STUDIES ON THE RUMEN PHYSIOLOGY AND METABOLIC FUNCTION WITH PRE- AND POSTPARTUM ADMINISTRATION OF RUMENSIN CRC IN THE DAIRY COW.

J.C.B. Plaizier¹, B. L. Green¹, B.W. McBride¹, and K. Leslie²

Department of Animal and Poultry Science¹, and Department of Population Medicine²

University of Guelph, Guelph, Ontario, Canada

Abstract

Monensin is now available for use in lactating dairy cattle as a controlled release capsule (CRC) to be placed intraruminally. This ionophore inhibits gram positive bacteria that produce acetate, butyrate, H⁺, lactate and formate. Propionate producing gram negative bacteria are generally monensin resistant. As a result of its effect on rumen bacteria, monensin changes the relative rates on VFA in favor of propionate and reduces methanogenesis in the rumen. By affecting lactic acid and total VFA concentrations, monensin can increase rumen pH, and can, therefore, reduce, but not prevent, ruminal acidosis in beef cattle and transition dairy cows on high concentrate diets. There are indications that monensin improves nitrogen utilization and reduces ammonia production. Few studies on the use of monensin in lactating dairy cattle have, so far, been conducted. These studies show that the product reduces the concentrations of keton bodies and increases the concentration of glucose in blood plasma, indicating that it has a therapeutic effect for the prevention of ketosis. The effect of monensin on milk production is not yet clearly understood, but no negative effects of this ionophore on milk volume, components, or any other adverse effects on health and production have been reported.

Introduction

The rapid increase in milk yield in the transition cow causes a very large increase in energy and nitrogen requirements. These cows are, therefore, changed from a roughage based diet to a transition diet which is high in concentrates. Even with this change in diet, transition and high producing dairy cows commonly experience a negative energy balance, which can result in clinical and subclinical ketosis (Sauer et al., 1989).

It is well documented that a rapid change to a high concentrate diet with a high content of readily fermentable carbohydrates can result in a decrease in rumen pH due to an increase in the concentration of lactic acid, resulting in ruminal acidosis (Underwood, 1992a). This condition can be acute, posing a life threatening situation, or subacute.

The ionophore sodium monensin is now available as a controlled release capsule (CRC) to be placed intraruminally. Monensin has been used in beef cattle for a considerable time. This has allowed the feeding of high levels of rapidly fermenting grains and low levels of roughage to these cattle without resulting in acute or subacute acidosis (Stock et al., 1990; Cooper and Klopfenstein, 1996). Additionally, in vitro research and experiments in beef cattle has indicated that monensin alters rumen fermentation in a way that will combat ketosis.

Only limited information on the use of monensin in lactating dairy cattle exist. As this product has the potential to prevent acidosis and ketosis, the use of monensin in transition dairy cattle could improve health and production of these cows.

Possible applications of this monensin to improve health and production of the lactating dairy cow and underlying rumen physiology, metabolic function, and systemic events are reviewed. Due to the scarcity of information of monensin in dairy cows, literature on the use of this ionophore in beef cattle is also included, and the implications of the latter research for dairy cattle are discussed.

Rumen Bacteria

The influence of monensin on rumen bacteria has been studied extensively. Dennis et al. (1981) studied the effects of monensin on lactate-producing and lactate-using rumen bacteria in vitro. Monensin inhibited growth of the major lactate-producing gram positive bacteria, i.e. Streptococcus and Lactobacillus, but it did not affect any of the major lactate fermenters, i.e. Anaerovibrio, Megasphera, Selenomons. Minimum inhibitory monensin concentrations in the media ranged from 0.38 to 3.0 m g/ml. Bergen and Bates (1984) argued that monensin inhibits gram positive, but does not effect gram negative bacteria by differences in the dependency on substrate level phosphorylation between these types of bacteria. They concluded that ionophores like monensin affect transmembrane ion fluxes and the dissipation of cation and protein gradients, thus obstructing primary membrane transport of cells and solute uptake coupled to this transport mechanism. Cells react to this reduced permeability by attempting to maintain primary transport by expending metabolic energy. Gram positive bacteria, which depend on substrate level phosphorylation of ATP cannot meet this increased demand and lyse. Gram negative bacteria, which are able to conduct some electron transport coupled with proton extrusion and/or ATP synthesis, will have an increased energy requirement for maintenance in the presence of ionophores, but are able to survive, grow, and proliferate.

