Objective—To compare the effects of meloxicam, carprofen, and flunixin meglumine administered IV on the concentration of prostaglandin E2 (PGE2) in the aqueous humor of dogs with aqueocentesis-induced anterior uveitis.
Animals—15 adult dogs with ophthalmically normal eyes.
Procedures—Each dog was assigned to 1 of 4 treatment groups. Treatment groups were saline (0.9% NaCl) solution (1 mL, IV), meloxicam (0.2 mg/kg, IV), carprofen (4.4 mg/kg, IV), and flunixin meglumine (0.5 mg/kg, IV). Each dog was anesthetized, treatment was administered, and aqueocentesis was performed on each eye at 30 and 60 minutes after treatment. Aqueous humor samples were frozen at −80°C until assayed for PGE2 concentration with an enzyme immunoassay kit.
Results—For all 4 treatment groups, PGE2 concentration was significantly higher in samples obtained 60 minutes after treatment, compared with that in samples obtained 30 minutes after treatment, which indicated aqueocentesis-induced PGE2 synthesis. For aqueous humor samples obtained 60 minutes after treatment, PGE2 concentration did not differ significantly among groups treated with saline solution, meloxicam, and carprofen; however, the PGE2 concentration for the group treated with flunixin meglumine was significantly lower than that for each of the other 3 treatment groups.
Conclusions and Clinical Relevance—Flunixin meglumine was more effective than meloxicam or carprofen for minimizing the PGE2 concentration in the aqueous humor of dogs with experimentally induced uveitis. Flunixin meglumine may be an appropriate pre-medication for use prior to intraocular surgery in dogs.
Objective—To compare effects of orally administered tepoxalin, carprofen, and meloxicam for controlling aqueocentesis-induced anterior uveitis in dogs, as determined by measurement of aqueous prostaglandin E2 (PGE2) concentrations.
Animals—38 mixed-breed dogs.
Procedures—Dogs were allotted to a control group and 3 treatment groups. Dogs in the control group received no medication. Dogs in each of the treatment groups received an NSAID (tepoxalin, 10 mg/kg, PO, q 24 h; carprofen, 2.2 mg/kg, PO, q 12 h; or meloxicam, 0.2 mg/kg, PO, q 24 h) on days 0 and 1. On day 1, dogs were anesthetized and an initial aqueocentesis was performed on both eyes; 1 hour later, a second aqueocentesis was performed. Aqueous samples were frozen at −80°C until assayed for PGE2 concentrations via an enzyme immunoassay kit.
Results—Significant differences between aqueous PGE2 concentrations in the first and second samples from the control group indicated that aqueocentesis induced uveitis. Median change in PGE2 concentrations for the tepoxalin group (10 dogs [16 eyes]) was significantly lower than the median change for the control group (8 dogs [16 eyes]), carprofen group (9 dogs [16 eyes]), or meloxicam group (9 dogs [16 eyes]). Median changes in PGE2 concentrations for dogs treated with meloxicam or carprofen were lower but not significantly different from changes for control dogs.
Conclusions and Clinical Relevance—Tepoxalin was more effective than carprofen or meloxicam for controlling the production of PGE2 in dogs with experimentally induced uveitis. Tepoxalin may be an appropriate choice when treating dogs with anterior uveitis.
Objective—To evaluate dogs with sudden acquired retinal degeneration syndrome (SARDS) for evidence of pituitary gland, adrenal gland, and pulmonary neoplasia and antiretinal antibodies and to evaluate dogs with neoplasia for antiretinal antibodies.
Animals—57 clinically normal dogs, 17 with SARDS, and 53 with neoplasia.
Procedure—Thoracic radiography, ultrasonography of adrenal glands, and contrast-enhanced computed tomography of pituitary glands were performed in 15 dogs with SARDS. Western blot analysis was performed on sera of all dogs; recoverin (23 kd) and arrestin (48 kd) retinal antibodies were used as positive controls.
Results—Neoplasia was not detected via diagnostic imaging in dogs with SARDS. Western blot analysis revealed bands in all dogs ranging from > 48 to < 23 kd. Prominent bands with equivalent or greater density than 1 or both positive controls at the 1:1,000 dilution, and present at the 1:3,000 dilution, were detected in 28% of clinically normal dogs, 40% of dogs with neoplasia, and 41% of dogs with SARDS. No bands in dogs with SARDS had a consistent location of immune activity, and none were detected at the 23-kd site. The area around the 48-kd site had increased immune activity in all 3 groups.
Conclusions and Clinical Relevance—The etiology of SARDS in dogs does not appear to be similar to cancer-associated retinopathy in humans on the basis of absence of differential antibody activity against retinal proteins. Although dogs with SARDS often have clinical signs compatible with hyperadrenocorticism, neoplasia of the adrenal glands, pituitary gland, or lungs was not detected.
OBJECTIVE To determine the efficacy of Bdellovibrio bacteriovorus 109J for the treatment of calves with experimentally induced infectious bovine keratoconjunctivitis (IBK).
ANIMALS 12 healthy dairy calves.
PROCEDURES For each calf, a grid keratotomy was performed on both eyes immediately before inoculation with Moraxella bovis hemolytic strain Epp63–300 (n = 11 calves) or nonhemolytic strain 12040577 (1 calf). For each calf inoculated with M bovis Epp63–300, the eyes were randomly assigned to receive an artificial tear solution with (treatment group) or without (control group) lyophilized B bacteriovorus 109J. Six doses of the assigned treatment (0.2 mL/eye, topically, q 48 h) were administered to each eye. On nontreatment days, eyes were assessed and corneal swab specimens and tear samples were collected for bacterial culture. Calves were euthanized 12 days after M bovis inoculation. The eyes were harvested for gross and histologic evaluation and bacterial culture.
RESULTS The calf inoculated with M bovis 12040577 did not develop corneal ulcers. Of the 22 eyes inoculated with M bovis Epp63–300, 18 developed corneal ulcers consistent with IBK within 48 hours after inoculation; 4 of those eyes developed secondary corneal ulcers that were not consistent with IBK. Corneal ulcer size and severity and the time required for ulcer healing did not differ between the treatment and control groups.
CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that B bacteriovorus 109J was not effective for the treatment of IBK; however, the experimental model used produced lesions that did not completely mimic naturally occurring IBK.