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1.
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.  相似文献   

2.
Sudden acquired retinal degeneration syndrome (SARDS) is a disease characterised by sudden and bilateral vision loss of dogs. Previous studies failed to identify the underlying cause [Mattson, A., Roberts, S.M., Isherwood, J.M.E., 1992. Clinical features suggesting hyperadrenocorticism associated with sudden acquired retinal degeneration syndrome in a dog. J. Am. Anim. Hosp. Assoc. 28, 199-202; Van der Woerdt, A., Nasisse, M.P., Davidson, M.G., 1991. Sudden acquired retinal degeneration in the dog: clinical and laboratory findings in 36 cases. Prog. Vet. Comp. Ophthamol. 1, 11-18] and earlier investigations about the occurrence of anti-retinal antibodies in SARDS patients showed inconsistent results. To provide a novel approach to those findings we designed a more detailed study. Autoantibodies of SARDS patients and normal controls were tested against the purified autoantigens S-antigen and cellular retinaldehyde binding protein (CRALBP) that play a role in human autoimmune uveitis. Next we tested the autoantibody binding pattern to whole retinal lysate. No difference in the incidence of autoantibodies could be found between SARDS patients and healthy controls while testing the well-known autoantigens S-antigen and CRALBP. Potential novel, yet unknown autoantigens were identified by a screening test using the retinal proteome as an autoantigenic source. In SARDS patients and normal controls, several retinal proteins were bound by IgG antibodies, but one band was strongly marked by SARDS patients. That band was excised, subjected to mass spectrometry (matrix-assisted laser desorption/ionisation-time of flight (MALDI-TOF/TOF)) and identified as neuron-specific enolase. Binding of the IgG autoantibodies of SARDS-affected dogs to this protein was verified using purified NSE, revealing 25% of NSE autoantibody-positive SARDS patients and 0% of negative controls. Our findings indicate that at least some dogs with SARDS have autoantibodies against NSE, although it is unclear whether these play a causative role in SARDS or whether they are the result of retinal destruction by another mechanism.  相似文献   

3.
OBJECTIVE: To determine the presence of serum antiretinal antibodies in sudden acquired retinal degeneration syndrome (SARDS) affected dogs and the size of the antigen to which these antibodies bind via the use of enzyme-linked immunosorbent assay (ELISA) and Western blot immunoassays. ANIMALS STUDIED: Serum was collected from 13 dogs affected by SARDS and five dogs with normal ocular examinations. PROCEDURES: All serum samples were subjected to ELISA with saline-soluble canine retinal tissue and Western blot analyses with SDS solubilized normal canine retinal tissue as the antigen. Antirecoverin (23 kDa) and antiheat shock cognate (65 kDa) antibodies were used as positive controls for both procedures. Affinity-purified goat antidog IgG and IgM labeled with horseradish peroxidase were used for all clinical samples and goat antirabbit IgG was used as the secondary antibody for the positive controls. RESULTS: ELISA demonstrated antibody reaction with all samples. Western blot immunoassays identified multiple bands in all canine serum samples, as well as in negative controls. Approximate sizes of the bands were 25 and 50 kDa, corresponding to IgG light and heavy chains, respectively. CONCLUSION: No antiretinal autoantibodies were identified in the serum of dogs affected by SARDS as compared to normal canine patients.  相似文献   

