Table 1.
Demographics, clinical characteristics, and serologic markers in adult patients with ocular toxocariasis.
Figure 1.
Funduscopic findings of ocular toxocariasis: Small amorphous posterior pole granulomas (A, B) with retinal nerve fiber layer defects (arrows), peripheral granulomas with round vitreous debris (C, arrow) and a tractional retinal fold (D), and vitreous findings, including tractional retinal detachment (E), whitish dot-like vitreous opacities, and vitreous veil (F).
Figure 2.
Spectral domain optical coherence tomography (SD-OCT) shows granulomas in the outer (A), inner (B), and all retinal layers (C) as reflective masses with posterior shadowing.
The masses remarkably distort the retina and may be accompanied by the epiretinal membrane (B, arrow) and photoreceptor disruption (within two arrowheads). Dotted lines denote the scanned area.
Figure 3.
Spectral domain optical coherence tomography (SD-OCT) images showing progressive retinal damage by ocular toxocariasis granulomas.
(A) Before discontinuous migration, a normal macular structure is visible, but scattered hyper-reflective dots indicate vitritis. (B) After discontinuous migration from the peripheral retina to the macula, a macular granuloma is observed in the inner retinal layers. (C) One month later, the inner retinal layers show severe distortion, a thick epiretinal membrane is present, and the granuloma extends to the outer retinal layers. (D) Three months after vitrectomy and epiretinal membrane removal, structural damage has not completely resolved.
Table 2.
Association between granuloma location and comorbidities in eyes with ocular toxocariasis.
Figure 4.
Clinical course of granuloma in ocular toxocariasis.
Fundus photographs taken at diagnosis (left column) and the last visit (right column) show several patterns. Complete resolution (A), partial resolution (B), partial resolution of retinal infiltrate with pigmented scar (C), and the remains of an inactive granuloma (D). Each photograph is labeled with the follow-up time in months (mo). Double arrow in B denotes retinal nerve fiber layer defect.
Figure 5.
Continuous (A–D) and discontinuous (E–H) migration of Toxocara granuloma.
(A) The granuloma shape is horizontally long, and the larva lies at the same level as the macula at the time of diagnosis. (B) Gradual inferior granuloma migration is observed. (C) The granuloma has turned toward the inferonasal side. The dotted line denotes a reference line connecting the fovea and inferior optic disc margin. (D) Retinal nerve fiber layer defect (double arrow) remains along the granuloma migration path 41 months after diagnosis. (E) Peripapillary granuloma with macular hard exudate. (F) Four months later, a new granuloma appears along the superotemporal arcade and a tractional membrane extends from the granuloma to the superotemporal vascular arcade and to the inferotemporal retina. A tractional membrane is also noted around the macula. (G) One month later, 2 novel granulomas appear in the macula and inferotemporal retina. (H) Ten months later, the inferior granuloma disappears and the macular granuloma is decreased in size, but multiple retinal nerve fiber layer defects remain (arrows).
Table 3.
Clinical course of granuloma in adult patients with ocular toxocariasis.
Table 4.
Treatment outcome in patients with ocular toxocariasis who were followed up for ≥3 months.
Table 5.
Probable sources of infection in adult patients with ocular toxocariasis.