A 9-year-old previously healthy boy was referred to our clinic with vitritis and visual acuity of 20/400 in 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 + flare 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 confirmed 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.
By the second visit, [day 5], initial labs had returned with a negative Toxoplasma immunoglobulin G (IgG), positive Toxoplasma IgM Antibody of 9.20 [high equivocal], negative rapid plasma reagin (RPR), and complete blood count (CBC) with an absolute eosinophil count of 883 [normal 15–500]; angiotensin-converting enzyme (ACE) and QuantiFERON-TB Gold test were negative. Based on these results, treatment was initiated for Toxoplasma gondii. Trimethoprim/Sulfamethoxazole (TMP/SMX) 800/160 mg was started. Four days after oral intake of TMP/SMX, oral Prednisone at 0.5 mg/kg daily was added to reduce posterior segment inflammation. At the same time his abnormal eosinophil count raised the suspicion of Toxocara infection.
At the next visit, [day 14], vitritis had slightly improved and visual acuity had improved to 20/200. A previously undiagnosed inferior tractional detachment was visualized a fibrotic band extending from the ora serrata to the disc, a classic presentation for ocular toxocariasis. Based on examination findings, 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.
One month later, his visual acuity in the left eye improved to 20/70. Anterior chamber inflammation 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 inflammation without any oral or topical medications. [Figure 1]