Purpose: We describe a unique case of ocular toxoplasmosis associated with concurrent neuroretinitis and a branch retinal artery occlusion (BRAO).

Observation: We report the case of a 35-year-old woman who presented with sudden-onset right inferonasal visual field loss and blurry vision. Initial clinical examination demonstrated visual acuity of 20/30, optic disc edema, macular exudates, subretinal fluid, and a filling defect in the superior temporal retina consistent with neuroretinitis and BRAO. Serologic testing was positive for both Toxoplasma IgM and IgG antibodies. The patient was treated with 160mg trimethoprim-800mg sulfamethoxazole twice daily for three months and a systemic corticosteroid taper. Visual acuity recovered to 20/20, and signs of intraocular inflammation resolved; however, a persistent inferonasal visual field defect remained due to the BRAO from the toxoplasmic retinochoroidal lesion. Follow-up over one year later showed no recurrence or new symptoms.

Conclusion: This case highlights a unique, concurrent presentation of neuroretinitis and BRAO caused by ocular toxoplasmosis. Prompt diagnosis and treatment resulted in favorable structural and visual outcomes. Toxoplasmosis should be considered in the differential diagnosis for neuroretinitis and retinal artery occlusions, especially in the presence of intraocular inflammation.

• Toxoplasmosis • Retinal artery occlusion • Neuroretinitis • Infectious uveitis • Posterior uveitis

Bahn JH, Abouodah H, Kim S, Conrady CD (2026) A Unique Case of Neuroretinitis and Branch Retinal Artery Occlusion Associated with an Acute Toxoplasmosis Lesion. JSM Ophthalmol 13(1): 1100.

BRAO: Branch Retinal Artery Occlusion; OCT: Optical Coherence Tomography

Toxoplasma gondii is a ubiquitous, obligate intracellular protozoan typically transmitted through infected fecal material, contaminated water, and undercooked meat [1-4]. Substantial differences in geographic distribution of T. gondii strains, their virulence, and ocular tropism is well established [3,4]. Approximately 2% of acquired cases of toxoplasmosis within the United States and 17.7% in Brazil will result in ocular complications and is the leading cause of posterior uveitis worldwide [1,3,5].Toxoplasmic retinochoroiditis classically presents with a unilateral, focal, full thickness necrotizing retinochoroiditis with overlying vitritis known colloquially as a “headlight in the fog.” Severe ocular manifestations may occur with drug resistant or more virulent protozoal strains, such as multifocal to widespread necrotizing retinochoroiditis, dense vitritis, substantial disc edema, and involvement of the macula, optic nerve, and/or central nervous system in the immunocompromised, elderly, or pregnant [1,6-9]. Diagnosis relies on the characteristic clinical findings with supportive serologic studies and ocular fluid analysis; however, atypical forms can present a diagnostic challenge and increase the risk of delayed treatment [1]. More rare posterior segment manifestations of toxoplasmosis include neuroretinitis, punctate outer retinal toxoplasmosis, occlusive retinal vasculitis, retinal neovascularization, pigmentary retinopathy, and optic nerve pathology [10,11]. We report a case of neuroretinitis and branch retinal artery occlusion (BRAO) secondary to an active toxoplasmosis lesion. To our knowledge, this is the first report of ocular toxoplasmosis associated with concurrent presentations of neuroretinitis and a BRAO.

The University of Nebraska Medical Center’s Institutional Review Board deemed this study exempt due to its de-identified nature. Informed consent was obtained from the patient for publication of this case report and accompanying images.

A 35-year-old white female patient presented with a one-week history of mild, right-sided headaches, sudden onset of a right inferonasal field defect, and blurry vision in the right eye (OD). She denied ocular pain, redness, discharge, diplopia, pain with ocular movement, or any similar symptoms previously. Past medical history was notable for hypertension, hyperthyroidism, and ocular migraines. An extensive review of systems and risk factors were unremarkable except for multiple tattoos, all of which were unremarkable and had been since getting them. She denied any previous travel outside the United States. The referring ophthalmologist had initiated 160 mg trimethoprim/800 mg sulfamethoxazole twice daily at the patient’s initial presentation when the patient was noted to be 20/30 in OD with an inferonasal visual field defect on confrontational visual fields under the assumption that this represented an atypical ocular toxoplasmosis presentation.

