Progressive retinal atrophy in Abyssinian and Somali cats in the Netherlands (1981-2001)

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.     

Familial non-rcd1 generalised retinal degeneration in Irish setters

Four Irish setters were diagnosed with bilateral retinal degeneration and cataracts at an age ranging from six to 11 years. In three of these dogs, progressive night blindness was reported from an age of eight to 11 years. In the fourth dog, aged six, no signs of visual impairment had been noticed. In all four dogs, the rod-cone dysplasia type 1 (rcd1) mutation was excluded as a cause, using an allele-specific PCR. From their three-generation pedigrees, a familial relationship was detected in three out of four dogs, which were also related to four additional Irish setter dogs with a history and clinical signs suggestive of late-onset progressive retinal degeneration. These results suggest the existence of a possibly hereditary, late-onset, progressive retinal atrophy in the Irish setter breed, that is distinct from rcd1.     

Control of inherited retinal degeneration in dogs and cats in the United Kingdom

The term progressive retinal atrophy (PRA) is synonymous with inherited blindness in both dogs and cats as the result of retinal degeneration. In fact several types of degeneration occur within this complex, but the ophthalmoscopic features are well recognised and practical disease control is possible through routine examination. However, effective measures demand the whole-hearted support of the breeds involved, and only extensively applied examination schemes in which there is a central pooling and use of results are likely to produce the degree of disease control necessary, Test-mating and electrorelinograph (ERG) examination also have a part to play in the identification of normal genotypes, but the application of routine ophthalmoscopic examination, perhaps associates with Kennel Club registration, currently offers the most effective way forward.     

Retinal degeneration in nine Swedish Jämthund dogs

The Jämthund is the fourth most common breed in Sweden with approximately 1600 pups registered each year. Although it has been known that some adult dogs go blind, so they cannot hunt, the Jämthund dog has historically not been screened for hereditary eye diseases. This report describes nine Swedish Jämthund dogs with retinal degeneration. These dogs represent all Jämthund dogs diagnosed with progressive retinal atrophy (PRA) by the Swedish Eye Panel and registered with the Swedish Kennel Club from January 1998 to September 2008. The dogs were examined with indirect opthalmoscopy and slitlamp biomicroscopy. Additionally, electroretinograms (ERGs) following ECVO guidelines were performed in two dogs (one affected and one normal) and the eyes from three affected dogs were examined by light‐microscopy postmortem. Typical findings were bilateral symmetric generalized retinal degeneration with tapetal hyper‐reflectivity, attenuation of blood vessels and pigment clumping in the nontapetal fundus. These retinal findings progressed with time in two dogs after re‐examination. Visual impairment, especially under dim light conditions, was observed in the affected dogs. ERG from one affected dog showed profoundly reduced rod responses, whereas cone responses were better preserved. Microscopic changes in the eyes from three dogs were characterized by a severe diffuse predominantly outer retinal degeneration and atrophy. Re‐sequencing of the prcd‐gene for eight of the nine investigated dogs revealed that none of the individuals carried disease allele that has been associated with prcd‐PRA in other breeds. In conclusion, ophthalmoscopic, electroretinographic, and light‐microscopic alterations observed in nine Jämthund dogs were compatible with PRA. The prcd mutation was excluded as a cause of this retinopathy.     

Effects of hereditary retinal degeneration due to a CEP290 mutation on the feline pupillary light reflex

Objective To understand how progressive rod cone degeneration due to a mutation in CEP290 affects the pupillary light reflex (PLR) in domestic cats. Animals studied Domestic cats identified as either normal wildtype (WT; n = 6), or homozygous for the rdAc mutation in CEP290 and having early stage retinal degeneration (stage 2, S2; n = 4), or advanced retinal degeneration (S4; n = 6). Methods The effect of light on pupil size was measured over a series of 10‐s pulses of white and chromatic light in cats lightly sedated with medetomidine. Results In WT cats, the PLR was characterized by a pronounced initial constriction that rapidly re‐dilated during the stimulus (pupil escape), to a stable or sustained constriction. There was then a marked constriction at stimulus offset. Each component of the PLR was retained in affected cats, but with progressively reduced irradiance sensitivity from early to advanced retinal disease. Conclusions The PLR of cats had multiple phases, with a remarkably high‐amplitude ‘paradoxical’ off‐constriction even in the absence of retinal disease. In rdAc cats, reduced irradiance sensitivity was consistent with progressive loss of rod and cone function. Based on previously characterized retinal pathology, this suggests the visual streak of the retina has a proportionally large contribution to PLR input. These findings support the hypothesis that the efficacy of planned therapeutic trials can be determined by careful evaluation of the PLR in cats.     

