Purpose: The purpose of this case was to report the inhibition of toxoplasma retinitis reactivation with long-term, low-dose antibiotics.Case summary: A 76-year-old woman complained of poor vision and floaters in her right eye. The corrected visual acuity (LogMAR) of the right eye was 0.5, and there was an area of yellow infiltration and dye leakage on the retinal fluorescein angiography images. Toxoplasma IgG were detected in the serum, the patient was diagnosed with toxoplasma retinitis, and the patient was advised oral trimethoprim-sulfamethoxazole, clindamycin, and steroids. Her visual acuity improved and the inflammation resolved. However, she again had decreased visual activity and retinal inflammation in her right eye after 5 months. The inflammation improved with oral steroids, but she was shifted to intravitreal dexamethasone because of the side effects of systemic steroids. Although the inflammation improved initially, there was worsening of inflammation (evidenced by vitreous opacity) after 2 months, which was treated with oral antibiotics. After vitrectomy for the removal of residual vitreous opacity, antibiotics were stopped because of the stable disease course. After discontinuation of the antibiotics, inflammation was noted again, and low-dose trimethoprim-sulfamethoxazole was administered. Low-dose antibiotics were continued for 5 months and the disease remained stable without any retinal inflammation. Conclusions Long-term, low-dose oral antibiotics may prevent reactivation of recurrent toxoplasma retinitis.

Purpose: To evaluate endothelial damage after cataract surgery in eyes affected by an angle-closure attack (ACA) and compare it to that in the unaffected fellow eyes (FEs) of patients with ACA and normal eyes (NEs). Methods: The medical data of eyes affected by ACA, FEs (with no history of acute glaucoma attack), and NEs of patients who underwent cataract surgery with simultaneous intraocular lens implantation were retrospectively reviewed. Endothelial cell density (ECD) and central corneal thickness (CCT) measured before surgery and at 1 week, 1 month, and 3 months after surgery were analyzed, and the percentages of loss in ECD and increase in CCT of the three groups were compared. Results: The study enrolled 140 eyes from 100 patients (50 eyes in the ACA group, 40 eyes in the FE group, and 50 eyes in the NE group). The mean ECD was significantly lower in the ACA group than in the other groups (p < 0.001). However, the percentage of ECD reduction was not significantly greater in the ACA group than in the other groups (p > 0.05). None of the eyes developed corneal edema at 3 months postoperatively. Moreover, the CCTs of the three groups were similar throughout the follow-up period (p > 0.05). Conclusions Phacoemulsification was not associated with greater endothelial cell loss in the ACA group than in the NE and FE groups. This finding shows that ACA history may not contribute to the exacerbation of corneal endothelial damage in cataract surgery.

Purpose: To evaluate endothelial damage after cataract surgery in eyes affected by an angle-closure attack (ACA) and compare it to that in the unaffected fellow eyes (FEs) of patients with ACA and normal eyes (NEs). Methods: The medical data of eyes affected by ACA, FEs (with no history of acute glaucoma attack), and NEs of patients who underwent cataract surgery with simultaneous intraocular lens implantation were retrospectively reviewed. Endothelial cell density (ECD) and central corneal thickness (CCT) measured before surgery and at 1 week, 1 month, and 3 months after surgery were analyzed, and the percentages of loss in ECD and increase in CCT of the three groups were compared. Results: The study enrolled 140 eyes from 100 patients (50 eyes in the ACA group, 40 eyes in the FE group, and 50 eyes in the NE group). The mean ECD was significantly lower in the ACA group than in the other groups (p < 0.001). However, the percentage of ECD reduction was not significantly greater in the ACA group than in the other groups (p > 0.05). None of the eyes developed corneal edema at 3 months postoperatively. Moreover, the CCTs of the three groups were similar throughout the follow-up period (p > 0.05). Conclusions Phacoemulsification was not associated with greater endothelial cell loss in the ACA group than in the NE and FE groups. This finding shows that ACA history may not contribute to the exacerbation of corneal endothelial damage in cataract surgery.