Treatment of ocular toxocariasis with albendezole: A case report

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1 Optometry (2009) 80, Treatment of ocular toxocariasis with albendezole: A case report Marcela Frazier, O.D., Michelle L. Anderson, O.D., and Sophocles Sophocleous, O.D. University of Alabama-Birmingham School of Optometry, Birmingham, Alabama. KEYWORDS Ocular toxocariasis; Albendazole; Vitritis; Vitrectomy Abstract BACKGROUND: Toxocara canis is a parasite that can infect the eye and create a significant inflammatory response that can be detrimental to the patient s vision. Its clinical presentation can mimic other causes of uveitis, and its diagnosis and treatment can be challenging. Prompt and accurate diagnosis of ocular toxocariasis is essential to prevent permanent visual loss. CASE REPORT: A 7-year-old Hispanic boy presented to the clinic with complaints of reduced visual acuity in the left eye. After a careful evaluation of his ocular health, he had ocular toxocariasis diagnosed and confirmed by enzyme-linked immunosorbent assay testing. Treatment with the anthelmintic, albendazole, and oral steroids was initiated. There was initial improvement of the vitritis with significant vitreous debris. However, 2 years later, reactivation occurred, and a vitrectomy was required. This case report reviews the management of a patient with active ocular toxocariasis, including clinical findings and treatment options. CONCLUSIONS: The differential diagnosis of ocular toxocariasis and review of the available treatments are presented. Optometry 2009;80: Ocular toxocariasis, or ocular larva migrans (OLM), is a known cause of vision loss in children. 1 The most common causative agent for ocular toxocariasis, Toxocara canis, is accidentally contracted in humans less than 4 years of age 2 most commonly by eating eggs in dirt and less commonly by contacting an infected puppy. 3 Toxocara canis, a roundworm parasite, infects puppies that ingest the eggs or larvae. The larvae travel throughout the puppies intestines where the adult worms produce eggs. Several thousand eggs are produced per day and are shed in an infected canine s feces into the soil where they can live dormant for several months to years. 4 Similarly, in humans, the Corresponding author: Michelle L. Anderson, O.D., Pediatric Ophthalmology and Strabismus, Inc., Two Landmark North, Suite 300, Route 19 North, Cranberry Township, PA manderson.od@gmail.com eggs hatch in the intestines, and the larvae penetrate the intestinal wall entering the circulation. As the larvae infects various somatic organs, visceral larva migrans (VLM) may occur. VLM is the most severe form of human toxocariasis, affecting many systems leading to fever, weight loss, bronchitis, limb and abdominal pain, hepatosplenomegaly, hypereosinophilia, and occasionally seizures. 5 Toxocara infection rarely shows concurrent VLM and OLM. 4 OLM results from larval infection of the posterior pole or peripheral retina. Otherwise healthy patients present with endophthalmitis, vitritis, retinochorioditis, fibrotic retinal bands, or retinal granulomas. 5 The seroprevalence of Toxocara antibodies in healthy adults in developed countries has been reported to range between 3% and 20%. 3,6 VLM is more prevalent in the south central and southeast regions of the United States, 7 likely because of the density of the dog population in these areas and the weather encouraging dogs to be outside. 4 The /09/$ -see front matter Ó 2009 American Optometric Association. All rights reserved. doi: /j.optm

