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2010 Aizawa t al, publih and licn Dov Mdical P Ltd. Thi i an Opn Acc aticlwhich pmit untictd noncommcial u, povidd th oiginal wok i poply citd.

Clinical Ophthalmology 2010:4 977979

Clinical Ophthalmology Dovepress

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Opn Acc Full Txt Aticl

DOI: 10.2147/OPTH.S13048

A ca of unilatal optic dic wllingwith chonic activ eptinBa viu infction

Naoko Aizawa1

Tou Nakazawa 1

Maahiko shimua2

1Dpatmnt of Ophthalmology,

Tohoku Univity Gaduat schoolof Mdicin , sndai, Miyagi, Japan;2Dpatmnt of Ophthalmology, NTTeat Japan Tohoku Hopita l, sndai,Miyagi, Japan

Copondnc: Naoko AizawaDpatmnt of Ophthalmology, TohokuUnivity Gaduat school of Mdicin,1-1 siyo, Aoba, sndai, Miyagi9808574, JapanTl +81-22-717-7294Fax +81-22-717-7298email [email protected]

Abstract: Ocular complications o chronic active EpsteinBarr virus (EBV) inection have

rarely been reported and are usually associated with systemic symptoms. We described a

17-year-old boy with unilateral optic disc swelling without any systemic symptoms at the initial

onset. Antibody titers to EBV were markedly elevated. Treatment with immunosuppressants

and corticosteroids dramatically relieved all his symptoms, including unilateral optic swellingand visual eld abnormalities.

Keywords: EpsteinBarr virus, optic disk swelling

IntroductionChronic active EpsteinBarr virus (EBV) inection (CAEBV) syndrome belongs to a

category o EBV-related disease. Ocular complications o CAEBV have rarely been

reported and are usually associated with systemic symptoms, including chronic atigue,

low-grade ever, pharyngitis, dark urine, and malaise, that are usually observed prior

to visual disturbances.1

We describe a rare case o unilateral optic disc swelling without any systemic

symptoms at the initial onset. It was not diagnosed as CAEBV until EBV-specic

immunological studies were done. Unilateral optic disc swelling was initial and unique

signs o CAEBV in this case.

Case reportA healthy, 17-year-old boy was diagnosed with visual eld abnormalities in his let

eye and reerred to our outpatient clinic or unilateral optic disc swelling. He had no

history o chronic atigue, recurrent ever, or other systemic symptoms. At his initial

visit, best-corrected visual acuity (BCVA) in his let eye was 20/20. Fundus examination

revealed prominent optic disc swelling and tortuous vessels (Figure 1A). Visual eld

abnormalities with enlargement o Marriotts scotoma (Figure 1B) and an aerent pupil-

lary deect were observed in his let eye. However, there were no ocular infammatory

symptoms. Magnetic resonance image results showed no intracranial abnormalities.

At that time, his blood tests revealed no abnormalities (white blood cell count: 4,900/

L, red blood cell count: 4.65 106/L, platelet count: 141 103/L, hemoglobin

level: 13.2 g/dL, glutamicoxaloacetic transaminase level: 36 IU/L, glutamicpyruvic

transaminase level: 44 IU/L, blood urea nitrogen level: 12 g/dL, creatinine level:

0.8 mg/dL, total cholesterol level: 110 mg/dL, sodium level: 140 mEq/L, and potas-

sium level: 3.9 mEq/L).

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Clinical Ophthalmology

28 August 2010
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Two weeks ater the onset o his ocular symptoms, acute

iridocyclitis and retinal vasculitis were observed in asso-

ciation with a slight ever. His let BCVA was decreased to

20/40. Specic viral immunological studies revealed elevated

levels o anti-EBV antibody (viral capsid antigen [VCA]-

immunoglobulin [Ig]G: 10,240, VCA-IgA: 1,280, VCA-IgM:

,10, early antigen [EA]-IgG: 2,560, and EA-IgA: 80; note

that each titer,10 is normal) and low titers o EpsteinBarr

nuclear antigen (EBNA: 40). DNA o EBV: 1,834 copy/0.2-g

DNA (B cells: 33 copy/100-ng DNA, T cells: 75 copy/100-ng

DNA, and natural killer [NK] cells: 1,100 copy/100-ng DNA).