Fluoroquinolone-induced retinal degeneration in cats

Although the exact mechanism of fluoroquinolone-induced retinal degeneration in cats remains to be elucidated, it appears from the literature that a similar retinal degeneration can be reproduced from either direct intravitreal injection of high concentrations of drug or exposure to UVA light and drug in laboratory animals. (19,25) The fluoroquinolone molecular structure is also similar structurally to other drugs that are known to directly induce retinal degeneration, including the cinchona alkaloids and halogenated hydroquinolones. Experimental evidence suggests that both the parent compound and its breakdown products via metabolism and photodegradation are active inducers of retinal degeneration. (18,25) Development of toxicoses also appears to be dependent on the maximum concentration of active drug, metabolite, or both reaching the retina over time. (18) Evaluation of the literature suggests that risk factors predisposing cats to fluoroquinolone-induced retinal degeneration may include the following: 1) large doses or plasma concentrations of drug, 2) rapid IV infusion of the antibiotic, 3) prolonged courses of treatment, and 4) age. Theoretically, other risk factors may also be involved including the following: 1) prolonged exposure to UVA light while the antibiotic is being administered, 2) drug interactions, and 3) drug or metabolite accumulation from altered metabolism or reduced elimination. To date, there are no published reports suggesting that the dose of fluoroquinolones should be reduced in geriatric cats or those with renal or hepatic failure. However, accumulation of fluoroquinolone metabolites in dogs and of the parent compound in humans with decreased renal function has been reported. (8-10) In humans with decreased renal function has been reported. (8-10) humans, fluoroquinolone doses are typically decreased in response to the degree of renal impairment. (28) In general, all fluoroquinolone antibiotics should be reserved for severe or recurrent infections, and whenever possible their use should be based on results whenever possible their use should be based on results of culture and susceptibility tests. When indicated, the fluoroquinolones, including enrofloxacin, can be used with limited risk of developing retinal degeneration in cats, provided the manufacturer's guidelines are adhered to and dose reduction is considered in geriatric cats or those with renal impairment. Dosing on renal impairment. Dosing on exact body weight using split dosing (2.5 mg/kg, PO, q 12 h) and avoidance of rapid IV infusions, and drug interactions may help to reduce the risk of retinal degeneration in some cases. Furthermore, monitoring cats for mydriasis and avoidance of UVA light while undergoing treatment may also be of benefit. Further evaluation of the pharmacokinetics of enrofloxacin and the other fluoroquinolones is required in geriatric cats or those with mild to moderate renal or liver impairment to determine whether drug accumulation, elevated peak concentrations of drug, or both may be occurring in this subset of cats. Therapeutic monitoring of drug concentrations may not always be feasible because of time and cost, but renal panels with dose or frequency reduction in response to the degree of renal impairment and the site and severity of infection may help to reduce retinal toxicosis.     

Functional and structural assessment of retinal sheet allograft transplantation in feline hereditary retinal degeneration

Purpose  To investigate whether sheets of fetal retinal allografts can integrate into the dystrophic Abyssinian cat retina with progressive rod cone degeneration.
Methods  Fetal retinal sheets (cat gestational day 42), incubated with BDNF microspheres, were transplanted to the subretinal space of four cats at an early disease stage. Cats were studied by fundus examinations, bilateral full-field flash ERGs, and indocyanine green and fluorescein angiograms up to 4 months following surgery. E42 donor and transplanted eyes were analyzed by histology and immunohistochemistry for retinal markers.
Results  Funduscopy and angiography showed good integration of the transplants in two of four cats, including extension of host blood vessels into the transplant and some scarring in the host. In these two, transplants were found in the subretinal space with laminated areas, with photoreceptor outer segments in normal contacts with the host retinal pigment epithelium. In some areas, transplants appeared to be well-integrated within the host neural retina. Neither of these two cats showed functional improvement in ERGs. In the other two cats, only remnants of donor tissue were left. Transplants stained for all investigated cellular markers. No PKC immunoreactivity was detected in the fetal donor retina at E42, but developed in the 4-month-old grafts.
Conclusions  Fetal sheet transplants can integrate well within a degenerating cat retina and develop good lamination of photoreceptors. Functional improvement was not demonstrated by ERG in cats with well-laminated grafts. Transplants need to be further evaluated in cat host retinas with a more advanced retinal degeneration using longer follow-up times.     

