In July, The British magazine "Cat World" published an unbalanced sensationalist article by British writer Roger Tabor against Munchkins and their derivative breeds. Tabor condemned them as "designer cats" and wrote that the public had been aghast when they first saw munchkins in his TV series and accompanying book about The Rise of the Cat (1991). He termed it "breeding to disadvantage an animal" and claimed that breeders were perpetuating a mutation for aesthetic reasons that would (or should) have been allowed to perish: "in recent times, some have been taken to produce novelty regardless of the cost to the cat". He added that non-threatening names were chosen for these short-legged mutants as part of a calculated marketing ploy and sincerely hoped that registries would not recognise some of the short-legged breeds.

Tabor quoted material for The Dwarf Cat Association website (without providing the website's name which would have allowed readers to visit it and make up their own mind) including their statement that intentional breeding or promotion of "physically limiting deformities" or health issues will not be accepted by the association. He claimed this was Orwellian doublespeak because the short-legged trait was a physically limiting deformity that prevented them climbing or moving like normal cats. Yet the wild Jaguarundi species of cat manages just fine with short legs and a long body as do non-feline predators with this body type (martens, polecats etc). Such mutations are part of ongoing evolution and may benefit the cat in its wild state by allowing them to exploit new ecological niches.

His article (polemic rather than balanced journalism) demonstrated an astounding degree of ignorance about the cats in question. This sort of statement not without precedent as Tabor's books had also given credence to the idea that the Golden Cat was an ancestor of the Siamese, that the Jungle Cat was an ancestor of the domestic cat (now ruled out by DNA studies) and perpetuated the myth of the tossable, ultra-docile, poor-pain-response Ragdoll (their pain response is completely normal). The designer cat article conveyed the opinion that short legged cats are cripples.

Nina Adkins responded with a letter regarding the Munchkin's very normal ability to jump and climb. While a short-legged cat might not jump as high as some of the long legged breeds, she pointed out that Mr Tabor's fish and chips would not be safe left unattended on a table! The short legged breeds are not hindered in running either and in games of chase with her other cats, the short-legged cats had the advantage of being able to run straight under furniture and turn corners much faster than her long legged cats. She also noted that far from always dying out, short legged feral cats exist to this day in Louisiana. It's worth noting that many mutations arise among free-breeding or feral cats - curled ears, rexed fur, bobbed tails - and that they can persist without human intervention and with no detriment to the cats.

The full text of my letter to the original misinformed article is reproduced below. Cat World published a greatly cut down version that omitted facts, background information and reasoning.

Dear Cat World

The mutation found in Munchkins is now thought to be pseudachondroplasia, which leaves head proportions unchanged, rather than achondroplasia.

Roger Tabor’s article conveniently ignored the fact that several generations of short-legged cats lived right here in the UK between the 2 World Wars, only dying out during wartime; a time during which many normal-statured cats also died and when some popular breeds went into serious decline.

Short-legged feral cats were recorded in England during the 1930s. In 1944, 4 generations of feral short-legged cats were documented in the Veterinary Record by Dr. H.E. Williams-Jones. He reported the case of an 8 1/2-year-old black female (described as having lived an extremely healthy life) who was normal in every way apart from her short legs. Her mother, grandmother and some of her own offspring were similar in appearance. The front limbs showed shortening, while the hind limbs were normal or less affected. Their gait was ferret-like. These cats were one of many established bloodlines that disappeared during World War II and the few surviving individuals had been neutered, losing the mutation altogether.

The Flatbush Mutation was another self-perpetuating Munchkin-type mutation; this time in the Vanderveer housing project in the neighbourhood of Flatbush (probably 1950s), Brooklyn, New York. A short-legged, short-tailed bicolour female cat appeared among the Flatbush stray population. More cats and kittens with this look appeared, spanning several generations of Flatbush cats. The mutation was eventually lost, but the short-legged cats did not need breeder intervention to perpetuate the mutation over several generations.

Short-legged cats have proven that they can survive and breed over multiple generations without human interference. This indicates a viable trait in cats and, in the right conditions, the potential for this highly successful predator to evolve and expand into further ecological niches, such as those occupied by the jaguarundi, marten or polecat. Sometimes abilities (such as jumping great heights) are traded off in the course of evolution. The fact a viable mutation has now been picked up and perpetuated by breeders suddenly makes it "bad".

