Now that the Canadian Food Inspection Agency (CFIA) has raised the safe rate for monensin to 48 parts per million per kilogram of dry matter from 33 ppm, Dr. Katie Wood wanted to know if the proven benefits to feeding monensin still held true at this higher rate.
Monensin is an ionophore that increases overall energy yield from feed, and improves animal performance. It does this by reducing gram-positive bacteria that favour fibre fermentation in the rumen, thereby increasing gram-negative bacteria that favour starch fermentation, and altering the volatile fatty-acid profile.
Gram-negative bacteria produce more propionate fatty acid, which is more energy dense than acetate, and reducing this acetate-propionate ratio is a known benefit to feeding monensin. Based on her work, Woods, a post-doctorate fellow at the University of Saskatchewan, says that benefit still holds true at the 48 mg/kg rate in barley-based finishing rations.
It fact it got better as the rate increased with the ratio dropping linearly from 1.9 without monensin, to 1.8, 1.4 and 1.3 as the monensin dose increased to 22, 33 and 48 mg/kg.
As expected with the increase in energy coming from the diet, dry-matter intake decreased from 10.0 kg/day without monensin to 9.9, to 9.3 and 9.1 as the monensin rate increased, and simple sugar digestibility increased progressively from 77.2 to 84.7, 88.0 and 94.0 per cent.
Small increases in average daily gain and feed-to-gain ratio were detected but were not statistically significant in this small-scale study that was designed to examine metabolic differences.
Rumen pH remained stable at the higher rates, and there was no effect on barrier function in the gastrointestinal tract, which is good news because disruptions in barrier function has implications for acidosis and liver abscesses.
Overall, Wood says, her work suggests the 48 mg/kg dose could be beneficial when bunk management is a challenge because it helps normalize feed intake without compromising performance.
On a seed stock operation five yearling bulls and five heifers suddenly dropped dead on May 10, four days after the animals in four pens went off feed. The attending vet performed necropsies on two and sent images as well as samples from the rumens, total mixed ration, and water for testing. Shortly after the two intact carcasses were delivered to the UCVM pathology lab.
Not knowing whether they were facing a disease outbreak, a nutritional deficiency or toxic poisoning the 150 bulls at this location were treated with antimicrobials and moved to pasture the next day as a stop-gap measure.
Some of the notable signs of distress, aside from being gaunt and dull, were severe breathing problems, extreme exercise intolerance and brisket edema.
The necropsy images and pathology exams found fluid retained in the intestines and some heart damage. Heart failure was the suspected cause of death and clues were starting to point to poisoning as the reason.
Fifteen more bulls and three more heifers died by May 14, after which a two-step treatment protocol was implemented. Animals that appeared sick were given 10 cc each of lasix (diuretic), dexamethasone (anti-inflammatory) and selenium/vitamin E, followed by a second treatment of lasix and dexamethasone a few days later.
Gray says the treatment seemed to help as noticeably sick animals that were treated were less likely to die than those that didn’t show signs and, therefore, went untreated.
A team from UCVM visited the ranch 12 days after the first deaths. Four heifers with clinical signs were examined and blood samples drawn to test for Troponin I, an enzyme that indicates acute heart damage in humans. Thanks to the close relationship between the veterinary school and medical college, Gray had picked up on the use of Troponin I that the UCVM faculty now uses for monitoring horses at the Calgary Stampede and asked if the test would be appropriate for this case.
Another post-mortem performed during that visit confirmed the pathology was consistent with a toxicological insult to the heart.
On June 5, blood samples were drawn from six animals that showed no clinical symptoms and samples of the liquid feed supplement were collected to test monensin level.
Lab reports indicated the four animals showing clinical signs did have elevated Troponin I levels, whereas those without clinical signs had only trace amounts of Troponin I in the blood. This finding, alongside the examinations of heart tissues, confirmed that the animals had died of heart failure.
Other test results for selenium/vitamin E in the blood, copper sulphate in the water, and the rumen contents were all normal. The toxicology report, however, showed monensin levels up to 2,200 ppm, 4.5 times what it should have been. The premix label indicated monensin should be fed in complete feeds at 22 ppm on a dry-matter basis.
Animals continued to die each day despite everyone’s best efforts, even though the feed supplement had been discontinued on May 6. The last bull died on May 27. One or two heifers continued to die each day until May 30. In all, 66 animals (11 per cent of those originally in the pens) died during this three-week nightmare.
A University of Saskatchewan researcher uncovered a real pellet puzzle during a recent small trial to see if a commercial binding agent could be used to improve byproduct pellets. Instead they found the pellets actually improved animal performance.
This was unexpected given that commercial binders have no nutritional value. Their purpose is solely to improve pellet durability, explains Dr. Katie Wood, a post-doctorate fellow at the university.
Unfortunately she found the binder didn’t improve the durability of either small or large pellets, yet the average daily gain on the heifers fed pellets with binder was 1.35 pounds compared to 1.00 pound for those fed pellets without binder.
The feed-to-gain ratio also improved when feeding binder pellets because total dry-matter intake (DMI) remained the same whether pellets included the binder or not.
Neither pellet size nor the binder made a difference to digestibility although gains were slightly better for the small-size binder-made pellets than large binder-made pellets.
The backgrounding ration for this trial was free-choice chopped grass hay and oat hulls with pellets fed individually at 0.09 per cent of body weight. Wheat screenings and wheat made up 59 per cent of the pellets, with another 36 per cent being pea screenings, oat hulls and canola screenings, along with small amounts of pea starch, molasses, salt and a mineral-vitamin mix, with and without commercial binders.
The trial involved eight heifers fitted with rumen cannulas to monitor pH and analyse rumen fluids.
Wood did note altered proportions of short-chain fatty acids (acetate, propionate, butyrate) in the rumen when pellets with the binder were fed. Short-chain fatty acids are the main products of fermentation and are rapidly absorbed into the bloodstream for energy.
This change in the rumen fermentation pattern is really the only clue that might explain the boost in performance, Wood says, adding that this is only speculation until further research answers the question.