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.     

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.     

Incidence of the gene mutation causal for rod-cone dysplasia type 1 in Irish setters in the UK

A survey to establish the UK prevalence of the gene mutation causing the rod-cone dysplasia type one (rcdl) form of generalised progressive retinal atrophy (gPRA) in Irish setters was carried out. The dogs were selected by members of two Irish setter breed societies to provide examples from most of the main breeding lines in the UK. A total of 210 Irish setters were tested and one bitch was found to be a carrier of the rcdl mutation. These results show that although a confirmed case of rcdl has not been reported in Irish setters in the UK for over a decade the gene is still present in the gene pool.     

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.     

RADIOGRAPHIC FEATURES OF AORTIC BULB/VALVE MINERALIZATION IN 20 DOGS

The radiographic features of aortic bulb/valve mineralization in 20 dogs were reviewed. Extent, shape, number, and location of mineralization were recorded. Five of the dogs had additional alternate imaging examinations, including bone scintigraphy, echocardiography, and thoracic computed tomography. A necropsy was done on one dog, and the area of mineralization was evaluated using routine histology. The median age was 10 (mean 9.7; SD +/- 2.7) years. There were five males, seven neutered males, one female, and seven neutered females. The breeds were: Irish setter (6); rottweiler (7); chow-chow (1); miniature dachshund (1); borzoi (1); English setter (1); English springer spaniel (1); great Dane (1); and greyhound (1). Dogs with both right and left lateral radiographs (n = 17) had mineralization visible on both views, more conspicuously on the right lateral radiograph (n = 12). Aortic bulb mineralization was identified on the ventrodorsal radiograph of only one dog. On lateral radiographs, the aortic bulb mineralization was localized within the 4th intercostal space and in the craniodorsal quadrant of the cardiac silhouette. In nine of the dogs, there were complex or multiple mineralizations and in 11 dogs, there was a single curvilinear mineral opacity oriented in a caudoventral to craniodorsal direction. In all radiographs, the mineralization was in the expected position of the aortic bulb, and echocardiography (n = 4), spiral computed tomography (n = 2), and necropsy (n = 1) confirmed that the mineralization was within the aortic bulb. Clinical pathologic data of the dogs suggested no reason for metastatic mineralization. Exact etiopathogenesis of the lesions were not determined in this study. Based on the histologic findings in one dog, the mineralization seen in the aortic root is similar to a form of dystrophic mineralization called Monckeberg's calcific arteriosclerosis in humans. No clinical signs attributable to the mineralization were observed.     

Leucocyte adhesion protein deficiency in Irish setter dogs.

Investigation of 12 Irish setter puppies from six litters with severe recurrent infections, neutrophilia and low body weight revealed a leucocyte adhesion protein deficiency with a total lack of CD11b and CD18. Their neutrophil function was severely impaired with a totally absent capacity to ingest C3b-opsonized particles, a significantly impaired capacity to ingest IgG-opsonized particles and significantly diminished adherence to nylon wool when compared with neutrophils from healthy control dogs. The chemiluminescence of patient neutrophils activated by C3b-opsonized particles was, consequently, significantly decreased compared with that of control neutrophils, while the respiratory burst assayed by phorbolmyristate acid (PMA) stimulated nitroblue tetrazolium (NBT)-reduction was normal in the patient group. Random migration and chemotactic responses of patient and control neutrophils, were similar. The etiology, pathogenesis and clinical manifestations of the Irish setter leucocyte adhesion deficiency were similar to that of the leucocyte adhesion deficiency in humans.     

Canine leucocyte adhesion deficiency in Irish red and white setters

Seventy-six Irish red and white setter samples were tested for the recently documented CD18 point mutation which manifests as canine leucocyte adhesion deficiency (CLAD) in Irish setters. Six carrier dogs were identified, all originating from a lineage within which sporadic deaths from symptoms consistent with CLAD had been observed. This is the first demonstration that the CLAD mutation exists outside the Irish setter population, confirming that the mutation is present in a significant minority of Irish red and white setters. Routine testing by breeders to identify carrier animals will enable the eradication of CLAD from the Irish red and white setter population.     

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.     

Cerebrospinal Fluid Analysis and Clinical Outcome of Eight Dogs With Eosinophilic Meningoencephalomyelitis

Eight dogs, 14 weeks to 5.5 years of age, had signs of diffuse or multifocal meningoencephalomyelitis. The total white cell counts of the cerebrospinal fluid (CSF) ranged from 11 to 5,550 cells/microliters; the percentage of eosinophils ranged from 21% to 98%. The total CSF protein content range was 19 to 1,430 mg/dl. On necropsy, two dogs had granulomatous encephalomyelitis due to protozoan infection. The other six dogs, of which three were Golden Retriever dogs, appeared to have an idiopathic eosinophilic meningoencephalitis; four of these dogs recovered. The significance of eosinophils in CSF and the possible emergence of a new encephalitic syndrome of dogs involving a hypersensitivity to an unknown agent is also discussed.     

