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alpha-Mannosidosis
While the potential for Murray Grey cattle to develop any bovine genetic abnormality, there is currently only 1 for which the American Murray Grey Association requires limited testing and a 2 for which some breeders are testing. The Alpha – Mannosidosis mutation was so pervasive in Australian Angus cattle, and by extension, derivative breeds during the 1960s, that the Murray Grey Beef Cattle Society implemented α – Manno testing across the breed. The American Murray Grey Association requires that all sires used in AI have a negative α – Mannosidosis test on file with the Association.
α-mannosidosis is a lethal disorder linked to a genetic condition affecting Angus, Murray Grey and Galloway cattle. There are two versions of the condition caused by two separate genetic mutations, one affects Angus and Australian Murray Greys; the other affects the Galloway breed. These two mutations cause the same disease and both affect the same gene. Affected calves express a number of symptoms including head tremors, uncoordination, aggression, nervousness and failure to thrive. Most calves die shortly after birth or within the first year and some are aborted during pregnancy.
Known α – Manno carrier bulls in the United States
Bimbadeen Westward Ho
Balmoral Elation
Cranbrook Lusty
Myostatin - Double-Muscling
Several Murray Grey breeders in the United States are testing for the myostatin mutation that causes double – muscling. While there have been very few actual double-muscled in the breed, there are carriers in the population and these breeders are being proactive in their testing.
According to an article on the American Shorthorn Association’s website,
“The double muscle condition arises from a genetic abnormality in the production of ‘myostatin’, which is a protein that acts on muscle cells' autocrine function to inhibit myogenesis: muscle cell growth and differentiation. It is encoded by the MSTN gene. An animal with the defective gene lacks the myostatin protein and hence muscle growth is unregulated.
The most obvious departure from normal in the phenotype of a double muscled animal is the enlargement of musculature, particularly in the rump and shoulder areas. There are however other traits which may or may not be significant, more particularly where the syndrome is fully expressed:
- Prominent creases between muscle groups
- Minimal fat cover and modified fat composition
- Shorter, thinner and less dense bones
- Delays in puberty, reduced fertility and reduced milk production
- Increased likelihood of dystocia
- Enlarged tongues in new born calves (Ed - making nursing difficult)
- Poorly developed genitals
- Increased susceptibility to respiratory disease probably due to increased demands on aerobic metabolic activity
- Increased meat tenderness and yield” 1
Known Myostatin carrier bulls in the United States
Cadella Park Minute Man
Thurloo Park Winchester
Cadella Park Jesse
Bundaleer X Road
Wallawong New Kid on the Block
Wallawong Vinnie Roe
Rockliffe Patron
Lochaber-Braes Diplomat
Member Reported Myostatin Reports
Contractural Arachnodactyly (CA) (“fawn calf syndrome”)
CA calves are normally born alive and most can walk, suckle and survive. The birth weight of CA calves is normal. The phenotype is subtle and hence CA may not initially be recognized as an inherited defect (Figures 1 and 2). Contractures which reduce the range of angular movement of the upper limb joints are present at birth in CA but are much less severe, without rigid joint contractures. Due to these contractures, CA calves at birth assume an abnormal crouched posture, resembling an elk or deer fawn, with the feet placed more to the rear that normal, hocks pulled up and back and the spine slightly arched. In their first days of life, CA calves are also flat down on their pasterns. Although there is a reduced range of movement ("contracture") in the upper limb joints, particularly the hip, stifle and hock, there is an increased extensibility of the lower limb joints, particularly the pasterns. CA affected calves are reported as taller and more slender, than their unaffected siblings.
Australian researchers assert that the inability to passively extend the hip, stifle and hock joints to the normal extent by pulling downwards on the foot of a newborn calf -- while it is held on its side on the ground -- is a valuable diagnostic sign in CA cases. Affected calves can show significant recovery and usually appear relatively normal by 4 to 6 months of age. As weanlings and yearlings, the CA calves appear lighter framed and lighter muscled, particularly in the hindquarters. Most perform poorly and remain tall, slender animals with poor foot conformation.
The more normal appearance of CA cases as mature adults makes early evaluation of the phenotype essential. Australian researchers have also reported the early onset of degenerative arthritis in cows that were CA-affected as calves, particularly in the stifle joints.
Contractural Arachnodactyly (CA) (“fawn calf syndrome”) carrier bulls in the US
The Glen Showboat (see AU database)
AMGA is consulting with these breeders to monitor their findings. There are currently no discussions regarding Association monitoring or mandating testing. |