2 176 Optometry, Vol 80, No 4, April 2009 prevalence of OLM was 1 case per 10,000 persons in a study of school children in Ireland 8 and about 1 to 11 cases per 1,000 persons in a survey of ophthalmology and optometry practices in Alabama. 9 At a uveitis referral center in Atlanta, Georgia, Schantz, et al. 3 found that 1% of all cases of uveitis resulted from ocular toxocariasis. Some suggest that there is a third form of infection in humans, overt toxocariasis (CT), which is a mild infection with vague symptoms and some clinical features of VLM. 8,10 Treatment of systemic toxocariasis (VLM) includes systemic anthelmintics. Treating the OLM and CT forms of toxocariasis with anthelmintic medication is controversial because of the risk of an increased immunologic reaction secondary to the release of by-products of dying larvae. However, one study found that the concurrent use of the anthelmintic, albendazole, and oral steroids was an effective treatment in 5 patients with OLM. 10 Case report A 7-year-old Hispanic boy presented to a University of Alabama-Birmingham (UAB) School of Optometry satellite clinic in Birmingham, Alabama for an eye examination in November 2004 with a chief complaint of reduced vision in the left eye that he related to a car accident 1 year earlier. The patient denied having eye pain, redness, photophobia, irritation, watering, or discharge. His mother reported that the child had no joint pain, coughing, malaise, shortness of breath, diarrhea, constipation, hearing loss, weight gain/ loss, or fever. They denied having a dog or cat for a pet, but they did reside near a chicken farm. The patient s medical history was unremarkable. The patient was not taking any medications and denied any allergies to medications. His entering uncorrected visual acuities were 20/30 in the right eye (O.D.) and 20/400 in the left (O.S.). Pupils were equal, round, and reactive to light with no afferent pupillary defect. The patient had leukocoria O.S. Versions were smooth and full in both eyes (OU) with no pain. Confrontation visual fields were full to finger counting O.D. and restricted 360 O.S. Cycloplegic refraction found a very mild hyperopic astigmatism O.D., and no retinoscopic reflex could be seen O.S. Slit lamp examination findings were unremarkable O.D. and showed pigmentary deposits on the anterior capsule of the lens O.S. and 41 cells and flare in the anterior chamber and anterior vitreous O.S. There were no keratic precipitates on the corneal endothelium and no Koeppe or Bussaca nodules on the iris O.S. Dilated fundus examination was unremarkable O.D., and 41 cells were seen throughout the vitreous O.S. There was no edema of the posterior fundus or optic nerves OU. The peripheral fundus O.S. was obscured because of the severe vitritis. Prednisolone acetate 1%, 1 drop every hour O.S., and homatropine 5%, 1 drop every day O.S. were prescribed. The patient was scheduled for a follow-up appointment the next day for further testing. Laboratory tests, including antinuclear antibodies, rheumatoid factor, erythrocyte sedimentation rate, fluorescent treponemal antibody absorption, purified protein derivitive of tuberculin (with anergy panel), angiotensinconverting enzyme, serum lysozyme, toxoplasma IgG and IgM, and Toxocara enzyme-linked immunosorbent assay (ELISA), were ordered for initial differentials of juvenile rheumatoid arthritis, syphilis, tuberculosis, sarcoidosis, toxoplasmosis, and toxocariasis. Other differentials to be considered were retinoblastoma and idiopathic pars planitis. 11 His entering visual acuities the next day were 20/20 O.D. and 20/200 O.S. Intraocular pressures were 12 mmhg O.D. and 14 mmhg O.S. by Goldmann applanation tonometry. The patient denied pain on palpation of the left eye. Exophthalmos was not present. B-scan ultrasonography O.S. showed a posterior vitreous detachment with an intact retina. Fundus photos were obtained (see Figure 1). The initial assessment was chronic vitritis with spillover in the anterior chamber O.S. Five days later, the patient reported no changes in his vision and good compliance with the medications. Ocular health remained stable. Results from laboratory testing showed a positive Toxoplasma IgG antibody with a negative Toxoplasma IgM antibody, establishing that the patient had a past infection with Toxoplasma gondii that was inactive at this time. The ordered Toxocara ELISA was not performed by the laboratory because of blood collection storage difficulties. All other laboratory results were negative. The patient was referred to his pediatrician for a physical examination to rule out any systemic signs related to his ocular inflammation. The patient was followed up closely to monitor the resolution of the vitritis and to monitor intraocular pressures caused by steroid use (see Figure 2). Three weeks from the initial presentation, the vitritis improved to 11 cells with 41 debris O.S. Peripheral fundus examination found a fibrotic band stretching across the superior temporal periphery to a granuloma O.S. (see Figure 3). Because of the clinical appearance of the lesion, the patient had ocular toxocariasis diagnosed O.S. Toxocara ELISA testing was performed later to confirm the diagnosis. In February 2005 (approximately 3 months after the initial presentation), the patient experienced a recurrence of the vitritis. Treatment with an oral anthelmintic to kill the Toxocara canis (T Canis) larvae and oral steroids to control the inflammation were prescribed: albendazole, 400 mg twice a day for 14 days, and prednisone, 5 mg 4 times a day for 14 days, then 5 mg 3 times a day for 14 days, 5 mg twice a day for 14 days, 5 mg once a day for 20 days. By March 2005 the vitritis resolved to trace vitreous debris O.S. The patient and his mother were educated about the high possibility for the need for a vitrectomy to improve the vision of his left eye. The patient did not have insurance until June 2006, which made obtaining medications and referrals for services difficult. In May 2006, his visual acuity was stable at 20/80 O.S. with residual vitreous debris. A local surgeon was willing to perform the surgery free of charge, but the surgeon felt that it was not necessary because his acuity was stable, and

Frazier et al Clinical Care 177 Figure 1 Initial presentation of the posterior pole. Notice the headlights in the fog appearance of the left optic nerve due to the vitirits.