In my opinion, Tabor's description of it being unable to move or jump like a "normal" cat is based on the erroneous idea that, having produced the "normal" domestic cat, evolution has ceased. Nature continues to produce new variations, some not viable (e.g. Twisty Kat) and others are viable in certain habitats (as with other short-legged, flexible bodied carnivores). Owners will tell you that Munchkins can jump, just not as high, and they are certainly not feline cripples as the article implied.

Despite the shorter legs, the unfamiliar Munchkin has fewer health problems than the more familiar Manx. Let's compare:

• Some Munchkins have been found to have a skeletal condition called thoracic lordosis, though this condition (affecting the back, chest, heart and lungs). This is uncommon in Munchkins and is not confined to short-legged cats. Widening the gene pool can reduce these problem. Early on, Munchkins were compared to short-legged dogs that had back problems; the feared problems did not arise due to the cat's more flexible spine. Small litter sizes indicate that 2 copies of the gene result in non-viable embryos absorbed at an early stage.
• In Manxes, spina bifida and pelvic problems are well documented; embryos inheriting 2 copies of the Manx gene having gross deformities and being resorbed or stillborn. Even those with 1 copy of the gene may have health and locomotory problems. (Robinson's Genetics For Cat Breeders; CFA president Richard H. Gebhardt).
• The Munchkin is not disabled by the short-legged trait and lordosis is rare but, in contrast, the serious nature of the Manx mutation has made that breed suitable for biomedical research into human spina bifida (Marc R. Raffe and Charles D. Knecht "Disorders of the Lumbosacral Plexus"; Michael S. Rand, DVM & Paula D. Johnson, DVM (various)) . However, I don't foresee Cat World publishing 2-page articles criticising the familiar home-grown Manx cat, perhaps because it would alienate subscribers, but a breed not bred in the UK provides a "safe" target and maybe an opportunity for a bit of "Yank-bashing" into the bargain.

The Munchkin article relies on our unfamiliarity with this more recent breed (even though the mutation is an old one) and an enduring British belief that all things out of the USA will be more extreme and less concerned with health than anything we sensible Britons would breed or build.

The Munchkin and many related breeds are recognised by The Dwarf Cat Association (TDCA) and some by TICA. The Bambino mentioned in the article duplicates the Minskin which has existed for much longer (http://www.minskin.com). I note that breed names, descriptions and quotes about "physically limiting deformities" in Tabor's article come straight from TDCA's website, but the TDCA is not credited (apart from a vague mention of "the association"). Out of courtesy, if nothing else, it should have cited its source even though it accuses the association of doublespeak. Its URL ( http://www.dwarf-cat.com/) wasn’t given; this would allow readers might investigate for themselves rather than accept someone else’s interpretation.

Tabor's article was, therefore, unbalanced and did not present full facts to Cat World readers. This obstructs readers in reading additional information to reach their own conclusions. Please, can we have some balance in such articles, not just one-sided pieces that selectively omit facts that an author evidently feels would compromise his argument? A conclusion based on selective information can never be sound. It is a tabloid newspaper tactic.

The short-legged mutation should also be considered in the light of really bad cases of breeding for deformity/disability or through morbid curiosity; for example the backyard breeding of Twisty Kats (radial hypoplasia) that were bred even though their forelegs lacked long bones.

As you have now opened the Pandora's Box on mutations affecting structure and function, perhaps it is high time to cover in depth the Recommendation by the Council of Europe's Convention for the Protection of Pet Animals already affecting cat breeders in Europe - a balanced piece please, not a tabloid-style article!

Footnotes:

"Disorders of the Lumbosacral Plexus", by Marc R. Raffe and Charles D. Knecht states "The Manx cat is bred for an absent or shortened tail, but additional deformities of the sacrum and spinal cord are common. Osseous deformities of the Manx cat are variable and range from spina bifida to sacrococcygeal dysgenesis."

In papers about the use of cats in biomedical research, Michael S. Rand, DVM & Paula D. Johnson, DVM (Assistant Veterinary Specialist- University Animal Care, University of Arizona, Tucson): "Spina Bifida: The spontaneous occurrence of this condition in the Manx cat has been offered by many investigators as a model through which to study the similar condition in humans. Detectable amounts of a-foetal protein in amniotic fluid have been reported in human pregnancies with neural tube defects. Similar detection has been verified in the Manx cat with neural tube anomalies. The clinical syndrome varies and can include megacolon, urinary incontinence with secondary predisposition to urinary infection, locomotor disorders, uterine inertia and chronic cystitis, along with the wide variety of bony anomalies. It appears to be an autosomal dominant trait with incomplete penetrance. The near absence of hydrocephalus and other CNS lesions in the cat model dims total homology, but this is the best known and most homologous model to date."