Genetic predictions for brisket disease a priority

Left: A calf showing the more obvious signs of brisket disease; swollen neck and chest. The condition gets its common name from the swelling in and around the brisket as a result of excess liquid pooling in the area. Center: A beef heart showing the results of brisket disease. Increased PAP causes the heart to work harder to pump blood into the lungs where it can be oxygenated. This in turn results in an enlarging of the right side of the heart (displayed on the left side of the image) and a thickening of the heart’s walls. Right: Brisket edema (swelling caused by fluid retention in tissues) in a steer that died from brisket disease. Clear edema fluid oozes from the incision. The skin over the brisket pits when pressed with a finger.

Pulmonary hypertension (PH), which is commonly referred to as brisket disease, has been observed in cow-calf and stocker operations where cattle are being grazed at high elevation for over 100 years. In addition, during the last decade death loss has doubled in feedlot cattle, with much of the increased loss coming at the end of the feeding period when animals are close or ready to market. This represents a tremendous economic loss to cattle feeders. There is increasing evidence that this sudden death loss in feedlots is due in large part to PH.

Anecdotal evidence reveals that the industry is feeding more cattle that are straightbred from breeds—particularly Angus—originally developed to thrive at low elevation. These breeds have certain bloodlines known to be prone to having high pulmonary arterial pressure (PAP) and increased incidence of PH. This can result in the sudden death observed in these market-ready cattle. Fortunately, this is heritable, which means it can be impacted through selection.

Pulmonary arteries carry blood from the right heart chambers to the lungs for oxygenation. When PAP increases, the heart must work harder to get blood into the lungs. The increased heart work load associated with high PAP can result in PH in cattle.

Work done at Colorado State University (CSU) reports high PAP results in excessive heart contractions, stretching of the heart muscle, and increased size of the right side of the heart. This also results in decreased animal performance. When the heart chambers exceed capacity, the heart walls thicken, which can result in heart failure and death loss. Research has also demonstrated that PAP increases in all cattle when they are being finished in feedlots, making them more susceptible to PH

As the indicator trait for susceptibility to PH, PAP can be tested for by trained veterinarians. It is important to sort seedstock for the trait because the decreased performance and death loss from PH has become an increasing problem throughout the different segments of the industry, including the finishing phase in feedlots.

In addition, feedlot cattle with compromised lung function caused by things like bovine respiratory disease (BRD) are also prone to higher PAP and potential PH. Therefore, producing genetic predictions to objectively describe animal’s susceptibility to PH has become an industry priority.

Feedlot managers have taken advantage of cheap gains from relatively low grain prices by feeding cattle to a fatter body composition. Much of this gain at the end of the feeding phase disproportionally results in increased carcass growth as opposed to the relatively stable size of the organs. This means lung capacity becomes proportionally smaller in relationship to body weight, which results in increased PAP and the potential for PH.

An EPD (expected progeny difference) to predict differences in animals’ susceptibility to PH will be based on the indicator trait of PAP, as well as genomic markers. Private businesses like Leachman Cattle of Colorado are currently calculating PAP EPDs, and CSU has been working with the American Angus Association to explore a genetic prediction for that breed.

CSU has found the heritability of PAP measured at high elevation to be .34, which is higher than weaning weight and yearling weight. They have also found the heritability of PAP taken at moderate altitude to be .29 and highly correlated (.83) with measures at high elevation. This means objective genetic predictions can be successfully calculated and susceptibility to PH can be decreased through selection.

Research has also demonstrated that PAP is a complex trait influenced by large number of genes. This means genomically-enhanced EPDs will increase the accuracy of PAP genetic predictions, so identifying informative markers needs to be researched for incorporation into PAP EPDs.

If lung function is compromised from something like pneumonia, PAP will also be increased, as well as the incidence of PH. This is why genetic predictions for BRD is also being explored. Research has demonstrated that BRD susceptibility is heritable, so EPDs can be calculated, and the susceptibility to BRD decreased through selection.

With the industry increasingly using cattle that are straightbred Angus, as well as other breeds developed at low elevations, the calculation of a PAP EPD is becoming an increasing priority. With cattle being fed to a fatter body composition in yards at moderate elevation, sudden death loss is increasing in cattle near market ready. This costly loss must be addressed for the industry to remain profitable. Luckily, the trait is heritable and responds to selection. — Dr. Bob Hough, WLJ correspondent

Dr. Bob Hough is the retired executive vice president of the Red Angus Association of America and a freelance writer.

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