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Blindness
Recently it has been found that blindness caused by the rdAc mutation is widespread among cat breeds and that Siameses and related breeds are the most affected by this disease. Read about the test at VGL at UC Davis
Fortunately there is a DNA test available for this autosomal recessive trait, which means that this problem is easily controlled in future litters, provided that the parents are tested and carriers are only mated to normal cats with respect to the mutation that gives PRA.
Ocicats have been found to be carriers already 2007 and there is published data of unrelated Ocicat carriers in the US and Europe (Menotti-Raymond et al, In Press; Narfstrom et al, 2009; Menotti-Raymond et al, 2007).
Any cat of any kind with double mutations will become blind with time. However, this do not mean that if a cat is tested and found normal it cannot become blind from other reasons. This is why it is prudent to submit a breeding cat to ophtamologic examination at least twice. Testing is done with blood or cheek swabs that can be ordered from Laboklin (Germany) or UC Davis. Results are ready within 10-30 days.
Menotti-Raymond, M., V. A. David, S. Pflueger, M. E. Roelke, J. Kehlera, S. J. O’Brien and K. Narfström (In Press). "Widespread retinal degenerative disease mutation (rdAc) discovered among a large number of popular cat breeds " The Veterinary Journal.
The recent discovery of a mutational variant in the CEP290 gene (CEP290: IVS50 + 9T>G), conferring recessive retinal degeneration in Abyssinian and Somali (long-haired Abyssinian) cats (rdAc) prompted a survey among 41 cat breeds (846 individuals) to assess the incidence, frequency and clinical consequence of rdAc. The rdAc allele displayed widespread distribution, observed in 16/43 (37%) breeds, exhibiting a high allele frequency (33%) in North American and European Siamese populations. Clinical evaluations demonstrated high concordance between rdAc pathology and the CEP290 (IVS50 + 9T>G) homozygous genotype (P = 1.1E−6), with clinical disease similar to affected Abyssinians/Somalis. This retinal degeneration has not been reported in breeds other than the Abyssinian/Somali and poses a significant health risk particularly in the Siamese breed group. Alertness of the veterinary community and the present availability of commercial diagnostic testing could synergistically enable breeders to reduce the incidence of rdAc blindness in pure-bred cat populations.
Narfstrom, K., V. David, O. Jarret, J. Beatty, V. Barrs, D. Wilkie, S. O'Brient and M. Menotti-Raymondt (2009). "Retinal degeneration in the Abyssinian and Somali cat (rdAc): correlation between genotype and phenotype and rdAc allele frequency in two continents." Vet. Ophthalmol. 12(5): 285-291.
Objective To characterize hereditary retinal degeneration in the Abyssinian cat (rdAc) in a recently established closed colony segregating for the rdAc mutation, and evaluate possible differences in the age of onset and progression of disease phenotype since the initial description of rdAc 25 years ago. The sample size of an earlier study was increased in order to det. the allele frequency in Abyssinian and Somali cats on a worldwide basis. Animals studied Twenty rdAc affected cats from the closed animal facility, 87 Abyssinian and Somali cats for study of genotype-phenotype concordance, and DNA from 131 Abyssinian and Somali cats from Scandinavia, the UK and Australia for evaluation of the rdAc allele frequency. Procedures DNA was extd. from blood and buccal swabs using com. available kits, followed by genotyping. Ophthalmic examns. were performed in the USA and Sweden by two board-certified veterinary ophthalmologists. Results A greater variation in the age of onset and progression of the disease was obsd. compared to that previously described. An excellent correlation between genotype and phenotype was obsd. A population genetic survey revealed that the rdAc allele is in moderate abundance in the Abyssinian breed in Europe and Australia. Surprisingly, homozygosity for the mutant allele was obsd. in a Siamese cat with ophthalmoscopic findings similar to those originally described for affected rdAc individuals. Conclusions Alertness to the potential of rdAc is needed on the part of the veterinary ophthalmol. community, not only in Abyssinian and Somali cats but possibly also in other related cat breeds. [on SciFinder (R)]
Menotti-Raymond, M., V. A. David, A. A. Schaffer, R. Stephens, D. Wells, R. Kumar-Singh, S. J. O'Brien and K. Narfstrom (2007). "Mutation in CEP290 discovered for cat model of human retinal degeneration." J. Hered. 98(3): 211-220.
