August 1966
Volume 5, Issue 4
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Articles  |   August 1966
Ocular Lesions Induced in C57 Mice by the Suckling Mouse Cataract Agent (SMCA)
Author Affiliations
  • ELIZABETH OLMSTED
    Buffalo Eye and Ear Hospital, Ophthalmologic Division of Deaconess Hospital, State University of New York at Buffalo, Buffalo, N. Y.
  • SHYAM PRASAD
    Department of Pathology, Deaconess Hospital, State University of New York at Buffalo, Buffalo, N. Y.
  • JOHN SHEFFER
    Department of Pediatrics, State University of New York at Buffalo, Buffalo, N. Y.
  • H. FRED CLARK
    Department of Bacteriology and Immunology, State University of New York at Buffalo, Buffalo, N. Y.
  • DAVID T. KARZON
    Department of Bacteriology and Immunology, State University of New York at Buffalo, Buffalo, N. Y.
Investigative Ophthalmology & Visual Science August 1966, Vol.5, 413-420. doi:
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      ELIZABETH OLMSTED, SHYAM PRASAD, JOHN SHEFFER, H. FRED CLARK, DAVID T. KARZON; Ocular Lesions Induced in C57 Mice by the Suckling Mouse Cataract Agent (SMCA). Invest. Ophthalmol. Vis. Sci. 1966;5(4):413-420.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

The biomicroscopic study of C57 mice inoculated with suckling mouse cataract agent (SMCA) presented the opportunity to observe the clinical evolution of a virus-induced cataract. It was possible to describe seven clinical stages of cataract development, progressing from minimal capsular changes to mature cataract formation followed by lens absorption. These changes progressed through five distinct patterns of cataract evolution. Histopathological studies showed that marked retinal, uveal, and lens changes preceded severe clinical lens changes by many days. Virus replication in the eye began very early and persisted during the development of the lenticular and retinal pathology. The data do not permit determination of whetherlens changes are secondary to viral retinitis and uveitis, or result from direct virus infection of the lens

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