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.     

A retrospective study on the prevalence of primary cataracts in two pedigrees from the German population of English Cocker Spaniels

Objective  Two pedigrees from the German English Cocker Spaniel population are presented to illustrate the familial occurrence of primary cataract (CAT) in single- and multicolored English Cocker Spaniels. The aim was to characterize similarities and differences in the prevalence and formation of CAT in these separately bred color variants of English Cocker Spaniels.
Materials  The study was based on the veterinary records for presumed inherited eye diseases of 1232 English Cocker Spaniels which were provided by the German panel of the European Eye Scheme for diagnosis of inherited eye diseases in animals (DOK, < http://www.dok-vet.de >). Data included information on 615 single-colored and 617 multicolored English Cocker Spaniels.
Results  CAT was diagnosed in 92 (14.96%) of the single-colored and 34 (5.51%) of the multicolored English Cocker Spaniels. The pedigree of the single-colored English Cocker Spaniels included 40 ophthalmologically examined dogs with 18 unaffected and 22 affected dogs. The pedigree of the multicolored English Cocker Spaniels contained 16 ophthalmologically examined dogs with 11 unaffected and five affected dogs.
Conclusions  In both color variants of the English Cocker Spaniels different forms of primary CAT with respect to location within the lens occurred among close relatives. Appearance of CAT was very heterogeneous without obvious sex differences. The sample pedigrees do not support the assumption of familial segregation of specific forms of primary CAT in English Cocker Spaniels.     

Fine Structure of the Choriocapillaris, Bruch''s Membrane and Retinal Epithelium of the Cow

The fine structure of the choriocapillaris, Bruch's membrane and retinal epithelium was investigated in both the tapetal and non-tapetal fundus of the bovine eye. In ail locations the retinal epithelium consists of a single layer of cuboidal cells. The epithelial cells are joined laterally by apically located tight junctions and throughout the retina display numerous basal infoldings and fine apical processes which enclose rod outer segments. All retinal epithelial cells are rich in smooth endoplasmic reticulum and mitochondria and contain phagosomes. Although not as abundant, profiles of rough endoplasmic reticulum and polysomes are also noted in all locations. In non-tapetal areas, melano-somes are numerous whereas over the central tapetum fibrosum they are absent. The absence of melanosomes over a functional tapetum is to be expected. While lysosomes are present throughout the epithelial layer, over the tapetal region they appear to be more numerous. The apparent increase in lysosomal numbers in this location may indicate an enhanced shedding of outer segment material over the tapetum. Although some retinal epithelial cells are modified to accomodate a tapetum lucidum their morphology is basically similar throughout the retina and probably indicates that ail regions of the retinal epithelium are capable of the normal functions of this indispensible retinal layer. The choriocapillaris is heavily fenestrated on the border facing the retina and overlying the tapetum also displays fenestrae on its choroidal edge. Bruch's membrane ( complexus basalis ) is pentalaminate throughout the retina and is slightly thicker in the posterior fundus.     

Fine structure of the retinal pigment epithelium, Bruch's membrane and choriocapillaris in the horse

The fine structure of the retinal pigment epithelium (RPE), Bruch's membrane and choriocapillaris was investigated by light and transmission electron microscopy in both the tapetal and non-tapetal fundus of the horse eye. In all locations, the RPE consisted of a single layer of low cuboidal cells. The epithelial cells were joined laterally by apically located tight junctions. These cells displayed numerous basal infoldings and abundant thin apical processes which enclosed the rod outer segments. The epithelial cell nuclei were large and located basally. Within the epithelial cells, smooth endoplasmic reticulum was very abundant, while rough endoplasmic reticulum was scarce, polysomes and mitochondria, which often display a ring-shaped structure, were abundant. Melanosomes were abundant in the non-tapetal area but absent in the tapetal area. Bruch's membrane was pentalaminate throughout the retina. The endothelium of the choriocapillaris was heavily fenestrated.     

Transpupillary diode laser retinopexy in dogs: ophthalmoscopic,fluorescein angiographic and histopathologic study

