Clinical, electrophysiological and morphological changes in a case of hereditary retinal degeneration in the Papillon dog

An autosomal recessive retinal disease with a late onset in Swedish Papillon dogs has recently been described. A 7-year-old Papillon dog showed no obvious signs of visual impairment and only minor ophthalmoscopic changes. Cone ERG b-wave amplitudes were within normal limits, while rod responses were nonrecordable or severely abnormal. Ultrastructural examination showed a generalized retinal degenerative disease, most prominent in the peripheral areas. The inferior retina was more severely affected than the superior areas. Both rods and cones showed morphological changes. The Papillon dog is another dog breed affected by progressive rod-cone degeneration, with similarities to the canine retinal disease given the gene symbol prcd .     

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.     

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.     

Assessment of retinal function and characterization of lysosomal storage body accumulation in the retinas and brains of Tibetan Terriers with ceroid-lipofuscinosis

OBJECTIVE: To characterize lysosomal storage body accumulation in the retina and brain of Tibetan Terriers with ceroid-lipofuscinosis and determine whether the disease in these dogs is accompanied by impaired retinal function and retinal degeneration. ANIMALS: Three 7- to 10-year-old Tibetan Terriers with ceroid-lipofuscinosis and 1 healthy 5-year-old Tibetan Terrier. PROCEDURE: Owners completed a questionnaire to identify behavioral and physical signs indicative of ceroid-lipofuscinosis. Neurologic, behavioral, and ophthalmologic evaluations, including full-field electroretinograms, were performed on each dog. Fluorescence, light, and electron microscopy were performed on specimens of retina, cerebral cortex, and cerebellum of all dogs postmortem. RESULTS: Behavioral assessments of the affected dogs revealed moderate visual impairment in low-light conditions but good vision in bright light. On funduscopic evaluation of these dogs, abnormalities detected ranged from none to signs of moderately advanced retinal degeneration. Compared with findings in the control dog, electroretinography revealed depressed rod cell function with some impairment of cone cell function in the affected dogs. Morphologically, disease-specific storage bodies were detected in retinal Müller cells and neurons, particularly in ganglion cells, and in cells of the cerebral cortex and cerebellum in affected dogs. Substantial photoreceptor cell loss and disruption of photoreceptor outer segment morphology appeared to develop late in the disease. IMPLICATIONS FOR HUMAN MEDICINE: The similarities between ceroid-lipofuscinosis in Tibetan Terriers and some forms of ceroid-lipofuscinosis in humans suggest that the canine disease may have a genetic and biochemical basis similar to that of one of the ceroid-lipofuscinosis disorders in humans.     

Clinical findings in early onset cone-rod dystrophy in the Standard Wire-haired Dachshund

OBJECTIVE: To describe the clinical findings and the age of onset of cone-rod dystrophy (crd) in the Standard Wire-haired Dachshund (SWHD) and to evaluate which clinical tests could be used to obtain a reliable diagnosis. ANIMALS: Sixty-eight SWHD and SWHD-derived dogs were used, including 23 affected with crd and 45 controls, respectively. PROCEDURES: The dogs were subjected to behavioral testing, examination of pupillary light reflexes (PLRs), indirect ophthalmoscopy and bilateral full field electroretinography (ERG). RESULTS: The majority of affected puppies (5-10 weeks) displayed pin-point sized pupils upon examination with focal light. All dogs in the control group, except one, displayed normal PLRs upon examination. In all crd-affected dogs there was a great variation both in age of onset and in clinical appearance of retinal changes upon fundoscopy. Two siblings displayed panretinal degeneration at the age of 10 months while other affected dogs showed early changes at the age of 3 years. Generalized bilateral retinal atrophy was the end stage of the disease. The maze test revealed no obvious differences among affected and unaffected groups. ERG recordings showed only slightly reduced rod, and mixed rod-cone responses, but severely reduced cone single flash a- and b-wave amplitudes, and cone flicker amplitudes were observed in all affected dogs. CONCLUSION: Presence of pin-point sized pupils in young SWHDs was found to be an important indicator of early onset crd. Fundoscopic changes and progression of disease at later stages resembled those previously described in the majority of progressive retinal atrophies in dog. ERG was found to be the most reliable diagnostic procedure to clinically diagnose crd in the SWHD.     

