Uveitis was induced in dogs by intracameral injection of canine lens protein. The lipoxygenase inhibitors phenidone and norhydroguaiaretic acid, and dimethyl sulfoxide decreased fibrin production at 0.5 and 1 hour after induction uveitis. Phenidone and norhydroguaiaretic acid also inhibited the initial increase intraocular pressure early in the course of inflammation. Leukotriene B4 in the aqueous was measured by use of radioimmunoassay at 1 hour after inflammation. In control dogs, 230 to 1,700 pg of leukotriene B4/ml was measured; in dogs treated with phenidone, leukotriene, B4 was not measured.

OBJECTIVE To compare tear cortisol concentrations between horses and ponies with pituitary pars intermedia dysfunction (PPID) and healthy nonaged (≤ 15 years old) and aged (≥ 20 years old) horses and to determine whether serum and tear cortisol concentrations were correlated. ANIMALS 11 horses and ponies with PPID and 20 healthy control horses and ponies (11 nonaged and 9 aged). PROCEDURES Paired tear and serum samples were obtained from PPID and control animals. All animals were free of active ocular disease. Tear and serum cortisol concentrations were measured with an ELISA and chemiluminescent assay, respectively. Groups were compared with Kruskal-Wallis and Mann-Whitney U tests, and Spearman correlation analysis was used to examine relationships between tear and serum cortisol concentrations within groups. RESULTS Median tear cortisol concentration was significantly higher in PPID animals than in aged control animals, despite comparable serum cortisol concentrations in PPID and aged control animals. Median tear-to-serum cortisol concentration ratios were also significantly higher in PPID animals than in aged control animals. Serum and tear cortisol concentrations were not significantly correlated in PPID or control animals. CONCLUSIONS AND CLINICAL RELEVANCE Some horses and ponies with PPID had increased tear cortisol concentrations, compared with concentrations in healthy aged animals. Localized cortisol production in the tear film or altered cortisol binding dynamics could have contributed to this increase. Further studies are warranted to evaluate these mechanisms and to determine whether increased tear cortisol concentrations are associated with delays in corneal wound healing in horses and ponies with and without PPID.

Blue eye disease, caused by a porcine rubulavirus (PoRV), is an emergent viral swine disease that has been endemic in Mexico since 1980. Atypical outbreaks were detected in 1990 and 2003. Growing and adult pigs presented neurological signs, mild neurological signs were observed in piglets, and severe reproductive problems were observed in adults. Amino acid sequence comparisons and phylogenetic analysis of the hemagglutinin-neuraminidase (HN) protein revealed genetically different lineages. We used cross-neutralization assays, with homologous and heterologous antisera, to determine the antigenic relatedness values for the PoRV isolates. We found antigenic changes among several strains and identified a highly divergent one, making up a new serogroup. It seems that genetically and antigenically different PoRV strains are circulating simultaneously in the swine population in the geographical region studied. The cross neutralization studies suggest that the HN is not the only antigenic determinant participating in the antigenic changes among the different PoRV strains.

Protein concentration was determined, using the Bradford technique, in tears from cats with normal corneas and from cats with corneal sequestrum. Tears from the former group contained 5.81 +/- 2.29 mg of protein/ml; those from cornmeal sequestrum-affected cats contained 6.21 +/- 2.21 mg/ml. Difference between the 2 values was not significant. Molecular weight determination was made, using 4 to 20% sodium dodecyl sulfate-polyacrylamide gels. Molecular mass of proteins ranged from 263 to 14 kDa. There was no detectable difference in the band patterns for the 2 groups.

Numbers of mast cells in the cornea, sclera, choroid, ciliary body, iris, and retina of sections of globes from 35 clinically normal dogs and 34 dogs with secondary glaucoma was determined. Fixed globes were trimmed along a vertical midsagittal plane and embedded in paraffin. Tissue sections, approximately 6 micrometer thick, were stained with toluidine blue for identification of mast cells. In normal globes, most of the mast cells were observed in the anterior portion of the uvea, and fewer mast cells were seen in the choroid and sclera. Mast cells were not observed in the retina and were seldom observed in the cornea of dogs with or without glaucoma. In sections of glaucomatous globes, mast cells were distributed evenly in the uvea and sclera, and fewer mast cells were present than in normal globes, regardless of the cause of glaucoma.