Objective To evaluate the ophthalmoscopic, fluorescein angiographic and light microscopic effects of diode laser retinopexy application in the tapetal and nontapetal fundus in the dog, and to ascertain appropriate laser power settings for production of photocoagulative lesions in these two regions. Animals studied Three adult female Beagle dogs. Procedures Laser burns were applied to selected areas in the fundus with an indirect headset delivery system using settings varying from 100 to 200 milliWatts (mW) and from 100 to 600 milliSeconds (mS) with total delivered energy ranging between 15 and 100 milliJoules (mJ). The dogs were then monitored by ophthalmoscopic examination and fluorescein angiography at regular intervals for 7–28 days. Histopathologic studies were performed at 7, 14 and 28 days after laser application. Results The diode laser produced ophthalmoscopically visible lesions in the nontapetal fundus with all laser settings used, and the appearance of these lesions corresponded to the energy levels used, and degree of pigment in the lased region. Gray‐white colored lesions with minimal subsensory retinal edema were seen with settings as low as 100 mWatts/150 mSeconds. In the tapetal fundus, laser burns were more difficult to produce, less repeatable, and required higher energy levels. Laser burns appeared as bronze, dark green or black discolorations of the tapetum with varying degrees of subsensory retinal edema. Lesions were more reproducible and were achieved with lower settings in the tapetal area of the tapetal/nontapetal junction. Ophthalmoscopically, depigmentation and repigmentation of the RPE (nontapetal fundus) and degenerative changes in the overlying retina (tapetal fundus) developed in the laser burns over the 28‐day study period. Fluorescein angiographic studies showed disruption of the blood–retinal barrier at the level of the RPE and fluorescein leakage into the subsensory retinal space was seen in most lesions at 24 h, was minimal at 3 days, and had resolved by 7 days. Histologically, grayish‐white lesions in the nontapetal fundus, and bronze to small black lesions in the tapetal fundus were typically characterized by outer retinal necrosis and RPE migration. Gliosis was considered minimal, was confined to the retina, and no inflammatory cells were seen. Peripheral intense white lesions (nontapetum) and lesions with a black center (tapetal fundus) were characterized by more extensive panretinal and choroidal necrosis. Most of the nontapetal lesions and a few in the tapetal fundus showed the formation of a central retinal detachment. Conclusions The diode laser effectively produces lesions suitable for retinopexy in both the nontapetal, pigmented fundus and the tapetal fundus, although variably so in the latter region. Initial laser settings of 100–150 mW/200 mS for the pigmented fundus, and 150 mW/200–300 mS for the peripheral tapetal fundus are recommended, and the clinician should gradually increase time interval settings to achieve a grayish‐white lesion in the nontapetum, and a bronze to slightly black lesion in the tapetal fundus. If possible, retinopexy should be applied to the peripheral tapetal area or tapetal/nontapetal junction.     

Breed variations in histopathologic features of chronic severe otitis externa in dogs: 80 cases (1995-2001)

OBJECTIVE: To compare pathologic changes of the horizontal ear canal associated with chronic severe otitis externa between Cocker Spaniels and dogs of other breeds. DESIGN: Retrospective study. ANIMALS: 80 dogs with severe otitis externa that required total ear canal ablation with lateral bulla osteotomy. PROCEDURE: Medical records were reviewed for breed, sex, and age at time of surgery. Histologic specimens from the horizontal ear canal were evaluated by a single examiner for overall tissue response pattern and scored for sebaceous gland hyperplasia, ceruminous gland hyperplasia, ceruminous gland ectasia, fibrosis, pigment-laden macrophages, and osseous metaplasia. RESULTS: 48 of 80 (60%) dogs were Cocker Spaniels. Thirty-five of 48 (72.9%) Cocker Spaniels had a predominately ceruminous tissue response pattern; only 9 of 32 (28.1 %) dogs of other breeds had the same pattern. Other breeds most commonly had a pattern dominated by fibrosis (n = 13 [40.6%]); fibrosis was the predominant pattern in only 4 of 48 (8.3%) Cocker Spaniels. Discriminant analysis and K-means clustering of 4 histopathologic criteria correctly classified 75% of the dogs as Cocker Spaniels or all other breeds. CONCLUSIONS AND CLINICAL RELEVANCE: Cocker Spaniels are at increased risk for chronic severe otitis externa requiring total ear canal ablation with lateral bulla osteotomy, indicating that earlier and more aggressive management of the primary otitis externa and secondary inflammation is warranted in this breed. Cocker Spaniels with chronic severe otitis externa have distinct differences in pathologic characteristics of the horizontal ear canal, compared with other breeds.     

Temporomandibular dysplasia in American Cocker Spaniels

Temporomandibular dysplasia was found in six American Cocker Spaniels related to each other. Clinical signs and diagnosis are described.     

Inherited retinal dysplasia and persistent hyperplastic primary vitreous in Miniature Schnauzer dogs

