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.

Results indicated that the PRTT and STT were both viable methods for measurement of tear production in Hispaniolan Amazon parrots. Topical application of an ophthalmic anesthetic agent did not have a significant effect on the PRTT values but significantly decreased the STT values.

The results of our study identified a population of ERU cases with an active intraocular Leptospira infectious process in the Southern United States. The diagnosis of intraocular leptospirosis required ocular fluid sampling for PCR or culture. Twenty-one percent of ocular fluid samples were positive by culture and forty-five percent by PCR; no control horses were positive by either culture or PCR. These findings are in contrast to a recent study from the Southeastern US that showed no evidence of bacterial DNA by PCR and supports the conclusion that a regional variation in Leptospira infections exists. The most common culture isolate was the serovar pomona; additionally, we report the first cases of serovar grippotyphosa outside of Europe. Title Role of intraocular Leptospira infections in the pathogenesis of Equine Recurrent Uveitis in the Southern United States.Abstract: Equine Recurrent Uveitis (ERU) has been linked to leptospirosis in Europe, however regional differences exist in reports from the United States. The objective of this study was to investigate the role of intraocular leptospiral infections in horses with ERU in the Southern United States. Blood and ocular fluid samples were collected from horses with ERU as well as normal controls. Leptospira serology was performed using microscopic agglutination test (MAT). Aqueous and vitreous humor samples were obtained and submitted for aerobic and Leptospira culture, PCR and MAT. Twenty-one control horses (40 eyes) and 31 ERU horses (46 eyes) were available. Serology was available for 48/52 horses: 16/21 control and 23/27 affected horses were positive for at least one serovar; bratislava was the most common serovar identified. Bacillus sp. and Micrococcus sp. were cultured from one control eye; Streptococcus sp. (n=1) and Leptospira (n=6) from the eyes of 6 ERU horses. Leptospira isolates belonged to serogroup pomona (n=4) and grippotyphosa (n=2). PCR results were positive in 14/31 (45%) horses with ERU; no control horses were positive by PCR (p=0.0001). MAT was positive for 17/24 of ERU horses (71%) and 1/21 (4.7%) of normal horses (p<0.0001). Horses with ERU had a high prevalence of Leptospira infection based on PCR and MAT results from intraocular fluids compared to controls. The diagnosis of intraocular infections was not aided by serology and required specific, invasive sampling of ocular fluid. Leptospira infection should be considered as a cause of ERU in the Southern United States.

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Fatal familial insomnia (FFI) is an inherited prion disease characterized by progressive insomnia and dysautonomia with only modest cognitive impairment early in the disease, associated with atrophy and gliosis in the medial thalamus, but without spongiform change. FFI is associated with an aspartic acid to asparagine mutation at codon 178 of the PrP gene (D178N) in conjunction with methionine at the codon 129 polymorphic site on the mutant allele (cis-129M). We report a pedigree with this genotype in which marked clinicopathologic phenotypic heterogeneity occurred including typical Creutzfeldt-Jakob disease, FFI, and what was thought to be an autosomal dominant cerebellar ataxia (ADCA)-like-illness, suggesting that the genotype-phenotype correlation is not as tight for this mutation as is frequently supposed.