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To determine the effect of α-chymotrypsin treatment on breaking strength and ultrastructural morphology of canine ciliary zonules.

Sample Population

Eyes from young random-source dogs from an animal shelter.


Eyes were obtained immediately after euthanasia of dogs. The enzyme α-chymotrypsin was applied to the ciliary zonules of 1 eye of each dog; the other eye was treated with saline solution as a control. The breaking strength of ciliary zonules was measured, using a linear actuator and force transducer. The lenses and ciliary bodies were then analyzed by scanning and transmission electron microscopy.


α-Chymotrypsin reduced the breaking strength of ciliary zonules by a mean ± SD 44 (± 20)%, compared with that for saline-treated control eyes. Increasing the volume of enzyme further decreased the breaking strength of the zonules. Differences in the appearance of the ciliary body by electron microscopy were not apparent between enzyme- and saline-treated specimens.

Conclusions and Clinical Relevance

Application of α-chymotrypsin to enucleated canine eyes at a concentration used in people significantly reduces the breaking strength of canine ciliary zonules without any apparent damage to the ciliary body. α-Chymotrypsin may be useful in the removal of subluxated canine lenses and in removal of cataractous lenses in young dogs, in which phacoemulsification often results in appreciable post operative capsular opacification. (Am J Vet Res 1998;59:335–339)

Free access
in American Journal of Veterinary Research


Objective—To determine histologic and immunohistochemical characteristics of the multifocal adherent plaques that commonly develop on the internal surfaces of the anterior and posterior lens capsules in dogs with cataracts.

Sample Population—31 anterior and 4 posterior capsular specimens collected during lens extraction surgery in dogs with cataracts.

Procedure—Specimens were evaluated, using light and transmission electron microscopy. Immunohistochemical techniques were used to localize cytokeratin, vimentin, α-smooth muscle-specific actin, fibronectin, tenascin, and transforming growth factor- β (TGF-β) within plaques.

Results—Histologically, plaques comprised elongated spindle-shaped cells that formed a placoid mass. Cells were embedded in an extracellular matrix containing collagen fibrils, often with duplicated or split basement membranes. Immunohistochemically, normal lens epithelial cells and cells within plaques stained for vimentin. Most cells and some areas of the extracellular matrix within plaques stained for TGF-β and α-smooth muscle-specific actin. Fibronectin and tenascin were also detected in the extracellular matrix.

Conclusions and Clinical Relevance—Canine lens capsular plaques are histologically and immunohistochemically similar to posterior capsule opacification and subcapsular cataracts in humans, which suggests that the canine condition, like the human conditions, is associated with fibrous metaplasia of lens epithelial cells. Transforming growth factor-β may play a role in the genesis of capsular plaques. Because severity of plaques was correlated with stage of cataract development, earlier surgical removal of cataracts may be useful to avoid complications associated with plaque formation. (Am J Vet Res 2000;61:139–143)

Full access
in American Journal of Veterinary Research



To evaluate the effectiveness of canine parvovirus monoclonal antibody (CPMA) as a treatment against canine parvovirus (CPV-2)–induced mortality and to support USDA product licensure.


28 purpose-bred Beagle dogs aged 8 weeks were randomized to the treated (n = 21) or control (7) group.


Dogs were challenged intranasally with 104.2 TCID50 virulent CPV-2b on Day 0 and monitored for 14 days for fecal viral shed and clinical disease. All dogs began shedding CPV-2 on Day 4 and were treated intravenously with a single dose of either CPMA (0.2 mL/kg) or saline (equal volume). No additional treatments were given to either group. Feces and sera were collected for quantitative analysis of fecal viral shed (hemagglutination) and antibody responses (hemagglutination inhibition and dot-blot ELISA), respectively. Dogs were monitored twice daily for parameters including lymphopenia, fever, vomiting, abnormal feces, inappetence, and lethargy. Humane endpoints triggered euthanasia by a veterinarian masked to treatment groups. The primary outcome variable was prevention of mortality as compared to controls.


Mortality was prevented in all CPMA-treated dogs compared to 57% mortality in the control group (P = .0017, Fisher exact test). Canine parvovirus monoclonal antibody–treated dogs also experienced less severe and/or shorter durations of diarrhea, fever, vomiting, CPV-2 shedding in feces, and lymphopenia. Both groups showed similar immunoglobulin M responses as measured by semiquantitative analysis.


Intravenous administration of CPMA can effectively improve clinical outcome when administered early in CPV-2 disease. Canine parvovirus monoclonal antibody treatment after proven infection does not interfere with adaptive immunity.

Open access
in Journal of the American Veterinary Medical Association