Toxoplasmosis is the most common cause of posterior uveitis in immunocompetent subjects. The infection can be congenital or acquired. Ocular symptoms are variable according to the age of the subject. For instance, young children present with reduced visual acuity, strabismus, nystagmus, and leucocoria, while teenagers and adults complain of decreased vision, floaters, photophobia, pain, and hyperemia. Toxoplasmic retinochoroiditis typically affects the posterior pole, and the lesions can be solitary, multiple or satellite to a pigmented retinal scar. Active lesions present as grey-white focus of retinal necrosis with adjacent choroiditis, vasculitis, hemorrhage and vitreitis. Cicatrization occurs from the periphery towards the center, with variable pigmentary hyperplasia. Anterior uveitis is a common finding, with mutton-fat keratic precipitates, fibrine, cells and flare, iris nodules and posterior synechiae. Atypical presentations include punctate outer retinitis, neuroretinitis, papillitis, pseudo-multiple retinochoroiditis, intraocular inflammation without retinochoroiditis, unilateral pigmentary retinopathy, Fuchs'-like anterior uveitis, scleritis and multifocal or diffuse necrotizing retinitis. The laboratory diagnosis of toxoplasmosis is based on detection of antibodies and T. gondii DNA using polymerase chain reaction (PCR). Toxoplasmosis therapy includes specific medication and corticosteroids. There are several regimens, with different drug combinations. Medications include pirimetamine, sulfadiazine, clindamycin, trimethoprime-sulphamethoxazol, spiramycin, azithromycin, atovaquone, tetracycline and minocycline. The prognosis of ocular toxoplasmosis is usually good in immunocompetent individuals, as long as the central macula is not directly involved.