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Ionophores are antimicrobial compounds which are routinely fed to ruminants to help feed efficiency. These antimicrobials specifically target the rumen bacterial population and alter the microbial ecology of the intestinal microbial consortium, resulting in increased carbon and nitrogen retention by the animal , increasing production efficiency

Monensin has been marketed for cattle as a methane inhibitor and propionate (the most efficiently utilized [gluconeogenic] VFA) enhancer.


Additional benefits of monensin usage include a reduction of dietary protein deamination, resulting in less ammonia urinary excretion, and a decrease in lactic acid production which results in a reduction in ruminal acidosis and liver abscesses.

Monensin and other ionophores benefits in sheep and cattle nutrition

-       Decrease of food consumption in addition to daily weight gain increase.

-       Improve in FCR

-       Light increase in quality features of the carcass.

-       Earlier maturation of the heifers(about 1 month).

-       Increase of propionic acid production and decrease of acetic acid in the rumen.

-       Probably save in consumption of ration protein(lower demand) or optimized consumption of it.

-       Decrease of methane production and improvement of fermentation process in the rumen.

-       Decrease of passing materials from rumen and decrease of decomposition-reconstruction of it's contents.

-       Increase digestibility of low quality forage.

-       Light increase in digestion of starch available in grain rich rations

-       Decrease of protein refraction inside the rumen and passing more organic compounds to digest in the intestine

-       Increase of protein stores and accumulation in calves that feed on low or mediate protein rations.

-       Significant control or decrease in severity and prevalence of coccidiosis especially with 30 gr ionophore per each ton of food.

-       Effects on gram positive bacteria(it is not effective on gram negatives)

-       Decrease in growth of streptococcus bovis and other lactate generating micro organisms of the rumen.

-       Relative regulation of food consumption in free feeding programs.

-       Decreases exceed amounts of hydrogen ion(saving energy).

-       Increasing cell membrane permeability to some ions

Responses to monensin consumption in improvement of growth

The use of antimicrobials as growth promotants in food animals has come under increased fire in recent years.

The best amount of monensin in the ration with 90% dry mater, 33 ppm. This amount of drug improves FCR approximately by 10.6%. this condition about cows with high roughage ration is present and food consumption does not increase, but increase in daily weight gain is about 14.7% and FCR improves relatively 15.3%. in pasture animals adding daily amounts of 200mg monensin to the ration is very beneficial in growth development.

Monensin toxicity

Monensin has some degree of activity on mammalian cells and thus toxicity is common. This is especially pronounced in horses, where monensin has an LD50 1/100th that of ruminants. Accidental poisoning of equines with monensin is a well-documented occurrence which has resulted in deaths.

In April 1984 a purebred sheep breeder in east central Saskatcewan encountered stiffness im a group of 100 lambs several days after stting the lambs on a new batch of 15% grower ration. Prior to the arrival ofthe newfeed, the lambs had been vaccinated for clostridial disease. The group, nsisng mainly of Suffolk and Hampshire breeds, was brought slowly onto the new ration. The previous creep ration was mixed with the grower rtion for four days. Then, only the grower ation was provided at a rate of 0.5 kg per head per day, along with hay and oats.

Monensin is safe and effective in target species, when used at recommended dosages. Ionophores have been used widely in the beef and poultry industry for improved feed efficiency and control of coccidiosis. However, intoxication may come after mixing errors that result in their inclusion in the diets of  nontarget species or in excessive concentrations in the diets of target species. The toxicity of monensin for cattle and other species is well documented and is known to be dose dependent. Due to their interference with membrane cation transport, polyether antibiotics can cause cell death by perturbing the intracellular ionic homeostasis and destabilizing biological membranes. Monensin toxicity is particularly evident in cardiac and skeletal muscle cells. There is no antidote or specific treatment for toxicoses induced by ionophores. Consistent lesions associated with monensin toxicosis in cattle are cardiac and skeletal muscle degeneration and necrosis, with secondary lesions from acute cardiac failure or chronic cardiovascular insufficiency. In Canada, the label warning prohibiting the use of monensin premix in lactating dairy cattle was removed in June 1996; since then, the use of monensin as an aid in the prevention of subclinical ketosis has become a common practice in lactating dairy cattle.

To our knowledge, this is the first report of monensin toxicosis in monensin-supplemented lactating dairy cattle and in lactating dairy cows in North America. In 1981, Wentink and Vente reported a case of monensin intoxication in dairy cattle where monensin had accidentally been added to the herd’s ration and there had been no previous exposure to lesser concentrations.

