MULTIMODAL IMAGING OF WEST NILE VIRUS CHORIORETINITIS DANIEL LEARNED, MD,* ERIC NUDLEMAN, MD, PHD,† JOSHUA ROBINSON, MD,† EMMANUEL CHANG, MD, PHD,† LORI STEC, MD,* LISA J. FAIA, MD,*† JEREMY WOLFE, MD,*† GEORGE A. WILLIAMS, MD*† Purpose: To report the results of multimodal imaging of West Nile virus chorioretinitis. Methods: Three patients with West Nile virus chorioretinitis were evaluated by color fundus photography, fluorescein angiography, enhanced depth optical coherence tomography, indocyanine green angiography, and fundus autofluorescence. Results: Imaging results demonstrate outer retinal and retinal pigment epithelial involvement with inner retinal sparing. Conclusion: Multiple fundus imaging modalities used during the diagnosis of West Nile chorioretinitis are consistent with outer retinal and pigment epithelial changes, suggesting outer retina and retinal pigment epithelium as the primary sites of ocular involvement. RETINA 34:2269–2274, 2014

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involvement, including meningitis, encephalitis, or meningoencephalitis, is estimated to occur in approximately 1 in 100 to 150 (0.67–1%) of infected individuals.7–9 Risk factors for developing neuroinvasive disease include environment (areas where primary infection is with Culex tarsalis or Culex quinquefasciatus mosquitoes), advanced age, immunosuppression, and male sex.9–14 Of the most severely affected individuals, 8% to 12% result in death.11,14 Currently, the treatment of neuroinvasive disease is supportive in nature. However, interferon alpha has been proposed as being an effective treatment. This is supported by in vitro studies, case reports with improvement of WNV encephalitis with treatment, and clinical trials based on similar arboviruses.15–18 Other proposed treatments have included ribavirin and intravenous immunoglobulin, which have failed to show a benefit in clinical trials.19–21 Ocular symptoms were first reported in 1956 and include decreased vision, photophobia, retrobulbar pain, diplopia, and floaters.22–28 West Nile virus chorioretinitis was first described as round, multifocal, “creamy” chorioretinal lesions, often arranged in a curvilinear pattern.24,26,29,30 Other ocular manifestations include occlusive retinal vasculitis, optic neuritis, congenital chorioretinal scarring, and uveitis without focal lesions.28 As with systemic manifestations, ocular symptoms are typically self-limited; however, persistent decreased vision has been reported.26,31 Ocular

est Nile virus (WNV) is a zoonotic pathogen transmitted from infected birds to humans by mosquitos.1,2 West Nile virus is a single-stranded RNA arbovirus within the Flaviviridae family first isolated in Uganda in 1937.1,3 The first documented case of human infection in North America was in New York in 1999 with subsequent increased incidence and rapid spread from coast to coast.4,5 Clinical manifestations of WNV infection are broadly classified into three categories: asymptomatic, West Nile fever, and West Nile meningoencephalitis. The majority of cases are asymptomatic (approximately 80%); however, when symptoms of West Nile fever occur, they typically follow a 3-day to 14-day incubation period and include high-grade fever, weakness, headache, myalgia, and gastrointestinal upset.2,4,6 These symptoms are often self-limited and tend to resolve within 1 week. Severe neurologic From the *Department of Ophthalmology, Oakland University School of Medicine, William Beaumont, Beaumont Eye Institute, Royal Oak, Michigan; and †Associated Retinal Consultants, Royal Oak, Michigan. None of the authors have any financial/conflicting interests to disclose. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.retinajournal.com). Reprint requests: George A. Williams, MD, Associated Retinal Consultants, P. C. Medical Office Building, Suite 344, 3535 W. 13 Mile Road, Royal Oak, MI 48073; e-mail: [email protected]

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disease typically only requires observation but can be treated with cycloplegia and topical steroids. Complications, such as macular edema, have been treated successfully with intravitreal anti–vascular endothelial growth factor medications.32 October 2012 saw the highest number of WNV cases reported in the United States to date.33 Of the 5,674 reported cases, 2,873 (51%) were categorized as neuroinvasive.33 The epidemic of 2012 has provided an opportunity to better define the disease using improved imaging modalities not available in 2003. We report three cases of classic WNV chorioretinitis using fundus autofluorescence (FAF), indocyanine green angiography (ICGA), spectral domain optical coherence tomography (OCT) with enhanced depth imaging (EDI), fluorescein angiography (FA), and color fundus photography.