His visual acuity was 3/600 O.S. with similar ocular findings to his initial presentation in November 2004.

3 Frazier et al Clinical Care 177 Figure 1 Initial presentation of the posterior pole. Notice the headlights in the fog appearance of the left optic nerve due to the vitirits. the amount of debris was low. The surgeon recommended that he wait for complete resolution. In October 2006, the patient presented with a reactivation of the infection and vitritis. His visual acuity was 3/600 O.S. with similar ocular findings to his initial presentation in November Treatment with oral albendazole and oral prednisone was reinitiated, and referral for a vitrectomy was made. On October 31, 2006, the vitrectomy was performed leaving the anterior vitreous intact to avoid cataract Figure 2 Pertinent ocular findings with initiated treatment throughout the course of the disease.

178 Optometry, Vol 80, No 4, April 2009 Figure 3 Fundus photo of the superior temporal retina O.S. Notice the band of fibrotic tissue (black arrows) that stretches to the granuloma from ora serrata.

At his most recent visit in October 2007 his visual acuity was stable at 20/50 O.S. He may not recover 20/20 vision because of anterior vitreous debris immediately behind the lens.

4 178 Optometry, Vol 80, No 4, April 2009 Figure 3 Fundus photo of the superior temporal retina O.S. Notice the band of fibrotic tissue (black arrows) that stretches to the granuloma from ora serrata. development. Findings from ELISA of the vitreous confirmed presence of Toxocara antibodies. Between October 2006 and November 2006, the patient s visual acuity improved to 20/50 O.S., and the granuloma became viewable during fundus examination (see Figure 4). At his most recent visit in October 2007 his visual acuity was stable at 20/50 O.S. He may not recover 20/20 vision because of anterior vitreous debris immediately behind the lens. Discussion Human toxocariasis can be a benign, asymptomatic, and self-limiting disease. Because humans are an intermediate Figure 4 Fundus photo of the superior temporal retina status post vitrectomy O.S. Notice the granuloma (white arrow) and the fibrotic band (black arrows) stretching to ora serrata. host for T canis, the larvae cannot develop into adult worms or multiply in an infected human, the disease process is noticed only when an immunologic reaction is activated in the host. 3,11 When second- and third-stage larvae enter the eye through the blood circulation, they burrow through the small blood vessels and into the vitreous, creating an eosinophilic, granulomatous response. 1,11 Ocular larva migrans typically occurs unilaterally and in young children but occasionally appears bilaterally in children and adults. The clinical appearance of OLM varies depending on the stage and degree of ocular involvement at the time of diagnosis. No clinical pattern is pathognomonic of OLM, so the clinician must rely on all available clinical and laboratory data to make the diagnosis. Furthermore, patients must be questioned about contact with puppies and about pica. The diagnosis of OLM is presumptive because a definite diagnosis requires actual demonstration of the larva in the human eye. Ocular manifestations include retinochoroidal granuloma, posterior or peripheral retinochoroiditis, vitreoretinal traction bands, optic papillitis, endophthalmitis, motile chorioretinal nematode, and even keratitis, conjunctivitis, and lens involvement. 11 The retinochoroidal granulomas can be macular or peripheral. If leukocoria is a presenting sign, the differential diagnoses of retinoblastoma, Coat s disease, persistent hyperplastic primary vitreous, retinopathy of prematurity, retinochoroidal coloboma, and congenital cataracts should be considered. Other differentials should include familial exudative vitreoretinopathy, idiopathic peripheral uveoretinitis, toxoplasmosis, histoplasmosis, idiopathic subretinal neovascular membrane, tuberous sclerosis, and optic neuritis. 5,11 Additional tests should be utilized when the diagnosis is unclear. B-scan ultrasonography is useful for differentiating a retinoblastoma. ELISA is usually the test of choice to find Toxocara antibodies in the serum. Western blot is another helpful technique in the immunodiagnosis of ocular toxocariasis. 12 A white blood cell count with differentials usually shows leukocytosis and hypereosinophilia in patients with VLM but typically is normal in OLM at the time of diagnosis. 3 The evaluation and cytology of aqueous enzymes may be helpful for confirmation of the diagnosis, but it is very involved. 2 There is no commonly accepted treatment regimen for ocular toxocariasis. One available treatment is the use of topical, intravitreal, or oral corticosteroids depending on the severity of inflammation. 4 Cycloplegic agents are used in the presence of an anterior segment inflammation to prevent posterior synechia. After treatment of our patient s initial presentation with steroids and cycloplegics alone, reinflammation occurred in approximately 3 months. Based on the outcome obtained with albendazole and steroid treatment by Barisani-Asenbauer et al., 10 the decision was made to start treatment with this anthelmintic. Once concurrent treatment with albendazole and oral prednisone was initiated, the inflammation resolved. Unfortunately, a relapse occurred approximately 20 months later. This recurrence was unexpected because the 7 patients treated by

