Ocular Toxocariasis Masquerading as Toxoplasmosis

Purpose To report panuveitis due to Toxocara, with positive Toxoplasma serology. Observation A nine-year-old boy presented with a panuveitis, intermittent headaches, and a visual acuity of 20/400 in his left eye. Slit lamp examination showed anterior chamber cells and are without keratic precipitates (KPs), vitreous cells and veils, and optic disc edema with a blurred fundus view. Initial lab values were positive for toxoplasmosis. Topical cycloplegic and steroid eye drops, in addition to trimethoprim/sulfamethoxazole (TMP/SMX) treatment, was initiated. Four days later, oral corticosteroids were started. As inammation cleared, the fundus examination showed an inferior tractional detachment, leading to an ultimate diagnosis of ocular Toxocariasis. High false positives on Toxoplasma serology and diffuse vitritis from toxocariasis limiting retinal visualization may confuse the initial diagnosis.


Introduction
Toxocariasis is a known, nevertheless uncommon, infection caused by the roundworms Toxocara canis and Toxocara cati. Active infection is more typical in children than adults, since children may eat contaminated soil containing embryonated eggs in the feces of pregnant or young dogs and cats. 1 .
Serological testing shows that 5.1-14% of the United States population has been in contact with Toxocara, with higher percentages in those living below the poverty line. [2][3] . Despite the prevalence of exposure, ocular toxocariasis, the result of the migration of a larva into the eye, is rather infrequent. A survey in collaboration with the American Academy of Ophthalmology found that in 2009-2010 there were only 68 cases of ocular toxocariasis presenting to ophthalmologists in the United States that year. 4 .
Unlike toxocariasis, toxoplasma is much more common, with an estimated 11% of the United States population over age six having been infected and with an estimated 2% of those infected having an episode of ocular toxoplasmosis. [5][6] . Like toxocariasis testing, serology is used to con rm a diagnosis.
For ocular infection, clinical evaluation is most important. Toxoplasma immunoglobulin M (IgM) testing has a high-false positive rates, (positive predictive value (PPV) of toxoplasma IgM is 22-45%), likely due to technical di culty with this test. 7 . We report a case of a boy with toxocariasis infection who was treated for toxoplasmosis initially due to a misleading Toxoplasma IgM.
2. Case Report his left eye. The child had had blurry vision for 5 months. He denied any fever or ocular symptoms including eye pain or light sensitivity, or any previous ocular problems, surgeries, or trauma. The patient did report mild intermittent headaches. On presentation [i.e. day 1], the patient's right eye was normal, but an afferent pupillary defect (+ APD) was found in the left eye. Anterior examination of the left eye showed 1 + cell and 1 + are without KPs. The vitreous had 3 + cells with haze and presence of vitreal veils. Grade 4 optic disc edema was visualized, but peripheral retinal examination was limited due to vitreous haze.
Spectral-domain optical coherence tomography (SD-OCT) showed normal foveal contour of both eyes.
Labs, ordered by the referring ophthalmologist, were pending. A preliminary diagnosis of neuroretinitis and panuveitis was made. Differential diagnoses included ocular toxoplasmosis, ocular toxocariasis, ocular bartonellosis, tuberculosis, syphilis, acute retina necrosis (ARN), Vogt-Koyanagi-Harada syndrome (VKH), and sarcoidosis. B scan was deferred since we did have a blurred view of an attached retina. A topical steroid drop and cycloplegic drop were started.
An infectious disease consult con rmed this 9-year-old lived in rural Florida and had had exposure to many animals, including cats, cows, pigs, chickens, a horse, and dogs. His parents did remember that the children played with a litter of hunting puppies and were covered in puppy stool afterwards. He suffered from eczema and seasonal allergies. He hunted and camped in the area and swam in local fresh water.
His travel was limited to Texas and Georgia and the family house was supplied by well-water. His history made the diagnoses of ocular toxoplasmosis, ocular toxocariasis and ocular bartonellosis more likely. previously undiagnosed inferior tractional detachment was visualized a brotic band extending from the ora serrata to the disc, a classic presentation for ocular toxocariasis. Based on examination ndings, previous high eosinophil count and history of playing with puppies, a Toxocara antibody test was ordered, as well as repeat Toxoplasma serology. This time, Toxoplasma IgG and IgM were negative and serum Toxocara antibody was positive (enzyme-linked immunosorbent assay (ELISA)). No titer information was available as the result was either positive or negative. The diagnosis of ocular toxocariasis was made. A fourteen-day course of Albendazole was ordered by pediatric infectious disease service because of the concern of visceral larva migraines while oral prednisone was tapered and topical eye drops continued.
resolved, but some vitreous cells and optic disc edema remained. The inferior tractional detachment was much better visualized and a peripheral granuloma was noticed. Four months later, his visual acuity had improved to 20/30 and his eye had no active in ammation without any oral or topical medications. [ Figure 1]

Discussion
In this case the diagnosis of ocular toxocariasis was supported by the positive IgG serology, classical presentation of a peripheral granuloma inducing retinal traction extending to the posterior pole, and a supportive social history. No invasive ocular biopsy was needed. Typically, ocular toxocariasis presents in one of three forms. While the most prevalent of these is debated, each form involves a larva in the subretinal space creating an overlying granuloma and frequently resulting in intraocular in ammation and retinal traction. The different subtypes are classi ed as a peripheral granuloma, posterior granuloma, or chronic endophthalmitis in which in ammation is so severe it mimics an infectious endophthalmitis and limits view of the retina. In this case the patient had tractional retinal detachment and a peripheral granuloma which was obscured by his vitritis.
Toxocara IgM is not commercially available and Toxocara IgG may be present in otherwise normal children in the US. While the de nitive diagnosis could be made with histology demonstrating the larva in the affected tissues, a cytologic study of aqueous humor or of a vitrectomy sample, these are rarely performed. ELISA is the typical test of choice. 1 . However, like other immunological testing, a positive IgG only implies previous contact with the infectious agent. It is helpful to obtain a good social history to include contact with kittens or puppies, or consumption of soil. In this case, the serum Toxoplasma IgM testing was misleading and his fundus view was obscured by the severe vitritis. Many experts now recommend repeat testing of both IgM and IgG prior to the diagnosis of Toxoplasma.
Anti-parasitic therapy, Albendazole, was utilized in this case because of an elevated eosinophilia count and complaint of headache, which is the standard of care by the American Academy of Pediatrics (AAP). 8 . Eosinophilia presents more commonly in visceral toxocariasis. The 2018 AAP Red book recommends treatment while acknowledging the parasite is likely already dead. The albendazole is fairly safe, so the bene t of ensuring the parasite is dead is worth the minor side effect of the drug. However, technically Albendazole is unproven to kill intraocular larvae. 9 Most of ocular manifestations are related to the strong in ammatory response against the presence of a dead worm in the sub-retinal space. Most providers recommend anti-in ammatory therapy to limit the intraocular complications of in ammation, with topical and oral steroids being used in this case; periocular injections of corticosteroids are an alternative treatment. Surgical therapy is considered in cases with complications of vitreal hemorrhaging, extensive tractional retinal detachment, rhegmatogenous retinal detachment, or macular pucker from an epiretinal membrane. Other interventions, although not relevant to this case, may include laser photocoagulation of live, motile larvae or intravitreal anti-vascular endothelial growth factor therapy to