The geographic form of retinal dysplasia in dogs is not always a congenital abnormality

To examine the congenital nature of the geographic form of focal/multifocal retinal dysplasia, we carried out a retrospective analysis of the medical records of dogs produced in a closed colony of service dogs who receive very thorough ophthalmologic examinations early in their life, and later, when they return for training. Medical records were reviewed from all dogs produced by The Seeing Eye, Inc. between October 1991 and September 1998, and which had a diagnosis of geographic retinal dysplasia coded. We identified 23 dogs of five different breeds or interbreed crosses that comprise the breeding and production program (Golden Retrievers, German Shepherds, Labrador Retrievers, Labrador Retriever/Golden Retriever cross and German Shepherd/Labrador Retriever cross) in which the results of at least two complete ophthalmic examinations were documented, the first before 10 weeks of age, and the second when the dog was a young adult. Of the 23 dogs, only one was identified as affected with the geographic form of retinal dysplasia when examined at 5–6 weeks of age. The remaining dogs were normal. Our findings indicate that, in most cases, the geographic form of retinal dysplasia is not present in dogs prior to 10 weeks of age. These findings indicate the need to revise recommendations for early screening of dogs for retinal dysplasia.     

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.     

Investigation of fellow eye of unilateral retinal detachment in Shih‐Tzu

Objective To investigate disease in the fellow eye, and consider the relation to rhegmatogenous retinal detachment (RRD) in Shih‐Tzus. Animals studied The fellow eyes of 49 Shih‐Tzus (27 male, 22 female; median age: 6.8 years) with unilateral RRD diagnosed by funduscopy or ultrasonography at Rakuno Gakuen University Teaching Animal Hospital were assessed in this study. Procedures Ophthalmic examinations (including menace response, pupillary light reflex, slit‐lamp biomicroscopy, and funduscopy) were performed in the subjects. Electroretinography was performed in 12 eyes that developed retinal degeneration. Maximum follow‐up period was 42 months. Results Cataracts and vitreous opacity were observed in 26 (53%) and 32 eyes (65%), respectively, by slit‐lamp biomicroscopy. Retinal degeneration with various degrees of hyper‐reflectivity of the tapetal fundus and/or attenuation of retinal vessels was observed in 35 eyes (71%) on funduscopy. A reduction of amplitude in rod, standard combined and 30 Hz flicker electroretingram was detected in 5 (42%), 10 (83%), and 6 eyes (50%), respectively. During the follow‐up period, RRD was detected in six eyes. Conclusion Retinal degeneration was frequently detected by funduscopy and electroretingrams in the fellow eye in Shih‐Tzus with RRD. In our subjects, vitreous degeneration was also observed frequently. It has been reported that peripheral retinal degeneration is one of the causes of RRD associated with vitreous degeneration in humans. We assume that primary retinal degeneration with secondary vitreous degeneration is one of the causes of RRD in Shih‐Tzus.     

Levels of trace elements in liver from Norwegian moose, reindeer and red deer in relation to atmospheric deposition

The levels of antimony, arsenic, cadmium, copper, lead, mercury, molybdenum, selenium and zinc were determined in liver of moose, reindeer and red deer from differen localities in Norway. Reindeer had considerably higher levels of mercury, lead and arsenic than moose and red deer. These findings are considered to be related to differences in feeding habits since reindeer on highland plateaus feed mainly on lichens which have been shown to accumulate trace elements. The levels of arsenic, and to some extent also selenium and cadmium, in moose and reindeer liver showed a north-south gradient closely related to the regional distribution of these elements in the forest moss. As regards lead, a north-south gradient and a relationship to moss levels, were found in moose liver only. It therefore seems that atmospheric deposition of the elements mercury, lead, arsenic, cadmium and selenium contribute to the body burden of these elements in cervides in Norway. There was no evidence of these elements accumulating to toxic levels.     

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.     

Hypertensive retinopathy and choroidopathy in a cat

Bilateral hypertensive retinopathy and choroidopathy with bullous retinal detachment was diagnosed in a 17-year-old, female spayed Domestic Short-haired cat. The underlying cause of the systemic hypertension could not be determined. The blood pressure was lowered successfully with the oral application of the L-type calcium channel blocker amlodipine besylate. The cat subsequently regained vision. The improvement in retinal function was documented using electroretinography.     

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

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

Excitotoxicity can be mediated through an interaction within the optic nerve; activation of cell body NMDA receptors is not required

Axonal trauma leads to a series of pathologic events that can culminate in neuronal death. Although the precise mechanisms of retinal ganglion cell death after optic nerve crush in the rat model have not been elucidated, glutamate antagonists can protect retinal ganglion cells after optic nerve axotomy. We therefore explored whether a glutamate congener was toxic if applied directly within the optic nerve, or if toxicity depended upon an interaction at the cell body level. NMDA reduced retinal ganglion cell survival when applied directly into the rat optic nerve. Glutamate can be toxic if administered within the optic nerve; a direct effect at the cell body is not necessary. Future work will help to additionally unravel the steps by which axotomy induces excitotoxic damage to ganglion cells, and perhaps indicate protective interventions.