Elevated levels o EBV T cells and NK cells along with clinical

symptoms o EBV inection indicated CAEBV.

Immediately ater the diagnosis, the patient received

systemic administration o immunosuppressants and corti-

costeroids. Three months ater chemotherapy, ocular infam-

mation and optic disc swelling gradually regressed, and his

BCVA returned to 20/20. As depicted in Figure 2, visual

eld abnormalities were also improved. Levels o anti-EBV

antibody were decreased (VCA-IgG: 1,280, VCA-IgA: 80,

EA-IgG: 160, and EA-IgA: 10) with low antibody titers o

EBNA: 40.

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Figure 1 Atth initial viit, A) visual eld by Goldmann perimeter indicated enlargement of Mariotts scotoma. B) Fundu photogaph of th lft y howd th ddih,

wolln optic dic.

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Figure 2 Aftth ytmic antinoplatic tatmnt, A) visual eld by Goldmann perimeter indicated no abnormalities. B) Fundu photogaph howd a nomal optic

dic appaanc.
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Optic dic wlling in patint with CAeBV

CommentsEBV is a DNA virus o the human herpes virus group, and

inection does not always cause generalized or local symptoms.

Primary inection with EBV leads to antibody ormation ol-

lowed, weeks or months later, by a serologic response to EBNA

with ormation o a virus carrier state that persists or lie.2Thus,

even under normal ocular conditions, the DNA o EBV can be

detected in the iris, ciliary body, retina, and choroid.3 Generally,

patients with CAEBV maniest persistently elevated antibody

titers o VCA and EA with low antibody titers o EBNA.4 In

this case, high levels o anti-EBV antibody present at the onset

and reduced levels present ater the regression o clinical signs

with chemotherapy indicated CAEBV.

Ocular involvement secondary to CAEBV is rare despite

that genomic DNA o EBV can be detected in various ocular

tissues, including the iris, ciliary body, retina, retinal pigment

epithelium, and choroid.3 Although it has been reported in

various ocular lesions,2,5 it is usually limited to a transient

ollicular conjunctivitis. Only two cases o unilateral optic

swelling due to CAEBV have been reported, and in both

cases, CAEBV with recurrent ever had been diagnosed

beore the onset o ocular symptoms.4 In our case, CAEBV

was not diagnosed until the onset o ocular symptoms.

Unilateral optic disc swelling without ocular infammation

was rst observed, and subsequently (2 weeks later), the

ocular infammation o uveitis and retinal vasculitis with a

slight ever was observed. The clinical course o this case

indicates that the activation o EBV initially occurred in the

optic neurons, which are the axons o retinal ganglion cells,

and then spread to the posterior segments o the choroid and

retina and to the anterior segment. Ophthalmologists should

be aware that the immediate onset o a unilateral visual dis-

turbance with optic disc swelling without any infammation

or intracranial disease may indicate CAEBV.

Acknowledgment/disclosureThe authors report no nancial support or confict o interests

in this work.

References1. Wong KW, DAmico DJ, Hedges TR III, Soong HK, Schooley RT,

Kenyon KR. Ocular involvement associated with chronic Epstein-Barr

virus disease.Arch Ophthalmol. 1987;105:788792.

2. Matoba AY. Ocular disease associated with Epstein-Barr virus inection.

Surv Ophthalmol. 1990;35:145150.3. Kimura H, Morita M, Yabuta Y, et al. Quantitative analysis o Epstein-barr

virus load by using a real-time PCR assay. J Clin Microbiol. 1999;37:

132136.

4. Yamamoto M, Ohga S, Ohnishi Y, Inomata H. Optic disk vasculitis

associated with chronic Epstein-Barr virus inection. Ophthalmologica .

2002;216:221225.

5. Morishima N, Miyakawa S, Akazawa Y, Takagi S. A case o uveitis

associated with chronic active Epstein-Barr virus inection. Ophthal-

mologica. 1996;210:186188.
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