OK - am waiting for the 2nd heifer of the day to calve and thought it an appropriate time to add a tid bit about Fawn Calf Syndrome (that someone asked about earlier). I stumbled on to it when a friend from Canada (sho I owe an email to) sent me to the Advantage Cattle Board because there was a discussion about deformed calves. Turns out there are some very intelligent and erudite individuals on this board and there was a long discussion about FCS. This is a disorder being investigated in Australia (OZ) and apparently traces to American Angus genetics.
The original discussion named names but since all Angus names to me are Rito or Bando or Frito of here, there, or everywhere and number 45 or 76 or 100 (and since the only Angus I know are Northern Improvement and Grizz) I have no idea who is involved. The entire post was pulled but then put back on without the names of the "potential dirty doers".
The people in OZ have done breeding trials, examination of calves and CT scans on calves trying to come up with a concise and clear definition of the condition. It appears to be autosomal recessive. There have been cases (apparently) in Canada and US ...here is a description that I wrote for something else
Fawn calf syndrome (FCS)
FCS is a newly described genetic defect of Angus and Angus composite cattle. Scientists from the University of Sydney, the University of New England, and NSW Agriculture have recently been contacted by beef breeders to investigate a possible new inherited syndrome in cattle called “Fawn Calf Syndrome”. The investigation has included pedigree analysis, examination and computer tomography (CT scan) of affected calves, and breeding trials. All cases studied so far by these researchers have traced to US Angus imported into Australia.
The key feature of FCS is muscle contractures at birth. The muscle contractures result in restricted movement of the joints. Passive movement of the limbs is restricted, which is obvious in severe cases, but may require measurements with a goniometer to appreciate the subtle lack of movement in mild cases. Though the contractures in FCS calves improve with age, muscle development always remains poor. Severe cases may show bilaterally symmetrical “hollowing out” of particular muscles in the hindquarters that are severely contracted from birth.
The calves also are taller than expected and there is increased angulation in the stifle and hock joints. While the entire clinical spectrum of the disorder has not been fully elucidated, the phenotypic expression of is extremely variable. Affected calves have been described at birth as having a fawn like appearance, and typically have longer and straighter than normal hind limbs and poor muscle development. Some severely affected animals also exhibit curvature in the middle of the back (dorsal scoliosis). Most affected calves have been culled at an early age due to inability to stand to nurse or walk, ill thrift and poor muscle development. Others have gone on to be fattened for slaughter but may produce undesirable carcasses. Some may be used as lightly muscled replacement females with apparently normal fertility. It is currently believed that FCS is a genetic disorder, with a simple recessive mode of inheritance, and that abnormalities of the protein fibrillin may be responsible. It also appears that FCS shares many features with the human disorder congenital contractural arachnodactyly (CCA) and thus could prove to be a useful model for studying the human disorder, as well as understanding the molecular biology of the development of the musculo-skeletal system.
It is important to note here that FCS is an emerging new disease syndrome - even in Australia. Proper characterization of the full spectrum of abnormalities in the disease is ongoing and more cases are needed to refine the diagnostic criteria. A number of cases from different pedigrees with common progenitors on the topside and bottomside of the pedigrees are required to complete this work properly. If you think you have a Fawn Calf contact Bryce Schumann at the AAA and the AI company/distributor.
The original discussion named names but since all Angus names to me are Rito or Bando or Frito of here, there, or everywhere and number 45 or 76 or 100 (and since the only Angus I know are Northern Improvement and Grizz) I have no idea who is involved. The entire post was pulled but then put back on without the names of the "potential dirty doers".
The people in OZ have done breeding trials, examination of calves and CT scans on calves trying to come up with a concise and clear definition of the condition. It appears to be autosomal recessive. There have been cases (apparently) in Canada and US ...here is a description that I wrote for something else
Fawn calf syndrome (FCS)
FCS is a newly described genetic defect of Angus and Angus composite cattle. Scientists from the University of Sydney, the University of New England, and NSW Agriculture have recently been contacted by beef breeders to investigate a possible new inherited syndrome in cattle called “Fawn Calf Syndrome”. The investigation has included pedigree analysis, examination and computer tomography (CT scan) of affected calves, and breeding trials. All cases studied so far by these researchers have traced to US Angus imported into Australia.
The key feature of FCS is muscle contractures at birth. The muscle contractures result in restricted movement of the joints. Passive movement of the limbs is restricted, which is obvious in severe cases, but may require measurements with a goniometer to appreciate the subtle lack of movement in mild cases. Though the contractures in FCS calves improve with age, muscle development always remains poor. Severe cases may show bilaterally symmetrical “hollowing out” of particular muscles in the hindquarters that are severely contracted from birth.
The calves also are taller than expected and there is increased angulation in the stifle and hock joints. While the entire clinical spectrum of the disorder has not been fully elucidated, the phenotypic expression of is extremely variable. Affected calves have been described at birth as having a fawn like appearance, and typically have longer and straighter than normal hind limbs and poor muscle development. Some severely affected animals also exhibit curvature in the middle of the back (dorsal scoliosis). Most affected calves have been culled at an early age due to inability to stand to nurse or walk, ill thrift and poor muscle development. Others have gone on to be fattened for slaughter but may produce undesirable carcasses. Some may be used as lightly muscled replacement females with apparently normal fertility. It is currently believed that FCS is a genetic disorder, with a simple recessive mode of inheritance, and that abnormalities of the protein fibrillin may be responsible. It also appears that FCS shares many features with the human disorder congenital contractural arachnodactyly (CCA) and thus could prove to be a useful model for studying the human disorder, as well as understanding the molecular biology of the development of the musculo-skeletal system.
It is important to note here that FCS is an emerging new disease syndrome - even in Australia. Proper characterization of the full spectrum of abnormalities in the disease is ongoing and more cases are needed to refine the diagnostic criteria. A number of cases from different pedigrees with common progenitors on the topside and bottomside of the pedigrees are required to complete this work properly. If you think you have a Fawn Calf contact Bryce Schumann at the AAA and the AI company/distributor.