A mutation in the CEP290 gene is reported in a cat pedigree segregating for autosomal recessive (AR) late-onset photoreceptor degeneration (rdAc). An initial screen of 39 candidate genes and genomic locations failed to detect linkage to cat rdAc. Linkage was ultimately established on cat B4 with 15 simple tandem repeat markers (logarithm of odds [LOD] range 4.83-15.53, Q = 0.0), in a region demonstrating conserved synteny to human chromosome 12, 84.9-90.63 Mb. The sequence of 10 genes with feline retinal expression was examd. in affected and unaffected individuals. A single-nucleotide polymorphism was characterized in intron 50 of CEP290 (IVS50+9T>G) that creates a strong canonical splice donor site, resulting in a 4-bp insertion and frameshift in the mRNA transcript, with subsequent introduction of a stop codon and premature truncation of the protein. A population genetic survey of 136 cats demonstrated that the rdAc mutation is in low frequency in Abyssinian populations (0.13, Sweden; 0.07, United States) and absent in breeds of non-Abyssinian heritage. Mutations in CEP290 have recently been shown to cause two human diseases, Joubert syndrome, a syndromic retinal degeneration, and Leber's congenital amaurosis, an AR early-onset retinal dystrophy. Human AR retinitis pigmentosa is among the most common causes of retinal degeneration and blindness, with no therapeutic intervention available. This identification of a large animal model for human retinal blindness offers considerable promise in developing gene-based therapies. [on SciFinder (R)]
Trost, K., L. Peiffer Robert, Jr. and B. Nell (2007). Goniodysgenesis associated with primary glaucoma in an adult European Short-haired cat. England: United Kingdom, Department for Small Animals and Horses, Clinic for Surgery and Ophthalmology, Veterinarplatz 1, 1210, Vienna, Austria.: 3-7.
A 9.5-year-old, male castrated European Short-haired (ESH) cat was presented with bilateral glaucoma associated with pectinate ligament dysplasia and an open iridocorneal angle (ICA) upon gonioscopy. The right eye (OD) was avisual and slightly enlarged; the left eye (OS) was still visual. Intraocular pressure (IOP) had been controlled with medical therapy over a 1.5 year-period in both eyes (OU). Eventually IOP could not be adequately controlled medically and the painful and blind right eye was enucleated and transscleral diode laser cyclophotocoagulation was performed twice in the left eye with less than optimal results and progressive loss of vision. Histopathology of the right eye showed goniodysgenesis characterized by failure of differentiation of the pectinate ligament, which existed as a solid sheet of uveal tissue at the entrance of a hypoplastic ciliary cleft, which contained loose mucoid mesenchymal tissue. The trabecular meshwork was hypoplastic and the scleral venous plexus could not be identified. Other findings of chronic glaucoma were inner retinal atrophy, optic nerve atrophy with disc cupping, scleral thinning, peripheral corneal vascularization and pigmentation, and mild focal iridal mononuclear inflammatory cell infiltrate. [on SciFinder (R)]
Rah, H. (2006). Development of novel feline model for inherited retinal degeneration: 140 pp.
Rah, H., J. Maggs David and A. Lyons Leslie (2006). "Lack of genetic association among coat colors, progressive retinal atrophy and polycystic kidney disease in Persian cats." J Feline Med Surg 8(5): 357-60.
