- Brief report
- Open Access
Retinal vasculitis in Toxocara canis neuroretinitis
© Besirli and Elner; licensee Springer. 2013
- Received: 11 September 2012
- Accepted: 12 September 2012
- Published: 3 January 2013
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.
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.
Ocular T. canis may present with retinal vasculitis in young patients in the setting of acute systemic infection.
- Toxocara canis
- Fluorescein angiography
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 , 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.
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 . In addition, retinal vasculitis is one of the common findings in animal models of ocular T. canis infection . 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.
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 work-up 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.
Informed consent was obtained from the mother of patient on his behalf for publication of this report and any accompanying images.
The authors wish to thank Richard E. Hackel, Department of Photography, WK Kellogg Eye Center, for his assistance with photographs.
- Stewart JM, Cubillan LD, Cunningham ET Jr: Prevalence, clinical features, and causes of vision loss among patients with ocular toxocariasis. Retina 2005, 25: 1005–1013. 10.1097/00006982-200512000-00009PubMedView ArticleGoogle Scholar
- Taylor MR: The epidemiology of ocular toxocariasis. J Helminthol 2001, 75: 109–118.PubMedGoogle Scholar
- Shields JA: Ocular toxocariasis. A review. Surv Ophthalmol 1984, 28: 361–381. 10.1016/0039-6257(84)90242-XPubMedView ArticleGoogle Scholar
- Fenoy S, Ollero MD, Guillen JL, del Aguila C: Animal models in ocular toxocariasis. J Helminthol 2001, 75: 119–124.PubMedGoogle Scholar
- Rubinsky-Elefant G, Hirata CE, Yamamoto JH, Ferreira MU: Human toxocariasis: diagnosis, worldwide seroprevalences and clinical expression of the systemic and ocular forms. Ann Trop Med Parasitol 2010, 104: 3–23. 10.1179/136485910X12607012373957PubMedView ArticleGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.