Chen and Wollin (1979) also studied the effect of monensin on the growth of methanogenic and rumen saccharolytic bacteria in vitro. The growth of gram negative Bacteriodes succinogenes and Bacteriodes ruminicola were delayed by addition of 2.5 m g of monensin per ml of medium, indicating that monensin induced a lag time for the growth of these bacteria. The gram negative Selenomonas ruminatum was insensitive to monensin. These authors argued that their results indicated that monensin acts in the rumen by selecting for the gram negative propionate producing Bacteriodes and S. ruminatum, and that this selection results in an increase in propionate formation in the rumen. This will affect the ratio between volatile fatty acids (VFA) in the rumen, and also the total amount of VFA produced during fermentation.

Newbold et al. (1993) grew the gram negative rumen bacteria Fibrobacter succinogenes, Prevotella ruminicola, and Veillonella parvula in medium containing increasing concentrations of monensin and another ionophore, tetronasin. Inhibition of bacterial growth, measured as the concentration of the ionophore which decreased growth by 50% in a 48 hr incubation, decreased substantially if bacteria had been previously grown in media containing the ionophores. The authors, therefore, concluded that these bacteria changed their physiological properties when they are grown in the presence of ionophores, and thereby became adapted to these components. Cross resistance between different ionophores was also observed, indicating a common mechanism of resistance to different ionophores.

Tung and Kung (1993) studied the susceptibility of cultures of gram positive Lactabacillus acidophilus and S. bovis to 2.5 ppm of monensin at pH 5.5 and pH 6.5. At pH 5.5 growth of S. bovis was not detectable during 50 h of incubation. At pH 6.5 growth of S. bovis was inhibited severely. At pH 5.5 monensin inhibited growth of L. acidophilus, but some growth was detectable after 74 h of incubation. At pH 6.5 the inhibition of the growth of L. acidophilus was much less than at pH 5.5.

In summary, monensin inhibits gram positive bacteria which produce acetate, butyrate, H⁺, lactate, and formate. However, propionate producing gram negative bacteria, especially after an adaptation period, are generally monensin resistant.

PH, lactate, and total VFA

Ruminal acidosis is initiated by bacteria which produce lactic acid, e.g. the gram positive Streptococcus bovis and Lactobaccilus sp., outnumbering the lactic acid utilizing bacteria (Russel and Hino, 1985). Normally, the rumen environment is anaerobic with a pH of 6.5, and has a microbial population of protozoa and predominantly gram negative bacteria. Subacute acidosis has been defined by rumen pH values between 5.2 and 5.6, whereas values below 5.2 signify acute acidosis (Cooper and Klopfenstein, 1996). These low pH values will reduce fermentation, as the gram-negative cellulolytic and methanogenic bacteria are severely affected when the rumen pH falls below 6.0 (Owens and Goetsch, 1988). The low pH values will also reduce rumen motility and negatively affect the protozoa population in the rumen (Slyter, 1976; Underwood, 1992a). Animals respond to this metabolic disorder by reducing Dry Matter Intake, and milk yield (Underwood, 1992a, Underwood, 1992b). Acidosis can further result in diarrhea, endotoxin production from gram-negative organisms, and cardiovascular and respiratory collapse (Underwood, 1992a). An increased rate of lactic acid production in the rumen leads to an increase in the effective osmotic pressure, resulting in a flow of water from blood to gastro-intestinal tract (Underwood, 1992a). Acidosis also causes mucosal damage leading to a deterioration of rumen epithelium tissue, which allows for the systemic invasion of bacteria responsible for liver abscesses (Underwood, 1992a). Ruminal acidosis has been widely reported in feedlot cattle on finishing diets (Cooper and Klopfenstein, 1996), but few reports on the incidence of subclinical and clinical acidosis in dairy cattle exist.

Nagaraja et al. (1985) induced ruminal acidosis in steers by intraruminal administration of a 50:50 mixture of finely ground corn and corn starch once daily for up to 4 days or until animals expressed severe ruminal acidosis indicated by a rumen pH of 4.5. Treatments included 0.11 kg and 0.22 kg salinomycin per kg body weight, and 0.66 lasalocid/ kg and 0.66 mg of sodium monensin per kg administered along with the corn and starch mixture and a control. A Latin-square design was used for the experiment. Hence, animals receiving ionophore treatment after the first period were previously exposed to ionophores, allowing for adaptation of the gram negative bacteria. Rumen fluid samples were collected before and at 6, 12, 24, 36 48, 54, 60, 72 and 78 hours after the initial administration of the corn and starch mixture. In the control cattle, severe acidosis was induced after two days of the ground corn and corn starch mixture. In the monensin treated animals administration of up to 72 hr was required to reach a rumen pH of 4.5. Monensin treated cattle had significantly higher rumen pH and rumen lactate concentrations at 48 and 54 hr. Rumen VFA concentrations were higher than those of the control cattle in rumen sample collected after 48 hrs. Ruminal pH decrease to below 5.0 in monensin treated cattle was not due to lactic acid, but to increased production of VFA. This contradicts the observation of Sauer et al. (1989) that monensin does not increase total VFA concentration in rumen fluid of lactating dairy cows, suggesting a diet by monensin interaction must be operating.