Electroretinography recordings using a light emitting diode active corneal electrode in healthy beagle dogs

Electroretinography (ERG) is a well-established diagnostic procedure for objectively evaluating retinal function. In this study, ERG in beagle dogs, which are a popular experimental animal, was performed to determine the normal range of ERG variables and assess differences between the left and right eyes. ERG findings including rod, combined rod-cone, single-flash cone, and 30-Hz flicker responses were recorded with an LED-electrode in 43 sedated beagle dogs. The subjects were divided into young (< 1 year old), adult (1~5 years old), and senile animals (≥ 6 years old). Normal ERG ranges were obtained. Significant differences in b-wave amplitude along with b/a ratio of the combined rod-cone response were found between the young and adult animals as well as young and senile dogs. No significant differences were observed between the left and right eyes. ERG variables in beagle dogs differed by age due to age-related retinal changes. Thus, we propose that normal ERG ranges should be determined according to age in each clinic and laboratory using its own equipment because each institution usually has different systems or protocols for ERG testing.     

Retinopathy associated with ivermectin toxicosis in two dogs

CASE DESCRIPTION: 2 dogs (dogs 1 and 2) were examined for sudden onset of blindness. Both dogs had mild obtundation and mydriasis in both eyes. It was thought that dog 1 may have ingested ivermectin; dog 2 had been treated with ivermectin for demodectic mange. CLINICAL FINDINGS: On initial examination, both dogs had mydriasis and decreased pupillary light reflexes in both eyes. Dog 1 had an absent menace response bilaterally. Fundic examination of both eyes in both dogs revealed regions of multifocal retinal edema and folds with low-lying retinal separation. The electroretinogram was extinguished in dog 1 and attenuated in dog 2. Ivermectin was detected in serum samples from both dogs. TREATMENT AND OUTCOME: Both dogs made a complete clinical recovery following cessation of exposure to ivermectin; electroretinographic findings improved, and retinal edema resolved with some residual chorioretinal scarring. CLINICAL RELEVANCE: To our knowledge, this is the first report of resolution of retinal edema and electroretinographic changes associated with ivermectin toxicosis in dogs. In dogs that develop blindness suddenly, fundic examination, electroretinography, and assessment of serum ivermectin concentration are diagnostically useful, even if exposure to ivermectin is unknown.     

Cerebellar cortical degeneration in adult American Staffordshire Terriers

Adult-onset cerebellar cortical degeneration recently has been reported in American Staffordshire Terriers. We describe the clinical and histopathologic features of this disease and examine its mode of inheritance in 63 affected dogs. The age at which neurologic deficits 1st were recognized varied from 18 months to 9 years, with the majority of dogs presented to veterinarians between 4 and 6 years of age. Time from onset of clinical signs to euthanasia varied from 6 months to 6.5 years, with the majority of affected dogs surviving from 2 to 4 years. Initial neurologic findings included stumbling, truncal sway, and ataxia exacerbated by lifting the head up and negotiating stairs. Signs progressed to obvious ataxia characterized by dysmetria, nystagmus, coarse intention tremor, variable loss of menace reaction, marked truncal sway, and falling with transient opisthotonus. With continued progression, dogs became unable to walk without falling repeatedly. Cerebellar atrophy was visible on magnetic resonance images and on gross pathology. Histopathologic findings included marked loss of Purkinje neurons with thinning of the molecular and granular layers and increased cellularity of the cerebellar nuclei. The closest common ancestor of the dogs was born in the 1950s and inheritance was most consistent with an autosomal recessive mode of transmission with a prevalence estimated at 1 in 400 dogs. This inherited disease is comparable to the group of diseases known as spinocerebellar ataxias in humans. Many spinocerebellar ataxias in humans are caused by nucleotide repeats, and this genetic aberration merits investigation as a potential cause of the disease in American Staffordshire Terriers.     