In cattle, the clinical signs of acute monensin toxicity are anorexia (24 to 36 h post ingestion), diarrhea, dullness, weakness, ataxia, dyspnea, prostration, and death within 3 to 14 d of the ingestion of the incriminated feed. The clinical signs seen in the outbreak described here started within 24 h of initial exposure to the monensin containing feed. Diarrhea, lethargy, and reduced feed intake of all the lactating cows were the most noticeable signs, which alerted the farmers that something was wrong. In this case, the rapid association of the clinical signs that the herd showed with the introduction of the new concentrate, followed by the prompt removal of the concentrate, may have allowed the farmer to avoid more severe consequences and losses. The monensin LD50 for cattle was estimated to range from 21.9 to 80 mg/kg BW, LD10 11.2 mg/kg BW, and the LD1 5.5 mg/kg BW.

It is apparent that, in cattle, a large safety range exists between the daily dose usually given and the single dose necessary to cause death. In this case, the average 600-kg dairy cow ingesting 3 kg of concentrate for a total of 3 feedings (24-h period) would have received a dose of 4.8 mg monensin/kg BW/d (2874 mg/head/d) and a total dose of 7.2 mg monensin/kg BW (4300 mg/head) in 36 h. This dose could have been sufficient to produce some deaths and was enough to produce evident clinical signs within 24 h of exposure and to decrease milk production. One possible explanation for this herd not presenting more severe symptoms is that it had been supplemented with monensin daily, prior to the toxic exposure and, therefore, that the rumen microflora had already adapted to the ionophore. Van Vleet et al found an apparent lack of enhancement of toxicosis in calves that were given 2 doses of 40 mg of monensin/kg BW at a 7-day interval, rather than 1 dose, indicating that the calves may have developed tolerance. Potter et al supported this observation and concluded that the greatest risk of intoxication occurs when cattle receive a feed containing monensin for the first time. Clinicopathologic changes induced by monensin are consistent with dehydration, electrolyte , and muscle damage. However, these changes have been shown to be dose dependent and nonspecific, with abnormalities reflecting generalized organ failure. Increased aspartate amino-transferase, creatine kinase, serum protein, blood urea nitrogen, creatinine, total bilirubin, urine protein, and decreased serum potassium, serum sodium, serum calcium and leukocytosis have been reported with monensin toxicosis. Cardiac troponin I has proven to be a highly specific and sensitive marker for myocardial cellular damage in many mammalian species. Blood concentrations of cTnI rise rapidly after cardiomyocyte damage, and the elevation persists for up to 8 d. Normal ranges for cTnI plasma concentrations have been established in horses, dogs, and cats, but not in cattle. In this case, the cTnI concentrations in the sampled cows were  0.1 ng/mL, compared with  0.1 and 0.9 ng/mL in 2 normal cows from the AVC herd used as controls. Because cTnI appears to be highly conserved among mammalian species and because the normal plasma cTnI concentration in peripheral blood of dogs, cats, and horses is similar to that of humans (0.0 to 0.4 ng/mL) , it is reasonable to assume that the human assay used for this report detected a human cTnI-like compound that was bovine cTnI and that the values obtained could be considered as

within normal limits. The near absence of clinicopathologic manifestations may have reflected the relatively low dosage of monensin received by the cows, the short duration of exposure, and the post exposure sampling


Intoxication treatment

As mentioned before, ionophores have low safe area and the metabolism and excretion of ionophores fails by using other drugs. So, the concentration of ionophores increases in tissues and the risk of toxicity increases. There is not any anti dote of monensin intoxication.

Feeding mineral oils at the primary hours of intoxication helps discharging of monensin residuals of GI system. IV injection of large amounts of isotonic liquids prevents dehydration and hypovolumic shock and kidney damages.



Impact of ionophores in Lactating and Dry Cow Rations

The improvement in feed efficiency shown in Table 1 reflects the shift in VFA (volatile fatty acid) production towards producing more propionic acid and reducing methane loss, improved nitrogen metabolism (less degradation of amino acids and peptides to ammonia), reduction of rumen bloat (cattle on pasture), and a decrease in lactic acidosis (shifting microbial population to reduce lactic acid accumulation). The increase in propionic acid results in higher blood glucose levels as the liver converts propionate to glucose. Decreases in ruminal production of acetic and butyric acids may also occur. Limited studies have shown that Holstein cows responded to Rumensin® more favorably than Jerseys.

In field studies using transition dairy cows, subclinical ketosis (when measured as 1200 to 2000 umol per liter of beta hydroxybutyric acid or BHBA), was reduced by 50% in 1010 cows from 25 commercial Canadian herds using a control release capsule (CRC) which provides 330 mg of Rumensin per day. In addition, the duration of subclinical ketosis and the incidence of displaced abomasums (DA) were reduced. Serum glucose levels in cows after calving receiving the CRC were increased 15%. Another Canadian study reported a 40% reduction in both clinical ketosis and DA’s. Retained placenta were numerically lower for cows fed Rumensin.

It was reported that body condition score (BCS) had an impact on milk production response. Cows classified as thin (BCS < 3.0) at three weeks before calving had no significant milk production response in the first 90 days after calving to Rumensin while cow’s classified with good BCS (3.25 to 3.75) had a significant increase in milk yield of 1.9 pounds or 0.85 kg, and heavy cows (> 4.0 BCS) increased milk by 2.6 pounds or 1.2 kg.