Early retinopathy in the Bernese Mountain Dog in France: preliminary observations

The objective of the study was to describe a form of early retinopathy in the Bernese Mountain Dog in France. Sixty-two Bernese Mountain Dogs (38 males and 24 females), whose ages ranged from 2 months to 9 years, were examined over a period of 3 years. Visual behavior, pupillary light reflexes, menace responses and ocular fundi were evaluated in all animals. Electroretinography (ERG) was performed on six of the affected dogs after dark adaptation. Fluorescein angiography (FA) was performed on one affected dog. Whenever possible, the pedigrees of the affected dogs were evaluated. A histological examination of the retina was performed on one of the affected dogs. Eight dogs (seven males and one female) were diagnosed with retinopathy with an early onset of clinical signs. (Four dogs were aged between 3 months and 1 year, two dogs were aged 2 and 3.5 years, and one dog was 7 years old.) Night vision was impaired in most of the dogs. Retinopathy was characterized ophthalmoscopically by a bilateral, symmetrical horizontal zone of tapetal hyper-reflectivity adjacent to and above the optic disc, and sometimes by peri-papillary hyper-reflectivity. ERG changes included a reduction in b-wave amplitude varying from one case to another. Fluoroscein angiography demonstrated an ischemic-type alteration with epitheliopathy opposite the hyper-reflective zone. Pedigree examinations suggested a familial predisposition. The histological examination indicated photoreceptor degeneration that was more pronounced in the central tapetal zone. In France, retinopathy in the Bernese Mountain Dog involves an early retinal degeneration that produces specific manifestations of the ocular fundus, night visual impairment or blindness, and has familial transmission.     

Mortality and morbidity due to gastric dilatation-volvulus syndrome in pedigree dogs in the UK

Objectives : To estimate breed-specific risk of death due to, and prevalence of, gastric dilatation-volvulus (GDV) in UK pedigree dogs. Methods : Data were available on the reported cause of and age at death and occurrence of and age at diagnosis of disease from the 2004 purebred dog health survey. A total of 15,881 dogs of 165 breeds had died in the previous 10 years; GDV was the cause of death in 65 breeds. There were 36,006 live dogs of 169 breeds of which 48 breeds had experienced ≥1 episodes of GDV. Prevalence ratios were used to estimate breed-specific GDV mortality and morbidity risks. Results : Gastric dilatation-volvulus was the cause of death for 389 dogs, representing 2.5% (95% CI: 2.2-2.7) of all deaths reported and the median age at death was 7.92 years. There were 253 episodes in 238 live dogs. The median age at first diagnosis was five years. Breeds at greatest risk of GDV mortality were the bloodhound, Grand Bleu de Gascogne, German longhaired pointer and Neapolitan mastiff. Breeds at greatest risk of GDV morbidity were the Grand Bleu de Gascogne, bloodhound, otterhound, Irish setter and Weimaraner. Clinical Significance : These results suggest that 16 breeds, mainly large/giant, are at increased risk of morbidity/mortality due to GDV.     

Original investigation of right-to-left shunting patent ductus arteriosus in an Irish setter puppy

A six-month-old, entire female, Irish setter was presented with a two-month history of progressive hindlimb weakness and collapse on exercise. Thoracic auscultation revealed a soft systolic murmur and a split second heart sound. Differential cyanosis and polycythaemia were not observed. Right-to-left shunting patent ductus arteriosus (r-PDA) was confirmed on contrast echocardiography ("bubble study") and selective right ventricular angiography. Comparison of blood gases from the metatarsal and auricular artery confirmed the presence of differential hypoxia. This technique is not known to have been described previously in the diagnostic investigation of r-PDA in dogs.     