An inherited form of progressive retinal atrophy (PRA) is recognized in Persian cats; however, the prevalence of PRA in the breed has not been determined. Breeders suggest that cats from only brown ('chocolate') or Himalayan ('pointed') lines are at risk for PRA, suggesting the disease is not widespread. This study was designed to evaluate whether PRA in Persian cats is associated with three coat colors, including chocolate, or with a highly prevalent inherited disease in this breed--polycystic kidney disease (PKD). Sixty related cats were evaluated for PRA by ophthalmic examination and genetically typed for PKD and the mutations that cause coat color variants in agouti, brown and color (producing the pointed coloration in Himalayan). No associations were identified among any of the traits, including between PRA and chocolate. These data suggest that PRA is not limited to cats with chocolate coat coloration and breeders and veterinarians should be aware that the prevalence of the disease may be higher than currently claimed. [on SciFinder (R)]
Rah, H., J. Maggs David, N. Blankenship Thomas, K. Narfstrom and A. Lyons Leslie (2005). "Early-onset, autosomal recessive, progressive retinal atrophy in Persian cats." Invest Ophthalmol Vis Sci 46(5): 1742-7.
PURPOSE: An early-onset retinal degenerative disease has been identified in Persian cats. This study genetically, clinically, and histologically characterized the disease. A breeding colony was established to assist with identification of the causative gene and to provide a resource for vision research. METHODS: Cats were produced from testcross breedings. Kittens underwent serial ophthalmic and neuro-ophthalmic examinations. Globes were harvested from age-matched affected, obligate carrier, and control cats and were evaluated by light microscopy. Fluorescein angiography assessed retinal and choroidal vasculature. RESULTS: Test breedings confirmed an autosomal recessive mode of inheritance. Rate and extent of disease progression were similar among individual affected cats. The earliest clinical signs (reduced pupillary light reflexes) were seen at 2 to 3 weeks of age. Retinal degeneration was virtually complete by 16 weeks of age. Histologic changes progressed rapidly and paralleled clinical findings. Histologic lesions were limited to the photoreceptors, outer plexiform layer, and retinal pigment epithelium in all but the terminal stages, when subtle changes were noted within the inner nuclear layer. CONCLUSIONS: Characterized in this study was an autosomal recessive, early-onset, retinal degenerative disease in Persian cats that is likely to be more prevalent in this breed than previously suspected. This feline disease model may identify a new gene or provide biological insight into some forms of early-onset retinitis pigmentosa (RP) in humans and genetic retinal degenerations in other species. A breeding colony that will assist in the identification of the causative gene has been established and is available for studies in vision research. [on SciFinder (R)]
Djajadiningrat-Laanen, S. C., M. M. A. R. Vaessen, F. C. Stades, M. H. Boeve and R. R. O. M. van de Sandt (2002). "Progressive retinal atrophy in Abyssinian and Somali cats in the Netherlands (1981-2001)." Tijdschr Diergeneeskd FIELD Full Journal Title:Tijdschrift voor diergeneeskunde 127(17): 508-14.
From 1981 to 2001, 248 Abyssinian and 127 Somali cats in the Netherlands were examined for hereditary eye disease. Distinct ophthalmoscopic signs consistent with hereditary progressive retinal atrophy (PRA) were observed in 11 Abyssinian cats, and subtle signs in 3 Abyssinian cats. A familial relationship was detected in 13 out of 14 of these cats, which supports a hereditary basis to the condition. Distinct funduscopic signs of retinal degeneration were observed at a median age of 4 years. One cat with advanced retinal degeneration was only 7 months old, whereas the remaining 10 cats were between 2 and 12 years old at the time of diagnosis. These differences in the age of onset are suggestive of at least two types of PRA occurring in Abyssinian cats in the Netherlands: a dysplastic, early-onset and a late-onset retinal degeneration. A large-scale and systematic examination programme for hereditary eye disease will be necessary to assess the incidence of PRA in the Dutch population of Abyssinian and Somali cats as a whole, and to provide a basis for a preventive breeding programme. [on SciFinder (R)]
Nilsson, S. F., O. Maepea, A. Alm and K. Narfstrom (2001). "Ocular blood flow and retinal metabolism in abyssinian cats with hereditary retinal degeneration." Invest Ophthalmol Vis Sci FIELD Full Journal Title:Investigative ophthalmology & visual science 42(5): 1038-44.