Burrin and Britton (1986) measured changes in ruminal components response to monensin level following an abrupt switch from a forage based to a concentrate based diet consisting of 75.5 % of high moisture corn in steers. Levels of sodium monensin used were 0, 150, and 300 mg/head daily. The experiment was conducted as a 3 x 3 Latin-square design. Steers were fed the high forage diet for at least 14 d before receiving the high concentrate diet. The latter diet was fed during a 48 h period. Before the concentrate feeding, the steers did not receive monensin. In all treatments groups ruminal pH decreased to around 5.5 at 12 h after the feeding of the concentrate diet, indicating that animals suffered from sub-acute acidosis, as this metabolic disorder has been defined by rumen pH values between 5.2 and 5.6 (Cooper and Klopfenstein, 1996). At 8 h and 16 h post-feeding higher dietary levels of monensin were associated with higher ruminal pH. Also higher dietary monensin levels were associated with lower lactate and total VFA concentrations. Ruminal pH had a higher correlation with total VFA concentration (r = -0.69, P < 0.01) , than with lactate concentration (r = -0.14, P < 0.10). Hence, the contribution of lactic acid to subacute acidosis was smaller than that of total VFA.

The study of Burrin and Britton (1986) shows that monensin can reduce the drop in rumen pH due to high dietary levels of concentrate, but that it cannot avoid acidosis. The important contribution of total VFA concentration to rumen pH was also highlighted. It has to be noted that the steers involved in the experiment did not receive monensin prior to the feeding of the high concentrate diet. Hence, the gram negative bacteria will not have had the opportunity to adapt to monensin. Had this adaptation been possible, then the effect of this ionophore on the gram negative bacteria and the total VFA concentration, and, therefore, rumen pH, might have been different.

Tung and Kung (1993) studied the effect of monensin in vitro. A diet containing 50% soluble starch, 21% glucose, 6% cellulose, 7% cellubiose, and 16% trypticase was added to buffered rumen fluid. Treatments included monensin (2.5 ppm) and a control. Incubation was carried out anaerobically at 39^oC. Samples were collected at 0, 3, 5, 6, 7, 9, and 22 hr of incubation. These samples were analyzed for VFA and D- and L-lactic acid, and pH was measured. The pH of monensin treated cultures was always higher than that of the controls. The pH of untreated cultures was below 5 after 6 h of incubation. In monensin treated cultures pH did not drop below 5 until after 9 hr of incubation. After 5 hr of incubation VFA was lower in control than in monensin treated cultures. However, following this time, total VFA concentration increased in monensin treated cultures but not in controls. Monensin reduced total lactate by more than 80% through 6 hr of incubation compared to the control. The concentration of L-lactate was about 10 to 20 times greater than that of D-lactate during the early hours of incubation, but by 22 h the ratio between these isomers was almost equal.

Cooper and Klopfenstein (1996) studied the effect of monensin supplementation on steers in a metabolism trial. Steers were summered on grass until the start of the trail in mid October. At the beginning of the trial steers received a 92.5 % concentrate diet with or without 25 g/ton of monensin. Steers were adapted to the finishing diet during a 20 day four step grain adaptation period. Ruminal pH was monitored continuously using submersible pH electrodes suspended through ruminal cannula. During the grain adaptation period, monensin did not affect average daily pH. In steers receiving monensin, the area of ruminal pH below 5.6, which indicated the time and intensity of exposure to clinical and sub-clinical acidosis, was lower during the first and the second period of 5 days on the finishing diet compared to the controls, but this difference was not significant in the first period. The magnitude of diurnal variation in rumen pH was not affected by monensin during the grain adaptation period. However, the variance of this variation tended to be lower for the monensin treated steers than for the controls. During the finishing period, average daily ruminal pH was 5.59 and 5.73 for the controls and the steers receiving monensin, respectively. Hence, the use of monensin resulted in a small rise of ruminal pH. Area of ruminal pH below 5.6 were 216.1 and 98.18 pH units for the control and the monensin treatment, respectively. This indicates that monensin reduced the severity of subacute acidosis, and illustrates that area under pH 5.6 is a better indicator for this severity than average pH.

