Osteochondrodysplasia in Scottish Fold Cats

Clinical Osteochondrodysplasia in Scottish Fold cats R MALIKa, GS ALLANa, CR HOWLETTb, DE THOMPSONc, G JAMESd, C McWHIRTERe and K KENDALLf Objective To better characterise the bone and joint problems which can develop in Scottish Fold cats. Design Retrospective study of cases seen in five veterinary clinics and radiographic survey of cats in a cattery. Results Six Scottish Fold cats (four castrated males, two spayed females) aged between 5 months and 6 years were presented for signs of skeletal disease including lameness, reluctance to jump, a stiff stilted gait, short misshapen distal limbs, swelling of plantar tarsometatarsal regions and short thick inflexible tails. A further four cases (one male, three females, 15 months to 11 years) were identified by radiographic screening of a cattery. A diagnosis of osteochondrodysplasia was based on characteristic radiological findings including irregularity in the size and shape of tarsal, carpal, metatarsal and metacarpal bones, phalanges and caudal vertebrae, narrowed joint spaces, and progressive new bone formation around joints of distal limbs with diffuse osteopenia of adjacent bone. A plantar exostosis caudal to the calca- neus was present in advanced cases. In all nine cases where pedigree information was available, affected cats allegedly originated from the mating of a Scottish Fold to a cat with normal ears. The severity and time of onset of phys- ical signs, and rate of progression and extent of radiographic abnormalities, varied from case to case. Limited histolog- ical observations suggested the underlying problem may be an osteochondrodysplasia, related to inadequate cartilage maturation. Clinical signs were ameliorated by administration of pentosan subcutaneously in two of three cats in which it was trialled, and one of these also benefited from an oral glycosaminoglycan preparation. Conclusions Clinical and radiological findings were ascribed to defective maturation and function of cartilage, partic- ularly in the distal limbs, ears and tail. As all Scottish Fold cats suffered from osteochondrodysplasia of some degree, the best solution would be to avoid using fold-eared cats for breeding and instead use Scottish shorthairs. Aust Vet J 1999;77:85-92 Key words: Cat, Scottish Fold, osteochondrodysplasia, osteodystrophy, chondrodysplasia, cartilage, autosomal dominant, lameness. Fold Scottish Fold PO Orally SFOCD Scottish Fold osteochondrodysplasia SC Subcutaneously he Scottish Fold is one of the Although fold-eared cats were first (prick, pert or upright) ears from this rarest purebred cats in Australia. bred in 1961 and registered in 1966, type of mating are known as ‘Scottish TThe defining feature of the breed there was no mention of any skeletal shorthairs’ in North America and is its ears, which fold forward (Figure 1). deformities until 1971 when progressive Australia (synonym: Scottish Fold S/E The ear fold is not present at birth but bony abnormalities and a crippling [straight ear], Scottish Fold variant; J develops at 3 to 4 weeks of age. The lameness were recognised.1,4 Inheritance Sternbeck personal communication). breed was developed in Scotland by studies were based on three different A limited description of SFOCD was mating a queen, affected by a natural types of matings: skeletally normal Folds given initially by Jackson,5 and more mutation, to local farm cats and British to skeletally normal Folds, affected Folds details for a single case were reported Shorthairs.1 Preliminary genetic analyses to skeletally normal Folds, and affected recently.6 The earliest and most consis- suggested that the defining genetic Folds to normal cats. Kittens with radio- tent finding is a tail with an abnormally abnormality, which causes the auricular logical lesions were only produced from thick and inflexible base. The feet are cartilage to fold, is inherited as a simple Fold-to-Fold matings.5 It was inferred short, and the underlying skeletal autosomal dominant trait, and the fold- that affected kittens are homozygous for changes result in reduced ability to ear allele is designated Fd.2,3 the Fd gene: thus normal cats are fdfd, support weight, an abnormal gait and skeletally normal Scottish Folds are ultimately lameness. In affected Fdfd, and Scottish Folds with osteodys- homozygous individuals, joint lesions aDepartment of Veterinary Clinical Sciences, The trophy are FdFd. It has been suggested progress until the cats are unable to University of Sydney, New South Wales 2006 bSchool of Pathology, The University of New that breeding of fold-eared cats should walk. Lesions are evident radiographi- 5 South Wales, Kensington, New South Wales 2052 be limited, and if used at all, they should cally in kittens aged 7 weeks. The meta- cKu-Ring-Gai Veterinary Hospital, 290 Bobbin be mated only to normal-eared cats.5 physes of metatarsal and metacarpal Head Road, Turramurra North, New South Wales The breed was banned in England in bones are distorted with widened 2074 dSylvania Veterinary Hospital, 335 Princes 1974, but continued to evolve in the