ocular damage may occur either from direct invasion of the protozoan or from immunological reactions against protozoan products. Toxoplasmosis is almost always congenital but may be acquired through inhalation of oocytes in cat feces or ingestion of contaminated pork or lamb meat. In both forms, an acute focal chorioretinitis lesion develops between ages 10 and 40 years. The lesions are usually single, posterior to the equator, and are often about one disk diameter in size; they commonly occur next to an area of scar.

Although a deÞnitive diagnosis of ocular toxoplasmosis can be made only by identifying the protozoa histologically, a supportive diagnosis is made on the basis of the clinical picture and serological tests. The serological tests most commonly used are the ELISA and the IFA test. The presence of high IgM anti-toxoplasma titers indicates a recent infection.

Treatment of toxoplasmosis retinochoroiditis with or without scleritis includes oral corticosteroids and antitoxoplasmic agents, such as sulfadiazine, pyrimethamine, and clindamycin; folinic acid should be added to avoid toxic depression of the bone marrow by pyrimethamine.

Any patient with scleritis and retinochoroiditis should be examined for toxoplasmosis.

7.4.2Helminthic Scleritis

7.4.2.1 Toxocariasis

Toxocariasis is a common parasitic disease in the USA; humans are infected after ingestion of the helminth Toxocara canis. The natural host for this parasite is the dog; droppings from which can contaminate sand and earth, which is later inadvertently ingested, primarily by children at play. Ocular manifestations, usually affecting individuals 6Ð40 years of age, include posterior pole and retinal periphery granulomas and chronic endophthalmitis [241]. Although a deÞnitive diagnosis of ocular toxocariasis can be made only by identifying the larva histologically, supportive diagnosis is made on the basis of the clinical picture and ELISA blood tests. Treatment

includes corticosteroids, either systemic or transeptal; thiabendazole also may be added.

Scleritis has not previously been described as a presenting manifestation of ocular toxocariasis [18, 241]. In our prior series of 172 patients with scleritis [13], one patient had toxocariasis (0.58%). The patient was a 70-year- old white female who developed recurrent nodular scleritis, anterior uveitis, dense cataract, and 360o posterior synechiae in her left eye. Visual acuity in the left eye was at the level of hand motions only. Because adequate examination of the posterior segment of the eye could not be done, ultrasonography was performed; this showed a temporal mass and vitreous membranes in the left eye. Review of systems disclosed a history of cervical cancer. Given the patientÕs age, history of cervical cancer, and the presence of an intraocular mass, a metastatic lesion versus a primary ocular melanoma was considered. Extracapsular cataract extraction, sphincterotomy, and pars plana vitrectomy were performed to improve visualization of the posterior segment. A granuloma temporal to the disk, subretinal exudates, and a tractional detachment of the retina were found. Biopsy of the scleral nodule and Þne needle biopsy of the intraocular mass were performed; nongranulomatous inßammation of the scleral specimen and granulomatous inßammation of the intraocular mass specimen were found with the absence of tumor cells from either lesion. An ELISA test for Toxocara was positive (titer, 1:64) and ocular toxocariasis was diagnosed. The patient was subsequently treated with topical and systemic corticosteroids; ocular inßammation, including scleritis was controlled, but the visual acuity did not improve.

Results of serology, and clinical and histological granuloma in the posterior segment of the eye, supported the diagnosis of toxocariasis in spite of the organism not being isolated, and the patient was beyond the age group normally associated with ocular toxocariasis.

Any patient who develops scleritis and posterior pole or peripheral retinal granuloma should be examined for toxocariasis.