Despite the abundance of research on the control of acidosis in feedlot and beef cattle, the information on the use of monensin for the prevention of acidosis in high producing dairy cattle remains lacking. This is partly explained by the fact that until recently ionophores were not approved for use in dairy cows in most countries. Weiss and Amiet (1990) studied the effect of lasalocid, an ionophore used in beef production to increase feed efficiency, on ruminal VFA patterns in mid lactation dairy cows. Diets were 65 % forage (alfalfa and corn silage) and 35 % concentrate. Treatments included addition of 340 mg / d lasalocid to the diet for 98 d and a control. Lasalocid did not affect production of milk and of fat corrected milk and did not have a substantial effect on performance and rumen function. This does not mean that no effect of monensin should be expected in all dairy cows. Weiss and Amiet (1990) provided the ionophore to mid and late lactation diary cows. These cows will not have received diets with a very high concentrate to forage ratio, as their daily milk yield must have been declining, and their rumen will also have been adapted to high concentrate diets. The energy and protein requirements of transition cows are higher than those of mid lactation cows, hence the requirement for high level of concentrate in their diets. Despite of these high concentrate levels transition cows will experience negative energy and protein balances. The rumen of these cows will also not yet have been adapted to high concentrate diets. The high concentrate diets, negative energy and protein balances, and the lack of adaptation to high concentrate diets in transition cows, explain why acidosis is more common in these cows than in mid-lactation cows and why a larger effect of monensin in transition cows can be expected.

Green (1997) compared a Monensin controlled-release intraruminal capsule (CRC) with a placebo and monitored rumen pH of periparturient cows once weekly. Highest average rumen pH were observed prior to the administration of the CRC at 3 weeks before expected calving and were 7.1 both the control group and the group about to receive the monensin CRC. Lowest average rumen pH were found at one week post calving and were 6.7 and 6.5 in the CRC group and the control group, respectively. The monensin CRC significantly increased rumen pH (P < 0.03). This data does not indicate a large incidence in acidosis in perparturient cows. However, Green (1997) only measured rumen pH weekly through a stomach tube, as the objective of her experiment was to study ketosis and not acidosis. Rumen pH shows a large diurnal variation (Cooper and Klopfenstein, 1996), frequent rumen pH measurements and calculation of the area under the pH curve are essential to study and quantify acidosis. Hence, the data from Green (1987) might not be fully indicative for the incidence of acidosis in transition cows.

Monensin can increase the ruminal pH in cows receiving a high concentrate diet, but not fully prevent ruminal acidosis. This ionophore influences rumen pH by affecting lactic acid and total VFA concentrations. To monitor the effect of monensin on rumen pH, measurement of rumen pH need to be conducted several times daily. Area under the pH curve provide a better quantification of acidosis than pH.

Relative rates of VFA

The relative rates of rumen volatile fatty acid production have been consistently altered by the use of monensin in vitro (Chalupa et al., 1980; Richardson et al., 1976) and in vivo (Richardson et al., 1976; Prange et al., 1978; VanMaanen et al., 1978; Rogers and Davis, 1982; Armentano and Young, 1983). The characteristic changes in the ruminal volatile fatty acid profile as a result of monensin are an increase in the concentration of propionate and a decrease in the concentration of acetate and butyrate (Chen and Wolin, 1979; Bergen and Bates, 1984; Schelling, 1984; Sauer et al., 1989; Weiss and Amiet, 1990).

Selection of gram negative bacteria allows enhanced propionate production from succinate because these bacteria have fumarate reductase an enzyme which is necessary to convert fumerate to succinate (Bergen and Bates, 1984). In a study with steers, Harmon et al. (1988) observed an increase in the net portal flux of propionate with monensin treatment, and after monensin was removed, the net portal flux of propionate and acetate decreased.

Methanogenesis and fermentation efficiency

Chen and Wollin (1979) observed that the growth of Ruminicoccus albus, Ruminicoccus flavefaciensis, and Butyrovibrio fibrisolvens were inhibited by 2.5 m g of monensin per ml of medium. As these bacteria contribute to methane production in the rumen, it was concluded that monensin could contribute to the reduction of methane production.