Abnormal dark-adapted ERG in cats heterozygous for a recessively inherited rod-cone degeneration

Purpose To study retinal function in cats homozygous and heterozygous for a recessively inherited rod‐cone degeneration. Methods Dark‐adapted electroretinograms (ERGs) were performed on early affected, heterozygous (ophthalmoscopically normal), and clinically normal, nonrelated cats. Responses to blue stimuli over a 3.9‐log unit range were recorded. Results Lower b‐wave amplitudes than normal were observed in heterozygotes and early affected cats. The amplitudes of the heterozygotes took an intermediate position between normal and early affected cats. Normalized amplitude/intensity data suggest a normal dynamic range in carriers. B‐wave implicit times in carriers were comparable to those of normal cats. Conclusions These results show that heterozygotes have an altered retinal function, although they are ophthalmoscopically normal. It is difficult to electrophysiologically differentiate heterozygotes from affected cats with the very early stage of retinal degeneration.     

A slowly progressive retinopathy in the Shetland Sheepdog

Objective To describe a slowly progressive retinopathy (SPR) in Shetland Sheepdogs. Animals Forty adult Shetlands Sheepdogs with ophthalmoscopic signs of SPR and six normal Shetland Sheepdogs were included in the study. Procedure Ophthalmic examination including slit‐lamp biomicroscopy and ophthalmoscopy was performed in all dogs. Electroretinograms and obstacle course‐test were performed in 13 affected and 6 normal dogs. The SPR dogs were subdivided into two groups according to their dark‐adapted b‐wave amplitudes. SPR1‐dogs had ophthalmoscopic signs of SPR, but normal dark‐adapted b‐wave amplitudes. Dogs with both ophthalmoscopic signs and subnormal, dark‐adapted b‐wave amplitudes were assigned to group SPR2. Eyes from two SPR2 dogs were obtained for microscopic examination. Results The ophthalmoscopic changes included bilateral, symmetrical, greyish discoloration in the peripheral tapetal fundus with normal or marginally attenuated vessels. Repeated examination showed that the ophthalmoscopic changes slowly spread across the central parts of the tapetal fundus, but did not progress to obvious neuroretinal thinning presenting as tapetal hyper‐reflectivity. The dogs did not appear seriously visually impaired. SPR2 showed significantly reduced b‐wave amplitudes throughout dark‐adaptation. Microscopy showed thinning of the outer nuclear layer and abnormal appearance of rod and cone outer segments. Testing for the progressive rod–cone degeneration ( prcd )‐mutation in three dogs with SPR was negative. Conclusion Slowly progressive retinopathy is a generalized rod–cone degeneration that on ophthalmoscopy looks similar to early stages of progressive retinal atrophy. The ophthalmoscopic findings are slowly progressive without tapetal hyper‐reflectivity. Visual impairment is not obvious and the electroretinogram is more subtly altered than in progressive retinal atrophy. The etiology remains unclear. SPR is not caused by the prcd‐mutation.     

Multifocal retinopathy of Great Pyrenees dogs

Forty-four related Great Pyrenees dogs were examined ophthalmoscopically. Focal retinal elevations, multiple gray-tan-pink subretinal patches, and discrete areas of tapetal hyper-reflectivity were seen in 19 dogs, ranging from 13 weeks to 10 years of age. These lesions varied in size from focal spots that were barely visible with the indirect ophthalmoscope to areas that were larger than the optic disc. Complete blood cell counts, serum biochemical profiles, urinalyses, and blood pressure measurements were completed on four affected dogs and all were within normal reference ranges. Photopic and scotopic electroretinography was completed and the a-wave and b-wave amplitudes and latencies were similar for affected and age-matched nonaffected Great Pyrenees and other normal dogs. Electroretinograms that were examined twice during a 3-year period on three affected adult dogs did not reveal significant progressive deterioration of the a or b-wave parameters. Fluorescein angiography was completed on four affected dogs of ages 1 (n = 2), 5, and 6 years. These angiograms were repeated in three of these dogs 1 year later. The blood ocular barrier was intact in these dogs but there was blocked choroidal fluorescence. Postmortem examination, light microscopy, scanning and transmission electron microscopy were performed on three affected puppies and two affected adult dogs. These examinations revealed that the lesions in the puppies were limited to bilateral multiple areas of retinal pigment epithelial vacuolation, hypertrophy, and apparent separation from Bruch's membrane, and multiple serous retinal detachments. The affected adult dogs had focal retinal degeneration and retinal pigment epithelial hypertrophy, hyperplasia and pigmentation. Pedigree analysis and test mating confirm that this condition is inherited, probably as an autosomal recessive trait. This condition develops at approximately 13 weeks of age and the focal areas of retinal detachment and retinal pigment epithelial vacuolation progress to permanent and stable focal areas of retinal degeneration, and retinal pigment epithelial hypertrophy and pigmentation.     