4.
OBJECTIVE: To evaluate dogs with sudden acquired retinal degeneration syndrome (SARDS) for evidence of pituitary gland, adrenal gland, and pulmonary neoplasia and antiretinal antibodies and to evaluate dogs with neoplasia for antiretinal antibodies. ANIMALS: 57 clinically normal dogs, 17 with SARDS, and 53 with neoplasia. PROCEDURE: Thoracic radiography, ultrasonography of adrenal glands, and contrast-enhanced computed tomography of pituitary glands were performed in 15 dogs with SARDS. Western blot analysis was performed on sera of all dogs; recoverin (23 kd) and arrestin (48 kd) retinal antibodies were used as positive controls. RESULTS: Neoplasia was not detected via diagnostic imaging in dogs with SARDS. Western blot analysis revealed bands in all dogs ranging from > 48 to < 23 kd. Prominent bands with equivalent or greater density than 1 or both positive controls at the 1:1,000 dilution, and present at the 1:3,000 dilution, were detected in 28% of clinically normal dogs, 40% of dogs with neoplasia, and 41% of dogs with SARDS. No bands in dogs with SARDS had a consistent location of immune activity, and none were detected at the 23-kd site. The area around the 48-kd site had increased immune activity in all 3 groups. CONCLUSIONS AND CLINICAL RELEVANCE: The etiology of SARDS in dogs does not appear to be similar to cancer-associated retinopathy in humans on the basis of absence of differential antibody activity against retinal proteins. Although dogs with SARDS often have clinical signs compatible with hyperadrenocorticism, neoplasia of the adrenal glands, pituitary gland, or lungs was not detected.  相似文献   

5.
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.  相似文献   

6.
Glaucoma and inherited retinal degeneration/dystrophy are leading causes of blindness in veterinary patients. Currently, there is no treatment for the loss of vision that characterizes both groups of diseases. However, this reality may soon change as recent advances in understanding of the disease processes allow researchers to develop new therapies aimed at preventing blindness and restoring vision to blind patients. Elucidating the molecular mechanisms of retinal ganglion cell death in glaucoma patients has led to the development of neuroprotective drugs which protect retinal cells and their function from the disastrous effects of elevated pressure. Identification of the genetic mutation responsible for inherited degenerations and dystrophies of the outer retina has enabled researchers using gene therapy to restore vision to blind dogs. Other patients may benefit from retinal transplantation, stem cell therapy, neuroprotective drugs, nutritional supplementation and even retinal prostheses. It is possible that soon it will be possible to restore sight to some blind patients.  相似文献   

7.
Pituitary dependent hyperadrenocorticism (PDH) shows a high morbidity and blindness is one of its complications. Compression of the optic chiasm (OC) by the hypophysis adenoma is one of the causes. Another cause could be due to vascular and metabolic alterations of the PDH. Out of a total of 70 dogs with confirmed diagnosis of PDH, 12/70 showed blindness. In only 2/12 the OC was compromised. Electroretinography in dogs without the OC being compromised showed altered A and B wave patterns. Ophthalmological Doppler showed an alteration of the blood flow only in blind dogs without OC compression. Cortisol concentrations (Co), triglycerides (Tg) and glycaemia (G) were greater in 10 dogs with non-compressive blindness vs. dogs with conserved vision. Loss of vision correlated with the increase in these variables. Blindness in dogs with PDH would be related to changes in retinal blood flow, associated to higher Co, Tg and G concentrations.  相似文献   

8.
We present a case of reactive histiocytic disease involving the orbit, optic nerve, retina, and choroid in a Border Collie dog initially presenting for vision loss. Long-term partial return of vision has been achieved with systemic immunosuppression. Anterior segment and ocular surface manifestations of reactive histiocytic disease in dogs are relatively common. Posterior segment and orbital involvement, however, are minimally documented in the existing literature. To the authors' knowledge, this is the first report of disease confined to the orbit and posterior segment as well as the first report of vision loss as a presenting complaint for reactive histiocytic disease. Clinical, magnetic resonance imaging, cytologic, and histopathologic findings are reviewed.  相似文献   

9.
Two cases of sudden onset of blindness associated with ocular protothecosis in dogs are reported. Both were adult, spayed female, mixed-breed dogs that lacked the usual clinical signs of systemic infection with Prototheca species. Physical abnormalities at the time of presentation were limited to the affected eyes which had serous discharge, hyperemic conjunctiva, and aqueous flare. The pupillary light reflexes were slow, and the menace reflexes were absent. Both dogs had glaucoma. Results of complete blood counts and serologic titres for antibodies to Blastomyces dermatitidis and Histoplasma capsulatum were within reference intervals. Protothecosis was diagnosed by cytologic analysis of vitreous humor and was confirmed at necropsy. These two cases were unusual because of their presenting signs and prolonged course of disease progression.  相似文献   