Bergen and Bates (1984) assumed that the increase in propionate production due to the selection for gram negative bacteria caused by monensin is associated with a decrease in methane production, as fumerate reductase is also the point in fermentation that diverts reducing equivalents and carbon to propionic acid formation. Propionate production is a sink for H⁺ therefore they are unavailable to methanogen bacteria as a substrate for methanogenesis (Van Nevel and Demeyer, 1977; Bergen and Bates, 1984; Russell and Stobel, 1989).

Losses of methane from eructation can represent up to 12% of the feed energy (Russell and Strobel, 1989). Monensin has been found to decrease methane production up to 31% in vitro and in vivo (Schelling, 1984). Armentano and Young (1983) found the fermentation efficiency of monensin was 6.3% higher than control fed animals based upon heats of combustion and measurement of daily CO₂, methane and hexose production. Therefore, by decreasing methanogenesis and increasing propionate at the expense of acetate monensin can potentially improve the efficiency of digestible feed energy fermentation and utilisation (Richardson et al., 1976; Armentano and Young, 1983; Russell and Strobel, 1989). In a review by Goodrich et al. (1984), feedlot and pasture fed cattle improved the efficiency of feed utilisation by 7.5% and 13.5% respectively.

Nitrogen utilization and ammonia production

The effect of monensin upon nitrogen utilisation and ammonia production has been a subject of interest and speculation for researchers in the past (Bergen and Bates, 1984). Monensin has been found to decrease the ruminal ammonia concentration (Van Nevel and Demeyer, 1977; Poos et al., 1979; Haimoud et al., 1995) and decrease dietary protein degradation (Van Nevel and Demeyer, 1977). Furthermore, in vitro experiments determined that the decrease in rumen ammonia was responsible for the increase in the flow of amino nitrogen into the small intestine (Russell and Strobel, 1989; Yang and Russel, 1993). Russel et al. (1988) found gram positive bacteria, which are monensin sensitive, had a higher specific activity for ammonia production than monensin resistant gram negative bacteria. These gram positive bacteria contribute to ammonia production because they utilise peptides and amino acids as an energy source instead of carbohydrate (Russell et al., 1988; Yang and Russell, 1993). Wallace et al. (1990) found ionophore treatment doubled the peak concentration of free peptides in rumen fluid after feeding in sheep.

Systemic events and ketosis

Sauer et al. (1989) supplemented the diets of second lactation and older cows with 15 g or 30 g monensin / ton of DM for three weeks postpartum. Feed intake was lower in the low monensin group, than in the control group, however no significant differences in body weight changes and milk production were observed between the three experimental groups. The low Monensin group has a significantly lower milk fat percentage than the control and the high monensin group. Monensin did not affect milk protein and milk lactose concentration, and did not result in any other adverse effects. Supplementation with monensin reduced the incidence of subclinical ketosis, which was defined as blood ketone concentrations in excess of 9 mg/100 ml blood. During the experimental period 50% of the cows in the control group, but only 33% and 8% and the low and the high Monensin group, respectively, experienced subclinical acidosis. Sauer et al.(1989), therefore concluded that Monensin can be used as a therapeutic agent for the prevention of bovine ketosis without adverse effects for milk production.

The improved availability of propionate resulting from the administration of monensin is important for both gluconeogenesis but also for a potential role in the regulation of ketogenesis. Propionate is the predominant precursor of glucose production and can contribute up 46% of the glucose output by the liver in the lactating cow (Lomax and Baird, 1983). In Holstein steers, 25 to 32% of the total glucose production originated from propionate (Armentano and Young, 1983). In ketogenesis propionate may play an indirect role in regulation. Methylmalonyl CoA is a regulator of the enzyme carnitine acyltransferase I which is involved in the initiation of fatty acid entry into the mitochondria for oxidation (Baird, 1982; Lomax et al., 1983). In an experiment by Brindle et al. (1985) methylmalonyl CoA, an intermediate in propionate metabolism was found to inhibit carnitine acyltransferase I in sheep liver mitochondria (Brindle et al., 1985).

Studies with lactating dairy cattle have found decreases in the b -HBA concentration and higher glucose concentrations with monensin treated animals compared to controls (Sauer et al., 1989; Abe et al., 1994; Duffield et al., 1996). In prepartum dairy cattle, higher glucose concentrations and decreased b -HBA and free fatty acid concentrations were observed (Stephenson, et al., 1994). Information is limited on the effect of monensin on free fatty acid circulation in lactating dairy cows. Studies have not shown a significant effect of monensin on free fatty acid circulation (Sauer et al., 1989; Abe et al., 1994) however there are indications that mobilisation is decreased (Abe et al., 1994).

