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Annual Student Case Report Challenge Optometry Students Become Optometry's Teachers Third Prize:
Congenital Toxoplasmosis in 6-Year-Old The mother hoped to improve her daughter's vision with glasses. An eye doctor in Mexico prescribed glasses six months earlier, but the patient did not comply with wearing them.
The girl's ocular history was negative for other conditions. She was born 22 days prematurely and spent 1-2 weeks in an incubator. Otherwise, her medical and family histories were unremarkable. The patient took no medications and had no known drug allergies. One additional note: The child was performing poorly in first grade and was not receiving any individualized instruction in school. Diagnostic Data We attempted confrontation fields but could not elicit a reliable response. Hirschberg's test revealed an estimated 20-25 LXT. Pupil testing revealed a +4 afferent pupillary defect in the left eye. Biomicroscopy was unremarkable in both eyes. IOP was 18mm Hg O.D.; we could not obtain a reading in the left eye due to poor fixation. Dilated fundus exam uncovered chorioretinal scars in both eyes. We located an 8-10 disc diameter scar in the right eye in the posterior pole, inferotemporal to the optic disc and partially involving the macula. A 10-12 disc diameter scar in the left eye was temporal to the optic disc and involved the entire macula. We also observed fibrosis in the posterior pole O.S. Optic atrophy was present in both eyes, but was greater in the left. Cup-to-disc ratios were difficult to grade. We detected no lesions, holes, tears or other pathology in the peripheral retina of either eye. Diagnosis Treatment and Follow-up
The patient returned to our low vision service 10 days later. At this visit, unaided distance acuity was 5/63 O.D., no light perception O.S. Acuity with the patient's new glasses was 5/32 O.D. at distance, 20/100 O.D. at 10cm. Color vision assessment with the Farnsworth D-15 panel test showed a protan defect O.D. The low vision service instructed the patient on using a 4x Magnaboite (dome magnifier) at near, which yielded 20/80 at 3-4 cm. A 2.2x FDTS was attempted at distance but yielded poor results. The child was uncooperative and disliked having a telescope mounted on her glasses. We decided to delay using low vision devices until she was older and willing to use them. We sent the mother a letter in which we described her daughter's condition and visual status. We also suggested that she seek educational assistance through the school, and provided her with instructions and phone numbers to do so. We also counseled the mother on adapting the home environment to maximize her daughter's residual acuity. The patient is scheduled for another low vision evaluation in one year. Discussion Transmission to humans usually occurs through direct contact with contaminated soil. Other means of transmission: ingestion of undercooked meats or other foods that contain the tissue cysts, or from mother to child during pregnancy.1-7 Patients who acquire the disease generally do not manifest ocular signs or symptoms. However, immunocompromised patients who become infected can develop extensive retinal lesions, which if left untreated may lead to severe visual impairment.2,4 A young adult who acquires an ocular Toxoplasma infection requires a detailed history to ensure proper management if you suspect HIV. The incidence of acquired infections is about 2-3%. Congenital infections transmitted during preg- nancy account for most cases.3 A pregnant woman who contracts a primary infection may transmit the infection to her unborn child. Subsequent children are not at risk if the mother is reinfected during later pregnancies because her antibodies combat the recurring infections.1,3 Children with congenital disease may have severe multiple organ problems at birth, or they may be asymptomatic at birth and develop neurological and ocular problems years later. Although 50% of infants with transplacentally-acquired toxoplasmosis are born healthy, the severity of systemic and ocular involvement varies according to the stage of pregnancy in which the mother contracts the infection.2,4,5 The brain and retina are especially susceptible to damage when the parasite is transmitted during the first trimester. Convulsions, intracranial calcifications and retinochoroiditis are pathognomonic for congenital toxoplasmosis.3 The ocular findings are the most common features of congenital toxoplasmosis. Affected infants usually are born with bilaterally healed chorioretinal scars in the posterior pole. Other ocular findings can include microphthalmos, cataracts, panuveitis, optic atrophy, strabismus, and nystagmus.6,7,8 We diagnosed this patient entirely by the clinical presentation: bilateral chorioretinal scarring, optic atrophy, strabismus, and nystagmus. Most active ocular Toxoplasma lesions in adults are a reactivation of a congenital infection. A newly reactivated lesion is classically seen next to an old, pigmented chorioretinal scar. Since the organism can remain viable in a non-proliferative form after initial infection, recurrent attacks are not uncommon. The first attack often occurs when the patient is in his or her 20s. The active retinochoroiditis that occurs usually presents as a focal, yellow-white, poorly demarcated lesion with an overlying vitritis. Clinicians often describe the presentation as a "headlight in the fog." The lesion begins in the superficial retinal layers, but the inflammation can progress to the deeper retinal layers, the choroid and the sclera. Patients usually present complaining of blurred vision, floaters, photopsia, pain and redness.1-5 Progression can lead to other ocular complications, including subretinal neovascular membranes, vessel occlusions, preretinal gliosis, retinal detachments, macular edema, papillitis, optic nerve atrophy, synechiae, cataracts and glaucoma.5 A dilated fundus exam can usually reveal an ocular lesion that's secondary to a Toxoplasma infection. Serologic testing can confirm the diagnosis. We didn't order serological testing for this patient for three reasons: the ocular findings pointed to a congenital toxoplasmosis infection; the fundus lesions appeared old, inactive and stable; and it would not have influenced our management. An active, ocular Toxoplasma lesion usually becomes self-limiting within 1-4 months and results in a chorioretinal scar. Treatment is warranted in any patient with HIV or AIDS regardless of the lesion's size or location, but usually is not indicated in immunocompetent patients. Two exceptions: if the lesion threatens or involves the macula, papillomacular bundle or optic nerve head; or if there's visual impairment secondary to a severe vitritis or retinal detachment.1-5 Conventional treatment involves a combination of sulfadiazine, pyrimethamine, folic acid and clindamycin.1,4,5 Some doctors add a systemic steroid such as prednisone to suppress inflammation. Manage an associated anterior uveitis with a standard regimen. Length of treatment varies depending on severity, but the usual course is 4-6 weeks.1,4 While the incidence of congenital toxoplasmosis is low, the severe neurological and ocular sequelae that can result from fetal infection have prompted most hospitals to screen pregnant women for Toxoplasma antibodies. No screening, however, is 100% effective in detecting the disease. Management initially aims to combat reactivated infections. Patient education is crucial to prevention. Since congenital infection al- most always presents with ocular signs, we must carefully monitor children inflicted with this disease to ensure that they also receive medical care and visual rehabilitation. Ms. Nguyen is a fourth-year student at University of Houston College of Optometry. Dr. Suarez is on the clinical faculty there. 1. Alexander
L. Exudative and nonexudative macular disorders. In: Primary Care of the
Posterior Segment. Norwalk, Conn: Appleton & Lange, 1994:277-344.
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