PURPOSE: To investigate if retinal blood flow decreases with progression of the disease in Abyssinian cats with progressive retinal atrophy (PRA), to examine if the choroidal blood flow was affected by the disease, and to determine the uptake of glucose and formation of lactate in the outer retina. METHODS: Local blood flow in different parts of the eye was determined with radioactive microspheres, in 9 normal cats and in 10 cats at different stages of PRA. Three blood flow determinations were made in each animal, during control conditions, after IV administration of indomethacin and after subsequent administration of N(omega)-nitro-L-arginine (L-NA). Blood samples from a choroidal vein and a femoral artery were collected to determine the retinal formation of lactate and uptake of glucose. RESULTS: In Abyssinian cats with PRA (n = 10), the retinal blood flow was significantly (P < or = 0.01) lower than in normal cats (n = 9) during control conditions, 6.4 +/- 1.7 compared with 14.1 +/- 1.9 g min(-1) x (100 g)(-1). The vascular resistance in the iris and ciliary body was significantly higher in the cats at a late stage of PRA, both compared with normal cats and to cats at an early stage of the disease, whereas the choroidal vascular resistance was not significantly affected. Indomethacin had no effect on ocular blood flows in normal cats, but in cats with PRA, iridal blood flow was more than doubled after indomethacin. The retinal formation of lactate was significantly (P < or = 0.001) lower in cats with PRA than in normal cats, 0.111 +/- 0.035 (n = 8) compared with 0.318 +/- 0.024 (n = 8) micromol x min(-1). The uptake of glucose was not significantly different in cats with PRA. CONCLUSIONS: Retinal blood flow is severely decreased in Abyssinian cats at a late stage of retinal degeneration, whereas the choroidal microcirculation is not significantly affected by the disease. At a late stage of retinal degeneration, vascular resistance in the iris is significantly increased, which at least in part could be caused by cyxlooxygenase products. [on SciFinder (R)]
Runte, M., G. Dekomien and J. T. Epplen (2000). "Evaluation of RDS/Peripherin and ROM1 as candidate genes in generalised progressive retinal atrophy and exclusion of digenic inheritance." Anim. Genet. FIELD Full Journal Title:Animal Genetics 31(3): 223-227.
Generalized progressive retinal atrophy (gPRA) is a heterogeneous group of hereditary diseases causing degeneration of the retina in dogs and cats. As a combination of mutations in the RDS/Peripherin and the ROM1 genes leads to the phenotype of retinitis pigmentosa in man we first performed mutation anal. to screen these genes for disease causing mutations followed by the investigation of a digenic inheritance in dogs. We cloned the RDS/Peripherin gene and investigated the RDS/Peripherin and ROM1 genes for disease causing mutations in 13 gPRA-affected dog breeds including healthy animals, obligate gPRA carriers and gPRA-affected dogs. We screened for mutations using single strand conformation polymorphism (SSCP) anal. Sequence anal. revealed several sequence variations. In the coding region of the RDS/Peripherin gene three nucleotide exchanges were identified (A277C; C316T; G1255A), one of which leads to an amino acid substitution (Ala339Thr). Various silent sequence variations were found in the coding region of the ROM1 gene (A536G, G1006A, T1018C, T1111C, C1150T, C1195T), as well as an amino acid substitution (G252T; Ala54Ser). By excluding the resp. gene as a cause for gPRA several sequence variations in the intronic regions were investigated. None of these sequence variations cosegregated with autosomal recessively (ar) transmitted gPRA in 11 breeds. The candidate gene RDS/Peripherin obviously does not harbor the crit. mutation causing the autosomal recessive form of gPRA because diseased individuals show heterozygous genotypes for sequence variations in the Miniature Poodle, Dachshund, Australian Cattle Dog, Cocker Spaniel, Chesapeake Bay Retriever, Entlebucher Sennenhund, Sloughi, Yorkshire Terrier, Tibet Mastiff, Tibet Terrier and Labrador Retriever breeds. In the following breeds the ROM1 gene was also excluded indirectly for gPRA: Miniature Poodle, Dachshund, Australian Cattle Dog, Sloughi, Collie, Tibet Terrier, Labrador Retriever and Saarloos/Wolfhound. Digenic inheritance for gPRA is practically excluded for both these genes in four breeds: Miniature Poodle, Dachshund, Labrador Retriever and Saarloos/Wolfhound. [on SciFinder (R)]
Van Veen, T., R. Cantera, K. Narfstroem, S. E. Nilsson, S. Sanyal, B. Wiggert and G. J. Chader (1989). "Postnatal development of photoreceptor proteins in mutant mice and Abyssinian cats with retinal degeneration." Prog. Clin. Biol. Res. FIELD Full Journal Title:Progress in Clinical and Biological Research 314(Inherited Environ. Induced Retinal Degener.): 275-89.