Ocular signs of canine monocytic ehrlichiosis: a retrospective study in dogs from Barcelona, Spain

Canine monocytic ehrlichiosis (CME) is a tick-borne disease caused by the rickettsia Ehrlichia canis. Ocular lesions are a common feature of the disease and can be present in all stages. The purpose of this retrospective study was to determine the prevalence, type and response to treatment of ocular lesions associated with monocytic ehrlichiosis in 46 affected dogs presented to the Autonomous University of Barcelona-Veterinary Teaching Hospital (UAB-VTH) from January 2000 to December 2002. Dogs were included in the study only if they had a positive serologic test for E. canis and information about the clinical outcome was available. Eighteen breeds were represented, with the German Shepherd dog (n = 6) being the most common. There were 25 intact and three castrated males, and 16 intact and two neutered females. Twenty dogs (43.4%) were between 5 and 10 years old. Seventeen dogs (37% of all cases of monocytic ehrlichiosis diagnosed during the study period) had ocular signs, and 11 dogs (64.7% of the ocular cases) had only ocular lesions without apparent systemic signs. Exudative retinal detachment was the most common ocular manifestation; other prevalent findings included anterior exudative uveitis and optic neuritis. Five of the 17 cases with ocular lesions (29.4%) had ocular bleeding disorders (hyphema or retinal hemorrhages). All the dogs with ocular disease presented with bilateral signs. Dogs with posterior segment disease had titers against E. canis that were > or = 1 : 320, while lower titers were noted in dogs with anterior exudative uveitis. Two dogs presented with chronic autoimmune panuveitis after ehrlichiosis treatment. Canine ehrlichiosis should be considered in the differential diagnosis of exudative retinal detachment and anterior uveal inflammatory lesions.     

Exocrine pancreatic insufficiency in dogs.

Pancreatic acinar atrophy (PAA) is by far the most common cause for the maldigestion signs of canine exocrine pancreatic insufficiency (EPI). The ability to diagnose PAA in the subclinical phase before the development of total acinar atrophy and manifestation of clinical signs has offered new possibilities to study the pathogenesis of the disease. Marked T-lymphocyte infiltration during the progression of acinar atrophy and the genetic susceptibility of the disease have been taken as a primary evidence of the autoimmune nature of the disease. The term autoimmune-mediated atrophic lymphocytic pancreatitis is preferred to describe pathologic findings. A single abnormally, low serum canine trypsin-like immunoreactivity (cTLI) concentration (< 2.5 mg/L), in dogs with typical maldigestion signs has been shown to be highly diagnostic for clinical EPI and is found in dogs with end-stage PAA. Repeatedly subnormal cTLI values (2.5-5.0 micrograms/L) in dogs with no clinical signs of EPI are valuable markers of subclinical EPI and highly suggestive for partial PAA. The primary treatment of EPI is supplementing each meal with pancreatic enzymes. The long-term treatment response for the nonenteric-coated enzyme supplements has been found to be good in half of these dogs, but the response varied considerably.     

Ophthalmic and cone derived electrodiagnostic findings in outbred Miniature Long-haired Dachshunds homozygous for a RPGRIP1 mutation