10.
The outcomes of dog's eyes with chronic (> 1 month) retinal detachment and giant retinal tears without therapy were compared with those treated with topical steroids and antiglaucoma medications, and with those that received a vitrectomy, retinal reattachment, endolaser therapy, and silicone oil tamponade. Fourteen of 16 eyes that did not receive therapy developed uveitis and secondary glaucoma, and were enucleated (4) or eviscerated (6); and 2 dogs were euthanized due to blindness and uveitis. Two eyes in 2 dogs remain without treatment, 1 and 3 years later. Fifteen of 19 eyes that received topical therapy developed nonresponsive uveitis and secondary glaucoma, and were enucleated (4) or eviscerated (9), 1 dog that was affected bilaterally was euthanized; and 3 eyes remain on topical anti-inflammatory therapy and the medication has been discontinued on 1 eye. Four of 6 eyes surgically reattached remain without clinical manifestations of uveitis and secondary glaucoma and 3 of these eyes have functional vision. Light microscopic observations completed on failed globes in the 3 groups were similar.  相似文献   

11.
Cataracts are a leading cause of blindness in both dogs and humans. Mutations in several genes have been associated with inherited forms of human cataract, but no mutations have been identified as the cause of any form of canine inherited cataract. We have used a candidate gene approach to investigate 20 genes, known to be associated with cataract in humans, for their potential association with the development of hereditary cataract (HC) in dogs. We have identified mutations in the HSF4 gene in Staffordshire Bull Terriers, Boston Terriers and Australian Shepherds affected by HC. Interestingly, different mutations in this single gene may be causing a recessive form of cataract in Staffordshire Bull Terriers and Boston Terriers and a dominant cataract in Australian Shepherds. Identification of the mutations that cause HC in these three breeds provides a method of controlling the disease within populations at risk using a simple diagnostic test, and also establishes cataract in these breeds as models for their human counterparts.  相似文献   

12.
Canine glaucoma is a group of disorders that are generally associated with increased intraocular pressure (IOP) resulting in a characteristic optic neuropathy. Glaucoma is a leading cause of irreversible vision loss in dogs and may be either primary or secondary. Despite the growing spectrum of medical and surgical therapies, there is no cure, and many affected dogs go blind. Often eyes are enucleated because of painfully high, uncontrollable IOP. While progressive vision loss due to primary glaucoma is considered preventable in some humans, this is mostly not true for dogs. There is an urgent need for more effective, affordable treatment options. Because newly developed glaucoma medications are emerging at a very slow rate and may not be effective in dogs, work toward improving surgical options may be the most rewarding approach in the near term. This Viewpoint Article summarizes the discussions and recommended research strategies of both a Think Tank and a Consortium focused on the development of more effective therapies for canine glaucoma; both were organized and funded by the American College of Veterinary Ophthalmologists Vision for Animals Foundation (ACVO‐VAF). The recommendations consist of (a) better understanding of disease mechanisms, (b) early glaucoma diagnosis and disease staging, (c) optimization of IOP‐lowering medical treatment, (d) new surgical therapies to control IOP, and (e) novel treatment strategies, such as gene and stem cell therapies, neuroprotection, and neuroregeneration. In order to address these needs, increases in research funding specifically focused on canine glaucoma are necessary.  相似文献   

13.
Achromatopsia was identified in three Labrador Retriever littermates. The dogs demonstrated day blindness, negotiating obstacles under low‐light conditions, but apparently blind when outdoors. One of the dogs presented with immature bilateral diffuse posterior cortical cataracts and clinical signs of day blindness became apparent following cataract extraction surgery. Electroretinography demonstrated an absence of a cone photoreceptor response to a bright stimulus and a flicker response of 30 Hz in all three dogs. No fundic lesions have been apparent ophthalmoscopically in any of the dogs as the initial presentation of each case. No abnormalities were detected with DNA screening for known mutations of the CNGB3 gene in any of the dogs.  相似文献   

