Spectral-Domain Optical Coherence Tomography Appearance of a Retinal Nematode

Case Report

A 65-year-old man presented with decreased visual acuity in his left eye of 10 days’ duration. His medical history was only remarkable for cataract surgery in the left eye. He was a farmer who lived in a rural region and had one dog and other animals.

Visual acuity was 20/30 in his right eye and 20/200 in his left eye. There was no afferent papillary defect. Slit lamp examination revealed a 2+ posterior subcapsular cataract in the right eye. The left eye was pseudophakic. There was no sign of inflammation in the anterior chamber or the vitreous cavity of either eye. Fundus examination findings were normal in the right eye. In the left eye, a live white nematode (roundworm), approximately 1 disc diameter in length, was observed close to the fovea (Figure 1, page E18). The body of the worm was tapered at one end and slightly rounded at the other end. There was no evidence of a worm track, vasculitis, or retinal hemorrhage. Systemic examination findings were unremarkable.

Figure 1. (A) Fundus photograph of the left eye at initial examination reveals a nematode inferonasal to the fovea of the left eye. (B) The body of the worm, which was roughly tapered at one end and slightly rounded at the other end, is visible at greater magnification.

Laboratory test results revealed a normal white blood count (5.1 × 10⁹/L), hemoglobin of 14.3 g/L, a normal platelet count (180,000), and no eosinophilia. The erythrocyte sedimentation rate, blood urea nitrogen, serum electrolyte, liver function test results, and abdominal ultrasonography findings were normal. Stool culture was normal with no ova or parasite in the stool. Serum levels of toxacara and fasciola hepatica antibody were negative. Enzyme-linked immunosorbent assays (ELISA) for hydatidosis and fasciolosis were negative.

Fluorescein angiography showed hypofluorescence near the fovea due to dye blockage by the nematode (Figure 2, page E18). Spectral-domain optical coherence tomography (OCT) showed a hyperreflective area in the retinal nerve fiber layer compatible with an intraretinal nematode (Figure 3, page E18).

Figure 2. Early-phase (A) and mid-phase (B) fluorescein angiograms of the left eye demonstrate hypofluorescence due to blockage by the nematode (arrows).

Figure 3. (A-C) Spectral-domain optical coherence tomography reveals a hyperreflective band in the nerve fiber layer and internal limiting membrane with the nematode (A, arrow). Optical coherence tomography from one end of the worm shows a hyperreflective band in the nerve fiber layer and internal limiting membrane compatible with the other end of the worm.

In the second week of follow-up, a small intraretinal hemorrhage occurred, close to the round end of the nematode (Figure 4, page E19). Four weeks later, the nematode spontaneously disappeared, as did the hypofluorescent area on fluorescein angiography. Visual acuity improved to 20/25 in the left eye (Figures 5 and 6, page E19). In all subsequent visits, the posterior pole and periphery of the retina were examined by indirect ophthalmoscope, slit lamp, and use of a 78 D lens. Fundus photography of the posterior pole and periphery of the retina was performed at each visit, but fluorescein angiography was performed only once, after disappearance of the nematode. The patient was examined monthly for 6 months with no sign of reappearance of the nematode.

Figure 4. (A-B) Fundus photographs of the left eye at the 1-week follow-up examination show a small intraretinal hemorrhage close to the nematode (A, arrow)

Figure 5. Fundus photograph of the left eye at 1-month follow-up reveals complete disappearance of the nematode.

Figure 6. Fluorescein angiogram of the left eye at 1-month follow-up shows no hypofluorescence in the macula after disappearance of the nematode.

Discussion

Loss of vision is an important symptom of nematode infection in the eye. The worm usually causes mild to moderate vitreitis, often associated with a multifocal gray-white lesion at the outer retina.^1–6 Indirect ophthalmoscopy is the most important measure, and diagnosis is generally made by fundus examination with visualization of the nematode or its tracks.² There are four more commonly known intraocular roundworms: Dirofilaria, Toxocara canis, Ancylostoma caninum, and Baylisascaris. However, other nematodes such as Loa loa filariasis, Onchocerca volvulus, Wuchereria bancrofti, and Angiostrongylus cantonensis have been reported to involve the eye. Humans usually acquire the infection by consuming food or water containing the nematode. The nematode can survive for several years in the human body. Direct microscopic evaluation is necessary for definitive diagnosis of the parasite.² This was not possible in our case because the nematode spontaneously disappeared. Interestingly, the nematode was located in the nerve fiber layer rather than in the subretinal space where worms are usually found.

There are some reports of imaging of intraocular nematodes and their sequelae.^7–9 One report described a case of ocular toxocariasis and exudative macular lesion.⁸ In this report, spectral-domain OCT imaging disclosed a highly reflective mass protruding above the retinal pigment epithelium from the macular granuloma, and angiography revealed dye leakage. After treatment, angiography revealed reticular hyperfluorescence surrounded by a hypofluorescent rim. A report by Suzuki et al⁹ described a migrating Toxocara larva in the retina. OCT of the lesion disclosed a highly reflective mass located in the nerve fiber layer, and fluorescein angiography revealed dye leakage from the lesion. However, another lesion was found in the macula after 3 weeks, and the OCT and fluorescein angiography findings were the same as for the first lesion. Fluorescein leakage was also observed along the presumed path of the migrating larva.

The treatment of choice, when possible, for a retinal nematode is direct laser photocoagulation of the worm, and in selected cases surgical removal of it. In our case, because of the nematode’s location in the nerve fiber layer, this treatment was avoided. The nematode would not have absorbed light energy sufficiently to be killed without causing too much damage to the retinal pigment epithelium, the retina, and its nerve fiber layer.