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Show J. C1in. Neuro-ophthalmol. 3: 267-274, 1983. Bilateral Toxocara Optic Neuropathy TERRY A. COX, MD. GREGORY E. HASKINS, MD. JOHN L. GANGITANO, MD. DEAN L. ANTONSON, MD. Abstract A 14-year-old girl had loss of vision in the right eye and bilateral optic disc swelling. After treatment with oral prednisone, the neuropathy resolved. An extensive evaluation led to a probable diagnosis of Toxocara optic neuropathy. The clinical appearance of ocular toxocariasis usually follows one of three patterns: 1) posterior pole granuloma, 2) peripheral granuloma, or 3) diffuse endophthalmitis. I Occasionally, the posterior pole granuloma arises near the optic disc. 2 .: 3 Apparent primary optic neuropathy is unusual; only three cases have been reported with clinical details4 - 6 and the fundus appearance in one other case has been illustrated. 7 All of these cases had involvement of one eye only. We report a patient who presented with bilateral optic disc involvement in whom the clinical history, serological testing, and final disc appearance led to the diagnosis of probable Toxocara optic neuropathy. Case Report A 14-year-old white girl developed fever, myalgias, and headache during the last week of her summer vacation on a Georgia farm. The acute illness resolved after 3 days, but fever up to 102° F and headache recurred daily for the next 4 weeks. Two weeks after onset of the acute illness, she noted "fuzzy spots" in her visual field that lasted for 1 day and did not recur. Four weeks after onset she was admitted to another hospital for evaluation of her fever, but when optic disc edema was noted she was transferred to the University of Nebraska Medical Center. The general physical examination was unremarkable. The visual acuity was R.E. 20/100 and L.E. 20/20. Color vision tested with AO pseudois- From the Departments of Ophthalmology (TAC, (;EH), Neurology (TAC), and Pediatrics (OlA). University of Nebraska Medical Center, Omaha, Nebraska; and Ehrling Bergquist USAF Regional Hospital. Offutt Air Force Base, Nebraska. OlG). December 1983 ochromatic plates was decreased on the right. Perimetry revealed enlarged blind spots in both eyes and a cecocentral scotoma in the right eye (Fig. 1). There was a relative afferent pupillary defect on the right. Slit lamp biomicroscopy showed trace cells in the anterior chamber on the right. The right optic disc was edematous, especially inferiorly (Fig. 2). There was a yellow-white mass involving the inferotemporal portion of the right disc and a superficial white infiltrate lay between the disc and the fovea. A small white infiltrate was visible in the retina 2 disc diameters superonasal to the right disc. The superior portion of the left optic disc was edematous with adjacent hemorrhage (Fig. 3). The disc swelling in both eyes progressed during the next few days. Fluorescein angiography done 3 days after admission demonstrated marked edema of the inferior portion of the right optic disc. There was late staining of both optic discs as well as staining of the retinal infiltrate superonasal to the right disc (Figs. 4-6). Four days after admission, the vision had decreased to counting fingers at 3 ft. in the right eye. Vision in the left eye remained 20/20. The anterior chamber on the right showed 1+ cells and flare, and the vitreous contained 1+ cells. An extensive evaluation was performed during the hospitalization. The erythrocyte sedimentation rate was elevated to 71 mm/hour (Westergren). The absolute eosinophil count was 760 mm.:l The alpha-2 globulin was 0.95 g/dl (normal 0.30-080 g/dl). The immunoglobulins were normal. Titers for typhoid 0 and H, paratyphoid A and B, proteus OX19, and brucella were normal. Fungal complement fixation tests for histoplasmosis, blastomyces, and coccidioides were negative. The indirect fluorescent antibody titer for toxoplasmosis was less than 1:32. The angiotensin converting enzyme level was normal. Cultures of blood, urine, CSF, bone marrow, liver, and bronchus were negative. The RPR was negative. The monospot test was negative. Total serum complement was normal. Liver function tests were normal. A pro (5 TU) skin test was negative; a monilia skin test showed 15 mm induration at 48 hours. The chest radiograph, liverspleen scan, and CT scans of the head, abdomen, and thorax were all normal. Two lumbar punctures 267 Toxocara Optic Neuropathy LEFT O.S. RIGHT 0.0. Figure 1. Initial visual fields. The blind spots are enlarged in both eyes and a cecocentral scotoma is present on the right. 