In a Dutch study, Rumensin reduced the rate of intra mammary infections (which was defined as above or below 250,000 somatic cells) by 13 percent (31 percent in control cows compared to 18 percent in supplemented cows). No changes were reported on the duration of intra mammary infections, lameness, cystic ovarian disease, or reproduction (days to first observed estrus and first service conception) when cows were fed Rumensin.


21 days prior to parturition, since the fetus growth is greatly high and because of milk production 21 days after parturition, the animal's need to glucose and energy, extremely increases. Drackley et al 2001, showed that during these 42 days, glucose consumption in Holstein cows increases from 1000- 1100 gr/day to 2500 gr/day.

In early breast-feeding, the amount of dry matter consumed by the mother is not adequate for production and maintenance and so the cow has negative balance of energy. To compensate this deficiency long chain fatty acids are broken down in adipose tissue and enter plasma and flow as NEFA in blood, then oxidize in the liver.

Changes in Milk Yield and Components

Research under pasture and confinement feeding systems has reported an average increase of 2.2 pounds (1.0 kg) of milk. Milk protein levels parallel milk volume increases while the milk protein percentage was constant. If a milk protein test response occurs, it could reflect improved amino acids available to the mammary gland to synthesize milk protein. Milk fat yield and percentage can vary when cows are fed Rumensin. Feed characteristics, type of oil, starch content, and/or NDF levels can lead to lower milk fat tests.

  • The amount of feed particles over 0.75 inch retained on the top screen on the Penn State Box can impact fat test due lower rumen pH. When Rumensin was supplemented to a low fiber ration, cows averaged 3.68% milk fat while cows fed Rumensin averaged 3.36%. Cows fed normal fiber diets however experienced smaller milk fat reductions compared to control cows 3.44 versus 3.60%
  • High levels of rumen fermentable starch can reduce rumen pH thereby leading to lower milk fat test with Rumensin due to excessive lactic acid and VFA production, less buffering from reduced saliva production, and changes in rumen turnover and passage rates.
  • Feeding unsaturated fatty acids can lead to excess formation of CLA or conjugated linoleic acids (trans-10, cis-12 C-18:2) when the rumen pH is low. Two conditions are needed for the production of trans-10, cis 12 CLA: an altered rumen fermentation and a source of polyunsaturated fatty acids.

For example, feeding soy oil lowered milk fat tests in combination with Rumensin further depressed fat test. In this study, cows fed the control diet produced 3.76% fat while cows fed control with Rumensin average 3.74%, however when soy oil was added to the control ration, fat test dropped to 3.14% fat, and the combination of soy oil and Rumensin resulted in cows producing milk with 2.43% fat. Feeding distillers grains (over 5 pounds of dry matter) has been shown to lower milk fat tests in combination with Rumensin in field observations. If dairy herds are at breed average or higher milk fat, no significant milk fat test drop occurred compared to herds that were 0.2 fat percentage point or more below breed average (for example, Holstein herds at or below 3.5% may experience lower milk fat tests).

Levels of Rumensin

The amount of Rumensin fed to lactating cows can vary from 11 to 22 grams per ton of TMR dry matter per day. Managers and nutritionists targeting the lower level of 11 grams per ton will add approximately 250 to 300 mg per cow per day for lactating cows. Following a step up program is legal for component fed herds. Allowing rumen fermentation to adjust to lower Rumensin levels can reduce the impact on milk fat tests. Because dry cows consume half of the dry matter of lactating cow, the higher level of 22 grams per ton is recommended which is approximately 250 to 275 mg/head/day. Another guideline is to add Rumensin at the rate of 0.3 milligrams per pound of body weight. For example, a 1000 pound Jersey cow would calculate to be 300 milligrams.

To calculate the amount of Rumensin fed, divide the level of Rumensin added to a ton of TMR dry matter (11 mg per ton for example) by two to get the milligrams per pound of TMR dry matter (for example, 11 g per ton / 2 equals 5.5 mg per pound of dry matter times 50 pounds of TMR equals 275 mg per cow per day). If excessive levels of Rumensin are accidentally fed, cows will go off feed in 24 hours, develop loose manure in 36 hours, and become sick in 48 hours.

Future Applications and Consideration

Dairy managers and consultants should considering strategic addition of Rumensin to dry cow and lactating cow rations. The impact of Rumensin on lowering lactic acid levels could reduce subacute rumen acidosis diminishing the need for direct fed microbial (DFM) products. The CRC used in Canada for dry and fresh cows that dispenses 330 mg for 90 days on a 24 hour/7 day basis is impressive for transition cows. Approximately 18 percent of Canadian dairy herds use CRC. Reducing methane production and increasing feed efficiency (less dry matter per pound of milk produced) will be environmentally important.




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