Figure 1. Anterior scleritis of the temporal aspect of the right eye.
Figure 2. Fundus photographs of the right eye. A, Mild optic nerve fullness and fine macular striae. B, Inferotemporal retina of the right eye showing a large chorioretinal scar with hyperpigmented edges and central retinitis with adjacent retinitis associated with overlying vitreous debris secondary to toxoplasmosis. C, After antibiotic therapy, the area of chorioretinitis decreased in size and developed pigmented edges.
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Rudich DS, Bhatnagar P. Scleritis Associated With Toxoplasmic Retinochoroiditis. Arch Ophthalmol. 2012;130(5):659–660. doi:10.1001/archophthalmol.2011.1527
Author Affiliations: Department of Ophthalmology, Mount Sinai School of Medicine, New York (Dr Rudich), and Department of Ophthalmology, Albany Medical College and Retina Consultants PLLC, Slingerlands (Dr Bhatnagar), New York.
Scleritis in conjunction with toxoplasmic retinochoroiditis has been reported rarely in the literature.1 We describe a case of toxoplasmic scleritis in a pregnant woman.
A 24-year-old woman who was 7 weeks pregnant visited the eye clinic with a 4-day history of pain, redness, blurry vision, and floaters in the right eye. Her medical history was unremarkable; in particular, she had no history of immunocompromise or immunosuppressive therapy. Her ocular history was significant for myopia. She also reported being told she had a “scar” in her right eye several years prior by an ophthalmologist. Best-corrected visual acuities were 20/30 OD and 20/20 OS. On examination, there was pain in the right eye with right gaze. Ishihara color plates were 9/10 OU. Anterior segment examination findings for the right eye were remarkable for 2+ sectoral scleral injection temporally (Figure 1), faint scattered keratic precipitates, and 1+ cell in the anterior chamber. Intraocular pressures were 14 mm Hg OD and 15 mm Hg OS. Dilated funduscopic examination of the right eye revealed an inferotemporal chorioretinal lesion with central retinitis and hyperpigmented edges as well as overlying vitreous debris. Adjacent was an area of active, elevated, white retinochoroiditis with overlying vitreous debris (Figure 2). Findings from anterior segment and funduscopic examinations of the left eye were unremarkable.
Treatment was started with prednisolone acetate, 1%, 4 times a day in the right eye. Owing to the contraindication of sulfa-based medications as well as pyrimethamine in pregnancy, oral azithromycin therapy with a 1-g loading dose followed by 500 mg/d was initiated in conjunction with her obstetrician.2,3 Findings from serologic studies for human immunodeficiency virus, rapid plasma reagin, Lyme antibody, and QuantiFERON for tuberculosis were all negative. Serum was negative for toxoplasmosis IgM antibody, and the IgG level was elevated at 2.81 IU/mL (reference range, 0.0-0.9 IU/mL).
Four days after antibiotic therapy was initiated, treatment with oral prednisone was started for the active vitritis. The anterior chamber reaction quickly subsided and the prednisolone acetate treatment was discontinued. During the following month, the area of active retinochoroiditis decreased in size and developed pigmented edges. The anterior scleritis resolved. Prednisone treatment was slowly tapered once improvement was seen in the vitritis, and the patient reported a resolution of her symptoms.
Toxoplasmosis is believed to be the most common cause of posterior uveitis.2 Scleritis in association with toxoplasmic retinochoroiditis is an uncommon entity.1 Accordingly, in a review of 243 patients with scleritis, no patient was reported to have toxoplasmic infection as a cause; furthermore, 37% had a systemic rheumatologic disorder, only 7% had an infection, and 44% had an associated medical disorder. Herpes zoster virus was the most commonly reported infectious cause and rheumatoid arthritis was the most common rheumatic disease.4
In cases of toxoplasmic scleritis, the inflammatory response is believed to extend from the active retinochoroiditis to involve the overlying sclera. Accordingly, pathologic specimens from eyes that were enucleated secondary to severe toxoplasmic scleritis displayed granulomatous inflammation of the retina, uvea, and episclera with associated retinal thickening. In many cases, the entire sclera extending outward from the retinitis was inflamed; however, in some cases, a region of uninflamed sclera separated the active scleritis from the underlying retinitis.1
Isolated toxoplasmic retinochoroiditis can rapidly spread and lead to severe permanent vision loss when treated with steroids alone.5 In our patient with scleritis, a dilated fundus examination revealed an area of typical toxoplasmic retinochoroiditis, allowing for prompt diagnosis and treatment with appropriate antibiotic therapy. The patient improved and maintained excellent visual acuity. This patient's course underscores the importance of a complete examination in cases of scleritis, including a dilated fundus examination, to rule out an infectious retinochoroiditis in association with the scleritis.
Correspondence: Dr Bhatnagar, Retina Consultants PLLC, 1220 New Scotland Rd, Ste 201, Slingerlands, NY 12159 (firstname.lastname@example.org).
Financial Disclosure: None reported.
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