physes, and similar but less marked Highway, Sylvania Heights, New South Wales USA where initial imports from the UK changes are evident in phalanges. This 2224 e were outcrossed to numerous other results in decreased length and abnormal Chatswood Veterinary Clinic, 80 Sydney Street, 1,4,5 Willoughby, New South Wales 2068 breeds. Fold-to-Fold matings were shape of these bones and shortening of fEast Chatswood Cat Clinic, 346 Penshurst Street, avoided, so only about 50% of offspring distal limbs. The caudal vertebrae are Willoughby, New South Wales 2068 had folded ears. Kittens with normal reduced in length, with widened Aust Vet J Vol 77, No 2, February 1999 85 Clinical endplates. After age 6 months, gross what small (1.3 kg) for her age (14 become arched and bilateral palpable plantar exostoses of tarsal and metatarsal weeks). It was presented for evaluation swellings of the tarsi became obvious to bones become clinically and radiograph- of left hindlimb lameness 5 weeks later, the owner. Radiographs demonstrated ically evident. Histologically, tissues weighing 1.8 kg. Lameness was thought changes consistent with SFOCD, and from affected kittens show defective to be worse in the mornings. The distal the cat was euthanased at its owners’ bone formation at growth plates, with hindlimbs were abnormally short and request. Necropsy was not permitted. disordered chondroblast proliferation misshapen, with excessively curved and irregular groups of cells arranged toenails. Radiographs of the distal Case 3 haphazardly. Physes are grossly extremities and tail at 21 weeks showed A 16-month-old male Fold (4.0 kg) expanded with deficient ossification, changes consistent with SFOCD, was presented for right forelimb lame- irregular mineralisation, defective including marked malformation of ness of 3 weeks duration. It had been remodelling and supernumerary centres metatarsal and metacarpal bones, considered normal when vaccinated at of ossification. phalanges and caudal vertebrae. The 14 weeks (1.8 kg), and castrated 6 weeks The original observations on SFOCD proximal tail was thickened and inflex- later. The affected paw was painful on were published in a journal not widely ible (Figure 2). No treatment was palpation. Radiographs under general available outside the UK. Subsequent prescribed and the kitten was spayed. anaesthesia demonstrated changes in the accounts paraphrase these observations, Radiographs at 6 and 11 months limbs consistent with SFOCD, but consider the problem as a chon- showed progression of skeletal abnor- including malformed metacarpal and drodysplasia.7 However, it was noted malities, with development of periartic- metatarsal bones and periarticular new that problems may occur later in life in ular new bone, narrowed joint spaces bone formation. The cat was treated some Folds, in which radiographic signs and apparent loss of bone density in with pentosan polysulphate (3 mg/kg are initially absent,1 and that heterozy- distal limbs. At this time the cat was said SC once weekly for 4 weeks), which gotes may develop skeletal disease that is to ‘seize up’ during play. Pentosan poly- produced some reduction in lameness. much milder than observed in homozy- sulphate (3 mg/kg SC every week for 4 The cat died after a traffic accident 1 gous Folds.4 weeks) was prescribed. According to the year later and was submitted for This article concerns six cats that owners, this reduced signs of dysfunction. necropsy. Tissues were collected for developed signs of SFOCD. At least five Current therapy is a complex glyco- histopathological examination. Inspec- of them were allegedly the progeny of saminoglycan preparation (Cartiflex, tion at necropsy showed foreshortening mating a Fold to a non-Fold. A radio- Pharmedica, 2 g PO daily for 30 days, of the distal limbs. graphic survey in a cattery suggested then 2 g twice weekly) that also appears that, contrary to contemporary wisdom, to reduce the cat’s discomfort. Case 4 this was likely a widespread problem in An 11-month-old male Fold was this breed. Case 2 presented for limping. The cat had been A 6-month-old castrated Fold was considered normal when vaccinated at Case reports presented for an abnormal gait which 18 weeks and castrated at 8 months. It Case 1 had become noticeable over the had been lame for several weeks, and A female Fold (Figure 1) brought in preceding 3 weeks. The cat’s movements appeared to avoid jumping from any for vaccination was considered some- had become stiff and stilted, its back had height. Hard, symmetrical, non-painful Figure 1. The cat in case 1. Note the forward-folding ears. Figure 2. The thickened, shortened, inflexible tail of the cat in case 86 Aust Vet J Vol 77, No 2, February 1999 Clinical swellings were palpable around hindclaws need regular trimming as they originated from the mating of a Fold to tarsometatarsal regions and similar but tend to grow abnormally. a cat with normal ears, this being a less prominent swellings were evident Scottish shorthair in seven instances, around carpometacarpal regions.

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