Idiopathic detrusor-urethral dyssynergia in dogs: a retrospective analysis of 22 cases

Results of a retrospective study of 22 dogs with signs of dysuria and/or stranguria in which a diagnosis of idiopathic detrusorurethral dyssynergia was made are presented. The diagnosis was based on the exclusion of detectable pathological conditions which could also cause urine outflow obstruction. The affected cases were 22 middle-aged male dogs (mean age 4·9 years) of large and giant breeds (mean bodyweight 36·7 kg). Nine dogs had had periodic clinical signs for longer than one year, one for seven months and eight for two to five weeks, while in four dogs signs had begun four to five days before referral. All dogs received the α-sympatholytic agent prazosin as an initial treatment and in 11 it remained the only therapy. There was a good effect in seven and a moderate response in the other four dogs. In one dog, prazosin was ineffective and was replaced by diazepam, which markedly reduced the signs. Three other dogs required frequent catheterisation and antibiotics were administered. These dogs responded favourably. Another three dogs with evidence of impaired bladder contractility were also treated with the parasympathomimetic agent carbachol. One did not improve and was euthanased. Four dogs developed bladder paralysis and severe infectious cystitis. Only one of these could be managed satisfactorily by long-term administration of prazosin, carbachol and antibiotics, and the others had to be euthanased.     

Morphologic features of degeneration and cell death in the neurosensory retina in dogs with primary angle-closure glaucoma

OBJECTIVE: To investigate cellular death in the neurosensory portion of the retina during the first 7 days after onset of clinical signs of overt primary angleclosure glaucoma (PACG) in dogs. SAMPLE POPULATION: 14 globes from dogs with PACG and 2 normotensive globes from dogs with PACG in the opposite eye. PROCEDURES: Retinas were examined via light microscopy and terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick end-labeling. RESULTS: Necrosis of ganglion cells and segmental degeneration of the nerve fiber layer rapidly progressed to scattered full-thickness retinal attenuation and disorganization. Apoptosis was detectable within 1 day after onset of PACG and was prominent by 3 days. Necrosis of ganglion cells was significantly greater in retinas affected for < or = 1 day, compared with retinas affected for > 1 day. In contrast, apoptosis in the ganglion cell layer was significantly greater in retinas affected for > 1 day, compared with retinas affected for < or = 1 day. End-stage retinal atrophy was seen by day 7. CONCLUSIONS AND CLINICAL RELEVANCE: The presence of necrotic ganglion cells within 1 day after onset of clinical signs suggests a narrow window of opportunity to initiate effective therapy in overt PACG. Photoreceptor death is an important and striking aspect of neurosensory retinal degeneration after acute onset of PACG.     

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.     

Senile cardiac amyloidosis in the dog

Thirty-two cases of senile cardiac amyloidosis from a routine necropsy material of 594 dogs were studied. The age of the affected dogs ranged from 10 to 16 years. Amyloid was observed in the intramural arteries and arterioles, predominantly in the ventricular myocardium. The vessels were often obturated with amyloid, and myocardial necroses and fibroses were common consequences of the vascular lesions. In three cases amyloid deposits were also observed in the main subepicardial coronary arteries. In contrast to man, only slight interstitial amyloid degeneration was found in four of the dogs observed. Amyloid in the mitral valves, tricuspid valves and aortic cusps was observed in six, two and three cases respectively. It was concluded that the distribution of senile cardiac amyloidosis in the heart of the dog differs considerably from that in man.     

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.     

Reference range and repeatability of a combined intestinal permeability and function test in clinically healthy Irish setter dogs

A reference range was determined for a combined test of differential sugar permeability, using lactulose (L) and rhamnose (R), and intestinal function, using D-xlylose (X) and 3-O-methylglucose (G), in clinically healthy adult Irish setter dogs. Urinary L/R ratios in 48 Irish setters from one to 12 years old varied from 0·03 to 0·18, with a mean ( ) of 0·10 (0·01); X/G ratios varied from 0·46 to 0·81, with a mean ( ) of 0·59 (0·01). There were no significant differences between L/R or X/G ratios of dogs of different sex (P>0·2) or age (P0·5), using analysis of covariance. Lactulose/rhamnose ratios of ≥0·18 and X/G ratios ≥0·43 were considered normal, defined by the respective mean ± 2 . Repeatability was established by performing three permeability and function tests at monthly intervals in twelve of the dogs. Analysis of repeated L/R and X/G ratios by means of linear models procedure revealed no significant differences between measurements made on successive occasions (P>0·15), confirming the repeatability of this test.     

Leucoencephalomalacia and Cerebral White Matter Vacuolar Degeneration in Two Related Labrador Retriever Puppies

Two Labrador Retriever dogs from a common dam had similar neurological deficits consisting of cortical blindness, dullness, and loss of previously learned habits. Both were examined at 5 months of age, and histopathological examination revealed leucoencephalomalacia and vacuolar degeneration of the cerebral white matter. Histopathologic findings in these 2 dogs differed from those reported previously in Labrador Retrievers with spongy degeneration of central nervous system white matter. A nonlittermate full sibling to 1 of these dogs was examined at 1.5 years of age for similar clinical signs that did not progress for the next 25 months.