Abyssinian Standard (FIFe)and Abyssinian Diseases
Head Shape: Wedge shaped, of medium proportions, wide at the top; the contours are soft and graceful. Nose: Medium long. In profile the head shows a soft curve, with neither a stop nor a straight nose. Chin: Firm and well developed. Muzzle: Not sharply pointed. A shallow indentation forming the muzzle is desirable, but a pinch is a fault.
Ears Shape: Relatively large, broad at the base; slightly rounded, with a thumb print and tufts of hair at the tips are desirable. Placement: Set well apart and pricked.
Eyes Shape: Large, almond in shape and set well apart. Colour: Brilliant and expressive; amber, green or yellow; pure, clear and intense colour; outlined with the colour of the ticking.
Neck Graceful.
Tail Fairly long and tapering; broad at the base.
Body Structure: Medium built, medium long; firm, lithe and muscular, having a firm feeling. Coat Structure: Short, fine and close, lying flat. Colour: 2 or 3 bands of colour on each hair with dark tips for preference. For colour varieties refer to the following tables.
Remarks: White is tolerated on the chin and the nostrils.
Faults:
Head - Too deep stop. -Too much marking on the face.
Ears -Small or pointed ears.
Eyes - Round eyes. - Unclear eye colour. - Absence of outline around eyes.
Body - Cobby appearance.
Tail - Rings on tail.
Coat - Cold or sandy tone in colour. - Ghost markings or other tabby markings on the body and legs.
Faults precluding the certificate:
Head - Siamese type. -Round head.
Legs - Bars on all four legs.
Tail - Whip tail.
Coat - Grey or too dark or too light undercoat. -Too little or lack of ticking in parts of coat where desired. - Unbroken necklaces. -Markings on belly and chest. - White locket. - White extending onto the chest.
Scale of Points - Total - 100
Head - 15 - General shape, nose, jaws and teeth, forehead, placement and shape of the ears.
Eyes - 10 - Shape and colour.
Body - 20 - Shape, size, bone structure, height of the legs, shape of the paws, shape and length of tail.
Coat - 25 - Body colour.
15 Ticking.
10 Texture.
Condition - 5
Recognized Colour Varieties - Coat colour
Body colour: as described in the General Part, with darker ticking according to the corresponding colour varieties.
Ground colour: as described in the General Part. Underside of the body, chest and innersides of the legs uniformly coloured with the ground colour, harmonizing with the upper parts of the body, without any ticking, bars, necklaces or markings on stomach or belly. Darker shading along the spine. White or off-white is only permitted above the lips, beside the nostrils and down the chin as long as it does not extend to the chest. The tips of the ears are in the same colour as the ticking. The back of the hind feet is dark, hairtufts between the toes are in the same colour as the ticking. The colour of the tail is an extension of the darker shading along the spine and ends in a solid dark tip, coloured with the colour of the ticking, without any rings.
Remarks: All remarks and faults described in the General Part also apply.
Colour - EMS Code
Ruddy/Blue/Sorrel/Beige-fawn - ABY n/a/o/p
Ruddy/Blue/Sorrel/Beige-fawn silver - ABY n/a/o/p s
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Abyssinian Diseases are very few but we do have some like all breeds.
Genetic testing for Pyruvate Kinase Deficiency (PK) in Abessinian and Somali cat´s PK - The Disease
Pyruvate kinase (PK) is an enzyme critical to the anaerobic glycolytic pathway of energy production in the erythrocyte. If erythrocytes are deficient in PK they are unable to sustain normal cell metabolism and hence are destroyed prematurely. This deficiency manifests as a hemolytic anemia of variable severity with a strong regenerative response. In cats, PK deficiency has been described in Abyssinian and Somalis. The feline disease differs from the canine disease in that affected aby´s can have a normal life span, only intermittently have anemia, and do not seem to develop either osteosclerosis or liver failure. The clinical signs of disease reflect the anemic status of the animal and include exercise intolerance, weakness, heart murmur and splenomegaly.
PK - The Trait of Inheritance
PK is inherited as an autosomal recessive condition. Heterozygotes (carriers) do not have any clinical signs of disease and live normal lives. They are able to propagate mutations throughout the population however and it is therefore important that carrier animals are detected prior to breeding. PK deficiency can be detected, using molecular genetic testing techniques. These tests identify both affected and carrier animals. It is also possible to identify animals deficient in PK activity through enzyme analysis in those breeds where a molecular genetic test is not available.
