Clinicopathological features of a congenital murine model of ocular toxoplasmosis

Abstract

Sequential clinical examination was carried out upon the eyes of mice that had been infected in utero with Toxoplasma gondii. Three patterns of clinical disease were seen. First, crystalliform cataracts, which either remained unchanged in character or occasionally became more extensive, were observed. Second, acute uveitis occurred in a small proportion of eyes, progressing into a chronic inflammatory disease with secondary opaque cataract. The third pattern comprised multiple discrete foci of deep retinal disturbance. It is suggested that these lesions were attributable to focal macrophage clusters in the sub-retinal space with overlying dome-shaped elevations of the photoreceptor matrix. The severity of disease, as assessed clinically, correlated with the underlying histopathology but not with the serological titres against Toxoplasma. Immunocytochemical staining for Toxoplasma antigen revealed only intra-retinal Toxoplasma cysts, but no free organisms or extracystic antigen were demonstrated. Selective photoreceptor destruction was the most prominent histopathological feature, implicating auto-immune mechanisms of tissue destruction.

Cataracts in congenital toxoplasmosis

“…Selective photoreceptor destruction was the most prominent histopathological feature. 15 In one study of a murine model, DNA deposition led to cataract formation. 16 It may be that both parasite replication and inflammatory cells arriving via the hyaloid artery during lens development cause such DNA deposition in the lens in congenital toxoplasmosis.…”