The development of opsin, transducin-a, and S-antigen in photoreceptor cells of mice homozygous or heterozygous for the rd or rds genes was similar to that in control mice during the 1st postnatal wk. While the abs. amts. of these proteins were low or decreased in the postnatal period, they persisted through the entire degeneration process. The major manifestation in the mutant retinae was a loss of polarity of the photoreceptor cells, without a loss in visual protein formation. In the Abyssinian cat model of progressive retinal atrophy, the development and cellular distribution of all proteins were similar in control and affected retinae until the beginning of stage 2 of the disease. At this point, the outer segments degenerated causing a loss of photoreceptors and of IRBP glycolipoproteins in the eyes. [on SciFinder (R)]
Curtis, R., K. C. Barnett and A. Leon (1987). "An early-onset retinal dystrophy with dominant inheritance in the Abyssinian cat. Clinical and pathological findings." Invest Ophthalmol Vis Sci FIELD Full Journal Title:Investigative ophthalmology & visual science 28(1): 131-9.
The clinical and pathological features of an early-onset autosomal dominant photoreceptor degeneration in the Abyssinian cat are described. Ophthalmoscopic evidence of retinal disease at 8-12 weeks of age was always preceded by marked dilatation of the pupils, impairment of the pupillary light reflex, and nystagmus. The electroretinogram was unrecordable in all but one of the affected individuals examined. Abnormal photoreceptor development was observed by both light and electron microscopy in retinas of a 22-day-old kitten; in this individual, no outer segment material was detected, and inner segments showed impaired development which was more severe towards the posterior pole. In a 40-day-old kitten, the inner segments were relatively well-formed, whereas the outer segments, though present, showed marked disorganization and degenerative change. The retinas of older individuals showed more advanced photoreceptor degeneration, with thinning of the neural retina. This early-onset retinopathy, which may be classified as a rod-cone dysplasia, is distinct from the hereditary retinal dystrophy (progressive retinal atrophy) previously described in this breed. The gene symbol Rdy has been adopted. [on SciFinder (R)]
Narfstrom, K. and S. E. Nilsson (1987). "Hereditary rod-cone degeneration in a strain of Abyssinian cats." Prog Clin Biol Res FIELD Full Journal Title:Progress in clinical and biological research 247: 349-68.
The retinal disease found in this strain of Abyssinian cats is a heritable disorder, primarily affecting the photoreceptors. The retina is, in most cases, ophthalmoscopically normal until the age of 1.5-2 years. The retinal changes that then appear are slowly progressive and lead to a generalized retinal atrophy in another 2-4 years. It is obvious that this cat retinal degeneration shows many similarities to human Retinitis Pigmentosa. Just as in RP the midperiphery/periphery is most severely affected at the earlier stages, and with progression of disease alterations become generalized, the central retina being the best preserved area until the very late stage. Rods are affected prior to cones, but later in the disease there is an involvement of both rods and cones. Also, the disease process is slow, starting off from an ophthalmoscopically normal appearing retina. This strain of Abyssinian cats, affected by the presently described retinal disease, therefore has the potential of becoming a new animal model in the study of hereditary visual cell disease processes. [on SciFinder (R)]
Narfstrom, K. and S. E. Nilsson (1986). "Progressive retinal atrophy in the Abyssinian cat. Electron microscopy." Invest Ophthalmol Vis Sci FIELD Full Journal Title:Investigative ophthalmology & visual science 27(11): 1569-76.
