The Case
The patient was a 56-year-old white woman who presented with new floaters and decreased vision in the left eye for two weeks and some temporal photopsias in the left eye for about four days. Her past ophthalmic history was unremarkable, and past medical history is remarkable for a positive lupus anticoagulant. She had a subclavian venous thrombosis 20 years ago leading to prophylactic coumadin and Plavix treatment. She discontinued these medications 10 years ago, and she said that her medical care providers have been aware and have not objected to her not being anticoagulated.
The visual acuity was 20/25 J1+ OD and 20/50 J10 OS. Ophthalmic examination of the right eye was unremarkable. The left eye had a quiet anterior chamber and posterior cells and debris, particularly over the area of retinal whitening above the disc. There were two areas of retinal whitening in the left eye, and there were plaques on nearby arteries. What is the most likely diagnosis? What treatment, if any, would you recommend?
Answer
The 6/4 color photograph showed retinal whitening above the disc and a smaller area of retinal whitening superonasal to the disc. There was vitreous debris in the posterior pole, including above superior white region and above the optic disc. Though it was difficult to discern in this photograph, the disc had a sharp margin. Some of the debris were clumped, resulting in darker spots best seen over the larger white lesion. There were plaques along arteries and veins near the white lesions. The OCT showed vitreous debris, retinal edema and disruption of the retinal laminations, and elevation of the RPE indicating a choroidal lesion. The 9/17 photograph revealed substantially reduced vitritis, a much sharper margin around the superior white lesion, and near-complete resolution of the superonasal lesion. The plaques along the blood vessels were also substantially improved.
This patient’s clinical presentation was consistent with primary toxoplasmosis infection. The infection can be multifocal, and the plaques on nearby blood vessels, particularly arteries, is commonly seen in this condition. Most patients with active toxoplasmosis chorioretinitis have reactivation of a prior infection. They present with retinal whitening adjacent to pigmented chorioretinal scars, and the primary infection is often in utero. In the absence of chorioretinal scarring, our patient was presumed to have a primary infection. The absence of severe vitritis is another indication that this was a primary infection. Patients with recurrent infection have a “headlight in a fog” clinical presentation of retinal whitening seen behind a haze of vitreous cells, because the immune system is reacting vigorously to a parasite to which it has been exposed previously. Our patient denied eating undercooked meat, but she did have feral cats who sometimes came inside her house. Her IgG for toxoplasmosis, which indicates infection at some point in her life, was positive, and this is commonplace in the population. Her IgM for toxoplasmosis was negative. Though IgM titers indicate more recent exposure, it can take several weeks after an acute infection for IgM titers to become positive.
Toxoplasmosis is almost always self-limited in immune-competent patients, and treatment is optional unless the fovea or optic nerve are threatened. To reduce the duration of infection, we
treated our patient with Bactrim after confirming that she did not have a sulfa allergy. The retinal whitening and vision improved markedly over the next several weeks.