The objectives of this study were to define the clinical syndrome of retinal dysplasia and persistent primary vitreous in Miniature Schnauzer dogs and determine the etiology. We examined 106 Miniature Schnauzers using a biomicroscope and indirect ophthalmoscope. The anterior and posterior segments of affected dogs were photographed. Four enucleated eyes were examined using routine light microscopy and scanning electron microscopy. A pedigree was constructed and related dogs were test-bred to define the mode of inheritance of this syndrome. Congenital retinal dysplasia was confirmed in 24 of 106 related Miniature Schnauzer dogs. Physical and postmortem examinations revealed that congenital abnormalities were limited to the eyes. Biomicroscopic, indirect ophthalmoscopic, and neuro-ophthalmic examinations confirmed that some of these dogs were blind secondary to bilateral retinal dysplasia and detachment (nonattachment) (n = 13), and the remainder had generalized retinal dysplasia (n = 11). Fifteen of these dogs were also diagnosed with unilateral (n = 9) or bilateral (n = 6) persistent hyperplastic primary vitreous. Nutritional, infectious, or toxic etiologies were not evident on physical, postmortem, light microscopic, or transmitting and scanning electron microscopic examination of four affected Miniature Schnauzers. We examined the pedigree and determined that an autosomal recessive mode of inheritance was most likely. Three test-bred litters including those from affected parents, carrier and affected parents, and carrier parents confirmed this mode of inheritance. This study confirms that retinal dysplasia and persistent hyperplastic primary vitreous is a congenital abnormality that is inherited as an autosomal recessive condition in Miniature Schnauzers.     

Inherited phosphofructokinase deficiency in an American cocker spaniel.

A 3-year-old female American Cocker Spaniel with a chronic hemolytic disorder and hemolytic crises was found to have M-type phosphofructokinase deficiency. This inherited erythroenzymopathy and myopathy is commonly diagnosed in English Springer Spaniels, but the family study of this Cocker Spaniel, although supporting an autosomal recessive mode of inheritance, did not reveal any English Springer Spaniel ancestors. Molecular genetic studies did, however, identify the same mutation in this dog as we previously reported in the English Springer Spaniel breed, suggesting that this mutation originated prior to the separation of these 2 breeds.     

Congenital hereditary cataract in Cocker Spaniels

Cases of congenital cataract in red Cocker Spaniels are reported. The investigation comprised clinical, histological and genetic studies. The common feature was bilateral, congenital, partial cataract of non-progressive nature.
Typically the cataract was localized subcapsularly at the anterior pole of the lens. In some cases it was of a more diffuse extent. In a few cases the cataract co-existed with persisting pupillary membrane, microphthalmia, hypotonia and rotatory nystagmus. Histopathological examination of affected eyes confirmed the clinical findings.
The disease appears to be of hereditary nature. The genetic studies on the condition in this breed of dogs showed that the mode of inheritance is presumably complex.     

Retinal dysplasia in dogs--a review

Retinal dysplasia is a developmental aberration of the neuroretina characterized by formation of retinal tubules, malformation rosettes and folding of the retina. Retinal dysplasia has been reported in Bedlington Terrier, Sealyham Terrier, Beagle, Labrador Retriever, English Cocker Spaniel, American Cocker Spaniel, English Springer Spaniel, Yorkshire Terrier and Rottweiler. A hereditary basis for retinal dysplasia has been proved or suggested for all breeds exhibiting retinal dysplasia except Beagle and Rottweiler. Ophthalmoscopically retinal dysplasia is characterized by vermiform streaks often radiating from the optic disc. The reflectivity of the tapetum is often altered in these areas. Accompanying retinal detachment or cataractous changes in the lens may be seen. Extensive retinal dysplasia and retinal detachment or cataract may result in visual impairment or blindness. Eyes exhibiting retinal dysplasia may be classified according to the number of layers from the retinal structure that are represented in the rosettes. Three-layer rosette. Two-layer rosette. Single-layer rosette. Primitive unilayer rosette. The etiology of retinal dysplasia includes viral disorders, irradiation, X-radiation, intrauterine trauma and heritable factors.     

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.     

Factor X deficiency in a Jack Russell terrier

Deficiency in factor X (Stuart-Prower factor) was identified in a 7-month-old spayed female Jack Russell Terrier following recurrent bleeding episodes. Various relatives were screened for factor X deficiency and low and subnormal levels were identified in the father and paternal grandmother, respectively. Factor X deficiency has been previously documented in a family of American Cocker Spaniels, in which the inheritance pattern appeared to be an autosomal dominant trait with variable expression. This is the first report describing this coagulopathy in the Jack Russell Terrier.     

Ophthalmoscopic characteristics in sheep and goats: comparative study

The ocular fundus was examined in 40 goat eyes and 40 sheep eyes by studying ophthalmoscopic characteristics and retinograms. Similarities and differing characteristics were described. In common: tapetal colour; peripheral yellowish area surrounding the Winslow stars; unpigmented areas in the non-tapetal zone; a great amount of myelin in the optic disc; the Bergmeister's papilla and the holoangiotic retinal vascular pattern. Differences: big size of the Winslow stars in goats; myelinizated fibre over the non-tapetal zone in sheep; shape, position and myelin distribution of the optic disc; and the presence of a 'primary artery' in goats.     