Intracapsular lensectomy and sulcus intraocular lens fixation in dogs with primary lens luxation or subluxation

Objective  To evaluate the postoperative results of lensectomy and sulcus intraocular lens fixation (SIOLF) via an ab interno approach in dogs with progressive lens subluxation or early luxation.
Study design  Retrospective study.
Animals studied  Twenty eyes from 19 dogs presented to the Animal Eye Clinic for lens luxation or subluxation between 1999 and 2006.
Methods  Medical records were reviewed to evaluate preoperative lens position, vision status, intraocular pressure (IOP), and whether surgery was performed on an emergent or elective nature. Lensectomy and SIOLF were performed and postoperative status including vision, glaucoma, and retinal detachment was assessed.
Results  Average age was 8.6 years (range 4–14 years) and 55% (11/20) were terriers. Patients were followed a mean of 29.2 months (range 1–92 months) after surgery. Retinal detachment or secondary glaucoma was observed in 1 of 20 (5%) and 5 of 20 (20%) eyes, respectively, with 1 of 20 (5%) exhibiting both. Mean preoperative IOP was 16 mmHg and preoperative lens position was equally divided between luxated and subluxated lenses. Surgery was performed more frequently as an elective procedure (18/20; 90%) due to normalized IOP vs. an emergency procedure (2/20; 10%). Vision was retained in 70% (14/20) of eyes with a mean time to vision loss of 41 months in the remaining eyes due to glaucoma, retinal detachment, or retinal degeneration.
Conclusions  Complications of glaucoma and retinal detachment after SIOLF in this study were less when compared with previously reported incidence rates in the literature for lensectomy alone which may reflect improved patient selection.     

N3 potentials in response to high intensity auditory stimuli in animals with suspected cochleo-saccular deafness

We describe a previously un-reported vertex-negative potential evoked by high intensity click auditory stimuli in some dogs and cats with suspected cochleo-saccular deafness. Brainstem auditory evoked potential tracings from 24 unilaterally or bilaterally deaf animals, 22 dogs and 2 cats, among which 21 belonged to breeds with high prevalence of suspected or histologically confirmed cochleo-saccular deafness, were studied retrospectively. Values for latency, amplitude and threshold of this potential in dogs were 2.15+/-0.23 ms, 0.49+/-0.25 microV, and 91.9+/-4.7 dB NHL, respectively (mean+/-SD). Latency and threshold values in cats were in the mean+/-2 SD range of the dog values. Sensitivity to click stimulus polarity and to click stimulus delivery rate pointed towards a neural potential instead of a receptor potential. The vertex-negative wave observed in these animals shares all characteristics with the N3 potential described in some deaf humans with cochlear deafness, where it is presumed to arise from saccular stimulation. The combined degeneration of cochlea and sacculus usually reported in deaf white dogs and cats suggest that N3 may have a different origin in these species.     