Patients and Methods This was a retrospective, noncomparative, observational study consisting of 3 patients evaluated between August and November of 2012. Institutional review board approval for the data collection and study was granted by the Western Institutional Review Board. The study was conducted in a Health Insurance Portability and Accountability Act complaint fashion, and the research adhered to the tenets of the Declaration of Helsinki. All patients had a diagnosis of West Nile chorioretinitis based on fundus examination and serologic testing. Diagnostic criteria for West Nile virus chorioretinitis included the following: 1) classic nummular lesions on fundus examination and 2) serologic testing showing elevated WNV-specific IgM. None of the patients had lumbar puncture to assess for pleocytosis or cerebrospinal fluid analysis. Fundus imaging included color fundus photography, FA, SDOCT with EDI, wide-field FAF, and ICGA. Classic chorioretinal lesions, as described above, were the only form of ocular disease included in this study. Fig. 1. Montage color fundus photography with inset enlargement of right (A) and left (B) eyes in the patient with West Nile chorioretinitis described in Case 1 showing deep, nummular yellow-white lesions in curvilinear distribution with asymmetric involvement of the right eye greater than left eye.



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No patient met criteria for the diagnosis of neuroinvasive WNV (meningitis, encephalitis, acute flaccid paralysis) as outlined by Sejvar et al.7 Treatment of all three patients described below consisted of supportive management and observation. None of the patients presented were treated with antiviral medications (interferon alpha, ribavirin), intravenous immunoglobulin, topical steroids, or cycloplegics. Topical steroids and cycloplegics were considered for all patients, but as a result of limited inflammation and lack of pain, these treatments were deferred. Results Case 1 A 56-year-old African American woman was initially evaluated and admitted to the hospital for diarrhea, nausea, vomiting, fever, back pain, and headaches in September 2012. Serum examination for IgM and IgG antibodies to WNV were positive at a level of 30.07 (normal limit, ,5.56) and 3.74 (normal limit, ,1.51), respectively. During the course of her stay at the hospital, the patient noted floaters in both eyes. Physical examination was significant for 20/ 20 corrected visual acuity in both eyes, normal anterior segments, and mild vitritis in both eyes. The optic disk and vessels were normal in both eyes. Scattered in the fundus of both eyes were multiple, 200-mm to 300-mm deep, nummular yellow-white opacities, with mild pigmentary changes. No cystoid macular edema was seen in either eye. The periphery in both eyes showed additional nummular lesions following a curvilinear distribution in the temporal and nasal equatorial periphery. The right eye was affected more significantly than the left eye (Figure 1, A and B). Fluorescein angiography demonstrated multiple nummular areas of hypofluorescence with a rim of peripheral staining corresponding to the deep creamy lesions noted on color fundus photography (Figure 2, A and B). Findings from ICGA revealed welldemarcated areas of focal, dense hypocyanescence

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persisting through the late phase (Figure 3) and corresponding with the center of the lesions seen on FA (Figure 2, A and B). Findings from SD-OCT with EDI revealed posterior vitreous opacities consistent with vitritis and deep retinal hyperreflective lesions extending from the outer nuclear layer to the retinal pigment epithelium, disrupting the normal outer retinal architecture (2 lesions depicted in Figure 4). No discernible changes were evident in the inner retina or nerve fiber layer overlying the deep lesions on OCT imaging. Two isolated lesions comparing color photographs, FA, ICGA, autofluorescence, and OCT images are demonstrated in Figure 4. Case 2 A 65-year-old white man presented with a 2-week history of decreased vision and floaters in the left eye. Review of systems was significant for a dull headache and associated flulike symptoms for 2 weeks to 3 weeks, including diarrhea and abdominal pain. Physical examination demonstrated best-corrected visual acuity of 20/20 in the right eye and 20/100 in the left eye. Findings from the anterior segment examination were normal in both eyes. Dilated fundus examination was significant for moderate vitritis in the left eye with multiple nummular yellow-white opacities, including numerous lesions arranged in a curvilinear pattern (see Figure, Supplemental Digital Content 1, http://links. lww.com/IAE/A251). In the right eye, fewer lesions were present but arranged in a similar distribution (see Figure, Supplemental Digital Content 1, http://links. lww.com/IAE/A251). A single lesion in the macula of the left eye was imaged by SD-OCT (see Figure, Supplemental Digital Content 1, http://links.lww. com/IAE/A251), which demonstrated a deep retinal lesion with focal disruption of the outer nuclear layer and retinal pigment epithelium, consistent with the