5 Frazier et al Clinical Care 179 Barisani-Asenbauer et al. 10 averaged a follow-up period of 13.8 months, with a range of 3 days to 24 months, and with no recurrences. A larger study with a longer observational period may be necessary to decide the effectiveness of this combination therapy. Anthelmintic agents have been used for the treatment of VLM, 2,4,13 with reports of clinical improvement. However, anthelmintic drugs are not commonly used for treatment of OLM because of the possibility of severe, sight-threatening immunologic reactions to the dying larvae. 3,14 A report from Austria described 5 cases of OLM (11 to 72 years of age) treated successfully with high doses of albendazole (400 to 800 mg twice a day) for 2 weeks with concomitant administration of oral steroids (tapered over 3 months) with no relapses during a mean follow-up period of 20.2 months. 10 Albendazole is a broad-spectrum anthelmintic that is effective against both the larval and adult stages of nematodes, cestodes, and trematodes. 3 Its mechanism of action is not completely known, but it is believed to selectively bind parasitic microtubules having a low human toxicity. 3,13 Side effects, which are reversible with discontinuation of treatment, include hepatotoxicity, leucopenia, and alopecia. 10 Albendazole is a category C drug so it should be avoided in pregnant women. 13 When compared with thiabendazole, which is another commonly used anthelmintic, in the treatment of VLM and OLM, both drugs were equally effective in achieving clinical improvement, but albendazole caused fewer adverse reactions. 13 Concomitant use of steroids is necessary to prevent a severe inflammatory reaction of dying larvae, but there is no risk of enhancing the infection because the larvae cannot multiply. 10 Vitreoretinal surgery is indicated if the inflammatory response results in an epiretinal membrane (ERM), tractional or traction-regmatogenous retinal detachment (RD), or a dense vitreous membrane. 4,15,16 Macular detachment can be caused by vitreomacular traction or ERM formation. If significant vitreoretinal traction is present, pars plana vitrectomy with scleral buckling is necessary. If no significant tractional component is present, scleral buckling alone may be sufficient. In certain cases, the vitrectomy may need to be combined with fluid gas exchange, silicone oil, membrane removal, or a lensectomy. Prognostic signs of visual recovery include good preoperative vision and absence of retinal folds throughout the macula. Timing of surgery is controversial. Control of inflammation before surgical intervention might decrease ERM formation postoperatively. However, in very young patients, earlier surgery might decrease the risk for amblyopia. Amblyopia treatment should be implemented aggressively in young patients to reach maximum visual potential. 16 It is hard to establish the efficacy of albendazole in the treatment of this patient with ocular toxocariasis. We cannot assess whether albendazole affected the immunologic response because our patient was treated concurrently with oral prednisone that may have counteracted an increased response. The intense inflammatory response from the infection produced residual vitreous debris in our patient. It cannot be determined whether the amount and density of debris would be significantly different had albendazole not been prescribed. The debris resulted in decreased and fluctuating vision between episodes and ultimately led to the necessity of a vitrectomy. Since the surgery, the patient s vision has improved and stabilized, but the role the anthelminthic played in this case remains uncertain. Conclusion When vitritis is diagnosed in a patient, it is important to identify the cause and treat the inflammation. T canis infection should be included in the clinical differential diagnoses, especially in unilateral cases. Clinical appearance, laboratory studies, and even cytology studies may be helpful in making the diagnosis. Retinal detachments, severe epiretinal membranes, and dense vitreous cyclitic membranes will require vitreoretinal surgery. Anthelmintic agents, such as albendazole, may be helpful when used concurrently with steroids to reduce the inflammation and to reduce the probability of recurrences. However, this case suggests that recurrences can occur, and this combination therapy does not eliminate recurrences. Patients must be closely followed up in case of recurrence and further treatment, such as vitrectomy, becomes necessary. Treatment of ocular toxocariasis with anthelmintics could become a viable option, but to evaluate the effectiveness of this therapy, a randomized, controlled trial would be necessary. Editor s note This article reports the case of a 7-year-old boy with ocular toxocariasis who is treated through a University of Alabama at Birmingham School of Optometry satellite clinic. The patient s mother, who has no insurance, brought her son into the clinic after hearing about its services through a video produced with the funds from an AOA Healthy Eyes Healthy People Ò grant, sponsored by Luxottica Group and VSP. Healthy Eyes Healthy People Ò is an ongoing AOA commitment to improve the visual health of all Americans. It is intended to reach beyond the patient in the exam chair and out into the community, to the individual who would benefit from optometric services but does not seek them out. P.B.F. References 1. Stewart JM, Cubillan LD, Cunningham ET Jr. Prevalence, clinical features, and causes of vision loss among patients with ocular toxocariasis. Retina 2005;25(8): Shields JA. Ocular toxocariasis. A review. Surv Ophthalmol 1984; 28(5): Schantz PM, Weis PE, Pollard ZF, et al. Risk factors for toxocaral ocular larva migrans: a case-control study. Am J Public Health 1980; 70(12): Glickman LT, Schantz PM. Epidemiology and pathogenesis of zoonotic toxocariasis. Epidemiol Rev 1981;3:

