Retinal vasculitis in Toxocara canis neuroretinitis

Background The purpose of this case report is to describe clinical and angiographic findings of retinal vasculitis in acute Toxocara canis neuroretinitis associated with systemic infection. Findings A 16-year-old male presented with a 1 week history of left eye pain, floaters, and decreased visual acuity. Ocular examination was consistent with neuroretinitis and retinal vasculitis. Fluorescein angiography demonstrated leakage of fluorescein from the optic nerve and the retinal veins. Clinical and laboratory evaluation were consistent with systemic Toxocara canis infection. Conclusions Ocular T. canis may present with retinal vasculitis in young patients in the setting of acute systemic infection.


Introduction
Toxocara canis (T. canis) is a ubiquitous parasite found worldwide. T. canis can only complete its lifecycle in dogs, and humans are accidental hosts [1,2]. Ocular T. canis is typically seen in children with an average age of diagnosis of 7.5 years [2,3]. The majority of patients present with blurred vision, pain, photophobia, and floaters. T. canis may demonstrate a localized disciform macular detachment, multifocal granulomas with interconnecting tracks, peripheral retinal detachment, papillitis, peripheral retinal mass, pars plana mass, vitritis, endophthalmitis, or cataract. The most common causes for vision loss in the setting of ocular T. canis are dense vitritis, cystoid macular edema, and tractional retinal detachment. Although animal models of T. canis infection uniformly demonstrate retinal vasculitis [4], this finding has not been previously reported in human eyes. We report a patient who presented with acute onset vision loss in the setting of constitutional symptoms and a positive T. canis ELISA. Interestingly, this patient had clinical and angiographic findings consistent with retinal vasculitis. To our knowledge, this is the first report of retinal vasculitis in ocular T. canis infection.

Case report
A 16-year-old male presented with a 1 week history of left eye pain, floaters, and decreased visual acuity. His review of symptoms was significant for headache, sore throat, and cough occurring 1 week prior to his visual symptoms. He did not have any known history of animal exposure and denied any recent direct contact with dogs. Visual acuity was 20/20 in the right eye and 4/200 in the left eye. The ophthalmic examination of the right eye was entirely normal. A relative afferent pupillary defect was present in the left eye. Anterior segment examination showed mild conjunctival hyperemia, fine keratic precipitates across the corneal endothelial surface, 3+ cells and flare in the anterior chamber, and 2+ anterior vitreous cells. Fundus examination showed mild posterior vitreous debris ( Figure 1a). The optic nerve was swollen with overlying exudates and surrounding subretinal fluid. Macula was thickened with underlying subretinal fluid extending from the optic nerve. There were multiple, track-like chorioretinal scars around the nasal portion of the retina, near the optic disk, and extending into the periphery (Figure 1a). Retinal veins showed mild phlebitis with areas of cotton wool spot-like exudates along the temporal vascular arcades.   T. canis ELISA and elevated eosinophil count at 8.2%. The rest of the laboratory work-up and chest X-ray were within normal limits. The patient's positive T. canis ELISA, eosinophilia, and systemic symptoms strongly indicated the diagnosis of systemic T. canis infection, and after consultation with the infectious disease service, he was treated with albendazole and oral prednisone. Two weeks later, the visual acuity remained at 20/200, and fundus examination showed improving macular star, optic nerve edema, and retinal exudates. Visual acuity improved to 20/80 17 months after his initial presentation (Figure 2b).

Discussion
Ocular manifestations of T. canis vary greatly and may include disciform macular detachment, multifocal granulomas, retinal tracks, peripheral retinal detachment, papillitis, peripheral retinal mass, pars plana mass, vitritis, endophthalmitis, and cataract. However, to our knowledge, retinal vasculitis has not been previously described in patients with ocular Toxocariasis. Our patient presented with clinical and angiographic findings of retinal vasculitis in the setting of T. canis neuroretinitis and evidence of concurrent systemic T. canis infection. His examination was significant for sheathing of the retinal veins and cotton wool spot-like exudates. Fluorescein angiography demonstrated dye leakage from retinal vessels with a venous predominance, consistent with the clinical findings.
Vasculitis is a well-documented finding in many organs in patients affected by systemic T. canis infection [5]. In addition, retinal vasculitis is one of the common findings in animal models of ocular T. canis infection [4]. Most patients with ocular T. canis are not seen in the acute phase of systemic infection. This may partly explain why retinal vasculitis is an uncommon finding in human ocular infections with T. canis and has not been reported previously. In our patient, the presence of constitutional symptoms, positive T. canis ELISA, and increased eosinophil count on blood analysis indicated concurrent systemic and ocular T. canis infection.

Conclusion
Although uncommon, T. canis infection needs to be considered in the differential diagnosis of neuroretinitis and retinal vasculitis in young patients. Evaluation for constitutional symptoms of T. canis infection as well as laboratory workup including T. canis ELISA and complete blood count may assist with diagnosis. Treatment with anthelmintic agents and systemic steroids may hasten recovery of ocular symptoms and funduscopic findings, though permanent posterior segment changes are common secondary to infectious and inflammatory factors. Visual outcome may be limited due to irreversible retinal damage despite the initiation of anthelmintics and anti-inflammatory agents.