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Health |
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Page under translation/construction... All cats - unregarding of breed - have health issues, more or less. But the problem with pure breeding is that you have a limited number of cats to mix and that increases the risk of inheriteble diseases. Pure breeding is acctually a form of inbreeding, and that makes us people responsible for maintaining a healthy breed. I do not think that Maine Coons are any unhealthier than any other cats, not as I have experienced during my time working at an animalhospital. The Maine Coons I have met have been at the clinic for vaccinations, castration, id-marking and for HD X-ray. But one cat in particular I still remember. A very sweet black silver classic tabby girl, six months old. She did not get much older than that since she had a bad heartcondition, my first experience with hypertrophic cardiomyopathy - HCM. PawpedsMaine Coon-katten (swedish) Today we have a healthprogram for Maine Coons here in Sweden for breeders to follow before they use their cats in breeding. This healthprogram was put up by Maine Coon-katten (a Maine Coon club), starting by the healthprogram for hipdysplasia. This was later followed by a second healthprogram for HCM, the most common heartdisease in cats. Today we also have added the DNA-test published by Meurs et al. a few years back as well. Hipdysplasia - HD I know a lot of pet owners that are very familiar with HD X-ray on dogs and not many of them think this is strange or funny in any way. But when I say that I do the same with my cats which I use in breeding I get some funny looks. "Why would you do that?" is a sort of standard question and the following is "Do the Maine Coons have more problems with HD than other breeds, coz I've never heard anyone do that to other cats?". Well no, I do not think that the Maine Coon is much different from any other breed regarding bad or good hips. Why should this be a problem only connected to dogs and the Maine Coon? It's just that some cats within the breed do have such high gradings on their hips that they most likeley will be troubled by it, those are the cats we're trying to avoid for the future generations. HD is inherited as a polygene recessive trait. Recessive means that you need the affected gene from both your parents to get the trait, and polygene means that there are a number of those genes involved in the penetrance of this trait. This means that you can mate two healthy cats and still get a litter with very bad hips. My boy is a very good example of that. His parents, and a number of cats behind them are said to have good hips. Still my male has one hip ranked as 1 (the Swedish scale, not comparable to OFAs!!!) and the other one good. His sister from the same litter has 2 and 3, respectively, on her hips. Well, HD traits are tricky and you could mate two HD cats and still end up with a litter with good hips. So why bother testing in the first place some people say? Yes, why? Well, maby I prefer aiming at breeding healthy cats, who could live a life without any problems. That's why I test all my breeding cats for HD, eventhough the parents may be ok. I want my kittens to have the best possible start in life, and if that could be helped in the right direction by a simple x-ray - why not? The Swedish grading of hips is "Good", "Borderline", "1", "2" and "3", these grades are NOT comparable to the rankings in OFA. In order not to exclude too many cats from breeding, since that would affect the breeding population to much at this point, the mildest form of HD is allowed in breeding, that is cats with "Borderline" or "1" is ok, as long as you mate that cat with at cat that has "Good" hips, to limit the risk of getting affected kittens. |
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Approved for breeding
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Not approved for breeding
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Hypertrophic cardiomyopathy - HCM HCM is not only a disease that affects Maine Coons, it is a very common heart disease in all cats, not to mention humans. In humans it has been established that there are a number of mutations in a number of genes that gives rise to this disease. At this moment there has only been one publication about one mutation in one gene in the Maine Coon. This gene is MyBPC3 (myosinbinding protein C 3), and the mutation transforms an alanine into a proline at position 31 in the protein which this gene is coding for. In a related population of cats this mutation seemed to be dominant and all carriers of the mutation developed the disease at some point in life. Cats with homozygote alleles of this mutation (sets of two affected alleles - mutation inherited from both parents) were more prone to develop the disease at earlier age and with more severe symptoms compared to heterozygote (one affected allele of two possible - mutation inherited from one parent). But this was seen in the related population of that study and another picture may arise when you look at the breed all together. Of the cats tested within the Swedish health program 47% of the cats diagnosed with HCM by ultrasound were carriers of this mutation in some form by the end of March 2008. But since there are thirteen genes affected in humans with over 200 known mutations that cause HCM, there will probably be more genes affected in the Maine Coon which have HCM as an end result. 53% of the HCM diagnosed cats in the Swedish health program did not carry this mutation but still had the disease. A second mutation in Maine Coon is said to be the one transforming an alanine into a tyrosine at position 74 in the MyBPC3-protein. Tests for this mutation are available in Europe and America, but since there has been no publication about this mutation to this point, the Swedish health program has not included this mutation into the program so far. Without published scientific data about this mutation it is hard to determine its relevance to the breeding population and wether or not it should be included to the health program at this point. MyBPC3 is a protein that stabilises the sarcomere in heart cells. The sarcomeres are responsible for contraction and relaxation of the cells, thereby cruical for the hearts ability to pump blood. Knock-out mice without MyBPC3 has been shown to survive without this protein, so it is not crucial for the sarcomere assemblance, but the stability of the sarcomer is still affected. A heart that does not have a functional heart cell compensates this with a new cell. If this cell still does not function properly another cell emerge... In the end the wall of the heart has thickened so much it is visible on ultrasound. In some cases this thickening takes long time to develop, in some cases it only takes a few months, like the kitten I mentioned earlier. The Swedish health program recommends that the cats heart is checked by ultrasound by one of the veterinarians connected to the programme (these veterinarians are specialist in HCM diagnosis, not just familiar with ultrasound examination, and the result from one of them should not be different from another). The first examination is done by the age of one year, second at two, third at three and then every second year after that. It is also recommended to test the cat for the "Merus"-mutation, the one changing an alanine into a proline (A31P) before breeding. At this point "Kochs"-mutation (A74T) is not included into the health program, due to non-published scientific data about this gene (which make it difficult to determine its relevancy to HCM). A cat diagnosed with HCM is not used in breeding. Cats diagnosed equivocal are retested one year later before it is being used or removed from breeding programs. Positive cats for Meurs mutation is not directly removed from the breeding population, but it is recommended to seriously reconsider how good it is to keep that cat in a breeding program. |
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Genetic health - what is that? updating in process... |
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