Patients with ocular toxoplasmosis carry a substantial and lifelong risk of developing a potentially severe functional impairment of vision. The mechanisms underlying ocular manifestations of the disease and their recurrence are poorly understood, thus, we are not in a position to prevent these events. A correct diagnosis of the disease is a necessary basis for estimating its clinical burden and functional consequences, as well as for designing and conducting clinical studies to test treatment strategies. Ocular toxoplasmosis may involve the anterior segment; however, in most instances, it predominantly affects the posterior segment of the eye. Initially, the process starts within the retina. However, reactivation of the disease may secondarily involve the choroid, thereby leading to retinochoroiditis. Toxoplasmic retinochoroiditis is a local event, which may fail to evoke a detectable systemic immune response. In doubtful cases, the aqueous humor can be analyzed for the presence either of parasitic DNA or of specific antibodies. However, the DNA content of the aqueous humor is low. A surer confirmation would necessitate puncturing the vitreous. A laboratory confirmation of the diagnosis can also be frustrated by false-negative results, which arise from marked individual differences in the time elapsing between the onset of clinical symptoms and the activation of specific antibody production. This article furnishes an overview of the clinical manifestations of ocular toxoplasmosis, of secondary tissue damage and of laboratory findings relating to the disease, as well as information regarding its functional consequences and recurrences.