FAWN CALF SYNDROME (FCS) and FRAME SCORE
Frame score is a relevant issue in any discussion of FCS - simply because FCS affected cattle have a higher frame score than their unaffected siblings.
At birth, FCS affected calves have longer than normal leg bones (the technical terms are “dolichostenomelia” and “arachnodactyly”), as demonstrated in Australia by measurements taken on radiographic images of the long bones in whole body CATScans of newborn FCS affected calves and their normal siblings. This greater than normal length of long bones in newborn FCS calves is maintained until maturity, as shown by more recent frame score measurements taken on the same animals now that they are mature adults.
It is quite possible that at some time in the past, selection for higher frame score was a significant factor in increasing the prevalence of the genetic mutation that causes this recessive genetic defect in the Angus breed. Although FCS calves that are severely affected at birth have a very undesirable phenotype as adults (tall and poorly muscled with weak foot and leg conformation), there is a bit of variation in the clinical severity between cases, as newborns and as adults. At least some of the calves with less severe signs of FCS at birth end up as adults that look reasonably normal to the untrained eye.
In my own small FCS research herd, it appears that the calves that were most severely affected at birth have become the tallest adults. Moreover, whilst the two tallest FCS animals are always “hard doers” that can be distinguished from their unaffected siblings at any time of year and would be very unattractive animals in any breeding program, the other two FCS cows are less severely affected and, when they are in fat condition, it can be difficult to distinguish them from their adult siblings that were normal at birth, unless they are standing side-by-side. These latter two FCS cows are however still a bit taller than their normal siblings and readily distinguished from them at the end of winter.
My conclusion from these observations is that at least some less severely affected FCS cases amongst a group of potential replacement heifers could appear to be acceptable as future breeders, particularly if selection is done at a time of year when all the heifers are in good body condition. With subcutaneous fat masking their poor muscling, a breeder seeking to increase frame score might even prefer some of the better looking FCS cases over the smaller normal heifers. Moreover, many less severely affected FCS cases may not be recognised at birth, even though clinical signs are always most pronounced at birth. In less severe cases, there is often a significant reduction in the severity of kyphosis (upwards arching of the spine) and joint laxity in the lower limbs within a few days of birth. Some FCS affected calves can appear relatively normal by 10 days of age, with no more than residual contractures in the hindlegs. Very few FCS cases are still “down on their pasterns” after the first 10 days. If these less severely affected FCS calves are not first observed until for a few days after birth they may not be classified as abnormal.
Until there is a test available to distinguish between non-carriers and heterozygous FCS carriers, there will also remain the possibility that the apparently normal heterozygous carriers are a little taller than their non-carriers siblings. If this is the case, selection for frame score in any population in which the mutation is present would likely result in an increasing prevalence of the FCS mutation in that population.
Frame score is a relevant consideration in FCS and vice versa.
It is true that FCS is a less severe defect in the individual newborn calf than a defect such as AM or NH. However, this does not mean that FCS is less important. The more insidious nature of FCS has probably allowed the mutation to become much more widespread in the Angus breed than other mutations that cause lethal defects.
The FCS phenotype is not just “different” or just “framier”. The FCS phenotype is commercially quite undesirable. In addition to the increased calf mortality under commercial field conditions, from weak calves that cannot get up and suckle quickly after birth, the persistent loose-jointedness in adult FCS cows predisposes them to the premature onset of degenerative arthritis and resulting early culling. Some FCS cases have had very severe osteoarthritis by six years of age.
Although the issue of unacceptable meat quality (lack of tenderness, not necessarily poor taste) is based on anecdotal reports and hence is speculative at this stage, this issue is something that requires investigation given that the basic biochemical defect in FCS appears to be in the connective tissue surrounding individual muscle cells. Some change in biomechanical properties of the meat would not be entirely unexpected in a syndrome like FCS where there appears to be a defect in the elasticity of muscle tissue at birth.
Although FCS may be a relatively “mild” phenotype defect and many FCS cases can survive to maturity and breed successfully, no sensible Angus breeder would want the FCS phenotype to become so common in the Angus breed that it was perceived as a normal Angus “type” by the wider cattle industry. These are not the type of cattle we want to breed, but they may become the cattle we do breed if some action in not taken.
The sooner we have a test available to clean up the FCS affected bloodlines the better.