a high-energy lactation diet, there was an advantage to MON application. Under the experimental protocol, milk fat percentage was unaffected by MON. When the results from the present study are combined with those in the literature, the benefits of MON are indicated, particularly when an MON CRC is introduced to periparturient cows.
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ACKNOWLEDGEMENTS
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The authors acknowledge the Israeli Cattle Breeder Board (Caesarea, Israel) and S. H. Design Engineering Ltd. (Herzelia, Israel) for financial support and Elanco for supplying the CRC. The authors would like to thank the dairy staff of Nir Galim for their cooperation.
Received for publication October 21, 2007.
Accepted for publication January 14, 2008.
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ABSTRACT
INTRODUCTION