Septic implantation syndrome in dogs and cats: a distinct pattern of endophthalmitis with lenticular abscess

Objective To summarize the clinical and pathologic findings in a group of dogs and cats with progressive clinical ocular disease, which were diagnosed with suppurative endophthalmitis and lens capsule rupture. Animals studied Twenty cats and forty‐six dogs that underwent unilateral enucleation or evisceration for intractable uveitis and/or glaucoma. Procedure Biopsy submission requests and microscopic case material were evaluated for clinical and histological features, including history of ocular trauma, duration of ocular disease, pattern of inflammation, and the presence of intralenticular microorganisms. Results The median duration for cats and dogs was 6 and 5 weeks, respectively. A history of trauma was reported for four (20%) cats and 18 (39%) dogs. All confirmed cases of trauma—three in cats and 14 in dogs—were caused by a cat scratch. Microscopically, all cases had suppurative endophthalmitis centered on the lens, lens capsule rupture, cataract, and lenticular abscess. Infectious organisms were identified by Gram stain within the lens of 14 (70%) cats and 30 (65%) dogs. Gram‐positive cocci were seen most commonly. Male cats were overrepresented as compared to females. There were no apparent gender, age or breed predilections in dogs. Conclusions A unique pattern of slowly progressive or delayed‐onset endophthalmitis with lens capsule rupture, lenticular abscess, and frequently intralenticular microorganisms is associated with traumatic penetration of the globe and lens capsule. The term Septic Implantation Syndrome (SIS) is favored in lieu of ‘phacoclastic uveitis’ to avoid confusion with phacolytic uveitis and to clearly implicate the role of intralenticular microorganisms in the pathogenesis.     

Retinal degeneration associated with the feeding of dog foods to cats

Retinal degeneration was observed in cats fed commerical dog food. The retinal degenerative lesions ranged in size from small areas of focal atrophy centered in the area centralis to generalized retinal atrophy. Blindness developed only in cats with generalized retinal atrophy. Analysis of the dog food diets, both dry and canned, revealed that taurine was absent or was present in very low concentrations when compared with control cat food diets. Plasma amino acid analysis also revealed taurine deficiency.     

Hereditary and congenital ocular disease in the cat

The aim of this review of hereditary and congenital ocular disease in cats is to present an overview of the most common disorders seen in this species, the pathogenesis of the problems and wherever possible, how they are treated. Several defects are common in breeds such as the Persian, Himalayan and Burmese cats and affect the anterior segment of the eye. Examples are agenesis of the eyelids, dermoids, entropion and corneal sequestrum. Other problems such as cataracts, lens luxation and retinal dysplasia, cause problems of the intraocular structures, but are less common in cats compared to dogs. Finally, various parts of the retina and in some diseases other parts of the eye, are specifically affected by hereditary diseases. Examples of these are lysosomal storage disease, Chediak-Higashi syndrome and progressive rod cone degeneration and rod cone dysplasia. Research of the latter two hereditary diseases, both described in the Abyssinian breed of cat, have made affected individuals important animal models for research into comparable diseases of humans.     

Multifocal chorioretinal lesions in Borzoi dogs

OBJECTIVES: To identify the prevalence of Borzoi chorioretinopathy in western Canada, characterize lesions with fluorescein angiography, determine if lesions were progressive, clarify the association of progressive retinal atrophy and investigate the etiology. MATERIALS AND METHODS: Serial ophthalmic examination, fundus photography, electroretinography, and fluorescein angiography were used to evaluate Borzoi dogs with lesions of Borzoi chorioretinopathy. Pedigree analysis and test breeding of two affected dogs were completed to determine the heritability of Borzoi chorioretinopathy. RESULTS: One hundred three Borzoi dogs were examined between 1998 and 2003. Focal, peripheral, tapetal, hyper-reflective and pigmented areas consistent with focal retinal degeneration and RPE pigmentation were identified in 12 dogs between 7 months and 7 years of age. Seven males and five female dogs were affected. Ophthalmoscopy and fundus photography over 5 years revealed individual lesions that did not progress or coalesce in 12 affected dogs. Electroretinography of affected and normal Borzoi dogs confirmed that retinal function was similar in normal and affected dogs up to 7 years of age. Fluorescein angiography was performed in three affected dogs and confirmed intact blood-ocular barriers, focal retinal pigment epithelium hypertrophy, and focal absence of choroiocapillaris corresponding to chronic, focal lesions. Pedigree analysis precluded simple dominant, X-linked dominant, or X-linked recessive inheritance. One male dog from the test-bred litter developed bilateral lesions at 14 months of age. Simple recessive, polygenetic, and acquired etiologies of these lesions cannot be ruled out at this time. CONCLUSIONS: Borzoi chorioretinopathy is an acquired condition that initially manifests as focal retinal edema and loss of choriocapillaris and tapetum. With time the retina degenerates becoming hyper-reflective and with RPE hyper-pigmentation and clumping within the borders of the tapetal lesions. Choriocapillaris remains hypofluorescent on fluorescein angiography. Progressive retinal atrophy was excluded as an etiology of multifocal chorioretinopathy in Borzois dogs. This condition is not inherited by simple autosomal dominant or sex-linked modes of inheritance.     