14.
A retrospective case series of 26 cats with diffuse retinal degeneration is presented. The most common presenting complaints included bumping into objects, dilated pupils, and reluctance to jump. Ophthalmic examination findings were consistent with those reported in dogs with progressive retinal atrophy. Breed predilection of the Siamese cat was observed. Cats with primary retinal degeneration presented late in the clinical course of their disease, when vision loss was severe. Early symptoms such as night blindness and secondary ocular complications (i.e., cataract and retinal detachment), reported in dogs with progressive retinal degeneration, were not observed in this study. All cats showed excellent adaptive capabilities to blindness.  相似文献   

15.
OBJECTIVE: To characterize the clinical and morphologic aspects of aqueous humor misdirection syndrome (AHMS) in cats and provide a hypothesis regarding its pathogenesis on the basis of detailed analysis of affected cats. DESIGN: Retrospective study. ANIMALS: 32 cats (40 eyes). PROCEDURE: Medical records of cats in which AHMS was diagnosed from July 1997 to August 2003 were reviewed. In certain cats, results of additional diagnostic testing were also obtained, including A-scan, B-scan, and high-resolution ultrasonography; streak retinoscopy; video keratometry; and infrared neutralizing videoretinoscopy as well as results of analysis of flash-frozen sections and histologic examination of enucleated globes. RESULTS: Cats had a uniformly shallow anterior chamber, intact lens zonules, and a narrowed approach to an open iridocorneal angle. Mean age of affected cats was 11.7 years (range, 4 to 16 years), and female cats were significantly more often affected than male cats. Clinical signs included mydriasis, decreased pupillary light reflex, decreased menace response, and blindness. Glaucomatous changes to the optic nerve, incipient cataracts, and eventual blindness were seen. Intraocular pressure was > or = 20 mm Hg (range, 12 to 58 mm Hg) in 32 of 40 eyes. Ultrasonography and histologic examination revealed a thickened anterior vitreal face interposed between the lens and ciliary body, partial ciliary cleft collapse, and cavitated vitreal regions. Various treatment modalities were used. CONCLUSIONS AND CLINICAL RELEVANCE: AHMS affects older cats, especially females, and may result in glaucoma, vision loss, and signs of ocular pain. Topical administration of carbonic anhydrase inhibitors decreased intraocular pressure.  相似文献   

16.
The most commonly encountered chronic enteropathies in dogs are inflammatory bowel disease (IBD), food allergies, and small intestinal bacterial overgrowth. Recent research in the field of immunopathogenesis of IBD and food allergy in human beings have made available new therapeutic options with immunomodulatory drugs. However, the mechanisms involved in the pathogenesis of canine IBD and food allergy have not been elucidated so far. Further studies focusing on the immunological dysregulation in the mucosa as well as clinical trials with new therapeutic modalities are needed to improve our knowledge and approach to these chronic diseases in dogs.  相似文献   

17.
The role of tumor suppressor genes in the pathogenesis of canine melanoma is incompletely understood. The genes encoding the tumor suppressors p53, Rb, p21 (waf-1), p16 (ink-4a), and PTEN have been postulated to contribute to the pathogenesis of melanoma in humans and experimental animal models. To assess whether inactivation of these genes similarly contributes to the origin and progression of canine melanoma, we examined their expression in seven distinct canine melanoma cell lines and in 31 retrospective samples (representing 29 dogs) of spontaneous canine melanoma. Various patterns suggestive of loss of tumor suppressor function emerged in these cell lines. The most frequently observed abnormality was loss or significant reduction of p16 expression in six of seven cell lines and in 21 of 26 tumor samples. Loss or significant reduction of PTEN expression was seen in four of seven cell lines and in 13 of 27 tumor samples. Although p53 was detectable in all the cell lines and in 24 of 30 tumors, exclusion of p53 from the nuclear compartment was observed in each of the cell lines and in 18 of 25 tumor samples. These results indicate that loss of function of these tumor suppressor proteins is a common occurrence that may contribute to the origin of canine melanoma. In our sample population, abnormalities in the expression or localization of one or more tumor suppressor proteins occurred with similar frequency in malignant and benign tumors; thus, additional work is necessary to determine how these proteins may impact disease progression and response to therapy.  相似文献   