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findings in Case 1 (Figure 4). Similarly, no changes were present in the inner retina or nerve fiber layer. Given the patient’s ophthalmic findings, WNV titers were drawn and found to be positive (IgM = 60.5; IgG = 6.0). Case 3 A 60-year-old white man with a history of nonproliferative diabetic retinopathy in both eyes, and a central retinal vein occlusion in the left eye, presented with decreased vision and floaters in the right eye for 2 weeks. Review of systems was significant for flulike symptoms, including headache and diarrhea, for which the patient was seen in the emergency department 1 week ago. He was found to have elevated WNV titers (IgM = 57.0; IgG = 4.8). On examination, his best-corrected visual acuity was 20/60 in the right eye and counting fingers at 2 feet in the left eye (unchanged in the left eye from his baseline). Anterior segments appeared normal in both eyes. A dilated fundus examination was significant for mild vitritis in both eyes with nummular yellow-white lesions similar in appearance and distribution to the above 2 cases (see Figure, Supplemental Digital Content 2, http://links.lww.com/IAE/A252). Multiple intraretinal hemorrhages were present in both eyes consistent with the patient’s history of diabetic retinopathy. Spectral domain OCT images through lesions in the macula of both eyes showed outer retinal and retinal pigment epithelial changes, consistent with Cases 1 (Figure 4) and 2 (see Figure, Supplemental Digital Content 1, http://links.lww.com/IAE/A251), however, more atrophic in appearance in Case 3 (see Figure, Supplemental Digital Content 2, http://links. lww.com/IAE/A252). Inner retinal changes revealed on OCT in Supplemental Digital Content 2 (see Figure, http://links.lww.com/IAE/A252) are attributed to

Fig. 2. Fluorescein angiography (left inset) and ICGA (right inset) of right eye posterior pole (A) and left eye posterior pole (B) in the patient with West Nile chorioretinitis described in Case 1. Fluorescein angiography images show nummular lesions with hypofluorescent centers and staining edges. The center of these lesions have well-demarcated borders with a blocking pattern in early and late phases on ICGA.

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Fig. 3. Indocyanine green angiography of the right eye with early phase at 1:23 (left inset) and intermediate phase at 10:46 (right inset) in the patient with West Nile chorioretinitis described in Case 1 demonstrating early and stable hypocyanescence throughout study.

the patient’s history of nonproliferative diabetes and history of vein occlusion in the left eye. The autofluorescence imaging from Case 3 (see Figure, Supplemental Digital Content 2, http://links.lww. com/IAE/A252) showed multiple hypoautofluorescent lesions compared with the hyperautofluorescent lesions in Figure 4 from the patient presented in Case 1. These differences are thought to be from a more subacute nature in this patient compared with that described in Case 1. These findings are supported by the OCT demonstrating a more atrophic appearance. All imaging modalities are consistent with outer retinal abnormality. However, it is important to note that ultrawide-field autofluorescence does have a lower resolution compared with 30° and 55° imaging modalities,

which leads some to question its validity clinically and could be a cause of the hypoautofluorescent lesions in the autofluorescence images in this case.

Discussion As first described in 2003, all 3 patients in our series presented with the classic findings of posterior to midperipheral “creamy” lesions on fundus examination, corresponding to “target” lesions on FA (central hypofluorescence with a rim of hyperfluorescence).24 As with previous reports,26,30 the lesions also demonstrate the characteristically curvilinear distribution and were associated with a mild vitritis.

Fig. 4. Color fundus photography, FA, ICGA, FAF, and SD-OCT with EDI imaging of two isolated “creamy” fundus lesions in the patient with West Nile chorioretinitis described in Case 1. Resolution of wide-field FAF has decreased compared with 35° or 55° imaging modalities. Clinical relevance for wide-field FAF has not yet been established. Color, wide-field color fundus photography; AF, autofluorescence; FA, wide-field fluorescein angiography; OCT, SD-OCT with EDI.