Objective To investigate ophthalmic and cone‐derived electrodiagnostic findings in outbred Miniature Long‐haired Dachshunds (MLHD) homozygous for a mutation in the RPGRIP1 gene previously associated with cone‐rod dystrophy 1 (cord1). Animals A total of 36 MLHD homozygous for the RPGRIP1 mutation and 23 dogs clear of the mutation (control group). Procedures The dogs underwent ophthalmic examination and photopic electroretinogram (ERG) recordings. Results None of the control dogs presented with clinical or ophthalmic signs consistent with cord1. Amongst the dogs homozygous for the mutation one presented with bilateral symmetrical total retinal atrophy. None of the other dogs in this group showed signs consistent with cord1. Photopic ERG recordings were available in 23 control dogs and 34 dogs homozygous for the mutation. Photopic a‐ and b‐waves following four light stimuli (3 cdS/m²) at a rate of 5.1 Hz were not significantly different between groups. The amplitudes of the 30 Hz flicker (128 flashes, 3 cdS/m²) response were significantly reduced in the dogs homozygous for the PRGRIP1 mutation. The difference in age between the two groups did not significantly affect the difference. Conclusion Homozygosity of the RPGRIP1 mutation does not invariably result in early onset cord1. However, cone derived ERG recordings show evidence of a reduced cone or inner retinal function in homozygous but clinically normal MLHD. Modifying genes that have yet to be identified may influence an individual dog’s risk of developing the blinding cord1 and also the age of onset and rate of progression.     

Progressive Juvenile Glomerulonephropathy in 16 Related French Mastiff (Bordeaux) Dogs

Background: Familial juvenile glomerulonephropathy (JGN) is reported in several breeds of dogs. The mode of inheritance and spectrum of pathological lesions vary among breeds. A progressive JGN was detected in a pedigree of French Mastiff (FM) dogs. Objectives: To describe clinical, laboratory, and histopathologic findings in related FM dogs suffering from progressive JGN and to determine the mode of inheritance of this condition. Animals: Sixteen affected and 35 healthy related FM dogs Methods: FM dogs <24 months of age and diagnosed with chronic kidney disease with evidence of proteinuria entered the study. Clinical, laboratory, histopathologic findings, and pedigree data were recorded. Results: Clinical signs were typical of progressive glomerulopathy with resultant renal failure. Increased blood urea nitrogen, creatinine and total cholesterol concentrations, and proteinuria were found in all patients. Affected dogs had abnormal kidney structure on abdominal ultrasound examination. Histopathologic examination revealed extensive cystic glomerular atrophy, glomerular hypercellularity, and capillary wall thickening without immune complex deposition when tested with immunohistochemistry or immunofluorescence. Electron microscopy did not disclose specific primary glomerular lesions. Mean age at death was 20 months and mean length of survival after diagnosis was 6 months. Both males and females from healthy parents were affected. An autosomal recessive mode of transmission is suspected, but a more complex mode of inheritance cannot be excluded. Conclusions and Clinical Importance: Progressive familial JGN occurs in FM dogs. Characterization of the pathogenesis and mode of inheritance of this disease warrants additional study.     

Multifocal retinitis in New Zealand sheep dogs

Thirty-nine percent of 1,448 working sheep dogs were affected with varying degrees of multifocal retinal disease on ophthalmoscopic examination. Lesions consisted of localized areas of hyperreflexia in the tapetal fundus, often associated with hyperpigmentation. Severely affected animals had widespread hyperreflexia with retinal vascular attenuation. Only 6% of 125 New Zealand dogs raised in urban environment were similarly affected. Both eyes of 70 dogs from New Zealand were examined histologically. Forty-seven of 70 dogs had ocular inflammatory disease. Ten other dogs had noninflammatory eye disease, and 13 dogs had normal eyes. Histologically, eyes with inflammatory disease were divided into three categories: Dogs 3 years of age or less with active inflammatory disease of the retina, uvea, and vitreous. Four dogs in this group had migrating nematode larvae identified morphologically as genus Toxocara. Diffuse retinitis and retinal atrophy in conjunction with localized retinal necrosis and choroidal fibrosis. Dogs in this category were severely, clinically affected. Chronic, low-grade retinitis with variable retinal atrophy. Most dogs in this category were over 3 years of age, and many were visually functional. The existence of a definable spectrum of morphological changes associated with inflammation, suggests that Toxocara sp. ocular larva migrans may be the cause of a highly prevalent, potentially blinding syndrome of working sheep dogs in New Zealand.     

