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- Author or Editor: Ken H. Lakhani x
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Abstract
Objectives—To assess the association between goniodysgenesis, ocular measurements, and glaucoma in Great Danes.
Animals—180 Great Danes.
Procedure—Eye examination and measurements were obtained from 180 Great Danes; for 30 of these dogs, depth of the anterior chamber, vitreal body length, and total depth of the globe were also measured. These data were merged with electronic pedigree information on 43,371 kennel club registered Great Danes. Relationships among goniodysgenesis, ocular measurements, and glaucoma and the heritability of goniodysgenesis were estimated.
Results—The degree of goniodysgenesis was significantly and positively associated with the likelihood of glaucoma. There was a significant association between the degree of goniodysgenesis in offspring and parents. The estimated heritability of the degree of goniodysgenesis was 0.52. The depth of the anterior chamber of the eye was also a good predictor of goniodysgenesis (ie, the dog was almost certain to have glaucoma if the depth was < 3.7 mm). If both parents had goniodysgenesis < 70%, then with 95% confidence, the occurrence of glaucoma in the ensuing offspring would be < 4/1000. This strategy translates to ensuring that the depth of the anterior chamber of the eye is > 3.7 mm for both parents.
Conclusions and Clinical Relevance—The strong and significant correlation among goniodysgenesis, other eye measurements, and glaucoma and the significant heritability of goniodysgenesis suggests that glaucoma may be heritable in Great Danes. If so, glaucoma can be controlled by breeding only from sires and dams with a minimum degree of goniodysgenesis. (Am J Vet Res 2001;62:1493–1499)
Abstract
Objective—To establish a model for inheritance of gluten-sensitive enteropathy (GSE) in Irish Setters.
Animals—44 dogs of a 6-generation family of Irish Setters with GSE and 7 healthy Irish Setters.
Procedure—Phenotype of each dog was determined after oral administration of gluten in the weaning diet, using morphometric evaluation of jejunal biopsies (all generations) and measurement of small intestinal permeability by use of a lactulose-rhamnose permeation test (generations 1, 2, and 3). Overall probability for each of 4 genetic models of inheritance (autosomal recessive, autosomal dominant, sex-linked recessive, and sex-linked dominant) accounting for segregation of partial villus atrophy within the entire family was calculated.
Results—The autosomal recessive model was most tenable and was 56,250 times more likely to account for segregation of partial villus atrophy than the autosomal dominant model, assuming disease prevalence of 0.8%. Both sex-linked models were untenable. These conclusions were robust to the error attached to estimation of disease prevalence. High intestinal permeability without morphometric jejunal abnormalities in 4 of 20 dogs in the 3 youngest generations suggested heterogeneity of lesions associated with GSE.
Conclusions—Genetic transmission of GSE is under the control of a single major autosomal recessive locus. (Am J Vet Res 2000;61:462–468)
