Abstract: Objective To retrospectively analyze the clinical characteristics and treatment outcomes of active ocular toxoplasmosis. Methods Clinical data were retrospectively analyzed from patients diagnosed with ocular toxoplasmosis. The diagnosis was confirmed through intraocular fluid and serological testing. Results The study included 12 cases(13 eyes), comprising 2 males(3 eyes)and 10 females(10 eyes). The age at initial diagnosis ranged from 17 to 73, with a mean of 37.4±16.7 years. The follow-up period ranged from 6 to 32 months, with a median duration of 8 months. At the initial visit, 12 eyes(92.3%)showed anterior segment inflammation, including 3 eyes(23.1%)with posterior synechiae. 4 eyes(30.8%)developed secondary ocular hypertension. All patients exhibited varying degrees of vitreous inflammatory haze, with 3 eyes(23.1%)showing severe vitreous opacity that nearly completely obscured the fundus view. Fundus manifestations were diverse. 10 eyes(76.9%)displayed necrotizing chorioretinal lesions, including 3 eyes(23.1%)with macular involvement. 2 eyes exhibited macular edema alongside extramacular lesions. 5 eyes(38.5%)had optic disc edema, among which 2 eyes showed yellowish-white peripapillary lesions approximately half a disc diameter in size. 6 eyes(46.2%)presented with pigmented chorioretinal scars adjacent to active lesions. Diagnosis was confirmed by intraocular fluid testing in 8 eyes(61.5%)during their first visit. However, 4 cases(5 eyes, 38.5%)were initially missed. Among them, 2 cases(2 eyes)showed significant optic nerve edema with peripapillary lesions; 1 case(1 eye)had a large necrotizing lesion involving nearly the entire superonasal quadrant; and 1 case(2 eyes)had severe vitreous opacity that prevented fundus examination. The intervals from initial visit to confirmatory intraocular fluid testing for these 4 cases were 0.87, 7.77, 0.45, and 1.0 months, respectively. All diagnosed patients received systemic and topical antibiotic, as well as corticosteroid therapy, with 3 cases undergoing vitrectomy. During follow-up, 1 patient experienced continuous deterioration, and another had recurrence with worsening after 2 years of stability. The remaining 11 eyes showed improvement and remained stable, with better log MAR BCVA at the last visit compared to initial presentation. Two eyes developed epiretinal membranes, and 1 eye developed vitreomacular traction. Conclusion Ocular toxoplasmosis presents complex and varied clinical manifestations. Necrotizing chorioretinal inflammatory lesions differ greatly in location and size. Specifically, small peripapillary lesions may be overlooked because of severe optic disc edema, while extensive necrotic lesions might cause diagnostic confusion. Moreover, inflammation frequently affects the vitreous, optic nerve, and macula. Patient prognosis largely depends on lesion severity. Clinical diagnosis should comprehensively consider patient history, symptoms, imaging, and laboratory tests. In suspected cases, timely testing of intraocular fluid and serum for Toxoplasma antibodies or DNA is essential. This approach facilitates early diagnosis and treatment, thereby improving patient outcomes.

Key words: Ocular toxoplasmosis, Clinical signs, Uveitis, Intraocular fluid testing, Prognosis