Seven adult Abyssinian cats at different stages of a recessively inherited retinal degenerative disease (progressive retinal atrophy) were studied ultrastructurally. At the stage of early disease, in 2-yr-old cats, disorganized and vesiculated discs were found in less than half of the rod outer segments in the periphery, while similar changes were seen in the central retina only infrequently or in patches. Cones appeared normal in all areas of the retina at the early stage. With progression of disease, the lesions were more advanced in all areas of the retina, and involved both rods and cones, with the most severe alterations found in the midperiphery. At the advanced stage, in a 6-yr-old cat, both rods and cones were lost, the inner nuclear layer thus being separated from the pigment epithelium by Muller cell processes and a few remaining outer plexiform processes only. Remnants of photoreceptor outer and inner segments, macrophages, and what appeared to be displaced photoreceptor cell nuclei could be found occasionally in the subretinal space, however. Clumps of pigment granules were often observed in the photoreceptor layer in the non-tapetal fundus. The pigment epithelium remained morphologically intact as a single layer of uninterrupted cells throughout the disease process, as did tapetal cells and choriocapillaris. There was no difference in the severity of disease between the peripheral tapetal and non-tapetal fundus. In the inner retina, only minor alterations were observed. These changes appeared at a later time than photoreceptor degeneration, and were considered secondary to the latter. [on SciFinder (R)]
Sarva, R. (1986). "Progressive retinal atrophy in the Abyssinian cat." Nord Vet Med FIELD Full Journal Title:Nordisk veterinaermedicin 38(6): 388-93.
Eight cases of hereditary progressive retinal atrophy in Abyssinian cats in Denmark are reported. Pedigree studies indicate direct lineage to affected cats of the same breed in Sweden. The disease is bilateral, progressive, and of the generalized type, and ultimately leads to blindness. [on SciFinder (R)]
Barnett, K. C. and R. Curtis (1985). "Autosomal dominant progressive retinal atrophy in Abyssinian cats." J Hered FIELD Full Journal Title:The Journal of heredity 76(3): 168-70.
Hereditary progressive retinal atrophy in Abyssinian cats in England is recorded. It is compared with another hereditary retinopathy in the same breed in Sweden and it is concluded that these are two distinct conditions, one occurring at an early age in kittens with an autosomal dominant mode of inheritance, the other occurring in young adult cats due to an autosomal recessive gene. The two diseases are bilateral, progressive, and of the generalized type, and are similar ophthalmoscopically. [on SciFinder (R)]
Narfstrom, K. (1985). "Progressive retinal atrophy in the Abyssinian cat. Clinical characteristics." Invest Ophthalmol Vis Sci FIELD Full Journal Title:Investigative ophthalmology & visual science 26(2): 193-200.
Ninety-four cases of a hereditary retinal degeneration in household Abyssinian cats were found in Sweden, mainly during a 3-year period. The disease was investigated by ophthalmoscopy, fluorescein angiography, electroretinography, and light microscopy. A bilateral retinopathy was usually first seen in affected cats at the age of 1.5-2 years. Fluorescein angiography did not demonstrate abnormalities of etiological significance to the disease process. A reduction mainly of a- and b-wave amplitudes in the ERG indicated a generalized photoreceptor disease. Light microscopy showed that the photoreceptor layer was primarily affected, while other retinal layers were mainly normal. The midperipheral and peripheral retina was affected more severely than the retina of the posterior pole until late stages of disease, when there was a generalized loss of photoreceptors. The clinical and laboratory findings suggest that PRA in these Abyssinian cats is a heritable photoreceptor degenerative disease with a fairly slow rate of progression. [on SciFinder (R)]
Narfstrom, K. and S. E. Nilsson (1985). "Hereditary retinal degeneration in the Abyssinian cat: correlation of ophthalmoscopic and electroretinographic findings." Doc Ophthalmol FIELD Full Journal Title:Documenta ophthalmologica. Advances in ophthalmology 60(2): 183-7.
