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Epstein–Barr virus associated acute retinal necrosis
  1. SUSANNE KRAMER
  1. Katharinenhospital Stuttgart, Kriegsbergstrasse 60, D-70174 Stuttgart, Germany
  2. University Eye Hospital, Department I, Schleichstrasse12, D-72076 Tübingen, Germany
  1. CHRISTOF BRUMMER,
  2. MANFRED ZIERHUT
  1. Katharinenhospital Stuttgart, Kriegsbergstrasse 60, D-70174 Stuttgart, Germany
  2. University Eye Hospital, Department I, Schleichstrasse12, D-72076 Tübingen, Germany
  1. manfred.zierhut{at}med.uni-tuebingen.de

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Editor,—Epstein–Barr virus (EBV) belongs to the group of herpesviruses. It may affect the eye in many different ways, most often as conjunctivitis or uveitis. For herpes simplex virus (HSV) and for varicella zoster virus (VZV) it is well known that they can cause acute retinal necrosis (ARN), but information regarding EBV retinitis is rare. To our knowledge we report the first case of a probable ARN associated with EBV infection.

CASE REPORT

In 1997 a 32 year old homosexual man presented for the first time to the University Eye Hospital, Tübingen. For 4 weeks he had suffered from an acute retinal necrosis of the left eye. His right eye was not affected. The visual acuity of the left eye was 0.1. The anterior segment of the eye showed corneal precipitates but no cells in the anterior chamber. Owing to massive cell infiltration in the vitreous the lower part of the fundus was not visible. There was a large necrotic area with bleeding and occlusive vasculitis in the upper nasal periphery (Fig 1). The patient claimed to be healthy, apart from an EBV infection with pericarditis which had occurred when he was 17 years old. Tests for HIV and syphilis were repeatedly negative, also for Lyme disease, toxoplasmosis, hepatitis B, HSV, and VZV. There were increased titres for EBV-IgA (1:128), EBV-IgG (1:1512), EBV nuclear antigen, and EBV early antigen (1:64), a constellation typical for an acute EBV infection. After therapy with aciclovir 5 × 400 mg, prednisolone 60 mg, acetylsalicylacide (200 mg), and topical prednisolone acetate the symptoms decreased.

Figure 1

Funduscopy of the left eye at presentation, showing peripheral necrotising retinitis with bleeding.

After 8 weeks his visual acuity increased up to 0.5 but dropped to 0.2 after 5 months as a result of vitreous haemorrhages because of neovascularisations. After clearance of the bleeding and peripheral laser coagulation the neovascularisations resolved. The fundus showed scars but no holes in the area of the necrotic retina (Fig 2). After 25 months the visual acuity was 0.2. The anterior parts showed mild cataracta complicata. Vitreous cell infiltration still persisted and the central part of the fundus was not clearly seen. The patient showed an absolute central scotoma and atrophy of the optic nerve, without treatment.

Figure 2

Funduscopy of the left eye after 6 months, showing peripheral scarring.

COMMENT

The role of EBV in ocular diseases is still not clear, because approximately 95% of adults are positive for EBV antigen and only a few suffer from ocular disease. Previously described cases of “EBV retinitis” only described inflammation of the posterior pole without scaring, which is not typical for viral retinitis. Proving an acute EBV infection usually is done with increased EBV titres. Such a constellation was found in our patient. The titres decreased during the following 12 weeks suggesting that EBV may play apart in this man's retinitis. The reported patient showed all criteria of the American Uveitis Society for ARN.

However, it is not possible to rule out that other herpesviruses have caused the retinitis. This probably could only have been proved with a diagnostic vitrectomy or anterior chamber tap which was refused because of improvement with treatment. Serological findings showed no signs of other herpes infections.

References

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