Primary ocular toxoplasmosis secondary to venison consumption

Abstract

Purpose: To describe primary ocular toxoplasmosis infection related to ingestion of undercooked venison.

Observations: This single site, retrospective case series reviewed 4 patients with primary ocular toxoplasmosis that was acquired by ingesting undercooked venison. De-identified data was collected regarding baseline patient characteristics including age, sex, past medical and ocular history, onset of symptoms, visual acuity (VA), response to treatment, and workup. All patients with acquired toxoplasmosis had similar chronology of systemic and ocular symptoms. Exposure occurred in October or November and systemic symptoms developed within 2 weeks, followed by ocular symptoms an average of 2.6 months later. Average age at onset was 56 ± 13 (age ± SD) years old and all were male. Average initial and final VA were 20/50 and 20/50, respectively. Positive anti-toxoplasma IgM and IgG serologies were found in all cases. All patients were treated with trimethoprim/sulfamethoxazole and achieved rapid improvement. Complications occurred in 50% of cases and included epiretinal membrane, cystoid macular edema, vitreoretinal traction, and neovascularization.

Conclusions and importance: Consumption of undercooked venison is a source of primary ocular toxoplasmosis even in immunocompetent hosts and has a clear chronology. A presentation of retinochoroiditis during the winter months should prompt questioning for exposure to wild game.

Keywords: Chorioretinitis; Ocular toxoplasmosis; Retinochoroiditis; Toxoplasmosis; Venison.

Fig. 1

(A) Fundus photographs of the left eye from Case 1 illustrating a focal area of retinitis in the inferior macula without any adjacent chorioretinal scar. The area of retinitis responded rapidly to initiation of trimethoprim/sulfamethoxazole with reduction in size and vitritis by day 11 and essentially complete resolution by 1 month. (B) Optical coherence tomography of the same patient at presentation showed inner retinal hyper-reflectivity with full-thickness retinal disorganization, retinal thickening, and posterior shadowing. The retinal thickening was greatly improved after 1 month of treatment (C) but an epiretinal membrane developed (D) which was visually significant.

Fig. 2

OCT raster through the retinal lesion showed focal vitreoretinal traction and overlying neovascularization. After treatment with trimethoprim/sulfamethoxazole, the neovascularization resolved, although residual vitreoretinal traction remained and was observed.