DEVON REX AND SPHYNX CATS

KIRLEE

Acknowledged to be the foundation cat in the Devon Rex breed.

Almost anyone interested in the Devon Rex will have read or heard about their origins.

It is thought that the gene responsible for the Devon's curly coat resulted from a spontaneous mutation in the domestic cat gene pool, but exactly when and where this occurred is unknown. The father of the Devon breed as we know it was an unnamed feral, curly-coated tom that lived around an abandoned tin mine near Buckfastleigh, Devon.  He mated with a straight-coated calico female who in 1960 produced a litter of kittens in the garden of cat lover Miss Beryl Cox and her friend Miss Margaret Croll. One of these kittens, a brownish-black male that Miss. Cox named Kirlee, had his father's short, curly coat.

At first, Kirlee was thought to be a Cornish Rex, another curly coated cat breed which had been discovered in Cornwall 10 years before.  Misses Cox and Croll heard about the Cornish Rex and eventually Kirlee was aquired by Brian Sterling-Webb who along with other breeders began a breeding programme for the breed, believing Kirlee to be a Cornish Rex.  However, after Kirlee mated with several different Cornish queens and produced only straight-coated offspring, it was concluded that the two breeds were unrelated. The name Devon Rex was adopted for the breed’s place of origin, and a breeding program was established. Test matings determined that the gene responsible for the curly coat was recessive. Breeders think that Kirlee’s parents must have been related, since a recessive gene must be inherited from both parents to manifest in offspring. To keep the breed healthy and expand the gene pool, Devon Rex cats have been outcrossed to several breeds including domestic shorthairs, Siamese and Persians.  However, in the United Kingdom, the Governing Council of the Cat Fancy now regulate the breeds which they consider to be approved outcrosses for the Devon Rex and include Abyssinian, Burmese, Korat, British and Asian Shorthairs.  Further details about the GCCF registration policy for Devon Rex can be found here.

Feline hypertrophic cardiomyopathy: (HCM) is by far the most common heart disease in cats. According to several studies, it is also the number one cause of spontaneous death in all indoor adult cats.

Just as rare as a superfit sports star who drops suddenly and dies on the field  – the same thing occurs in cats. Except, in cats, sudden death due to HCM is surprisingly common, and often the first – and only - symptom. In people HCM is generally diagnosed whereas in cats, the first time the owner may be aware of there being a problem, is a symptom that may be a clot.  The problem is that these stroke-like events continue and typically worsen. 

I often wonder whether our Sonny had HCM as he was affected on two occasions with stroke like events, the second causing him being put to sleep.  Unfortunately so far as I am aware, feline HCM was not particularly well known at the time of his death and we did not proceed with any diagnostic procedures after the first episode, nor was any further investigation recommeded by my Vet. 

The ramifications of this is that as this disease is a genetically inherited from an autosomal dominant gene which means that Sonny must have inherited it from one of his parents and will have passed the gene onto some of his progeny.  Luckily, not too many of his kittens went into breeding programmes, but some may have. 

HCM does not usually show until a cat is adult, meaning that affected cats can produce kittens before anyone is aware of the problems.  Fortunately is does not appear to be a disease which Devons suffer from in any large degree, but if you are interested in reading further go to this site.

Luxating Patellae: is found with a greater incidence in Devon Rex according to Dr. Susan Little, the well known President of The Winn Feline Foundation.  The kneecap slips out of the groove where is would normally sit and causes the cat pain and distress.  In some cats an operation is a viable option to deepen the groove.  This has to be carried out as early as possible to prevent tendons stretching and loosing their elasticity.  Many cats seem to deal quite well with this problem.

Inherited Myopathy (Spacticity): This dreadful disease, the bane for many years of the Devon Rex is a recessive inherited disease.  Look at this site for more information.  This gives several papers and links that provide detailed information about the disease. 

Briefly, it manifests itself in a variety of ways, the typical gait - stiff leg, the head flexed at a bizarre angle, protruding shoulder blades, megaesophagus which can cause inhalation of food into the lungs leading to pneumonia and a general air of fragility.  It can appear from the age of 3-23 weeks, by which time most kittens are in their new homes. 

This site leads to a video which shows affected cats and kittens, do be aware that although the cats and kittens are well cared for, this is quite distressing to watch.

Vitamin K dependent Coagulopathy: is exactly what it says it is.  A few Devons have been diagnosed with this disease which manifests itself usually only at the time of an operation when the cat will not stop bleeding.  A boost of Vitamin K usually rectifies this, as it can in humans who have problems with coagulation.  This link gives access to academic veterinary papers.

Neonatal Isoerythrolysis: Breeders and owners of Devon Rex and Devon Rex Variants are recommended to blood type test all their cats but more especially all breeding stock. Blood type A kittens resulting from a mating between a type A stud and a type B queen may die within the first few days of life if allowed to suckle their mother's colostrum. It is also important to know that cats with type B blood can die if given a transfusion of the common type A blood.

Anyone conducting a mating between a type B female and type A male has to be aware of the 16-24 hours recommended whereby any kittens resulting from this mating will require to be hand fed, either by gastric tube or syringe. 

A type B cat will produce powerful antiA antibodies  and these are found in high numbers in the colostrum of the mother.  These antibodies react to the surface proteins of the red blood cells, and destroy them; this process is called isoerythrolysis. This can cause acute anaemia, and usually produces noticeable signs of jaundice as the kittens’ immature livers struggle to clear them of the dead blood cells. The destruction of the oxygen-carrying red cells and the resulting anaemia may cause necrotic damage to the kittens’ vital internal organs, and/or necrosis of their extremities, such as the tips of ears or tails. Typically, affected kittens will pass characteristically dark brown or red-coloured urine, due to the excretion of the dead blood cells. In cases where isoerethrolysis is a risk or is suspected, the kitten may be stimulated to urinate onto a pad of white cotton wool or tissue to check for the characteristic discolouratioFailure to do so will result in the loss of those type A kittens absorbing the antibodies throught the gut wall into the bloodstream.  After 16-24 hours (depending on whose research you read) the antibodies cannot pass through the gut membrane and so the problem has passed and the kittens are able to suckle as normal.  For more information this site

http://www.winnfelinehealth.org/Pages/Feline_Blood_Types_and_NI_Web.pdf 

will help.