Bilateral neuro-retinitis with zoster infection

Citation
T. Nicaeus et H. Wilhelm, Bilateral neuro-retinitis with zoster infection, KLIN MONATS, 214(3), 1999, pp. 175-177
Citations number
6
Categorie Soggetti
Optalmology
Journal title
KLINISCHE MONATSBLATTER FUR AUGENHEILKUNDE
ISSN journal
00232165 → ACNP
Volume
214
Issue
3
Year of publication
1999
Pages
175 - 177
Database
ISI
SICI code
0023-2165(199903)214:3<175:BNWZI>2.0.ZU;2-L
Abstract
Background Infections with varicella tester virus may involve the optic ner ve and the retina. Different pathomechanisms have been discussed. We presen t a case with an autoimmune inflammatory reaction according to the clinical course. Patient A 69-year-old female was referred to our clinic because of suspecte d bilateral anterior ischemic optic neuropathy. She complained of severe vi sual loss the day before admission. Her ophthalmological and general histor y was unremarkable apart from treatment with 5 to 7.5 mg prednisolone alter nately because of rheumatoid arthritis. Best corrected visual acuity was 1/ 15 OD and 0.1 OS. A relative afferent pupillary defect on the right eye was present. Optic disc oedema with multiple hemorrhages of the retina extendi ng into the peripheral fundus, slightly attenuated retinal arteries and mac ular oedema were seen fundoscopically in both eyes. Therapy and clinical outcome After immediate treatment with steroids (initi al dose 250 mg prednisolone per day) visual acuity improved. Because of a c linically suspected and serologically proven active varicella-zoster infect ion an additional virostatic therapy with valaciclovir was started and ster oids were lowered gradually. Within 2 months, visual acuity increased to 0. 8 OD and 1.0 OS. Oedema of optic discs and macula resolved and retinal hemo rrhages disappeared. Conclusion A severe hemorrhagic neuro-retinitis involving the optic discs w as seen in the course of a varicellazoster infection, possibly reactivated by chronic steroid therapy of a rheumatoid arthritis. Because of the normal ization of visual function an ischemic pathogenesis is unlikely. An autoimm une inflammatory reaction seems to be the predominant mechanism, supported by the good effect of steroid and valaciclovir therapy.