268 Figure 2. Initial appearance of right optic disc. inferior part of the disc and the small white superonasdl to the disc. Note the infiltrate involving the lesion located 2 disc diameters Journal of Clinical Neuro-ophthalmology December 1983 Cox, Haskins, Gangitano, Antonson Figure 3. Initial appearance of left optic disc. The superior portion of the disc is edematous. Figure 4. Fluorescein angiogram of right fundus. The inferior disc vessels are elevated by the underlying edematous nerve tissue and infiltrate. 269 Toxocara Optic Neuropathy Figure 5. Fluorescein angiogram of right fundus, late phase. There is staining of the optic disc and the retinal lesion superonasal to the disc. Figure 6. Fluorescein angiogram of left fundus. late phase. The left optic disc stains. 270 Journal of Clinical Neuro-ophthalmology Cox, Haskins, Gangitano, Antonson Figure 7. Fundus of right eye, showing macular star exudate. were nonnal. Biopsies of conjunctiva, liver, minor salivary gland, scalene node, and bronchus were all nonnal. A bone marrow aspirate showed mild eosinophilia. Based on the fundus appearance, we felt that the most likely diagnosis was sarcoid optic neuropathy. Because of the rapid deterioration of vision, we started oral prednisone 60 mg daily on the fourth hospital day. Three days after starting prednisone, the vision had improved to 20/400 in the right eye and the disc swelling in both eyes was noticeably decreased. A macular star exudate was noted on the right (Fig. 7). After 8 days of treatment, the vision was 20/150 in the right eye, the hemorrhages in the left eye had resolved, and the disc swelling in both eyes continued to decrease. After 2 weeks of prednisone therapy, the acuity was 20/80 in the right eye. One week later, the visual acuity had improved to 20/30 in the right eye. The steroids were gradually tapered and discontinued 3 weeks later. Three weeks after stopping steroids, the vision was 20/25 in the right eye and 20/15 in the left, with some macular exudates and mild disc edema remaining in the right eye. The left disc was nonnal (Fig. 8). Four months after hospital admission, the vision was 20/25 in the right eye. A few strands of fibrous tissue were apparent on the right disc at 2 and 6:00. Six months later, the vision was 20/15 in both eyes. The fibrous tissue on the right optic disc was more prominent (Fig. 9). A defect persisted in the nasal superior visual field in the right eye. The visual field was normal in the left eye (Fig. 10). December 1983 Three months after the initial evaluation, blood was sent to the Center for Disease Control in Atlanta for a Toxocara ELISA titer and a repeat toxoplasmosis titer. The toxoplasmosis titer was less than 1:8. The Toxocara titer was elevated to 1:128. A history of exposure to puppies during the previous summer was obtained. Discussion Toxocara canis is an extremely common roundwonn infection of dogs. Virtually every puppy born in tropical and temperate zones of the world is infected with this parasite.s Studies in Georgia and Louisiana have shown Toxocara eggs in 2030% of backyard soil samples.9 • 1o Contaminated soil is frequent in parks and playgrounds. Ocular toxocariasis results from ingestion of eggs containing larvae of T. canis. These eggs hatch in the small intestine. The larvae then invade the wall of the intestine, migrate to the liver, pass to the lung, and then enter the systemic circulation. When the larvae reach blood vessels too small to allow passage, they actively penetrate into surrounding tissue. Clinical signs and symptoms in the eye may result from tracks of hemorrhage and necrosis caused by larval migration; however the most severe manifestations are usually caused by inflammation resulting from the death of the larva. Ocular signs may first occur years after the initial infestation. Bilateral ocular involvement occurs in less than 3% of cases. 11 Simultaneous systemic and ocular symptoms are 271 Toxocara Optic Neuropathy Figure 8. Left fundus 4 months after presentation. The disc and macula are normal. figur" 9. RighI funaus 4 montns atter presentation. There is a small amount of fibrous tissue overlying the inferior half of the optic disc. said to be uncommon with ocular toxocariasis.