Ocular toxoplasmosis.

Dear Editor: Acquired Toxoplasma gondii ocular infection usually presents with necrotizing retinochoroiditis with dense vitritis and vasculitis. Atypical disease has been observed in im-munocompromised states such as malignancy and AIDS 1 or after iatrogenic systemic 2 or local 3 immunosuppression. Intravitreal triamcinolone acetonide (TA) is used frequently by ophthalmologists for conditions like uveitis and diabetic macular edema. However, its unscrupulous use may have dismal consequences. We recently managed a case of fulminant retinal necrosis after intravitreal TA in a patient with previously undiag-nosed ocular toxoplasmosis. This 53-year-old Malay woman with diabetes consulted an ophthalmologist for blurring of vision in the left eye. On examination, her left eye's best-corrected visual acuity (BCVA) was 20/1200. There was an area of intraretinal whitening at the fovea, with flame and blot hemorrhages in the posterior pole and proximal in-ferotemporal arcade, vessel engorgement and tortuosity, and mild vitreous haze (Fig 1A [available at http://aaojournal.org]). She was diagnosed by her attending ophthalmologist with nonischemic central retinal vein occlusion with branch mac-ular artery occlusion. She received macular grid laser with concomitant intravitreal TA (4 mg/0.1 ml). Vision initially improved to 20/200 but dropped to hand movements (HM) after 2 months. Retinal necrosis with elevated intraocular pressure was detected. She was referred subsequently to the Singapore National Eye Centre for further management. When she consulted at Singapore National Eye Centre, BCVAs were 20/30 (right eye) and HM (left eye). There was a grade 3 left relative afferent pupillary defect. Intraoc-ular pressures were 18 mmHg (right eye) and 40 mmHg (left eye). There was mild anterior segment inflammation with 1–2ϩ cells. There was widespread deep retinal necro-sis associated with disc pallor and arterial sheathing with 2ϩ vitritis (Fig 1B–D [available at http://aaojournal.org]). No residual TA was detected. A clinical diagnosis of progressive outer retinal necrosis of presumed viral etiology was made. However, vitreous analysis by polymerase chain reaction was positive for Toxoplasma gondii but negative for viruses (cytomegalovirus, varicella-zoster, herpes simplex). A serum Toxoplasma immunogloblin G titer of1/256 was detected. Human immunodeficiency virus serology was negative ; CD4 and CD8 levels were normal. She received a full course of anti-Toxoplasma therapy. Although the retinitis resolved, vision did not recover. The diagnosis of ocular toxoplasmosis depends largely on the presence of typical lesions, with retinochoroiditis as a key feature, and is supported by serologic and/or molecular testing. Although this may be associated with vasculitis or vascular occlusion, the latter may …