Case of the Month | December 2021

Case of the Month
December 20, 2021

The Case

The patient was a 17-year-old woman who had stable, decreased vision in the left eye for one month. She had longstanding pain around the left eye that radiated down to her neck, and there had been no recent change in the amount of pain. The visual acuity was 20/20 OD and 20/100 OS. The anterior segment examination was remarkable for 1+ anterior chamber cells. On posterior segment examination, there was 1+ vitreous cells and juxtafoveal whitening with mild associated chorioretinal scarring.

What was the most likely diagnosis? What treatment, if any, would you recommend?

This patient’s clinical presentation was typical of toxoplasmosis retinitis. There was retinal whitening associated with a chorioretinal scar, indicating reactivation of a prior lesion. OCT showed juxtafoveal thickening with disruption of all retinal layers extending to the nasal half of the fovea. There was decreased vision and a threat of substantial, permanent central visual loss. She was given intravitreal clindamycin and prescribed Bactrim DS BID and prednisone 40 mg QD for 5 days with a plan for subsequent steroid taper. She experienced rapid resolution of the acute retinitis, leaving her with a chorioretinal scar and a visual acuity of 20/300, J5 at three weeks. There are plans for using Bactrim DS three times per week for at least one year.

The diagnosis of toxoplasmosis retinitis relies primarily on the clinical findings, and laboratory testing is sometimes helpful. Many people in the general population have positive IgG titers to the organism, indicating prior exposure. A positive IgM titer indicates more recent infection, but this can be negative in the setting of reactivation limited to the eye. PCR of anterior chamber or vitreous fluid has a sensitivity of about 67%. Our patient had a positive IgG titer, a negative IgM titer, and a negative PCR of anterior chamber fluid.

Toxoplasmosis retinochoroiditis is an infectious process due to the protozoan Toxoplasma gondii. Most infections in the United States occur in utero, but it can occur later due to ingestion of the organism, often from undercooked meat. The organism resides in normal-appearing retinal tissue in an encysted form, and acute infection occurs when it becomes unencysted and invades adjacent tissues. Often the infection is next to a chorioretinal scar, which developed after a prior episode of retinitis. The amount of associated vitreous cells depends on whether there has been prior retinitis, the severity of prior retinitis, and the degree of immunocompetence of the patient. The clinical picture sometimes resembles a “headlight in a fog”, in which vitreous cells result in a hazy view of the retinal whitening.

The natural course of the disease involves gradual enlargement of the area of retinitis over 1-2 weeks and then fading over several months, leaving an area of chorioretinal atrophy and hyperpigmented scarring. Antibiotic treatment, including systemic or intravitreal clindamycin, pyrimethamine (Daraprim), sulfadiazine, or trimethoprim-sulfamethoxazole (Bactrim), can shorten the duration of active retinitis. Corticosteroids are often used if the fovea is threatened. After the acute retinitis has resolved, choroidal neovascularization at the edge of a chorioretinal scar can result in loss of central vision.

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This patient’s clinical presentation was typical of toxoplasmosis retinitis. There was retinal whitening associated with a chorioretinal scar, indicating reactivation of a prior lesion. OCT showed juxtafoveal thickening with disruption of all retinal layers extending to the nasal half of the fovea. There was decreased vision and a threat of substantial, permanent central visual loss. She was given intravitreal clindamycin and prescribed Bactrim DS BID and prednisone 40 mg QD for 5 days with a plan for subsequent steroid taper. She experienced rapid resolution of the acute retinitis, leaving her with a chorioretinal scar and a visual acuity of 20/300, J5 at three weeks. There are plans for using Bactrim DS three times per week for at least one year.

The diagnosis of toxoplasmosis retinitis relies primarily on the clinical findings, and laboratory testing is sometimes helpful. Many people in the general population have positive IgG titers to the organism, indicating prior exposure. A positive IgM titer indicates more recent infection, but this can be negative in the setting of reactivation limited to the eye. PCR of anterior chamber or vitreous fluid has a sensitivity of about 67%. Our patient had a positive IgG titer, a negative IgM titer, and a negative PCR of anterior chamber fluid.

Toxoplasmosis retinochoroiditis is an infectious process due to the protozoan Toxoplasma gondii. Most infections in the United States occur in utero, but it can occur later due to ingestion of the organism, often from undercooked meat. The organism resides in normal-appearing retinal tissue in an encysted form, and acute infection occurs when it becomes unencysted and invades adjacent tissues. Often the infection is next to a chorioretinal scar, which developed after a prior episode of retinitis. The amount of associated vitreous cells depends on whether there has been prior retinitis, the severity of prior retinitis, and the degree of immunocompetence of the patient. The clinical picture sometimes resembles a “headlight in a fog”, in which vitreous cells result in a hazy view of the retinal whitening.

The natural course of the disease involves gradual enlargement of the area of retinitis over 1-2 weeks and then fading over several months, leaving an area of chorioretinal atrophy and hyperpigmented scarring. Antibiotic treatment, including systemic or intravitreal clindamycin, pyrimethamine (Daraprim), sulfadiazine, or trimethoprim-sulfamethoxazole (Bactrim), can shorten the duration of active retinitis. Corticosteroids are often used if the fovea is threatened. After the acute retinitis has resolved, choroidal neovascularization at the edge of a chorioretinal scar can result in loss of central vision.

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