~ However, Raistrick and Hartl~ have reported an adult who had malaise, anorexia, and night sweats for 1 week prior to visual symptoms. They stated that they had seen six other adults with similar presenting symptoms. We have seen one other 272 adult with Toxocara endophthalmitis who had preceding systemic symptoms. One feature of Toxocara optic neuropathy that suggests the diagnosis is the proliferation of fibrous inflammatory tissue in the chronic phase. This finding was prominent in the cases of Bird et al.,4 Journal of Clinical Neuro-ophthalmology Cox, Haskins, Gangitano, Antonson LEFT O.S. RIGHT 0.0. Figure 10. Visual fields 10 months after presentation. The left field is normal. The right eye has a mild superior altitudinal defect. Phillips and Mackenzie,5 and Duguid, and was less apparent in Molk's case.6 In our patient, fibrous proliferation progressed between exams 4 months and 10 months after onset. Treatment of Toxocara optic neuropathy with steroids in the acute phase has been attempted in only two previous cases. In the patient of Bird et al.,4 there was no apparent effect; Molk6 had good results with periocular steroid injections. The dramatic response to treatment in our case suggests that timing of steroid therapy is more important than the method of administration. The ELISA test (enzyme-linked immunosorbent assay) is currently the best serological test for diagnosing human ocular toxocariasis. Pollard et al. la found this test to be positive with a titer of 1:8 or more in 37 of 41 patients with clinically diagnosed Toxocara ocular infections. The titer was positive in six of 65 control patients. The corresponding figures for the series of Shields et al. 14 were 18 of 22 positive in patients and none of 20 positive in controls. Combining these two series, the sensitivity of the ELISA test is 87.3% and the specificity is 92.9% at a titer of 1:8. A study by Schantz et al. 15 suggests that higher titers are more likely early in the course of the disease. Three of their 17 patients had titers of 1:64 or higher, and all three had signs and symptoms for 1 month or less. However, one patient had a titer of 1:32 14 years after the original diagnosis. The ELISA test, the subsequent funduscopic appearance, and the history of exposure to puppies all support the diagnosis of Toxocara optic neuropathy in our patient. We suggest that Toxocara be December 1983 considered as an etiology in any unusual inflammatory or infiltrative optic neuropathy. References 1. Wilkinson, CP., and Welch, R.B.: Intraocular Toxocara. Am.]. Ophthalmol. 71: 921-930,1971. 2. Pollard, l.F.: Ocular Toxocara in siblings of two families. Arch. Ophthalmol. 97: 2319-2320, 1979. 3. Ashton, N.: Larval granulomatosis of the retina due to Toxocara. Br.]. Ophthalmol. 44: 129-148, 1960. 4. Bird, A.C, Smith, ].L., and Curtin, V.T.: Nematode optic neuritis. Am. ]. Ophthalmol. 69: 72-77, 1970. 5. Phillips, CI., and Mackenzie, A.D.: Toxocara larval papillitis. Br. Med.]. 1: 154-155, 1973. 6. Molk, R.: Treatment of Toxocaral optic neuritis. ]. C1in. Neuro-ophtha!mol. 2: 109-112, 1982. 7. Duguid, I.M.: Features of ocular infestation by Toxocara. Br. ]. Ophtha!mol. 45: 789-796, 1961. 8. Glickman, L.T., and Schantz, P.M.: Epidemiology and pathogenesis of zoonotic toxocariasis. Epidemiol. Rev. 3: 230-250,1981. 9. Beaver, P.C: Observations on the epidemiology of ascariasis in a region of high hookworm endemicitv. ]. Parasito!. 38: 445-453, 1952. . 10. Headlee, W.H.: The epidemiology of human ascariasis in the metropolitan area of New Orleans, Louisiana. Am. ]. Hyg. 24: 479-521, 1936. 11. Brown D.H.: Ocular Toxocara canis.]. Pediatr. Ophthalmol. 7: 182-191, 1970. 12. Raistrick, E.R., and Hart, J.CD.: Adult Toxocaral infection with focal retinal lesion. Br. Med.]. 3: 416, 1975. 13. Pollard, l.F., Jarrett, W.H., Hagler, W.5., Allain, D.5., and Schantz, P.M.: EUSA for diagnosis of ocular toxocariasis. Ophthalmology 86: 743-749, 1979. 273 Toxocara Optic Neuropathy 14. Shields, J,A., Felberg, NT, and Federman, J,L.: Discussion of presentation by Dr. Zane F. Pollard, et al. Ophthalmology 86: 750-752, 1979. 15. Schantz, P.M., Meyer, D., and Glickman, L.T.: Clinical, serologic, and epidemiologic characteristics of 274 ocular toxocariasis. Am. J, Trop. Med. Hyg. 28: 2428,1979. Write for reprints to: Dr. Terry Cox, Department of Ophthalmology, University of Nebraska Medical Center, 42nd and Dewey, Omaha, Nebraska 68105. Journal of Clinical Neuro-ophthalmology [VBtoxoplasmosis] |