Toxoplasma gondii infections are a major source of visual loss and blindness. Ocular toxoplasmosis may occur as a result of congenital or acquired infections and as a manifestation of immunosuppression, particularly as a result of transplantation of AIDS (acquired immunodeficiency syndrome). Due to the recent resurgence of acquired ocular toxoplasmosis in Brazil and the worldwide complications of toxoplasmosis in HIV (human immune deficiency virus) infections, we initiated studies to develop a model of acquired toxoplasmosis to evaluate the molecular mechanisms of pathogenesis and therapeutic strategies. We have developed an animal (murine) model of ocular toxoplasmosis that is characterized by retinal inflammation, chorioretinal scarring, retinal disorganization, and cyst formation. Retinal disease occurs in three different strains of mice following inoculation with toxoplasmosis by the subcutaneous or intraperitoneal routes. This model of acquired ocular toxoplasmosis is being used to evaluate the efficacy of new antiparasitic agents in controlling the development of retinal cyst formation and retinal inflammation.