Nutritional Problems in Cats: Taurine Deficiency and Vitamin A Excess

Two nutritional problems of the cat are reviewed. One represents a deficiency of taurine, the other vitamin A toxicity. Taurine deficiency in cats is insidious because the progressive retinal degeneration induced may go unnoticed until the damage is advanced and irreversible. Both rods and cones undergo degeneration along with the underlying tapetum lucidum. The hyperreflective focal lesion is easily observed in the area centralis with an ophthalmoscope and has been previously identified as feline central retinal degeneration. This lesion is not reversed by taurine supplementation, even though the remaining retina may be saved from further degeneration. The cat requires dietary taurine, found in meat and fish, because it cannot synthesize enough to meet demands for bile acid conjugation and tissue metabolism, especially those of muscle and central nervous system.

Vitamin A toxicity is not commonly observed in cats but may occur if cats are fed beef liver in which appreciable vitamin A is stored. Cats exhibit muscle soreness and hyperesthesia, especially along the neck and forelimbs where bony exostoses of cervical verterbrae and longbones are common. The diagnosis is readily made from radiographs. The response to removal of vitamin A from the diet is generally rapid and, unless the toxicity has been chronic in young kittens, recovery is generally satisfactory.

     

Progressive retinal atrophy in the Abyssinian cat

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.     

Feline glaucomas

Cats are usually presented at a very late stage in the course of glaucoma when the eye is already blind. Secondary glaucoma because of another underlying ocular lesion is the most common form of glaucoma in the cat and is frequently associated with chronic anterior uveitis or intraocular neoplasia. Chronic stages of glaucoma in the cat are characterized by buphthalmus, anterior lens luxation, and exposure keratitis secondary to the enlarged globe. Ophthalmoscopic signs of glaucomatous retinal degeneration are only noticed in very advanced stages. Treatment of glaucoma in cats is usually aimed to keep the eye comfortable and within a normal intraocular pressure range. However, many antiglaucoma medications that are successfully used in humans and dogs are not very well tolerated by cats and, therefore, the selection of recommended drugs is limited in this species.     

Electrophysiologic differentiation of homozygous and heterozygous Abyssinian-crossbred cats with late-onset hereditary retinal degeneration

OBJECTIVE: To develop a method to electrophysiologically differentiate heterozygous-carrier Abyssinian-crossbred cats from homozygous-affected Abyssinian-crossbred cats before clinical onset of inherited rod-cone retinal degeneration. ANIMALS: 14 back-crossed Abyssinian-crossbred cats of unknown genotype (homozygous or heterozygous) for inherited rod-cone retinal degeneration, 24 age-matched mixed-breed control cats, 6 age-matched heterozygous Abyssinian-crossbred cats, and 6 homozygous Abyssinian cats. PROCEDURE: Electroretinography (ERG) of heterozygous and homozygous cats revealed differences, especially for scotopic recordings. Frequent ophthalmoscopy and ERG (2 to 5 times; at intervals of 3 to 6 months) of back-crossed cats were performed. Amplitudes and implicit times were analyzed by use of a graphic representation of results. Ratios for amplitudes of the b-waves to amplitudes of the a-waves (b-wave:a-wave) were compared. RESULTS: 8 back-crossed cats had decreased a-wave amplitudes, increased b-wave implicit times, and abnormal ERG waveforms. Values for the b-wave:a-wave for the highest scotopic light intensity were significantly higher for those same 8 cats. CONCLUSIONS AND CLINICAL RELEVANCE: The 8 back-crossed Abyssinian-crossbred cats with abnormal results developed fundus changes over time consistent with disease. A graphic representation of ERG results can be used to differentiate between genotypes prior to funduscopic changes. Values for the b-wave:a-wave ratio provide confirmation. These ERG analyses may be applied clinically in the diagnosis of retinal degenerations in various species. IMPACT FOR HUMAN MEDICINE: Cats with hereditary rod-cone degeneration may be a useful model for comparative studies in relation to retinitis pigmentosa in humans. Similar evaluations of ERG results could possibly be used for humans with suspected generalized retinal degeneration.