18.
Z Chester  W T Clark 《The Veterinary record》1988,123(26-27):668-671
A telephone survey of 50 owners of blind dogs was made in order to assess how well visually deprived dogs can cope within their environment. Ten of the 50 dogs surveyed died or were euthanased as a direct result of their blindness or ocular disease. Three owners were unable to come to terms with their pet's visual loss. Two dogs died as a result of accidents directly associated with blindness and five dogs were euthanased due to pain caused by glaucoma. Twenty-seven owners reported permanent behaviour or temperament changes in their pets. Behavioural changes included a more cautious approach to the environment and closer contact with the owner. Owners were aware of an obvious compensatory reliance on the senses of hearing and smell. Permanent temperament changes were reported in only two dogs both of whom became more aggressive. Only six of the surveyed dogs were unable or unwilling to find their way around in familiar surroundings. The most consistent measures undertaken by owners to ensure the dogs' safety was to prevent access to roads and to ensure that there was minimal movement of furniture within the home. Six dogs lost interest in exercise after the onset of blindness but a further six were still allowed to roam at large. Of the 32 owners who accompanied their dogs eight reported that restraint on a lead was unnecessary. Twenty-eight owners had encountered people who had suggested it was unkind to keep a blind dog.  相似文献   

19.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited myocardial disease seen in dogs, cats, and humans. A common entity in Boxers and the related English bulldog, the disease is characterized by fatty or fibrofatty replacement of the myocardium, ventricular arrhythmias, and the potential for syncope or sudden death. In some individuals, concomitant left ventricular involvement results in systolic dysfunction and a progression to congestive heart failure. The clinical and pathological characteristics of ARVC share many similarities in dogs and humans, and Boxers serve as an important spontaneous model of the disease.Although multiple mechanisms have been implicated in the pathogenesis of ARVC, the disease is ultimately considered to be a disorder of the desmosome. Multiple causal genetic mutations have been identified in people, and over 50% of affected humans have an identifiable mutation in desmosomal proteins. To date, only a single genetic mutation has been associated with ARVC in Boxer dogs. Other as-yet-undiscovered genetic mutations and epigenetic modifiers of the disease are likely. Treatment of ARVC in dogs is focused on controlling ventricular arrhythmias and associated clinical signs. This article will review the pathophysiology, clinical diagnosis, treatment, and prognosis of ARVC in the dog.  相似文献   

20.
Progressive retinal atrophy was studied in 17 Tibetan Terriers. The diagnosis was made on the basis of clinical signs of the disease, retinal histopathologic findings, or both. Affected dogs were the progeny of matings of affected or ophthalmoscopically normal dogs. Results of the mating supported a simple autosomal recessive mode of inheritance. The disease initially could be diagnosed by findings of night blindness and ophthalmoscopic signs of tapetal hyperreflectivity in affected dogs that were approximately 1 year old. Electroretinograms recorded from affected dogs, compared with those of clinically normal dogs of the same age, did not reveal appreciable abnormalities until affected dogs were 10 months old, at which time a reduction in the amplitude of the b wave was seen in response to a Ganzfeld white-light stimulus. The peak times of the response were unaffected. With progression of the disease, the electroretinographic b-wave amplitude was gradually reduced, and the electroretinographic response was extinguished in affected dogs by the time they were 30 months old. Early in the disease, rod and cone functions were affected equally, with more rapid loss of rod function developing only later in the disease. Fluorescein angiography of affected dogs did not reveal abnormalities earlier than could be detected by ophthalmoscopy. Despite the electroretinographic findings, histopathologic findings included patchy disorientation and disorganization of the outer segments of rods and cones in affected dogs as young as 9 weeks. With progression of the disease, rods were lost at a faster rate than cones, and atrophy of the inner retinal layer was observed.  相似文献   

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