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Abstract
A longitudinal biomicroscopic study of lenses and fundi of over 2,000 Peromyscus maniculatus (deer mice) which have cataracts as an autosomal recessive trait has been correlated with histologic development of cataracts. By selective breeding, early-onset cataracts (Type I), which are frequently associated with abnormal closure of the fetal fissure and hyaloid vascular abnormalities, have been separated from later-onset (Type II) cataracts, which are more heterogeneous. Type I cataracts occur in syndactylous deer mice, develop rapidly, and histologically may show backward migration of disrupted lens bow cells before lens opacity is apparent biomicroscopically. Posterior subcapsular cataracts then develop and spread centrally and inferonasally to the equatorial area and then to the entire equator. The nucleus opacifies in either a "shell" pattern or as isolated dots. Anterior cortical opacification progresses to mature cataract. Histologically, abnormal migration and proliferation of lens epithelium and enlargement and vacuolar degeneration of the basal (posterior) process of cortical lens fibers are early changes in Type I cataracts. Disruption of the lens bow with failure of differentiation and inward turning of lens epithelium to become lens fibers occurs concurrently. Type II cataracts may follow the developmental pattern of Type I but are rarely associated with severe hyaloid vascular abnormalities and progress more slowly. About 6% of animals develop diabetes, which is not associated with the cataract-webbed trait.