Forty‐four related Great Pyrenees dogs were examined ophthalmoscopically. Focal retinal elevations, multiple gray–tan–pink subretinal patches, and discrete areas of tapetal hyper‐reflectivity were seen in 19 dogs, ranging from 13 weeks to 10 years of age. These lesions varied in size from focal spots that were barely visible with the indirect ophthalmoscope to areas that were larger than the optic disc. Complete blood cell counts, serum biochemical profiles, urinalyses, and blood pressure measurements were completed on four affected dogs and all were within normal reference ranges. Photopic and scotopic electroretinography was completed and the a‐wave and b‐wave amplitudes and latencies were similar for affected and age‐matched nonaffected Great Pyrenees and other normal dogs. Electroretinograms that were examined twice during a 3‐year period on three affected adult dogs did not reveal significant progressive deterioration of the a or b‐wave parameters. Fluorescein angiography was completed on four affected dogs of ages 1 (n = 2), 5, and 6 years. These angiograms were repeated in three of these dogs 1 year later. The blood ocular barrier was intact in these dogs but there was blocked choroidal fluorescence. Postmortem examination, light microscopy, scanning and transmission electron microscopy were performed on three affected puppies and two affected adult dogs. These examinations revealed that the lesions in the puppies were limited to bilateral multiple areas of retinal pigment epithelial vacuolation, hypertrophy, and apparent separation from Bruch’s membrane, and multiple serous retinal detachments. The affected adult dogs had focal retinal degeneration and retinal pigment epithelial hypertrophy, hyperplasia and pigmentation. Pedigree analysis and test mating confirm that this condition is inherited, probably as an autosomal recessive trait. This condition develops at ≈ 13 weeks of age and the focal areas of retinal detachment and retinal pigment epithelial vacuolation progress to permanent and stable focal areas of retinal degeneration, and retinal pigment epithelial hypertrophy and pigmentation.

Three cats with indolent corneal ulcers and one cat with bilateral corneal sequestration and normal aqueous tear production were found to have rapid tear break-up times (BUTs). Tear BUTs in clinically affected cats averaged 2.5 +/- 1.29 s and 2.33 +/- 0.58 s for the right and left eyes, respectively. Palpebral conjunctival biopsies were harvested from consistent sites from each eye of affected cats (n = 7 affected eyes), and age-and breed-matched controls (n = 2 unaffected eyes). Light microscopy revealed a marked decrease to complete absence of conjunctival goblet cells (average goblet cell (GC):epithelial cell (EC) density = 18:50), conjunctival epithelial dysplasia, squamous metaplasia, and neutrophilic and mononuclear cell submucosal infiltration in affected cats. Specimens from the control cats had an average GC:EC density of 34:50, and minimal submucosal inflammatory infiltrate. The corneas (n = 7 eyes) healed following surgical keratectomy with (n = 2 eyes) or without (n = 1 eye) conjunctival pedicle flaps, superficial keratectomy and striate keratotomy with (n = 2 eyes) or without (n = 2 eyes) third eyelid flaps, and mucinomimetic tear supplementation (n = 5 eyes). Goblet cell regeneration was confirmed after 5 months of mucinomimetic supplementation (n = 2 eyes). The etiology for these mucin deficiencies remains unknown.

Silicone tubing was used to divert aqueous humor from the anterior chamber of the right eye to the rostral compartment of the right frontal sinus in four clinically normal mixed-breed dogs. Biomicroscopic examination, and pneumoapplanation tonometry and tonography, completed for up to 18 weeks postoperatively, confirmed gonioimplant function in all four cases. The dogs were euthanized at 6, 8, 16 and 18 weeks postoperatively. Gonioimplant patency was further confirmed by postmortem examination of the globes, implants and frontal sinuses. Gross and light microscopic examinations revealed iridal attachments to the implant (n = 4), mild anterior uveitis (n = 3), anterior subcapsular cataracts (n = 4), and focal corneal (n = 3) and scleral (n = 3) scarring in the operated globes. Light microscopic examination of frontal sinus specimens revealed mild lymphocytic proliferation and fibrosis immediately adjacent to the implant entrance site. There were no bacteria detected on aerobic or anaerobic cultures of the frontal sinuses or light microscopic examination of the globes or frontal sinuses. Results indicate that the frontal sinus shunting of aqueous humor is a safe and effective means of extraorbital aqueous diversion with potential applicability in the management of glaucoma.

Ocular sarcoma was diagnosed by light microscopic examination in enucleated globes (n = 4), orbital tissue biopsy (n = 1) and ocular evisceration contents (n = 1) from six cats. To determine if feline leukemia virus (FeLV) or a replication-defective FeLV, feline sarcoma virus (FeSV), was present in these ocular sarcomas, immunohistochemistry (IHC) and polymerase chain reaction (PCR) for FeLV were utilized. Immunohistochemical staining for FeLV glycoprotein 70 (gp70) was performed on all six formalin-fixed, paraffin-embedded tumors using an avidin-biotin complex technique. DNA was extracted from each specimen and a 166 bp region of the FeLV long-terminal repeat (LTR) was amplified by PCR. All tumors were composed primarily of spindle cells; two neoplasms had PAS-positive basement membrane enveloping areas of spindle cells. All tumors involved the uvea and five of six tumors showed transcleral extension, one of which invaded the optic nerve. Immunohistochemical staining for FeLV gp 70 was negative. PCR to amplify a portion of the FeLV LTR was negative. Based on these findings of these limited number of cases, FeLV/FeSV may not play a role in the tumorigenesis of feline ocular sarcomas. However, additional tumors representing all morphological subtypes should be investigated for the presence of viral antigen and DNA. It is important to determine the etiology and pathogenesis of these malignant ocular sarcomas. If the cell of origin and pathogenesis involve ocular and lenticular injury, and FeLV/FeSV is not present, then the clinical management of cases of feline ocular trauma, uveitis and glaucoma may prevent the development of this tumor.