Sphynx cat

The Canadian Sphynx breed was started in 1966 in Toronto, Ontario when a hairless male kitten named Prune was born to a black and white domestic shorthair queen (Elizabeth).[3] The kitten was mated with his mother (called backcrossing), which produced one more naked kitten. Together with a few naked kittens found later, the cat Prune was the first attempt to create a hairless breed.

After purchasing these cats in 1966 and initially referring to them as "Moonstones" and "Canadian Hairless", Ridyadh Bawa, a science graduate of the University of Toronto, combined efforts with his mother Yania, a longtime Siamese breeder,[5] and Keese and Rita Tenhoves to develop a breed of cats which was subsequently renamed as Sphynx. The Bawas and the Tenhoves were the first individuals able to determine the autosomal recessive nature of the Sphynx gene for hairlessness while also being successful in transforming this knowledge into a successful breeding program with kittens which were eventually capable of reproducing.[6] The Tenhoves were initially able to obtain for the new breed provisional showing status through the Cat Fanciers' Association (CFA) but ultimately had the status revoked in 1971, when it was felt by the CFA Board that the breed had concerns over fertility.[5]

The first breeders had rather vague ideas about Sphynx genetics and faced a number of problems. The genetic pool was very limited and many kittens died. There was also a problem with many of the females suffering convulsions. In 1978, cat breeder Shirley Smith found three hairless kittens on the streets of her neighborhood. In 1983, she sent two of them to Dr. Hugo Hernandez in the Netherlands to breed the two kittens, named Punkie and Paloma, to a white Devon Rex named Curare van Jetrophin.[7] The resulting litter produced five kittens: two males from this litter (Q. Ramses and Q. Ra) were used, along with Punkie's half-sister, Paloma.[5]

The first noted naturally occurring foundation Sphynx originated as hairless stray barn cats in Wadena, Minnesota, at the farm of Milt and Ethelyn Pearson.[4] The Pearsons identified hairless kittens occurring in several litters of their domestic shorthair barn cats in the mid-1970s.[4] Two hairless female kittens born in 1975 and 1976, Epidermis and Dermis, were sold to Oregon breeder Kim Mueske, and became an important part of the Sphynx breeding program.[7][4] Also working with the Pearson line of cats was breeder Georgiana Gattenby of Brainerd, Minnesota, who outcrossed with Cornish Rex cats.[7]

In 2010, DNA analysis confirmed that Sphynx hairlessness was produced by a different allele of the same gene that produces the short curly hair of the Devon Rex (termed the "re" allele), with the Sphynx's allele being incompletely dominant over the Devon allele and both being recessive to the wild type.[8] The Sphynx's allele is termed "hr", for hairless. The only allowable outcross breeds in the CFA are now the American Shorthair and Domestic Shorthair. Other associations may vary, and the Russian Blue is a permitted outcross in the Governing Council of the Cat Fancy (GCCF).[9] In Europe, mainly the Devon Rex has been used for outcrosses.

The Sphynx's hairlessness is produced by a mutation in the same gene that produces the short curly coat of the Devon Rex.[8] Moreover, it was found that the curly coat of Selkirk Rex cats is also associated with this gene.[10]

The gene encodes keratin 71 (KRT71) and is responsible for the keratinization of the hair follicle. The Sphynx's mutation leads to a complete loss of function where the structure of the hair is damaged so that the hair can be formed but is easily dislodged. In the Devon Rex mutation, a residual activity of the protein still exists.[8] The Selkirk Rex allele (sadr) is dominant over the wild type gene, which is dominant over the Devon Rex allele (re) and the Sphynx (hr), which forms an allelic series of : KRT71SADRE > KRT71+ > KRT71re > KRT71hr.[10]

The breed does have instances of the genetic disorder hypertrophic cardiomyopathy (HCM). Other domestic cat breeds prone to HCM include Persian,[22] Ragdoll, Norwegian Forest cat, Siberian cats, British Shorthair and Maine Coon;[23] however, any domestic cat including mixed breeds can acquire HCM.[24] Studies are being undertaken to understand the links in breeding and the disorder.[25] Cats are screened for HCM disease with echocardiography (ultrasound of the heart), as well as with additional tests determined by the veterinarian cardiologist including electrocardiogram (EKG, ECG), chest radiographs (X-rays), and/or blood tests.[24]

The Sphynx cat has a high rate of heart disease, either as HCM or mitral valve dysplasia. In a 2012 study of 114 Sphynx cats, 34% were found to have an abnormal heart, with 16 cats having mitral valve dysplasia and 23 cats having HCM.[26] These prevalences were found in cats with an average age of 2.62 years. Males cats developed more severe disease than female cats and often developed it earlier, at an average age of 19 months for males and 29 months for females.[23] Since the prevalence of genetic heart disease is high in this breed, many breeders will recommend screening for HCM yearly.

As HCM progresses into an advanced stage, cats may experience congestive heart failure (CHF) or thromboembolism.[24]

Congenital myasthenic syndrome (CMS) previously referred to as muscular dystrophy, myopathy or spasticity, is a type of inherited neuromuscular disorder associated with alpha-dystroglycan deficiency, found in Sphynx and in Devon Rex cats as well as variants of these breeds, which can occur between the first 3 to 23 weeks of their life.[27][28][29] This condition has also been described, but is rarely seen.[30][28] Cats affected by CMS show generalized muscle weakness and fatigue, as well as ventroflexion of the head and neck, head bobbing, and scapulae protrusion.[27]