Funduscopic findings following cataract extraction by means of phacoemulsification in diabetic dogs: 52 cases (1993-2003)

OBJECTIVE: To determine prevalence of retinal hemorrhages and microaneurysms in dogs with diabetes mellitus following cataract extraction by means of phacoemulsification and identify potential risk factors. DESIGN: Retrospective study. PROCEDURE: Medical records of dogs undergoing phacoemulsification between 1993 and 2003 were reviewed, and information was recorded on signalment, history, physical examination findings, ophthalmic examination findings, results of laboratory testing, electroretinographic findings, and surgical findings. Glycemic control was classified as poor, intermediate, or good on the basis of baseline blood glucose concentration, perioperative body weight loss, daily insulin dosage, and presence of glucosuria and ketonuria. Data from diabetic and nondiabetic dogs were analyzed to determine prevalence and risk factors for development of retinal hemorrhages or microaneurysms following phacoemulsification. RESULTS: 11 of the 52 (21%) dogs with diabetes mellitus developed ophthalmoscopic signs of retinal hemorrhages or microaneurysms, compared with 1 of the 174 (0.6%) nondiabetic dogs. Median time from onset of diabetes mellitus to diagnosis of retinopathy was 1.4 years (range, 0.5 to 3.2 years). No risk factors for development of retinopathy were identified. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that retinal hemorrhages and microaneurysms may be more common and develop earlier in diabetic dogs than previously reported. This may affect treatment, as diabetic dogs survive longer with improved glycemic control.     

Familial glomerulonephropathy in the Bullmastiff

Glomerular disease was diagnosed by histopathologic examination in 11 related Bullmastiff dogs, and clinical and laboratory data were collected retrospectively. Four female and seven male dogs between the ages of 2.5 and 11 years were affected. Clinical signs, including lethargy and anorexia, were nonspecific and occurred shortly before death or euthanasia. In five affected dogs serial blood samples were obtained, and dramatically elevated blood urea nitrogen and creatinine levels were demonstrated up to 2.75 years before death. Protein-creatinine ratios were elevated in six of six dogs and were above normal 3.5 years before death in one dog. The kidneys appeared grossly normal to slightly smaller than normal at necropsy. Histologic abnormalities of the kidneys were consistent with chronic glomerulonephropathy with sclerosis. Examination of the pedigrees of related affected dogs yielded evidence supporting an autosomal recessive mode of inheritance.     

Risk factors associated with outcome in dogs with tetanus: 38 cases (1987-2005)

OBJECTIVE: To assess the clinical course of disease and risk factors associated with outcome in dogs with tetanus. DESIGN: Retrospective case series. ANIMALS: 38 dogs with tetanus. PROCEDURES: Data were collected from medical records of dogs with tetanus, including signalment; wound characteristics; initial clinical signs; severity of worst clinical signs; time to wound management, antimicrobial treatment, and antitoxin administration; and 28-day survival rate. Statistical analyses were performed to evaluate relationships between the potentially predictive variables and disease progression and outcome. RESULTS: The 28-day survival rate was 77% (among 35 uncensored dogs). The most common initial clinical signs in affected dogs were ocular (n = 18) and facial (11) abnormalities. Nineteen dogs progressed to recumbency with severe muscle spasms, and 14 dogs had high or low heart rate or blood pressure values. Eight dogs died or were euthanized because of complications of tetanus. There was a significant association between younger age and development of more severe clinical signs. Furthermore, a significant inverse relationship between development of severe clinical signs and survival was identified. There was no association between earlier initiation of wound management, antimicrobial administration, or antitoxin administration and either progression of signs or 28-day survival rate. Wound type was not associated with 28-day survival rate. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that younger dogs with tetanus may be more likely to develop severe clinical signs. The prognosis for survival in dogs with tetanus is good if abnormalities in heart rate or blood pressure values do not develop.     

