Ocular toxocariasis was first identified in 1956 by Nichols. Human infection occurs via ingestion of embryonated eggs from contaminated soil. Ocular toxocariasis typically presents as optic papillitis, endophthalmitis, or posterior peripheral granuloma.1 Inflammatory complications include cataract, vitreous opacification, epiretinal membrane formation, falciform folds, or rhegmatogenous retinal detachment.
Serum enzyme-linked immunosorbent assay (ELISA) for Toxocara was introduced in 1979 and improved the clinical diagnosis of ocular toxocariasis, resulting in better differentiation from retinoblastoma in children. Serum titers of 1:8 or greater are 90% sensitive and specific for prior infection.2
Ocular toxocariasis usually affects children in their first decade of life. A recent retrospective of Goldmann–Witmer and ELISA analysis of aqueous and vitreous samples from patients with posterior uveitis of undetermined origin identified Toxocara in 3 of 12 children and 0 of 37 adults.3 ELISA testing of aqueous or vitreous humor can detect ocular toxocariasis in the absence of positive serology or a history of visceral larva migrans.4,5
A 66-year-old woman with a history of type 2 diabetes mellitus, hypertension, and arthritis had progressive vision loss in her left eye associated with papillitis of unclear etiology. Prior to onset of symptoms, she cared for two puppies in rural Puerto Rico; there was no exposure to cats. Serology was for positive for toxoplasma IgG and negative for Bartonella and syphilis.
Angiotensin-converting enzyme, lysozyme, purified protein derivative, and chest x-ray were negative. She was treated with combinations of pyrimethamine, prednisone, doxycycline, and clindamycin, but her vision continued to deteriorate. Twenty-eight months after onset of symptoms, she was referred for analysis of anterior chamber fluid.
At the time of referral, examination of the right eye was unremarkable. Visual acuity in the left eye was hand motions with an afferent pupillary defect. Intraocular tensions were normal. There was trace anterior chamber cell, posterior synechiae, and anterior cortical lenticular changes. There was also moderate vitreous haze. Taut fibrovascular membranes extended superiorly and superonasally from the disc (Fig. 1). A large tractional retinal detachment involved the fovea and extended to the superonasal periphery. A yellow, vascularized lesion was seen anterior to the equator at the 10-o’clock position. On fluorescein angiography, there was diffuse leakage at the macula, along the inferotemporal venule, and from the disc to the periphery at the 10-o’clock position. Contact B-scan ultrasound further demonstrated a 2.0-mm subretinal lesion with 3.0 mm of overlying fibrotic tissue at the 10-o’clock position near the equator (Fig. 2). The lesion demonstrated low reflectivity. Polymerase chain reaction of anterior chamber fluid aspirate was negative for toxoplasma and Bartonella henselae. ELISA for Toxocara IgG from this fluid was quantified at 1.74 index value (normal = less than 0.8). Serum antibody to Toxocara was not detected.
Fundus photographs of the left eye showing progression from presentation (left) to 28 months later at the time of anterior chamber enzyme-linked immunosorbent assay (middle and right). Photograph to the right shows a fibrovascular membrane in the superonasal periphery.
Transverse and longitudinal B-scan of the left eye at the 10-o’clock position (left and middle) and A-scan (right) ultrasonography at presentation showing a subretinal lesion, traction retinal detachment, and a non-mobile, highly reflective membrane.
Pars plana vitrectomy and membrane peeling were elected to repair the traction retinal detachment. Surgery was preceded by a 5-day course of mebendazole 1 gram by mouth daily, sub-Tenon injection of 40 mg of triamcinolone acetonide, and intravitreal injection of 1.25 mg/0.05 mL of bevacizumab to the left eye. ELISA of dilute vitreous aspirate obtained at the time of surgery for Toxocara IgG was 1.29 index value. Polymerase chain reaction of the aspirate was negative for toxoplasma. Two weeks after surgery, the patient developed a recurrent retinal detachment requiring scleral buckle placement, pars plana lensectomy, 360º relaxing retinectomy, and silicone oil placement. Four months postoperatively, the visual acuity was hand motions and the ophthalmic examination was stable.
Treatment with oral anti-helminthic agents is indicated for visceral larva migrans. In ocular toxocariasis, clinical symptoms may begin when death of the nematode incites an inflammatory response. Favorable outcomes in patients with ocular toxocariasis have been reported when anti-helminthics are combined with oral prednisone to reduce inflammation.6
Successful surgical management of Toxocara endophthalmitis or tractional/rhegmatogenous retinal detachment as a consequence of Toxocara granuloma has been reported,7,8 including 10 cases of macular traction secondary to ocular toxocariasis managed with combinations of vitrectomy, membrane peeling, scleral buckling, silicone oil, and gas–fluid exchange.9
This case highlights the importance and utility of ELISA testing of the anterior chamber fluid and/or vitreous aspirate for ocular toxocariasis, even if systemic antibodies to Toxocara cannot be detected. The case also shows that the diagnosis of Toxocara should be entertained in adult individuals with a suggestive history. We believe that this patient is one of the oldest patients described to have active ocular toxocariasis. The oldest previously reported case was in a 51-year-old man.10
- Carter RC. Intraocular nematodiasis, with special reference to Toxocara canis, the dog ascarid, as a causative agent in nematode endophthalmitis. Am J Ophthalmol. 1958;45:853–869.
- Pollard ZF, Jarrett WH, Hagler WS, Allain DS, Schantz PM. ELISA for diagnosis of ocular toxocariasis. Ophthalmology. 1979;86:743–752. doi:10.1016/S0161-6420(79)35465-3 [CrossRef]
- De Visser L, Rothova A, De Boer R, et al. Diagnosis of ocular toxocariasis by establishing intraocular antibody production. Am J Ophthalmol. 2008;145:369–374. doi:10.1016/j.ajo.2007.09.020 [CrossRef]
- Biglan AW, Glickman LT, Lobes LA Jr, . Serum and vitreous Toxocara antibody in nematode endophthalmitis. Am J Ophthalmol. 1979;88:898–901.
- Felbert NT, Shields JA, Federman JL. Antibody to Toxocara canis in the aqueous humor. Arch Ophthalmol. 1981;99:1563–1564. doi:10.1001/archopht.1981.03930020437005 [CrossRef]
- Barisani-Asenbauer T, Maca SM, Hauff W, Kaminski SL, Domanovits H, Theyer I, Auer H. Treatment of ocular toxocariasis with albendazole. J Ocul Pharmacol Ther. 2001;17:287–294. doi:10.1089/108076801750295317 [CrossRef]
- Treister G, Machemer R. Results of vitrectomy for rare proliferative and hemorrhagic diseases. Am J Ophthalmol. 1977;84:394–412.
- Hagler WS, Pollard ZF, Jarrett WH, Donnelly EH. Results of surgery for ocular Toxocara canis. Ophthalmology. 1981;88:1081–1086. doi:10.1016/S0161-6420(81)80039-5 [CrossRef]
- Amin HI, McDonald HR, Han DP, et al. Vitrectomy update for macular traction in ocular toxocariasis. Retina. 2000;20:80–85. doi:10.1097/00006982-200001000-00015 [CrossRef]
- Raistrick ER, Hart JC. Adult toxocaral infection with focal retinal lesion. Br Med J. 1975;3:416. doi:10.1136/bmj.3.5980.416 [CrossRef]