Green et al. (1996) and Green (1997) compared a monensin CRC placed intraruminally with a placebo in lactating Holstein cows. Capsules were administered three weeks prior to expected calving date. Cows were fed ad libitum for two weeks postpartum. Subsequently, during weeks three to five, postpartum animals were restricted to 90% of their ad libitum intake. Blood serum samples were collected twice weekly and were analysed, among others, for b -hydroxybutyrate (b -HBA) and glucose. b -HBA and glucose profiles are given in figures 1 and 2, respectively. The b -HBA and glucose concentration in the prepartum period was not different (P>0.05) between the treatments and the pattern of change for b -HBA and glucose concentration during the experiment was the same (P>0.05) for both treatments. However the mean b -HBA concentration for the six week postpartum period was lower (P<0.01) and the mean glucose concentration was higher (P<0.001) in the monensin treated cows than in the controls. The monensin treated cows maintained a b -HBA concentration below the 1.2 mmol/l threshold indicative for subclinical ketosis, during the first two weeks postpartum and in the final week of the experiment. During the restriction period the b -HBA concentration of the monensin cows was above the threshold however it was below 1.8 mmol/l which is in upper range for diagnosing subclinical ketosis in other experiments (Dohoo and Martin, 1984; deBoer et al., 1985; Mills et al., 1986; Nielen et al., 1994). The b -HBA concentration of placebo treated cows was above the threshold immediately postpartum and remained elevated throughout the experiment. In the last two weeks of the restriction period the b -HBA concentration was greater than 2.5 mmol/l and within the range for clinical ketosis. Monensin decreased, on average, the b -HBA concentration by 35.1% and increased glucose concentration by 14.8%. Therefore, monensin decreases the occurrence of subclinical ketosis.

Hayes et al. (1996) studies the effect of a intraruminal monensin CRC on reproductive performance and milk production of dairy cows fed on pasture in New Zealand. The authors assumed that monensin could improve milk production and fertility in their cattle, as their pasture had sufficient protein, but inadequate energy for high milk production. These cattle did not receive concentrate. The monensin CRC treated cows produced more milk fat, milk protein and litres of milk than controls, but reproductive performance was not affected.  

In summary, the net effect of monensin upon altering the rumen fermentation pattern is a decrease in circulating free fatty acids and ketone bodies while increasing glucose concentration.

Conclusions

Monensin affects bacteria populations in the rumen and selects for gram negative bacteria and inhibits growth of gram positive bacteria. As a result of this, monensin alters rumen fermentation, thereby increasing ruminal propionate, reducing ruminal methanogenesis, reducing the production of lactic acid, increasing rumen pH, and decreasing ruminal degradation of dietary protein. Monensin also reduces rumen ammonia, increases blood glucose, and decreases blood levels of ketone bodies. Hence, monensin has a therapeutic effect for the prevention of ketosis.

However, beneficial effects of monensin on milk production, milk fat, milk protein have so far not yet been demonstrated in the limited number of studies on the use of this ionophore in lactating dairy cows. The relative increase in propionate compared to other VFA, which was documented in beef cattle, also occurs in lactating dairy cattle. Hence, the beneficial effect of this increase reported in beef cattle can also be expected in dairy cattle.

Results from studies on the effect of monensin on milk production are inconclusive However, no negative effects of this ionophore on milk production have been reported. Also no other adverse effects of monensin for the lactating dairy cow were reported in the reviewed literature.

Research with beef cattle on high concentrate diets, and the limited research on the use of monensin in periparturient dairy cows has indicated a possible role for the prevention of ruminal acidosis in transition cows. Ruminal acidosis is a common problem in these cows, as they are abruptly changed from a roughage based diet to a concentrate based diet. As ruminal acidosis results in several averse effects on the cow’s health, this area merits further investigation. In such experiments rumen pH needs to be monitored several times daily, and contamination, e.g. with saliva, needs to be avoided. To quantify ruminal acidosis the area under the pH curve needs to be calculated.

Monensin has the potential to improve health and production of lactating dairy cows on high concentrate diets. More research on the effect of this ionophore on ruminal acidosis and milk production is required.

Acknowledgements

We wish to acknowledge the support provided by Drs P. Dick and R. Bagg form Elanco/Provel and the Ontario Ministry of Agriculture, Forestry and Rural Affairs (OMAFRA).

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