You have a phenomenal show heifer; she has an amazing set of EPDs and won grand champion every show she has gone to. You breed her to an equally impressive bull in hopes of having offspring that are just as good as she is. Little did you know that she was a carrier of a genetic defect, and the bull you used, he was a carrier of the same defect.
Now, let’s fast forward about nine months to when the cow is ready to have her calf. The calf that was supposed to be outstanding, was born dead because you as a breeder failed to know that they were carriers of genetic defects.
Genetic defects occur in all species, no matter how big or small. Some defects cause little to no harm, while others can be fatal. In beef cattle there are many different genetic defects, some of the fatal genetic defects include Tibial Hemimelia (TH), Pulmonary Hypoplasia with Anasarca (PHA), Curly Calf Syndrome (CCS) and Neuropathic Hydrocephalus (NH). There are also non-lethal genetic defects such as Fawn Calf Syndrome.
Pulmonary Hypoplasia with Anasarca (PHA) is a genetic defect documented mostly in the Shorthorn, Maine Anjou and Chianina breeds. This defect is a recessive trait and is always lethal in a homozygous state. Calves affected with this defect have an excess amount of fluid collected in the skin and body, which leads them to have an increased size and weight, and in most cases they have small, underdeveloped lungs. Because of the increased size and weight of the calf, the cow often suffers dystocia.
Tibial Hemimelia (TH) is a genetic defect primarily found in the Shorthorn breed, but is also found in Chianina, Maine Anjou, and Simmental. This defect is a recessive trait, and is always lethal in the homozygous state. Tibial Hemimelia is a defect of the tibia, a bone in the lower hind legs. Calves with this defect can be born alive but because they are unable to stand, walk and nurse, they do not survive. The number of carriers of Tibial Hemimelia are substantial, but there are DNA tests to reveal an animal’s status.
Curly Calf Syndrome (CCS) Is found primarily in Angus cattle. Calves affected with this defect are born dead. They have bent and twisted spines, rigid, sometimes hyperextended legs, and are small and thin, with little muscle development. Because of their phenotype, calving difficulties can occur.
Neuropathic Hydrocephalus (NH) is a defect primarily found in Angus cattle. Affected calves are born dead, weighing only 25-35 pounds. These calves also have enlarged skulls with the skull plates loosely organized. There is no recognizable brain tissue, but just fluid is present. There is also no spinal tissue present. Like the other genetic defects it is recessive and is always lethal in the homozygous state.
When both parents have the defective gene, there is a 25 percent chance the calf will be lethally affected, a 50 percent chance they will be carrier of the defect, and a 25 percent chance they will have both a normal phenotype and genotype. When a carrier is mated to a non-carrier, there is a 50 percent chance it will be a carrier, and a 50 percent chance it will have a normal genotype; there is a zero percent chance, however, that it will be lethally affected.
There are also non-lethal genetic defects, one of these being Fawn Calf Syndrome (FCS). Calves affected with Fawn Calf Syndrome have feet placed more to the rear than normal, hocks pulled up, and their back and spine is arched. They tend to have reduced range in movement in the hips, stifle and hock, and they have an increased extensibility of their lower limb joints. They tend to have a normal birth weight, but they are taller and more slender than calves that are not affected. Calves can slowly recover from Fawn Calf Syndrome, and can appear normal after four to six months, but tend to be lighter framed and muscled, and most remain tall and slender. Cows that were affected as calves often get an early onset of degenerative arthritis.
Genetic defects can be easily prevented just by simply not using sires that are carriers of the defected genes.
As a breeder, you are accountable for knowing what animals are carriers of genetic defects. This is rather easy because most breed associations have tested and documented the results of many sires. Thanks to technology, this information can be found in a simple Internet search. It is also important to know what you have in your own cow herd. DNA test can be performed very easily by testing the semen or by pulling hair samples.
If you have a calf that is born with a defect, make sure that you report it to your breed association. I believe that we as breeders should also start to discourage A.I. sire companies from selling seamen of carrier bulls. These defected animals often as a side effect are able to produce animals with desirable traits for club calf breeders, such as good hair coats. For a steer, having a defected gene is fine because it will have no chance of reproducing, but if you have a heifer, she now has a defective gene that could potentially cause difficulties in her future as a breeding animal.
Genetic defects are easily preventable, if you as a breeder have proper knowledge. The best thing you can do is know that the sire you are using is free of genetic defects, and that your cow is also free of genetic defects. Don’t lose profit because of something that could have easily been prevented.
Jessica Carlson is a freshman at Princeton High School and lives on her family’s cattle farm in rural Malden.