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A 26-year-old man with a blind spot in his left eye
Digital Journal of Ophthalmology 2013
Volume 19, Number 3
September 26, 2013
DOI: 10.5693/djo.03.2013.07.001
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Alfred White Jr, MD | USF Eye Institute, University of South Florida
Timothy Saunders, MD | USF Eye Institute, University of South Florida
Peter Reed Pavan, MD | USF Eye Institute, University of South Florida
Diagnosis and Discussion
This clinical presentation is consistent with Toxoplasma neuroretinitis, which was confirmed by serology. Patients with neuroretinitis typically present with decreased visual acuity, from 20/50 to 20/200, and visual field defects usually in the ceocentral or central distribution. Stellate maculopathy and disc edema are the hallmark findings and may coincide with an adjacent serous retinal detachment.(2) Disc edema is often the initial sign followed by macular star formation approximately 1 week later with resolution of the peripapillary exudate. Vitreous cells usually are present without an anterior chamber response.(6) Recurrence, although rare, is most commonly associated with ocular toxoplasmosis.(2)

Fluorescein angiography findings typically include late phase disc staining. Capillaries supplying the optic nerve head demonstrate leakage that usually persists after resolution of the edema. Perifoveal capillary leakage is virtually nonexistent.(6)
Most cases of ocular toxoplasmosis are acquired instead of congenital.(7) The classic lesion in ocular toxoplasmosis is a focus of active retinochoroiditis adjacent to an old scar. The theory for the pathophysiology of this lesion is reactivation of Toxoplasma tissue cysts in the retina.(8)

Ultimately, our patient exhibited a toxoplasmic neuroretinitis, making this an atypical presentation of ocular toxoplasmosis. Other atypical forms include occlusive retinal vasculitis, retinal detachment, pigmentary retinopathies, panuveitis, optic neuropathy, and scleritis.(9) The presentations of toxoplasmosis are numerous and diverse.
Toxoplasma infection begins with ingestion of oocysts present in contaminated food and water sources.(4) While hematogenous spread is the most widely accepted route of infection, it has also been postulated that Toxoplasma can demonstrate a predominantly neuronal spread to the eye by way of the brain and optic nerve.(8) This is supported by the preponderance of juxtapapillary lesions seen in certain patient populations.(8) One retrospective study of 51 patients with active ocular toxoplasmosis with optic nerve involvement differentiated lesions into five categories:(10)

• Juxtapapillary retinochoroiditis—chorioretinal lesion contiguous with a swollen optic disc (33.3%)
• Pure papillitis—swollen optic disc, peripapillary vein sheathing plus a healed toxoplasmic scar (5.9%)
• Neuroretinitis—swollen disc, papillomacular or macular serous detachment, and hard exudates in the macula
• Distant lesion—swollen disc and a distant active lesion (43.1%)
• Mixed—any combination of the previous categories (15.7%)

The most serious potential complication of ocular toxoplasmosis is Toxoplasma encephalitis. This fatal complication is typically seen in immunocompromised hosts.11 A PubMed search revealed only one reported case of ocular toxoplasmosis with encephalitis in an immuncompetent person.(12) The patient had Toxoplasma retinochoroiditis without neuroretinitis. Despite the absence of large studies on the incidence of encephalitis in patients with Toxoplasma neuroretinitis, likely due to its rarity, one should have a high index of suspicion and rule-out brain involvement in all patients with neurologic findings. In fact, it may be prudent to obtain baseline neuroimaging in all patients with suspected Toxoplasma neuroretinitis.

Ocular toxoplasmosis remains a clinical diagnosis, typified by a focus of retinochoroiditis with vitreous inflammation and an adjacent chorioretinal scar. Serology, while useful in identifying primary infection, is limited in differentiating between recurrent acquired and recurrent congenital infection. IgM confirms primary infection, and remains positive for approximately a year. In contrast, IgG is detectable for life, in both congenital and acquired infections.(11) One study detected measurable rises of IgG in patients with active recurrent disease (typical and atypical) compared to patients with latent disease or seropositive nonspecific uveitis.(13) When serologies are equivocal, PCR analysis of intraocular fluid for parasites provides more robust diagnostic data.(14) Our patient was both IgG and IgM positive, which suggests a recently acquired infection.

Triple therapy for ocular toxoplasmosis is classically a combination of pyrimethamine, sulfadiazine, and prednisone. Due to high rates of intolerance and serious adverse effects, alternative treatment, such as trimethoprim/sulfamethoxazole and clindamycin, may be employed, and is supported by published trials yielding comparable results.(6,15)

Although toxoplasmosis rarely presents as neuroretinitis, the disease may have severe, even fatal, complications; thus it should be regularly considered as part of the differential diagnosis.
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