Ophthalmoscopic and electroretinographic (ERG) findings were correlated in a group of Abyssinian cats affected by a slowly progressive and hereditary retinal degenerative disease. According to ophthalmoscopic findings the disease was divided into stages. At stage 1 and 2 retinal changes were minor; showing a gray discoloration most often in the peripheral and midperipheral tapetal fundus. At stage 3 discoloration was generalized and there was marked vascular attenuation. A generalized retinal atrophy was found at stage 4. ERG recordings showed an abnormally depressed stimulus response curve for the b-wave at stage 1 of disease when 30-Hz cone flicker responses were indistinguishable from normal. With progression of disease there was a successive decrease of a- and b-wave amplitudes before there was a significant reduction also of the c-wave amplitude (first seen at stage 3). The ERG was nonrecordable at stage 4. These findings suggest that the photoreceptors are affected primarily by the disease, before there is a functional involvement also of the pigment epithelium. The rod system seems to be affected early in the disease as compared with the cone system. A staging of the disease by ophthalmoscopy correlated more to the function of the rods than to that of the cones. [on SciFinder (R)]
Narfstrom, K. L., S. E. Nilsson and B. E. Andersson (1985). "Progressive retinal atrophy in the Abyssinian cat: studies of the DC-recorded electroretinogram and the standing potential of the eye." Br J Ophthalmol FIELD Full Journal Title:The British journal of ophthalmology 69(8): 618-23.
DC-recorded electroretinography (ERG) and direct recordings of the standing potential (SP) were performed on a group of normal cats and Abyssinian cats affected by a hereditary retinal degenerative disease with similarities to human retinitis pigmentosa. A significant reduction of a- and b-wave amplitudes was found at an early stage of disease at a time when there were no major alterations in the c-wave and SP. At later stages both the c-wave and the SP oscillations were significantly reduced or absent. These findings indicate a primary photo-receptor disorder. Threshold studies for the scotopic b-wave showed a loss of retinal sensitivity early in the disease at a time when 30 Hz flicker responses were normal, which could indicate an earlier involvement of the rods than of the cones. There were no major alterations in the timing of the ERG in the affected animals tested. [on SciFinder (R)]
Narfstrom, K. (1983). "Hereditary progressive retinal atrophy in the Abyssinian cat." J Hered FIELD Full Journal Title:The Journal of heredity 74(4): 273-6.
Progressive retinal atrophy (PRA), a hereditary eye disease leading to blindness, was found in the Abyssinian breed of cat. Sixty-eight cases of a bilateral generalized retinopathy, at different stages of the disease process, were seen in the breed during ophthalmoscopic examinations of cats throughout Sweden during a 2-year period. Forty-five percent of cats aged 2 years or older were affected in the examined group. The earliest case was diagnosed in a 16-month-old cat. At the age of 3-4 years a bilateral retinal atrophy was usually present in affected cats. Genetic analysis indicates that PRA in the Abyssinian cat is caused by an autosomal recessive gene. [on SciFinder (R)]
Narfstrom, L. K. and S. E. Nilsson (1983). "Progressive retinal atrophy in the Abyssinian cat: an update." Vet Rec FIELD Full Journal Title:The Veterinary record 112(22): 525-6.
[on SciFinder (R)]
Giuliano, E. A. and A. van der Woerdt "Feline retinal degeneration: clinical experience and new findings (1994-1997)." J Am Anim Hosp Assoc FIELD Full Journal Title:Journal of the American Animal Hospital Association FIELD Publication Date:1999 35(6): 511-4. FIELD Reference Number: FIELD Journal Code:0415027 FIELD Call Number:.
A retrospective case series of 26 cats with diffuse retinal degeneration is presented. The most common presenting complaints included bumping into objects, dilated pupils, and reluctance to jump. Ophthalmic examination findings were consistent with those reported in dogs with progressive retinal atrophy. Breed predilection of the Siamese cat was observed. Cats with primary retinal degeneration presented late in the clinical course of their disease, when vision loss was severe. Early symptoms such as night blindness and secondary ocular complications (i.e., cataract and retinal detachment), reported in dogs with progressive retinal degeneration, were not observed in this study. All cats showed excellent adaptive capabilities to blindness. [on SciFinder (R)] FIELD Check Tags:Female; Male
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