Doreen Krist1, Hartmut Wenkel. 1. Department of Ophthalmology, University Erlangen-Nürnberg, Schwabachanlage 6, D-91054 Erlangen, Germany.
Abstract
OBJECTIVE: To report on the clinical findings in a patient with posterior scleritis associated with infection with Borrelia burgdorferi. DESIGN: Interventional case report. PARTICIPANT: A 39-year-old male ranger who experienced posterior scleritis after several tick bites with erythema migrans. TESTING: Extensive ophthalmic and systemic workup, including serologic testing and imaging techniques. RESULTS: Sonography and contrast-enhanced computed tomography showed a large scleral mass (16 x 12 x 13 mm) in a patient with painful proptosis in the left eye with episcleral vascular dilation, reduction in bulbar motility, and chorioretinal folds in the upper temporal quadrant. Treatment with high-dose corticosteroids resulted in rapid regression of clinical symptoms and of the scleral mass. Intensive workup revealed immunoglobulin M antibodies (enzyme-linked immunoassay, Western immunoblot) and a positive lymphocyte transformation assay against B. burgdorferi. No other cause for posterior scleritis could be identified. CONCLUSIONS: Posterior scleritis should be added to the list of ocular manifestations associated with Lyme disease. Because corticosteroids alone resulted in rapid improvement of clinical symptoms, the scleritis might be mediated by autoimmunologic mechanisms.
OBJECTIVE: To report on the clinical findings in a patient with posterior scleritis associated with infection with Borrelia burgdorferi. DESIGN: Interventional case report. PARTICIPANT: A 39-year-old male ranger who experienced posterior scleritis after several tick bites with erythema migrans. TESTING: Extensive ophthalmic and systemic workup, including serologic testing and imaging techniques. RESULTS: Sonography and contrast-enhanced computed tomography showed a large scleral mass (16 x 12 x 13 mm) in a patient with painful proptosis in the left eye with episcleral vascular dilation, reduction in bulbar motility, and chorioretinal folds in the upper temporal quadrant. Treatment with high-dose corticosteroids resulted in rapid regression of clinical symptoms and of the scleral mass. Intensive workup revealed immunoglobulin M antibodies (enzyme-linked immunoassay, Western immunoblot) and a positive lymphocyte transformation assay against B. burgdorferi. No other cause for posterior scleritis could be identified. CONCLUSIONS:Posterior scleritis should be added to the list of ocular manifestations associated with Lyme disease. Because corticosteroids alone resulted in rapid improvement of clinical symptoms, the scleritis might be mediated by autoimmunologic mechanisms.