A Case Report of Longstanding Toxoplasmosis Chorioretinitis

Introduction Congenital toxoplasmosis (CT) can elicit severe damage to several organs, especially the eye, and may be manifested at birth or later. The diagnosis of ocular toxoplasmic infection is based primarly on the characteristic of ocular findings and supportive serologic evidence. It is generally well agreed that macular lesions, involving the optic nerve, and cases with intense inflammation should be treated. Objective To describe a clinical presentation and reviews the current management options of reactivation of ocular inflammation, typical of a ocular toxoplasmosis with evidence of congenital infection, a satellite scar or an inactive lesion in the other eye, in which antibodies titer remain as a chronic infection. Material and methods This is a retrospective case report of a 13 years old boy presented with complaints of decreased vision in his left eye for 4 weeks and did not refer clearly for the vision in the right eye. Examination of the fundus oculi noticed cikatricial chorioretinal macular area in the right eye with visual acuity 1/10, and active chorioretinitis, preretinal and intraretinal bleeding in the left eye with visual acuity 1/10. The serology resulted positive for Toxoplasma gondii. He was treated at our Pediatric Department of Infectious Disease Service with classic therapy Pyrimethamine, Sulfadiazine with supplemental leucovorin (folinic acid) to minimize pyrimethamine associated hematologic toxicity and oral steroids for 4 weeks. Results The fact that our patient presented initially with such severe anterior inflammation suggests us that this was a longstanding infection. This is further supported by the results of his blood work, IgG for Toxoplasma gondii resulted positive, 650. The patient had presumed ocular toxoplasmosis from his mother, which also resulted IgG positive for Toxoplasma The therapeutic outcome showed improvement in acute case, treatment resulted in reducted retinal area of left eye, without cikatricial signs and no vitreal inflammation with a visual acuity of left eye 10 / 10, and no change in visual acuity of right eye 1/10 with cikatricial central area. Monitoring of blood counts showed no bone marrow suppression after therapy. Conclusion This case shows a severe presentation of a relatively wellknown clinical entity. Although ocular toxoplasmosis may be self-limiting in immunocompetent individuals, prompt diagnosis and proper management can improve visual outcome. Suddenly blurred vision in the quiet eye in the young adult could be chorioretinal inflammation and scar caused by Toxoplasma gondii. In a case such as this, it is important to utilize the current management options to fight the infection and as well to control inflammation and minimize long-term ocular damage. It is necessary to suspect this pathology in every children attending consultation with vision disorder. Diagnosis should be confirmed by charachteristic lesions of fundus oculis and any serological value of Toxoplasma IFI and treatment should be indicate as fast as possible in active lesions.