Cell proliferation kinetics in the hair root matrix of dogs with healthy skin and dogs with idiopathic seborrhea

Cell proliferation kinetic values were established for the hair root matrix of primary anagen follicles of 14 Beagles and 4 Cocker Spaniels with healthy skin and 9 Cocker Spaniels with primary idiopathic seborrhea. Indices were established by intradermal pulse labeling with tritiated thymidine, followed by cutaneous biopsy and autoradiography. The hair root matrix cell labeling index was 23.4 +/- 3.5% for Beagles, 24.4 +/- 4.0% for healthy Cocker Spaniels, and 24.9 +/- 4.3% for seborrheic Cocker Spaniels. These values indicate a rapidly proliferating cell population. Differences among these cell kinetic data for the 3 groups of dogs were not statistically significant. Although significant cell kinetic differences have been reported for other epidermal structures (interfollicular epithelium, upper hair follicle external root sheath, sebaceous glands) in seborrheic Cocker Spaniels, proliferation of hair root matrix cells apparently remains unaffected.     

Cell proliferation of epidermis, hair follicles, and sebaceous glands of beagles and cocker spaniels with healthy skin

Cell proliferation kinetic values were established for the epidermis, hair follicle epithelium, and sebaceous glands of 10 Beagles and 4 Cocker Spaniels with healthy skin and coats. Values were established by intradermal pulse-labeling injections of [3H]thymidine, examination of cutaneous biopsied tissues, and autoradiography. The epidermal basal cell-labeling index was 1.41 +/- 0.46% for Beagles and 1.71 +/- 0.56% for Cocker Spaniels. The hair follicle basal cell-labeling index was 1.46 +/- 0.78 and 1.07 +/- 0.42%, respectively. Calculated epidermal cell-renewal time for viable layers of the epidermis was 23.38 +/- 5.93 days for Beagles and 20.97 +/- 4.92 days for Cocker Spaniels. Differences between cell kinetic data for the 2 breeds were not significant (P greater than 0.05). The basal cell-labeling index for the sebaceous gland was significantly (P = 0.009) lower for Cocker Spaniels (0.40 +/- 0.18%) than for Beagles (1.81 +/- 1.08%). Seemingly, epidermal and follicular cell proliferation kinetics in healthy dogs was similar between the 2 breeds, whereas sebaceous gland basal cells were less proliferative in healthy Cocker Spaniels than in healthy Beagles.     

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.     

Glomerular Ultrastructural Findings Similar to Hereditary Nephritis in 4 English Cocker Spaniels

Renal disease affecting 3 male and 1 female English Cocker Spaniels was studied. Clinical features of the disease included proteinuria and progressive deterioration of renal function. Dogs were 11 to 27 months old when euthanized because of severe chronic renal failure. Grossly, the renal cortices were thin. Light microscopic evaluation revealed diffuse glomerular disease characterized by mesangial thickening, glomerular fibrosis, periglomerular fibrosis, and glomerular obsolescence. Based on these clinical and pathologic features, familial nephropathy of English Cocker Spaniels was suspected despite the fact that the individual dogs were not closely related. On transmission electron microscopy, a distinctive ultrastructural lesion was observed in the glomerular basement membranes (GBM) of all dogs. The GBM exhibited extensive thickening, multilaminar splitting, and fragmentation. Electron dense deposits, suggestive of immunocomplex glomerular disease, were notably absent. A similar ultrastructural GBM lesion is found in human beings and Samoyeds with hereditary nephritis, diseases caused by mutations in the type IV collagen genes. Familial nephropathy in English Cocker Spaniels may be a form of hereditary nephritis caused by a mutation in one of the collagen IV genes.     

A cardiomyopathy in the English Cocker Spaniel: a clinico-pathological investigation

This report describes some of the characteristics of a cardiomyopathy in English Cocker Spaniels. Forty-nine dogs from a kennel with a history of a cardiomyopathy were assessed clinically, electrocardiographically and radiographically. Angiography, haemodynamic and post-mortem examinations were carried out on selected dogs. On electrocardiographic (ECG) and radiographic criteria the dogs were classified into five groups. Twenty-six dogs (Group 1) were normal. Seven dogs (Group 2) showed ECG changes compatible with left or biventricular hypertrophy in the absence of radiographic abnormality. This was interpreted as concentric hypertrophy. Seven dogs (Group 3) showed ECG and radiographic evidence of cardiac hypertrophy with five of the seven exhibiting enlargement of both chambers. The changes were considered to be compatible with eccentric hypertrophy. Post-mortem findings in dogs with ECG characteristics of Groups 2 and 3 have shown concentric hypertrophy in three cases and eccentric hypertrophy in one case. Six dogs (Group 4) had right axis deviations. Three dogs (Group 5) showed left axis deviations. It is suggested that a cardiomyopathy exists in English Cocker Spaniels initially developing as a concentric hypertrophy and progressing to eccentric hypertrophy. At present the aetiology is unknown.