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In addition to the findings in WNV chorioretinitis, retinal manifestations of WNV include optic neuritis, congenital chorioretinal scarring, occlusive retinal vasculitis, and uveitis without focal lesions.28 Chorioretinitis has previously been described as the most common ocular manisfestion.28 However, Sivakumar et al34 suggested that there may be a group of patients with retinitis being much more common than choroiditis. Varying viral strains, different patient population, and increasing awareness of WNV may all contribute to the differences in presentation among studies. Previous reports35 have speculated that the curvilinear pattern of chorioretinitis associated with WNV may be a result of contiguous spread to the retina from the central nervous system along nerve fibers. Indeed, an association between WNV meningoencephalitis and chorioretinitis has been reported.24 We present a series of patients who did not meet criteria for the diagnosis of neuroinvasive disease presenting with classic WNV chorioretinitis lesions. Using FAF, ICGA, and SD-OCT with EDI, we demonstrate deep retinal lesions that spare the inner retina and nerve fiber layer, which may be more consistent with hematogenous spread of the virus to the eye through choroidal circulation. Previous reports28,36–39 of occlusive vasculitis and microvasculature obstruction in patients with WNV may further support the notion of hematogenous spread. The classic lesions seen on color fundus photography and FA have already been well characterized in the literature.23,24,26,28–30 However, the corresponding lesions on ICGA and SD-OCT with EDI reported are less well understood, and closer analysis may help offer additional insight into pathophysiologic characteristics of this disease. The intensely hypocyanescent lesions on ICGA have previously been attributed to an inflammatory hypoperfusion at the level of the choriocapillaris as with other inflammatory conditions including the “white dot syndromes.”40–42 Multimodal imaging in this case may call that etiologic explanation into question. First, it is unclear why hypoperfusion within the choriocapillaris layer in itself would cause such a welldemarcated, intensely hypocyanescent area on ICGA that dramatically attenuates the signal from the underlying larger choroidal vessels in the early frames. Second, hypoperfusion would not explain why these hypocyanescent lesions persist into the intermediate phase (at least 10 minutes). As shown in Figure 3, these hypocyanescent areas are present from the earliest frames and persist largely unaltered when reimaged 10 minutes later. As time passes, bound indocyanine green will escape through the fenestrations within the choriocapillaris and diffuse into the choroidal stroma.42 This is evident by the

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nearly complete obliteration of the details of the deeper choroidal vasculature in later frames. This diffusive process would also extend laterally to blur the sharp edges of even the pinpoint hypocyanescent lesions in this case, if the lesions were secondary to hypoperfusion. Moreover, unlike the “iceberg effect” as is the case with other causes of chorioretinitis, the lesions on ICGA in this case are smaller than the lesions imaged with color photography, FA, or FAF.40 Also, the hyperfluorescent rim revealed on FA and the more amorphous hyperautofluorescent lesion revealed on FAF (Figure 4) have no correlates on ICGA imaging. Indocyanine green angiography is fundamentally different from FA, and as such, areas of hypocyanescence cannot be analyzed using the same paradigm.42 This is largely because ICGA uses a longer wavelength that readily penetrates many physiologic and pathophysiologic entities that commonly cause “blocking” in FA. For the reasons outlined above, analysis of the hypocyanescent areas on ICGA in this case seems to be more consistent with a blocking phenomenon than simply a choroidal hypoperfusion mechanism. However, it is unclear what material and in what layer is causing the blocking. In looking at a given lesion using the various imaging modalities, exemplified by 2 lesions in Figure 4, it is reasonable to posit that the deep “creamy” lesion revealed clinically corresponds to an area of outer retinal and pigment epithelial hyperreflectance on SD-OCT with corresponding choroidal shadowing. This area exactly corresponds to the hypofluorescent portion of the lesion on FA and to the deeply hypocyanescent lesion on ICGA. Another possible source for the perceived blocking phenomenon on ICGA could be an aggregation of inflammatory cells or microscopic granuloma within the choriocapillaris itself. A less likely alternative could be a full-thickness choroidal granuloma; however, some lesions appear too finely punctate for this to be plausible. It is also difficult to support the existence of a choriocapillaris granuloma from the OCT images in this case. Referring to this ocular manifestation of West Nile virus infection as a “chorioretinitis” implies that it is characterized by primary choroidal involvement with secondary overlying pigment epithelial and outer retinal damage. We believe that the virus typically gains access to the eye hematogenously and likely through choroidal circulation, rather than directly from the central nervous system by means of ganglion cell axons.35 The multimodal imaging analysis reported here calls into question the extent of choriocapillaris involvement and the widely accepted interpretation of these ICGA findings as primarily secondary to choriocapillaris hypoperfusion. Rather, these results support the outer retina and retinal pigment epithelium as the primary location of the disease activity.

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Key words: angiography, chorioretinitis, fluorescein angiography, fundus autofluorescence, indocyanine green angiography, spectral domain OCT with enhanced depth imaging, uveitis, West Nile virus. References 1. Craven RB, Roehrig JT. West Nile virus. JAMA 2001;286: 651–653. 2. Petersen LR, Marfin AA. West Nile virus: a primer for the clinician. Ann Intern Med 2002;137:173–179. 3. Smithburn KC, Hughes TP, Burke AW, Paul JH. A neurotropic virus isolated from the blood of a native of Uganda. Am J Trop Med 1940;20:471–492. 4. Nash D, Mostashari F, Fine A, et al. The outbreak of West Nile virus in the New York city area in 1999. N Engl J Med 2001; 344:1807–1814. 5. Hayes EB, Komar N, Nasei RS, et al. Epidemiology and transmission dynamics of West Nile virus disease. Emerg Infect Dis 2005;11:1167–1173. 6. Mostashari F, Bunning ML, Kitsuatani PT, et al. Epidemic West Nile encephalitis, New York, 1999: results of a household-based seroepidemiological survey. Lancet 2001;358:261–264. 7. Sejvar JJ, Haddad MB, Tierney BC, et al. Neurologic manifestations and outcome of West Nile virus infection. JAMA 2003;290:511–515. 8. Petersen LR, Roehrig JT, Hughes JM. West Nile virus encephalitis. N Engl J Med 2002;347:1225–1226. 9. Debiasi RL. West Nile virus neuroinvasive disease. Curr Infect Dis Rep 2011;13:350–359. 10. Lindsey NP, Kuhn S, Campbell GL, Hayes EB. West Nile virus neuroinvasive disease incidence in United States, 20022006. Vector Borne Zoonotic Dis 2008;8:35–39. 11. Center for Disease Control (CDC). West Nile virus activity—United States, 2009. MMWR Morb Mortal Wkly Rep 2010;59:769–772. 12. DeSalvo D, Roy-Chaudhury P, Peddi R, et al. West Nile virus encephalitis in organ transplant recipients: another high-risk group for meningoencephalitis and death. Transplantation 2004;77:466–469. 13. Kleinschmidt-DeMasters BK, Marder BA, Levi ME, et al. Naturally acquired West Nile virus encephalomyelitis in transplant recipients: clinical, laboratory, diagnostic, neuropathological features. Arch Neurol 2004;61:1210–1220. 14. O’leary DR, Marfin AA, Montgomery SP, et al. The epidemic of West Nile virus in the United States, 2002. Vector Borne Zoonotic Dis 2004;4:61–70. 15. Morrey JD, Day CW, Julander JG, et al. Effect of interferonalpha and interferon-inducers on West Nile virus in mouse and hamster animal models. Antivir Chem Chemother 2004;15:101. 16. Anderson JF, Rahal JJ. Efficacy of interferon alpha-2b and ribavirin against West Nile virus in vitro. Emerg Infect Dis 2002;8:107. 17. Sayao AL, Suchowersky O, Al-Khathaami A, et al. Calgary experience with West Nile virus neurological syndrome during the late summer of 2003. Can J Neurol Sci 2004;34:194. 18. Kalil AC, Devetten MP, Singh S, et al. Use of interferon alpha in patients with West Nile encephalitis: report of 2 cases. Clin Infect Dis 2005;40:764. 19. Chowers MY, Lang R, Sassar F, et al. Clinical characteristics of West Nile fever outbreak, Israel, 2000. Emerg Infect Dis 2001;7:675. 20. Planitzer CB, Modrof J, Kreil TR. West Nile virus neutralization by US plasma-derived immunoglobulin products. J Infect Dis 2007;296:435.



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Multimodal imaging of west nile virus chorioretinitis.

To report the results of multimodal imaging of West Nile virus chorioretinitis...
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