|Ocular tumor model|
Toxoplasma cyst in the retina.
Retinal folds and mild inflammation in the two mice inoculated with T. gondii.
More cysts in the retina of a mouse treated with interferon gamma.
Severe inflammatory responses in a mouse inoculated with T. gondii and treated with interferon gamma.
Murine acquired ocular toxoplasmosis
Ocular toxoplasmosis is the leading cause of ocular infection in immunocompetent patients and the second leading cause of ocular infection in AIDS patients. Although the great majority of ocular toxoplasmosis is thought to be congenital, studies indicate that it may also occur after birth, in particular, in the AIDS patients. Therefore, the use of an experimental model to study acquired ocular toxoplasmosis becomes mandatory.
Acquired ocular toxoplasmosis is induced in C57BL/6 mice by infection of an avirulent strain of Toxoplasma gondii (T. gondii) ME49 cysts. (Gazzinelli et al. Experimental Parasitology 1994; 78: 217-229). Multiple CNS lesions and focal ocular inflammation, mainly T lymphocytic infiltration, and RPE involvement usually develop 15 days after T. gondii infection. Four weeks after infection, a stable number of cysts is observed in the brain but cysts are rarely seen in the eye. In most ocular lesions, the parasite are unable to detect even when using PCR. We have reported that IFNg and TNFa play a protective role in ocular toxoplasmosis.
The model parallels the clinicopathological findings of T lymphocytic infiltration and rarity of T. gondii in fetal eyes of congenital toxoplasmosis.