Uveitis was induced in dogs by intracameral injection of canine lens protein. The lipoxygenase inhibitors phenidone and norhydroguaiaretic acid, and dimethyl sulfoxide decreased fibrin production at 0.5 and 1 hour after induction uveitis. Phenidone and norhydroguaiaretic acid also inhibited the initial increase intraocular pressure early in the course of inflammation. Leukotriene B4 in the aqueous was measured by use of radioimmunoassay at 1 hour after inflammation. In control dogs, 230 to 1,700 pg of leukotriene B4/ml was measured; in dogs treated with phenidone, leukotriene, B4 was not measured.

To compare the effect of intraperitoneal administered Carvacrol with bevacizumab in an oxygen-induced retinopathy (OIR) model in rats. Twenty-eight newborn rats were included in the study and the OIR model was created with the 50/10% oxygen style. The study consisted of 4 groups and each rat in the groups received an intraperitoneal injection of 0.01 mL once on the postnatal 14th day. While the OIR model was not created in Group I (control group), it was created for Groups II, III, and IV. Groups I and II were injected with 0.9% NaCl solution, Group III with bevacizumab, and Group IV with carvacrol. The rats were sacrificed on the postnatal 18th day.Histopathological and immunohistochemical studies showed that the number of retinal vascular endothelial cells (RVECs) and nuclear factor (NF)-κB levels decreased similarly in Group III and Group IV compared to Group II. RVECs values for Group I, Group II, Group III and Group IV were measured as 1.26±0.80, 27.10±3.63, 7.54±1.38, and 6.22±1.22, respectively and it differed significantly between groups (p<0.001). Likewise, NF-κB levels were recorded as 0.61 ± 0.30, 4.36±0.65, 2.68±0.44, and 2.85±0.58, respectively and it differed significantly between groups (p<0.001). On the other hand, RVECs and NF-κB levels were similar between Group III, and Group IV (p values were 0.58 and 0.91, respectively).The study demonstrated that carvacrol significantly reduced retinal pathological neovascularizations, RVECs, and NF-κB levels. Moreover, the observed effects were comparable to those of bevacizumab.

An ELISA for detection of Toxoplasma gondii-specific IgA in feline serum was developed. A group of cats (n = 7) was inoculated orally with T gondii bradyzoites. Toxoplasma gondii-specific serum IgM, IgG, and IgA responses were followed sequentially by use of the ELISA for 34 weeks. Serum IgA was detected later than IgM or IgG, and was detected in most cats on week 34 after inoculation. None of the cats was seropositive for IgA during the oocyst-shedding period. A group of client-owned cats with suspected clinical toxoplasmosis and a group of healthy cats were tested for T gondii-specific IgA in serum. A trend toward association of T gondii-specific IgA in serum of cats with ocular disease was observed.

OBJECTIVE To characterize the distribution and intensity of cyclooxygenase (COX)-2 expression in the eyes of cats with and without uveitis and to determine whether COX-2 expression is correlated with severity of inflammation. SAMPLES Archived ocular tissue specimens from 51 cats with and 10 cats without ocular disease. PROCEDURES Specimens from only 1 eye were evaluated for each cat. Specimens were stained with H&E stain or immunohistochemical stain for detection of COX-2 and reviewed. For each eye, the type, severity, and distribution of inflammation and the distribution and intensity of COX-2 expression were determined for the uvea and other ocular tissues. Correlation between COX-2 expression and inflammation severity was also assessed. RESULTS COX-2 was not expressed in any nondiseased eye. Of the 51 diseased eyes, 20 had histologic evidence of lymphocytic-plasmacytic uveitis, 13 had neutrophilic uveitis, 11 had diffuse iris melanoma with uveitis, and 7 had diffuse iris melanoma without uveitis. Of the 44 eyes with uveitis, COX-2 was detected in the uvea of 16, including 11 eyes with lymphocytic-plasmacytic uveitis, 4 with neutrophilic uveitis, and 1 with diffuse iris melanoma–induced uveitis. Inflammation was severe, moderate, or mild in 10, 5, and 1 of those eyes, respectively. Cyclooxygenase-2 was detected in the cornea of 21 eyes with uveitis and 1 eye with diffuse iris melanoma without uveitis. Uveitis severity was positively correlated with COX-2 expression in both the uvea and cornea. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that COX-2 is an inflammatory mediator in feline uveitis but not diffuse iris melanoma.