A 39-year-old male presented to the Emergency Room complaining of progressive blurring of vision in the right eye. The patient underwent best-corrected visual acuity testing, full ophthalmic slit-lamp examination of the anterior and posterior segments, (SD-OCT), and fluorescein angiography. Visual acuity was 20/22 in the right eye and 20/20 in the left eye, without correction. Anterior segment examination in both eyes was unremarkable and intraocular pressure was 18 mmHg. Fundus examination of the right eye showed 1 disc diameter whitish yellow inflammatory lesion inferotemporal to the macula not involving the fovea with focal vitritis. The fundus examination of the left eye was normal. SD-OCT in the right eye showed subertinal fluid and retinal thichening indicating an active retinochoroiditis. Fluorescein angiography showed early hypofluorescence of the lesion and involved vessels with progressive hyperfluorescence due to leakage of the dye in addition to leakage from the involved blood vessels indicating vasculitis (Fig. 1). A serologic search for Toxoplasma gondii infection was positive for immunoglobulin G (133 UI/mL, reference value, 10 UI/mL), whereas immunoglobulin M levels were normal, indicating prior exposure to Toxoplasma. A syphilis screen and other tests, including for tuberculosis, toxocariasis, sarcoidosis and autoimmune diseases were all negative. A presumptive diagnosis of toxoplasma retinochoroiditis was made, and a regimen of spiramycin 1gm 3 times daily was started and planned for 6 weeks. Gradual reduction of the retinal edema was noted after 2 weeks of presentation and the patient was started on oral prednsolone 1 mg/kg/day with weekly tapering dose. 2 weeks later (1 month from presentation), mild reduction of visaul acuity in the left eye to 20/28 was noted and on fundoscopic examination, there was flattening and pigmentation of the lesion which indicate scarring, with the development superficial retinal folds involving the macula indicating traction at superficial macular layers. SD-OCT showed Vitreoretinal traction involving the superficial layers of the macula (Fig. 2). Patient was being closely followed up to detect any progression of traction. 2 months after complete resolution, the patient has developed a chorioretinitis lesion on the border of the previous scar which and on fundus fluorescine angiography it has shown a characteristic early hypofluoresence with late leakage (Fig. 3) indicating a toxoplasmosis satellite chorioretinal lesion for which another cycle of spiramycin has started for 45 days.