Toxoplasma gondii is a ubiquitous organism able to infect almost all mammals and birds and has been estimated to infect one third of the global human population with a great variation of prevalence between different countries [1, 2]. Generally, ocular toxoplasmosis (OT) represents the most common cause of posterior uveitis. OT might develop as a complication of both acquired and congenital infections. OT may develop during the acute phase of infection, but is particularly characterized by active attacks and recurrences during the chronic phase. Severity of OT may be influenced by variations in the strain/genotype of T. gondii, parasitic load, infectious stage of parasite (infection by oocyst or tissue cyst), moment of infection (congenital or postnatally acquired), and host-related factors such as immune status and age [2, 3]. OT manifests typically as focal chorioretinitis with a tendency to recur in the adjacent retinal areas. The factors responsible for recurrences are unknown, but trauma, hormonal changes, and cellular and/or humoral immunosuppression appear to contribute to the release of parasites from tissue cysts [3]. In addition, autoimmune processes were also pointed out as possible (co-)factors for the recurrences and severity of OT [4, 5]. The prevalence of recurrences was reported to be 55 % in 5 years of follow-up after the first episode [6]. Holland et al. reported that the risk of recurrence was the highest immediately after an episode of active disease and that recurrence had a tendency to occur in clusters [7]. Further, younger patients had a higher risk on an active OT episode compared to older patients [8]. Treatment for OT commonly includes a combination of various systemic antiparasitic drugs sometimes with addition of corticosteroids to lessen the inflammatory reaction and its possible complications [3]. Visual prognosis is mainly determined by the location of the retinal lesion; macular lesions and lesions adjacent to the optic disk have a worse visual prognosis.
