Objectives To determine the accuracy and precision of the Icare® TONOVET Plus rebound tonometer and the Tono‐Pen AVIA Vet™ applanation tonometer for intraocular pressure (IOP) measurement in normal ex vivo canine eyes and comparison to earlier models of these tonometers. Animals & procedures The anterior chambers of six normal dog eyes were cannulated ex vivo. IOP was measured with the TONOVET (TV01), TONOVET Plus, Tono‐Pen Vet™, and Tono‐Pen AVIA Vet™ at manometric IOPs ranging from 5 to 70 mm Hg. Data were analyzed by linear regression, ANOVA and Bland‐Altman plots. A P value ≤ .05 was considered significant. Results Intraocular pressure values obtained using the TONOVET Plus and TV01 were significantly more accurate than with the Tono‐Pen VET and Tono‐Pen AVIA Vet, particularly at higher IOPs (30‐70 mm Hg). Accuracy was not significantly different between any of the devices in the low to normal physiologic IOP range (5‐25 mm Hg). Level of precision was high for all devices, though the TONOVET Plus was more precise than the Tono‐Pen Vet in the 5‐25 mmHg range and the TV01 was more precise than the Tono‐Pen AVIA Vet over the whole IOP range. Conclusions All devices underestimated IOP, particularly at higher pressures. Rebound tonometers were more accurate over the full range of IOP tested and in the high IOP range; however, there were no significant differences in accuracy among devices in the physiologic IOP range. All tonometers can provide clinically useful IOP readings in dogs, but rebound and applanation tonometers should not be used interchangeably.
rdAc cats show preservation of the central retina with maintenance of EZ integrity, which recapitulates findings in human patients.
The cat is emerging as a promising large animal model for preclinical testing of retinal dystrophy therapies, for example, by gene therapy. However, there is a paucity of studies investigating viral vector gene transfer to the feline retina. We therefore sought to study the tropism of recombinant adeno-associated viral (rAAV) vectors for the feline outer retina. We delivered four rAAV serotypes: rAAV2/2, rAAV2/5, rAAV2/8 and rAAV2/9, each expressing green fluorescent protein (GFP) under the control of a cytomegalovirus promoter, to the subretinal space in cats and, for comparison, mice. Cats were monitored for gene expression by in vivo imaging and cellular tropism was determined using immunohistochemistry. In cats, rAAV2/2, rAAV2/8 and rAAV2/9 vectors induced faster and stronger GFP expression than rAAV2/5 and all vectors transduced the retinal pigment epithelium (RPE) and photoreceptors. Unlike in mice, cone photoreceptors in the cat retina were more efficiently transduced than rod photoreceptors. In mice, rAAV2/2 only transduced the RPE whereas the other vectors also transduced rods and cones. These results highlight species differences in cellular tropism of rAAV vectors in the outer retina. We conclude that rAAV serotypes are suitable for use for retinal gene therapy in feline models, particularly when cone photoreceptors are the target cell.
Pathogenic variants in retinol dehydrogenase 5 (RDH5) attenuate supply of 11-cis-retinal to photoreceptors leading to a range of clinical phenotypes including night blindness because of markedly slowed rod dark adaptation and in some patients, macular atrophy. Current animal models (such as Rdh5−/− mice) fail to recapitulate the functional or degenerative phenotype. Addressing this need for a relevant animal model we present a new domestic cat model with a loss-of-function missense mutation in RDH5 (c.542G > T; p.Gly181Val). As with patients, affected cats have a marked delay in recovery of dark adaptation. In addition, the cats develop a degeneration of the area centralis (equivalent to the human macula). This recapitulates the development of macular atrophy that is reported in a subset of patients with RDH5 mutations and is shown in this paper in seven patients with biallelic RDH5 mutations. There is notable variability in the age at onset of the area centralis changes in the cat, with most developing changes as juveniles but some not showing changes over the first few years of age. There is similar variability in development of macular atrophy in patients and while age is a risk factor, it is hypothesized that genetic modifying loci influence disease severity, and we suspect the same is true in the cat model. This novel cat model provides opportunities to improve molecular understanding of macular atrophy and test therapeutic interventions for RDH5-associated retinopathies.
Leber Congenital Amaurosis (LCA) is a group of debilitating inherited retinal diseases that cause retinal degeneration and eventual blindness in children. 1 About 20% of LCA cases are caused by mutations in the centrosomal 290 kDa (CEP290) gene. 1 Mutations in this gene have been associated with a broad spectrum of diseases, ranging from neonatal lethal syndromes to retina-only phenotypes. [2][3][4][5][6][7][8][9] The most common retinal phenotype caused by mutations in this gene is LCA, with the commonest mutation being a mutation in intron 26 (c.2991 + 1655A > G) that creates a strong splice donor site, leading to the introduction of a cryptic exon in the CEP290 transcript. 10 The additional
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