Congestive heart failure in feedlot cattle research
According to Brian Vander Ley and his colleagues at a recent bovine congestive heart failure workshop, congestive heart failure in feedlot cattle is increasingly recognized as an emerging condition in the western Great Plains of the U.S. and Canada.
Producers and veterinarians in the Panhandle of Nebraska began noticing these cases several years ago. Dale Grotelueschen, a University of Nebraska-Lincoln Extension veterinarian, who was previously stationed at the Panhandle Research and Extension Center in Scottsbluff, examined many of these cases and found that they did not seem to be caused by other common causes of congestive heart failure. These cattle had not been exposed to high altitude and did not have any of the infections that can also cause heart failure
“I think it was an issue for a long time, but efforts to understand it have really gained momentum in just the last few years,” he said.
When Vander Ley joined the UNL team, a strong effort was underway to address the potential genetic component of congestive heart failure. The effort began by collecting feedlot cases of congestive heart failure that were matched with healthy pen mates to test the hypothesis that EPAS 1, a gene previously associated with high-altitude heart failure, was associated with the condition seen in feedlot cattle.
If that didn’t turn out to be the case, Vander Ley said, the search for a genetic cause would continue with the same set of samples. This work began in 2017 with 102 case/control pairs. The team depended upon feedlot personnel to identify the affected animals, and he said they did so with unparalleled accuracy. Clinical signs of the disease include enlarged brisket, elbows pulled out, jugular pulses, jugular distension and fluid-filled, distended abdomens.
Once cases were identified, samples were taken from both the case and a healthy pen mate that displayed no signs of heart failure during the feeding period. The sampling phase of the project was completed in the spring of 2018. Vander Ley’s collaborators at the U.S. Meat Animal Research Center, ran tests to determine if EPAS 1 was also associated with the congestive heart failure observed in feedlot cattle. EPAS 1 was not associated with heart failure; consequently, efforts to find a genetic link are ongoing. The results of the study were to be presented in January by Mike Heaton at an international meeting, but that meeting was prevented by the government shutdown.
“The interpretation of the results from EPAS 1 genotyping indicate that EPAS 1 is not related to congestive heart failure seen in feedlot cattle,” Vander Ley said. “It’s too early to say conclusively that congestive heart failure in feedlot cattle is different than heart failure seen in cattle at high altitude, but the differences in genetic risk may indicate that the cause of the heart failure might be different.”
With EPAS 1 out of the way, the focus of the genetic research has shifted to identify other potential genetic causes. Whole genome sequencing technology is being used to search for genetic differences between cases and controls. While whole genome sequencing is a powerful, effective way to detect genetic causes of diseases like congestive heart failure, the process takes time. In the meanwhile, whole genome scanning using SNP chips is being used to take a “peek” into the problem.
“The good news is that we have some early indications that there is something that’s highly associated with these feedlot congestive heart failure cases, so that’s encouraging,” he said.
Vander Ley, an epidemiologist, is also interested in other risk factors associated with congestive heart failure in feedlot cattle. As he is relatively new to Nebraska, he had little experience with congestive heart failure prior to taking on his current role at UNL. He has spent a lot of time talking with people involved with cattle feeding and quickly discovered that people have strong impressions about why congestive heart failure is such a problem. Common themes from these conversations indicate that producers feel that most cattle die late in the feeding period and that industry emphasis on production characteristics may have resulted in cattle outgrowing their cardiac capacity.
“During our case/control collections, we noticed that a lot of the cases didn’t fit these impressions,” he said. “With some of those impressions in mind, we started going back in the data from some feedlots to find out if these impressions were correct. We are using existing health records to test these impressions.”
The project is still ongoing, but current results indicate that many impressions are not accurate. While many cases develop late, cases have developed throughout the feeding period.
“We have one case in our set that weighed about 600 pounds and developed heart failure on day one of the feeding period, so it’s not just a late-fed calf problem,” said Vander Ley.
Based on their data, he is working on the theory that a proportion of cattle are genetically predisposed to congestive heart failure and are pushed into clinical disease by environmental or management factors. Declining frequency of cases toward the end of the feeding period might indicate that there are not many potential cases left by the time cattle are finished. Ongoing efforts to identify genetic links will help test this theory.
“We’ve got two things to figure out and the genetic link will probably be the one we’ll get first,” he said. “That will help us figure out what the environmental or management risk factor is. It might be more than one thing, it could be stress, nutrition, rapid growth or something we don’t even suspect. It will be difficult to know until we can separate out which calves are a genetic risk from ones that aren’t.”
Vander Ley said the ideal outcome is the identification of the genetic cause that will allow cattlemen to breed it out of their cattle, much like they have other unwanted genetic traits.
The team is also working to develop tools and strategies to help cattle producers until the permanent solution is in place. The team is working to identify tests that can be used to quickly and easily diagnose congestive heart failure cases, and potentially even predict which calves may become cases. Recently the team had the opportunity to intensively monitor two animals with high pulmonary arterial pressures that were not yet clinical cases. These animals were moved from about 4,000 feet of elevation to about 2,000 feet of elevation to determine whether their pulmonary arterial pressures would decrease. After a six-week observation period, the animals were euthanized, and post mortem examinations were performed. While pulmonary arterial pressures did go down, post mortem examination showed severe heart damage was still present in both animals.
While research continues, it appears that genetics play a role and that other risk factors alone, aren’t sufficient to cause heart failure.
“We finish millions of cattle in this country that weigh 1,400 plus pounds that are technically obese that don’t have heart failure,” he said. “Those two things by themselves aren’t enough to cause heart failure so we’re confident that there is a genetic cause that has another risk factor superimposed on top of it to create the problem, but we don’t have the evidence just yet. We’re working on that.” ❖
— Gabel is an assistant editor and reporter for The Fence Post. She can be reached at firstname.lastname@example.org or (970) 392-4410.
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