Presentation
Features
Posterior pole granuloma
A focal, white subretinal or intraretinal nodule (with or without pigmentation) evident in the posterior pole, with or without inflammation and vitreous haze
Peripheral granuloma
A focal, elevated, white mass in the retinal periphery (with or without intraocular inflammation) accompanied by variable folding of the surrounding peripheral membranes, tractional retinal detachment, and/or pigmentary changes
Chronic endophthalmitis
Panuveitis presenting with conjunctival injection, pain, and diffuse intraocular inflammation
Atypical presentation
Iridocyclitis, focal iris nodules, cataracts, optic disc swelling, motile subretinal larvae, and diffuse chorioretinitis
Color fundus photograph shows posterior pole granuloma along with retinal exudates (courtesy of Se Joon Woo, MD)
Color fundus photograph (a) and optical coherence tomography (b) show choroidal neovascularization secondary to ocular toxocariasis (courtesy of Se Joon Woo, MD)
Color fundus photograph (a) and optical coherence tomography (b) show the formation of macular hole secondary to ocular toxocariasis
Color fundus photograph shows epiretinal membrane with peripheral granuloma secondary to ocular toxocariasis (courtesy of Se Joon Woo, MD)
Color fundus photograph shows peripheral granuloma with vitreous traction and tractional retinal detachment (courtesy of Se Joon Woo, MD)
Color fundus photograph (a) shows vitreous haze obscuring the disc and retinal vessels. Ultrasonography (b) shows severe vitreous opacity (courtesy of Se Joon Woo, MD)
Anterior segment photographs show cataract formation (a, b) in patients with ocular toxocariasis (courtesy of Se Joon Woo, MD)
Fundus photographs show optic disc edema without granuloma at initial presentation (a). At 2 months later, vitritis and macular exudates appear with newly developed granuloma (b)
Serial color fundus photographs show intraocular migration of granuloma. This case shows continuous (a, b) and discontinuous migration (c, d)
Vitritis is the most common cause of vision loss in patients with ocular toxocariasis, followed by cystoid macular edema, tractional retinal detachment, and epiretinal membrane formation (Stewart et al. 2005). In addition, granuloma development may damage the retina and photoreceptors, triggering significant vision loss (Ahn et al. 2014b). Thus, the causes of vision loss in eyes with ocular toxocariasis can be grouped into three categories: intraocular inflammation; retinal comorbidities, including epiretinal membrane formation, vitreous opacity, tractional/rhegmatogenous retinal detachment, macular edema, cataracts, and macular holes; and retinal damage caused by granulomas per se.
Serology
Serological data supposedly supporting a diagnosis of ocular toxocariasis can be misleading and are inherently limited by the fact that no reliable in vivo gold standard for the confirmation of the presence of T. canis larvae is yet available (Chieffi et al. 2009). In contrast to systemic toxocariasis, in which eosinophilia is a cardinal feature, patients with ocular toxocariasis do not typically exhibit high serum eosinophil counts (Paul et al. 2009). Historically, no confirmatory, or even suggestive, laboratory test supported a clinical diagnosis of ocular toxocariasis prior to the advent of enzyme-linked immunosorbent assays (ELISAs) (Rolda’n et al. 2010). Today, the standard diagnostic test is an indirect ELISA for excretory/secretory T. canis antigens. An ELISA titer ≥0.250 is usually considered positive, affording a sensitivity and specificity of 92.2% and 86.6%, respectively (Jin et al. 2013). The serum immunoglobulin E (IgE) level plays a supportive role in the diagnosis of ocular toxocariasis. However, eosinophilia is usually absent in ocular toxocariasis, in contrast to the patients with systemic toxocariasis. A recent study found that 69.6% of patients diagnosed serologically and clinically with ocular toxocariasis had elevated IgE levels but that only 11.6% exhibited eosinophilia (Ahn et al. 2014b).
Intraocular Assays
ELISA-mediated detection of anti-Toxocara antibodies in ocular fluid may assist in the diagnosis of ocular toxocariasis (Alabiad et al. 2010; Sharkey and McKay 1993; Shields 1984). However, the cutoff value remains controversial; the ELISA-positive rate was only 33% among patients with ocular toxocariasis when the serum cutoff level was used (Ahn et al. 2014b). Remnant Toxocara organisms were occasionally evident in vitrectomy specimens obtained during surgery (Maguire et al. 1990). Currently, the detection rates afforded by vitreous cytology or biopsy remain unclear; further work is required to define optimal cutoffs.
Molecular Analysis
Efforts have been made, via PCR, to detect Toxocara DNA in the aqueous or vitreous humor. A few reports detected T. canis eye infections using molecular methods (Olave et al. 2016; Van De et al. 2013). However, in general, T. canis may not shed tissue into the vitreous.
Management
We know little about the pathogenesis, diagnosis, or optimal treatment of human toxocariasis. Thus, minimizing human exposure to Toxocara species is important. Reductions in raw meat consumption should reduce both systemic and ocular diseases. Management of ocular toxocariasis must reflect the severity of inflammation and the presence of any retinal comorbidities that might trigger permanent visual impairment. No consensus on optimal treatment has yet emerged. It is imperative to reduce inflammation, eliminate the infective organisms, and address vitreoretinal sequelae. Individualized approaches must be tailored to the visual manifestations associated with, and the severity of, intraocular inflammation and modified by reference to clinical responses.
Anti-inflammatory Therapy
Anti-inflammatory corticosteroids are used to treat both ocular and systemic inflammation, and may reduce the vitreoretinal sequelae causing vision loss secondary to ocular toxocariasis. Systemic, periocular, and topical corticosteroids reduce intraocular inflammation and improve inflammation-associated vitreoretinal complications. Cycloplegics prevent the development of anterior and posterior synechiae in inflamed anterior segments.
Anti-helmintic Therapy
The results of a few controlled trials of anti-helmintic drugs used to treat systemic toxocariasis have been published. However, any role for such drugs in patients with ocular toxocariasis remains controversial; it is not clear that anti-helmintics kill intraocular Toxocara larvae. Albendazole (400 mg twice daily for 7–14 days) is often prescribed. Thiabendazole (50 mg/kg/day for 3–7 days) is recommended for patients resistant to albendazole, but liver status should be closely monitored because of its liver toxicity.
Others
Surgery is indicated in cases with structural complications, including a dense or opaque vitreous membrane, retinal detachment, an epiretinal membrane, or a macular hole. In a recent study, 32 of 101 patients (31.7%) required surgery to remove epiretinal membranes (n = 19), to treat a vitreous opacity (n = 9), and/or to remedy retinal detachment (n = 2). Surgery was successful in 68.4%, 88.9%, and 50% of such patients, respectively (Ahn et al. 2014b). Choroidal neovascularization can be combined with retinal granuloma due to ocular toxocariasis. Repeated intravitreal injections of anti-VEGF agents can be efficacious for regressing CNV (Yoon and Woo 2018).
Full access? Get Clinical Tree