Clinical and imaging findings,treatments, and outcomes in 27 dogs with imaging diagnosed trigeminal nerve sheath tumors: A multi‐center study

The clinical behavior of canine trigeminal nerve sheath tumors and benefits of previously reported treatments are incompletely defined. Aims of this retrospective, multicenter, observational study were to describe clinical signs, tumor localization characteristics, treatments, and clinical outcomes in a group of dogs with this neoplasm. Databases at four hospitals were reviewed for dogs with a trigeminal nerve sheath tumor diagnosis, magnetic resonance imaging (MRI) studies, and presentation between 2004 and 2014. A single observer recorded medical record findings and two observers recorded MRI characteristics by consensus. A total of 27 dogs met inclusion criteria (15 treated with stereotactic radiation therapy and 12 unirradiated). Two unirradiated dogs were excluded from outcome analyses. The most common presenting signs were masticatory muscle atrophy (26 dogs), neurologic signs referable to intracranial disease (13), and ocular disease (12). Based on MRI findings, all dogs had disease extending centrally at the level of the brainstem. The most commonly affected trigeminal nerve branches were the mandibular (26 dogs), maxillary (22), and ophthalmic (10). Of 15 dogs treated with stereotactic radiation therapy, one had improved muscle atrophy, and six had poor ocular health after treatment. Neurologic signs improved in 4/5 dogs with intracranial signs. Overall median survival time for the 10 unirradiated dogs with available follow‐up was 12 days and 441 days for the 15 stereotactic radiation therapy dogs. Mean survival times between these groups were not significantly different (mean 95% CI for unirradiated dogs was 44–424 days and mean 95% CI for stereotactic radiation therapy dogs was 260–518 days).     

Acute blindness in dogs: Sudden acquired retinal degeneration syndrome versus neurological disease (140 cases, 2000–2006)

Objective  To evaluate dogs with amaurosis and compare signalment, history, ophthalmic examination and neurologic abnormalities between dogs diagnosed with sudden acquired retinal degeneration syndrome (SARDS) versus neurological disease (ND). Animals Studied-140 dogs with acute vision loss and ocular abnormalities insufficient to account for visual deficits. An electroretinogram (ERG) was performed on each dog.
Procedures  Medical records were reviewed and information was collected for all dogs meeting the inclusion criteria. Dogs diagnosed with SARDS were compared to those with ND based on signalment, duration of clinical signs, past medical problems, clinicopathologic findings, and ophthalmic and physical examination abnormalities.
Results  120 dogs were diagnosed with SARDS and 20 dogs with ND based on ERG results. Mixed-breed dogs were most commonly diagnosed with SARDS as well as ND. Pure breed dogs frequently diagnosed with SARDS included the Miniature Schnauzer and Dachshund. Dogs with SARDS did not differ significantly from those with ND based on age or sex distribution. Cushing's-like symptoms were reported more frequently in SARDS dogs as well as conjunctival hyperemia and retinal vascular attenuation. Papilledema and asymmetric visual deficits were observed more frequently in dogs with ND. Dogs with ND were no more likely than SARDS dogs to have additional neurological deficits.
Conclusions  Appreciable overlap of clinical signs exists between dogs with SARDS and dogs with ND resulting in acute vision loss. As a significant portion of dogs (14%) in the present study were diagnosed with ND, an ERG to rule out ND is indicated in dogs with amaurosis.     

Familial progressive nephropathy in young Bull Terriers

The clinical, clinicopathological and pathological findings are described in three Bull Terrier bitches with advanced renal disease. The bitches were less than four years old and showed variable presenting signs but anorexia, lethargy and polydipsia were the most frequent. All three dogs were azotaemic and isosthenuric. Urinary protein was measured in two of the three cases. Both were proteinuric. At necropsy all dogs had shrunken kidneys. Histological examination revealed nephron loss, atrophy of glomerular tufts, interstitial fibrosis, and mineralisation of basement membranes.

The progressive renal disease in these dogs was similar to the condition reported in Bull Terriers in Australia, and is probably familial and inherited.