Ebola Virus

Ebola virus disease (EVD) was first discovered in 1976 near the Ebola River in Congo. The virus is transmitted through direct contact with blood or body fluids or needles/syringes from a person who is sick or who has died from Ebola infection. Sexual contact with semen from a man who has recovered from Ebola is debated as a possible mode of transmission. Symptoms are fever, bruising, headache, weakness and fatigue, nausea and vomiting, and abdominal pain. Patients with acute EVD may experience conjunctivitis, conjunctival hemorrhage, and acute vision loss of unclear etiology. Symptoms may appear 2–21 days after initial exposure. There is no vaccine or curative medication for EVD; treatment is aggressive supportive care.

Survivors of EVD may experience “post–Ebola virus disease syndrome,” which can include arthralgias, myalgias, fatigue, weight loss, headache, neurocognitive deficits, and psychosocial issues. Uveitis can affect Ebola survivors. In 1 patient, Ebola virus was isolated from aqueous humor 9 weeks after viremia resolved. Iris heterochromia and uveal edema may develop (Fig 11-21). Retinal pigment epithelial cells may be a potential reservoir for the virus. Patients may have episcleritis, interstitial keratitis, anterior uveitis, chorioretinal lesions (Fig 11-22), or optic neuropathy. Uveitis relapses may occur up to 13 months after a negative PCR test on serum.

Figure 11-21 Late-onset panuveitis and iris heterochromia in an Ebola survivor. A, Slit-lamp photograph of right eye with corresponding anterior segment optical coherence tomography at baseline. B, At day 11, the iris of the left eye has turned green and shows edema. C, By day 32, the iris has reverted to its original blue color and the iris edema has improved. D, Ultrasound biomicroscopy (UBM) image shows normal ciliary body anatomy of the right eye. E, At day 12, UBM of the left eye shows ciliary body swelling (arrowheads) and supraciliary/choroidal effusion (arrows) consistent with progressive panuveitis, choroiditis, and evolving hypotony. F, Repeat UBM shows decreased ciliary body swelling and resolution of supraciliary/choroidal effusion (arrows) by day 32. G, B-scan ultrasound imaging shows choroidal thickening at day 11 (arrowheads). H, At day 32, the choroidal thickening has resolved.

(Reprinted with permission from Shantha JG, Crozier I, Varkey JB, et al. Long-term management of panuveitis and iris hetero-chromia in an Ebola survivor. Ophthalmology. 2016;123[12]:2626–2628.e2.)

Figure 11-22 Inactive chorioretinitis in a recent Ebola survivor. A, Fundus photograph of the right eye shows clear media and a retinal opacity temporal to the optic nerve (arrow). B, A corresponding fluorescein angiogram image shows hyperfluorescence with staining of the retinal lesion temporal (arrow) and 3 small lesions nasal to the nerve. C, Fundus photograph of the inferotemporal retina shows a hyperpigmented scar with a hypopigmented halo.

(Reprinted with permission from Shantha JG, Crozier I, Varkey JB, et al. Long-term management of panuveitis and iris hetero-chromia in an Ebola survivor. Ophthalmology. 2016;123[12]:2626–2628.e2.)

Excerpted from BCSC 2020-2021 series: Section 9 - Uveitis and Ocular Inflammation. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.