6 180 Optometry, Vol 80, No 4, April Thomann KH, Marks ES, Adamczyk DT. Primary eyecare in systemic disease, 2nd ed. New York: McGraw Hill; 2001: Marmor M, Glickman L, Shofer F, et al. Toxocara canis infection of children: epidemiologic and neuropsychologic findings. Am J Public Health 1987;77(5): Lampariello DA, Primo SA. Ocular toxocariasis: a rare presentation of a posterior pole granuloma with an associated choroidal neovascular membrane. J Am Optom Assoc 1999;70(4): Good B, Holland CV, Taylor MR, et al. Ocular toxocariasis in schoolchildren. Clin Infect Dis 2004;39(2): Maetz HM, Kleinstein RN, Federico D, et al. Estimated prevalence of ocular toxoplasmosis and toxocariasis in Alabama. J Infect Dis 1987; 156(2): Barisani-Asenbauer T, Maca SM, Hauff W, et al. Treatment of ocular toxocariasis with albendazole. J Ocul Pharmacol Ther 2001;17(3): Alexander LJ. Primary care of the posterior segment, 3rd ed. Spain: McGraw-Hill; 2002: Magnaval JF, Malard L, Morassin B, et al. Immunodiagnosis of ocular toxocariasis using Western-blot for the detection of specific anti- Toxocara IgG and CAP for the measurement of specific anti- Toxocara IgE. J Helminthol 2002;76(4): Sturchler D, Schubarth P, Gualzata M, et al. Thiabendazole vs. albendazole in treatment of toxocariasis: a clinical trial. Ann Trop Med Parasitol 1989;83(5): Dernouchamps JP, Verougstraete C, Demolder E. Ocular toxocariasis: a presumed case of peripheral granuloma. Int Ophthalmol 1990; 14(5-6): Amin HI, McDonald HR, Han DP, et al. Vitrectomy update for macular traction in ocular toxocariasis. Retina 2000;20(1): Werner JC, Ross RD, Green WR, et al. Pars plana vitrectomy and subretinal surgery for ocular toxocariasis. Arch Ophthalmol 1999;117(4):532-4.

Moncef Khairallah, MD

Moncef Khairallah, MD Department of Ophthalmology, Fattouma Bourguiba University Hospital Faculty of Medicine, University of Monastir Monastir, Tunisia INTRODUCTION IU: anatomic form of uveitis involving