PK - The Mutation-based Test and its Advantages
The genetic defect leading to the disease has been identified. By DNA testing the responsible mutation can be shown directly. This method provides a very high accuracy test and can be done at any age. It offers the possibility to distinguish not only between affected and clear cats, but also to identify clinically healthy carriers. This is essential information for controlling the disease in the breed as carriers are able to spread the disease in the population, but can not be identified by means of common laboratory diagnostic. If a particularly valuable animal turns out to be a carrier, it can be bred to a non-affected animal, and non-carrier kittens can be saved for the next round of breeding.
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About 1-2 years we also started doing the Genetic testing DNA for Progressive Retinal Atrophy (PRA). I think that today all serious Aby and Somali breeders are doing it to all their breeding cats.
Progressive retinal atrophy (PRA) is a hereditary disease of the eye that causes blindness. The retina is the tissue lining the back wall of the inside of the eye and is composed of two classes of photoreceptor cells called rods and cones; the rods function in dim light, and the cones in bright light. A PRA affected aby begins to have difficulty seeing in dim light, then gradually loses the ability to see in bright light, eventually becoming completely blind. As the vision fails, the pupils become increasingly dilated, and may take on a shiny or iridescent quality. When properly trained and managed most aby´s can adjust to blindness well.
PRA is a blanket term for many types of retinal diseases, all of which result in blindness. There are two groupings of PRA - early onset, and late onset. In early onset PRA poor vision in low light may be detectable shortly after birth, with total blindness occurring from 1 to 5 years. In late onset forms, night blindness occurs from 1 to 5 years, progressing to total blindness anytime after 3 years of age
PRA is diagnosed by ophthalmoscopic examination by a Veterinary Ophthalmologists.The pupils are dilated with eyedrops and the eyes examined. The exam takes less than five minutes and the cost is variable, depending on whether the exam is performed at a public eye clinic or through private practice or a teaching hospital.
If an eye exam diagnoses retinal changes potentially associated with PRA, a more sensitive test may be needed in order to confirm that the aby has PRA. The electroretinograph (ERG) measures the response of the rods and cones to specific colors of light. Some ophthalmologists will do the ERG procedure without anesthetizing the aby, but the rigorous demands for accuracy in the research program we are following dictate that the ERG be performed while the aby is anesthetized. When properly performed, an ERG provides the most definitive diagnosis, and is so sensitive that it can detect the presence of disease long before it can be seen by clinical examination.
PRA is hereditary and is always assumed to be an autosomal recessive trait until proven otherwise. (A recessive trait requires two copies of the defective gene. An affected aby must have two copies of the defective gene. A aby with only one copy of the gene is a carrier and will never have PRA, but will be able to pass that defective gene on to approximately half its offspring.
At the present time, the only way to determine if an aby is a carrier is if one of its parents is affected, or if one of its offspring is affected. Identifying carriers is imperative in order for breeders to make informed decisions and minimize the risk of producing PRA affected aby. To do this, all Abyssinians must have yearly eye exams, regardless of age or breeding status. PRA affected aby´s should be registered in the Aby & Somaliringens database. Silence in this case will increase the chances of producing aby´s with PRA.
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Early Neutering?
Early neutering is when you are neutering the cat before the age of 6 month.
The cats I have bred have so far never been neutered in a young age as less than 6 month.
But I’m not against it or afraid of doing it.
Being a breeder is not as easy as people may think. Instead of letting the new “Mummy” and “Daddy” taking care of the neutralisation, it could be easier to do it before the kitten leaving your home.
The kittens that are sold as pets do have breed restrictions or will be neutered before the leave
Here in Sweden it’s still a bit controversial to neuter the cats around 3-4 month. But as I’m a speaker of not using all cats for breeding and not using my males too much as young cats it seams to be much easier for everybody.
Some people may say that it could interfere with the breed stock or increase the cat’s gene pole but that is for me just rubbish.
To buy a kitten/cat for breeding means much more knowledge and demands on you as a buyer.
I can recommend reading Susan Little’s – The WINN Foundation one of the greatest Veterinarians in The Felines and about this issue.
http://www.winnfelinehealth.org/Pages/Early_Age_Altering_Web.pdf