Purpose: We report a case of acute retinal necrosis caused by Epstein-Barr virus (EBV) infection.
Case: The patient in this case was a 67-year-old man who visited a local physician for decreased visual acuity and floaters 9 days before visiting our hospital. At the time of examination, bleeding at the posterior pole of the retina and white lesions on the temporal side of the retina were observed. Accordingly, uveitis was suspected, and the patient was referred to our department. Retinal whitening and vitreous opacity in the fovea were observed at the time of examination at our department. His serum viral antibody titers were positive for the varicella-zoster virus (VZV), herpes simplex virus (HSV), and cytomegalovirus (CMV) only for immunoglobulin (Ig) G antibody, whereas serum toxoplasma antibody titers, β-D-glucan, and T-SPOT were all negative. As his vitreous opacity increased, vitrectomy was performed on the 30th day after the first visit. Intraoperative fundus examination revealed retinal necrotic lesions in the macula and peripheral retina, but no union lesions. Polymerase chain reaction (PCR) of the vitreous humor samples collected during vitrectomy was negative for the HSV type 1, HSV type 2, and VZV, but positive for EBV. The concentration of EBV in the vitreous humor at the time of the initial surgery was as high as 389,750 copies/mL. Vitreous opacity exacerbated again, and re-vitrectomy was performed on the 40th day. Intraoperative fundus examination revealed retinal necrotic lesions in the peripheral retina and the progression of vessel sheathing. Blood tests showed high levels of EBV IgG and low levels of EBV IgM, suggesting a reactivation of previous EBV infection. The amount of EBV DNA in the vitreous humor obtained during the two surgeries and in the blood samples obtained during the second surgery was analyzed using real-time PCR. The results showed that the amount of EBV DNA in both vitreous humor samples was > 20 times higher than that in whole blood, indicating that local ocular EBV infection developed secondary to the systemic reactivation of EBV.
Conclusion: EBV retinal necrosis can occur because of the reactivation of previous EBV infection.
Nippon Ganka Gakkai Zasshi (J Jpn Ophthalmol Soc) 126: 1057-1063,2022.
