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RETINA QUIZ Red Eye, Blurred Vision Signal by Mark T. Dunbar, O.D A 51-year-old white male noted pain, redness and blurry vision in his right eye for the past
week. He assumed it was "pink eye" and would resolve on its own, but he grew concerned when his vision became increasingly blurred. His medical and
Best-corrected visual acuities were 20/50 O.D. and 20/20 O.S. Confrontation fields were full to careful finger counting. The pupils were equally round and reactive. There was suggestion of an afferent pupillary defect in the right eye. Slit lamp examination of the right eye revealed diffuse injection of the conjunctiva, and the cornea showed scattered keratic precipitates on the endothelium. Present in the anterior chamber were 2+ cells and trace flare. The iris was normal, the lens clear. The anterior segment of the left eye was normal. Applanation tonometry was 21mm Hg O.D. and 18mm Hg O.S. Dilated fundus exam of the right eye showed a moderate vitritis. The optic nerve appeared hazy but showed a small cup with good rim coloration and perfusion. Less than one disc diameter from the optic nerve along the superior arcade was a fluffy, white lesion extending superiorly (figure 1). Adjacent to the lesion was a localized area of hyperpigmentation. Fundus exam of the left eye was normal. Quiz
Discussion
Toxoplasmosis is caused by an intracellular parasite, toxoplasma gondii. Recent studies suggest that acquired infections are more prevalent than we thought. Acquired toxoplasmosis may be transmitted via unwashed vegetables, uncooked or undercooked meats, unpasturized bovine milk and even contaminated drinking water. Exposure to contaminated soils and litter boxes may also be a source of acquired toxoplasmosis. Our patient admitted that he frequently ate wild game, often not adequately cooked. In congenital toxoplasmosis, patients generally present with an inactive chorioretinal scar. Often these scars are located in the posterior pole or directly in the macula. Reactivation of a congenital infection can occur, generally adjacent to an old scar. Acquired infections often present as a single lesion. They typically occur unilaterally with a predilection for the mid-peripheral fundus. There can also be a reactivation of an acquired infection. Like the congenital form, it often occurs adjacent to the original infection. It can appear identical to a congenital reactivation. Our patient has reactivation of the disease as evidenced by the pigmented chorioretinal scar adjacent to the active retinochoroiditis. Active toxoplasmosis retinochoroiditis typically has a feathery white or creamy-yellow appearance. The lesions may appear thick or slightly elevated. Other findings include vitritis, papillitis, perivasculitis and vessel sheathing. There's often a spill-over inflammation of the anterior chamber. Notice in figure 1 the sheathing of the retinal vessels and localized areas of vasculitis. There's also a serous detachment inferior to the pigmented scar. That combined with the vitritis may be responsible for the reduced acuity. How should this patient be managed? Toxoplasmosis is a self-limiting disease in healthy patients. Yet, uveitis specialists agree that there are certain indications for treatment.1 These include an area of active retinitis threatening either the macula or the optic nerve, or a significant reduction in visual acuity due to a severe vitritis in an active lesion. Other indications include an active lesion larger than one disc diameter as well as any case occurring in an immunocompromised patient.2 Peripheral lesions that don't affect visual acuity generally can be followed without treatment. There's less agreement on which medications to use to treat the active disease. Popular initial regimens include pyrimethamine with sulfonamides or clindamycin with sulfonamides.1,2 Either combination may include the use of corticosteroids. Don't use steroids alone because it could result in recurrent infection. In one study among uveitis specialists regarding which medications to use in treating active toxoplasmosis, less than one-third agreed on treatment regimens. 1 Thirty-two percent used pyrimethamine, sulfadiazine and folinic acid along with a corticosteroid; 27 percent used the same regimen plus clindamycin. Our patient proved difficult to treat. He was treated initially with pyrimethamine, sulfadiazine, a corticosteroid and folinic acid but did not seem to improve. Clindamycin was added and after several months the lesion began to improve (figure 2).
1. Engstrom R, Holland G, Nussenblatt R, Jabs D. Current practices in the management of ocular toxoplasmosis. Am J Ophthalmol 1991; 111:601-610.
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