Poststreptococcal syndrome (PSS) involves the development of systemic nonsuppurative inflammation after a streptococcal infection. The inflammation is sterile and thought to represent an autoimmune reaction between streptococcus-sensitized lymphocytes and host tissue because of "molecular mimicry."1 Common manifestations of PSS include acute rheumatic fever, reactive arthritis, and acute glomerulonephritis. Recently, uveitis was described as a sign of PSS.2- 4 This intraocular inflammation also develops after the bacterial infection. One report claims PSS uveitis can be recurrent.4 Herein, we confirm the findings of that single case and report that the length of time between episodes may be as long as 27 months.
A 10-year-old white boy developed photophobia, ocular redness, and blurred vision bilaterally following an episode of streptococcal pharyngitis. Medical history was otherwise noncontributory. Examination noted vision of 20/80 OU with 3+ cells in the anterior chambers. Workup revealed an elevated antistreptolysin O (ASO) titer (760 IU/mL) (normal range, 0-125 IU/mL) and an elevated erythrocyte sedimentation rate (27 mm/h) (normal range, 0-15 mm/h). Titers for antinuclear antibodies, rheumatoid factor, toxoplasmosis, Lyme disease, and angiotensin-converting enzyme were normal. Chest x-ray films, urinalysis, complete blood cell count, and chemistry panel were unremarkable. Symptoms resolved with cycloplegics and topical steroids. Twenty-seven months later he developed blurred vision, ocular tenderness, and photophobia bilaterally 10 days after streptococcal pharyngitis. Medications included a 10-day course of a combination product consisting of amoxicillin and clavulanate (500 mg twice daily). He denied other PSS symptoms. On examination, visual acuity was 20/50 OU. Pupils, motility, visual field, and tonometry were normal. Slitlamp examination revealed mild bulbar conjunctival hyperemia in both eyes. Both anterior chambers had 2+ cells and flare. Fine white keratic precipitates were present on the inferior cornea bilaterally. Irides demonstrated no nodules or atrophy. Anterior vitreous contained mild cells in both eyes. Fundus examination disclosed disc hyperemia with a few fine peripheral vitreous precipitates bilaterally, but no "snow-banking" or vascular sheathing. Blood testing revealed an elevated ASO titer (753 IU/mL), an elevated erythrocyte sedimentation rate (27 mm/h), and an HLA-DR2 haplotype. Complete blood cell count, HLA-B27, rapid plasma reagin, and angiotensin-converting enzyme levels were unremarkable. Treatment was begun with aggressive topical 1% prednisolone acetate and cycloplegics. Within 6 weeks, all inflammation resolved, and visual acuity returned to 20/20 OU.
We believe this patient had recurrent PSS uveitis. However, we are aware of only 1 other case of recurrent PSS uveitis.4 In our patient, both episodes of inflammation were preceded by a culture-positive streptococcal pharyngitis with elevated ASO titers, and demonstrated findings and a clinical course typical for PSS uveitis.2- 4 The patient's HLA-DR2 typing is interesting, as this haplotype has been seen in association with rheumatic fever and other PSS.1 Recurrent PSS uveitis is not surprising since other PSS entities may be recurrent, even with a subclinical infection.1
Confirmation that PSS uveitis may be recurrent could be important for its diagnosis, prevention, and treatment. We agree with Leiba et al4 that all patients with ocular signs and symptoms of PSS and active streptococcal infection or a history of PSS should receive eye examinations. Examining blood ASO titers may be useful in patients with idiopathic uveitis and a history of a streptococcal infection.
This study was supported in part by the Heed Ophthalmic Foundation (Dr Wirostko), and an unrestricted grant from Research to Prevent Blindness Inc, New York, NY.
Reprints: Thomas B. Connor, Jr, MD, The Eye Institute, 925 N 87th St, Milwaukee, WI 53226 (e-mail:firstname.lastname@example.org).
Wirostko WJ, Connor TB, Wagner PF. Recurrent Poststreptococcal Uveitis. Arch Ophthalmol. 1999;117(12):1649-1650. doi: