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Man has 3-day history of OD pain, decreased vision, other symptoms: What is diagnosis?


Man has 3-day history of OD pain, decreased vision, other symptoms: What is diagnosis?




Travis C. Rumery, DO, Clinical Lecturer, Ophthalmology and Visual Sciences, University of Michigan

Blake V. Fausett, MD, PhD, Resident, Ophthalmology and Visual Sciences, University of Michigan

Jonathan D. Trobe, MD, Professor, Ophthalmology and Visual Sciences; Professor, Department of Neurology, University of Michigan

Shahzad I. Mian, MD, Associate Professor, Ophthalmology and Visual Sciences; Residency Program Director, Ophthalmology and Visual Sciences, University of Michigan


Photography: Richard E. Hackel, MA, CRA


No financial interests for anyone listed above.



A 79-year-old Hispanic man presented with a 3-day history of right periocular pain and decreased vision in the right eye. He also had new-onset nausea, vomiting, fevers, chills, and confusion.

The patient’s medical history included transient ischemic attack, hypertension, hyperlipidemia, iron-deficiency anemia, and coronary artery disease with coronary artery bypass grafting. His ocular history was significant only for pseudophakia. A retired construction worker, he had been a previous smoker, having quit more than 20 years prior.

Consultation by a neurologist found only slight inattentiveness. The ophthalmology service was consulted.


Visual acuity with correction was 20/200 OD and 20/20 OS. Pupils were equal in size and constricted to light but with a right relative afferent pupillary defect. Motility and alignment exams were normal. Confrontation visual field testing revealed constriction inferiorly OD and was full OS.

Anterior segment exam disclosed only pseudophakia OU. Fundus examination revealed only vitreous syneresis overlying the posterior pole OD.

Clinical course

MRI of brain and orbits was normal. Lumbar puncture showed glucose 52 mg/dl, protein 61 mg/dl; white cells 86/mm3 with 43% neutrophils, 29% lymphocytes, and 22% histiocytes. VDRL, AFB, flow cytometry, cytology, PPD, RPR, toxoplasmosis IgM and IgG, and Lyme titers were negative.

For a diagnosis of bacterial meningitis or possibly herpes simplex encephalitis, he was treated with intravenous vancomycin, ceftriaxone, and ampicillin as well as intravenous acyclovir.

On hospital day 2, dilated fundus examination of the OD showed a slightly swollen optic disc and many round, whitish, deep choroidal lesions, attenuated retinal arterioles, and 3-4 dot-blot hemorrhages in the superior retinal periphery (Figure 1). Fundus examination of the OS was normal.

Chorioretinitis in the setting of meningitis was diagnosed. As causes, we considered syphilis, tuberculosis, histoplasmosis, coccidioidomycosis, bartonella, toxoplasma, diffuse unilateral sub-acute neuroretinitis (DUSN), Lyme disease, nocardia, aspergillus, cryptococcus, meningococcus, ophthalmomyiasis, onchocerciasis, cysticercosis, non-Hodgkin’s large-cell lymphoma, and sarcoidosis.

But on further questioning, the patient’s family reported he was an avid camper and that on occasion he slept outside in a tent in his own back yard.

Arbovirus IgM (West Nile Virus) titer was positive. Antibiotics were discontinued and he was treated supportively. He was discharged after 6 days of hospitalization.


When he was seen as an outpatient 15 days after presentation, both eyes were involved (Figure 2). Visual acuity was 20/500 OD and 20/40 OS. The vitreous of both eyes showed rare cells. Optic disc pallor was present OD.

Two-month follow-up

Visual acuity was 20/80 OD and 20/40 OS. Trace vitreous debris was still present OU. Atrophic chorioretinal lesions were now present OU (Figure 3).

Discussion and diagnosis

WNV is a single-stranded RNA arbovirus belonging to the Flaviviridae family, which includes Japanese encephalitis, St. Louis encephalitis (SLE), yellow fever, dengue, Murray Valley encephalitis, Kunjin encephalitis, and Western equine encephalitis viruses.1 Wild birds serve as the primary natural hosts.2 Mosquitos are responsible for transmission from birds to humans and other mammals.2,3 The WNV was first detected in the United States in 1999 during an outbreak in New York.

Only 20% of infected individuals experience systemic symptoms, including malaise, fever, rash, anorexia, and lymphadenopathy.4 Reported ocular symptoms include photophobia, retrobulbar pain, and diplopia.5 Approximately 1 in 150 infections results in meningitis or encephalitis6 with a mortality rate of 5% to 10% in this group.7 Ages more than 50 years and diabetes have been identified as risk factors for severe neurologic disease and death.3,8

Common intraocular manifestations include bilateral, multifocal chorioretinitis with circular “target-like” lesions scattered in the mid-periphery and often arranged in a radial linear pattern.9 Other intraocular findings include mild iridocyclitis, anterior uveitis, vitritis, occlusive retinal vasculitis, optic disc edema, and optic neuritis.6,9 While patients may suffer an initial significant decline in vision, visual acuity tends to recover to near-baseline levels, with chorioretinal involvement not typically extensive.9 However, the less frequent ocular lesions, including optic neuritis and occlusive vasculitis, frequently induce persistent and likely permanent visual deficit.7

The diagnosis of systemic WNV infection relies on a high index of clinical suspicion and specific laboratory test results. The most efficient diagnostic method is detection of IgM antibody to WNV in serum or CSF using the IgM antibody-capture ELISA assay. Because IgM antibody does not cross the blood-brain barrier, its presence in CSF strongly suggests infection of the central nervous system.6

The pathogenesis of WNV-associated chorioretinitis remains speculative. It has been hypothesized that hematogenous dissemination of WNV to the choriocapillaris during viremia may seed the choroid to produce a multifocal granulomatous chorioretinitis with scattered or linear distribution of chorioretinal lesions.10 One report showed mononuclear perivascular inflammation in pathologic specimens of neuro-invasive cases with WNV infections.11 However, Khairallah et al.12 argue that the linear pattern of WNV-associated chorioretinitis is related to retinal nerve fiber organization. Their findings suggest a contiguous spread of WNV from central nervous system via the optic nerve fibers into the eye, rather than a hematogenous dissemination to the choriocapillaris.

Treatment of WNV infection is supportive.


WNV disease must be included in the differential diagnosis of a patient experiencing an acute febrile illness associated with symptoms suggestive of encephalitis or meningitis.13

The unique pattern of multifocal chorioretinitis in patients with systemic symptoms of WNV infection can help to establish the diagnosis while serologic testing is pending, highlighting the importance of the dilated fundus examination in patients who are suspected of having WNV infection.6

To understand and manage better the full spectrum of ocular disease caused by WNV virus infection, all patients who have suffered a WNV-induced meningoencephalitis should be referred for ophthalmologic evaluation.14


1. Mukhopadhyay S, Kuhn RJ, Rossman MG. A structural perspective of the Flavivirus life cycle. Nat Rev Microbiol. 2005;3:13-22.

2. Craven RB, Roehrig JT. West Nile virus. JAMA. 2001;286:651-653.

3. Petersen LR, Marfin AA. West Nile virus: a primer for the clinician. Ann Intern Med. 2002;137:173-179.

4. Mostashari F, Bunning ML, Kitsutani PT, et al. Epidemic West Nile Virus encephalitis, New York, 1999: results of a household-based seroepidemiological survey. Lancet. 2001;358:261-264.

5. Weiss D, Carr D, Kellachan J, et al. Clinical findings of West Nile virus infection in hospitalized patients, New York and New Jersey, 2000. Emerg Infect Dis. 2001;7:654-658.

6. Khairallah M, Ben Yahia S, Ladjimi A, et al. Chorioretinal involvement in patients with West Nile Virus. Ophthalmology. 2004;111:2056-2070.

7. Chan CK, Limstrom SA, Tarasewicz DG, Lin SG. Ocular features of West Nile virus infection in North America. Ophthalmology. 2006;113:1539-1546.

8. Nash D, Mostashari F, Fine A, et al. 1999 West Nile Outbreak Response Working Group. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med. 2001;344:1807-1814.

9. Myers, J, Leveque, T, Johnson MW. Extensive chorioretinitis and severe vision loss associated with West Nile virus meningoencephalitis. Arch Ophthalmol. 2005;123:1754-1756.

10. Garg S, Jampol LM. Systemic and intraocular manifestations of West Nile virus infection. Surv Ophthalmol. 2005;50:3-13.

11. Sampson BA, Armbrustmacher V. West Nile encephalitis: the neuropathology of four fatalities. Ann N Y Acad Sci. 2001;951:172-178.

12. Khairallah M, Ben Yahia S, Attia S, et al. Linear pattern of West Nile virus-associated chorioretinitis is related to retinal nerve fiber organization. Eye (Lond). 2007;21:952-955.

13. Hershberger VS, Augsburger JJ, Hutchins RK, et al. Chorioretinal lesions in nonfatal cases of West Nile Virus infection. Ophthalmology. 2003;110:1732-1736.

14. Anninger WV, Lomeo MD, Dingle J, et al. West Nile virus-associated optic neuritis and chorioretinitis. Am J Ophthalmol. 2003;136:1183-1185.



Figure 1 Retcam fundus photos demonstrating numerous round, whitish, deep choroidal lesions involving the posterior pole OD and normal fundus OS.

Figure 2 Composite fundus photos demonstrating multifocal chorioretinal scars involving posterior pole OU and optic disc pallor OD.

Figure 3 Optos fundus photos demonstrating numerous areas of chorioretinal atrophy OU, with linear pattern of atrophic chorioretinal lesions superior to optic disc OS, and optic disc pallor OD > OS. (Illustrations courtesy of Richard E. Hackel, MA, CRA)


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