Ten days after developing symptoms, the patient was evaluated in our clinic and was found to have a visual acuity of 20/30 OD and 20/25 in the left eye (OS). Intraocular pressure was 19 mmHg OD and 15 mmHg OS. Confrontational visual field testing reaffirmed a defect in the inferior nasal quadrant OD but was full OS. The anterior segment was notable for fine keratic precipitates, rare cell without flare in the anterior chamber, and 0.5+ cell without haze in the vitreous OD. Dilated fundus exam revealed blurring of 270° of the disc margins, macular exudates consistent with an incomplete macular star, retinal whitening along the superior arcade, and peripapillary subretinal fluid OD (Figure 1a). Anterior and posterior segment examination was unremarkable OS. Optical coherence tomography (OCT) revealed superior retinal hyperreflectivity of all retinal layers with associated subretinal fluid and intraretinal exudates consistent with a full thickness retinochoroidal lesion and partial macular star OD, respectively (Figure 1a, d-e). There was also inner retinal hyperreflectivity in the temporal macula consistent with a recent sectoral retinal ischemic event such as a branch retinal artery occlusion (BRAO) [Figure 1d]. Fluorescein angiography OD was notable for leakage of the disc and surrounding vessels. There was also a filling defect in the superotemporal retina consistent with a BRAO, while peripapillary indocyanine green (ICG) angiography hypofluorescence was consistent with a full thickness retinochoroidal lesion (Figure 1b-c). All imaging was unremarkable in OS.

A clinical diagnosis of toxoplasmic-associated neuroretinitis complicated by the development of BRAO secondary to the retinochoroidal lesion OD was made. Due to the paucity of literature on BRAOs and the atypical nature of the retinal vascular occlusion with ocular toxoplasmosis, neuroimaging of the brain and vessels was performed and unrevealing. Systemic laboratory evaluation for infectious and autoimmune etiologies was performed and notable for elevated T. gondii IgM and IgG titers. Commonly associated infectious causes of a macular star with or without retinochoroiditis, such as syphilis, tuberculosis, Lyme, Bartonella henselae and quintana, and Rocky Mountain Spotted Fever serologies were unremarkable. Intraocular fluid was not analyzed per patient request. Testing for other systemic inflammatory, blood and vascular disorders such as ANCA-associated vasculitis, serum sarcoidosis markers, and a coagulopathy panel were unremarkable. Due to positive serological testing for toxoplasmosis and symptomatic improvement with ongoing treatment, the clinical findings were felt to represent an ocular complication of toxoplasmosis infection.

Treatment with 180 mg trimethoprim/800 mg sulfamethoxazole twice per day for three months, 1% topical prednisolone acetate taper (tapered 1 drop every 2 weeks), and an oral prednisone taper starting at 60mg and tapered weekly were initiated. Intravitreal clindamycin was considered but not available at our institution due to ongoing supply issues. After 3 months of treatment with 180 mg trimethoprim/800 mg sulfamethoxazole and corticosteroid taper, the intraocular inflammation, retinal exudates, and subretinal fluid had resolved (Figure 1e). Central visual acuity improved to 20/20, but the right inferior nasal field defect persisted. OCT showed resolution of intraretinal exudates and subretinal fluid but revealed significant inner retinal thinning in the temporal macula along the superior arcade consistent with a prior BRAO (Figure 1g-h). The patient has continued to demonstrate stability off medication without new symptoms over the past year.

Figure 1 Neuroretinitis, a full thickness retinochoroidal lesion, and branch retinal artery occlusion from toxoplasmosis. Colored fundus photo at presentation (a) demonstrated peripapillary subretinal fluid (white *), a white lesion superior to the nerve, and a partial macular star (blue *). There was a superior filling defect (white *) and blockage on fluorescence and ICG angiography from the lesion (b-c). OCT of the macula at presentation (d) revealed exudates (blue *) and inner retinal hyperreflectivity (white *) consistent with a macular star and BRAO. An OCT through the lesion 2 weeks later (e) demonstrated a full thickness lesion (white *) with nearly resolved subretinal fluid. Two months after treatment there were sclerotic vessels within the superior macula, resolution of subretinal fluid, improvement in intraretinal exudates and the retinochoroidal lesion (f). There was inner retinal thinning temporally (white *) consistent with a BRAO and the retina was now atrophic in the area of prior retinochoroidal lesion (blue *) (g-h).

Ocular toxoplasmosis occurs most commonly in otherwise healthy, immunocompetent adults via acquired disease associated with various risk factors such as proton pump inhibitor use and consumption of contaminated food or water or through reactivation from congenitally or postnatally acquired infections [2,12]. Diagnosis is often clinical but may be aided by additional diagnostic tools such as serum or ocular fluid serologies and intraocular fluid PCR analysis. These additional ancillary tests are especially helpful in severe or atypical ocular toxoplasmosis characterized by widespread chorioretinitis, severe vitritis, and pervasive retinal vasculitis, which can be difficult to distinguish from other devastating diseases such as virally-mediated acute retinal necrosis or even endophthalmitis [3,13-15]. Unfortunately, the sensitivity of PCR detection of T. gondii is lower than rates seen with herpetic etiologies and a negative result does not necessarily rule out the pathogen’s presence, so response to therapy should be monitored closely and diagnosis re evaluated with suboptimal therapeutic responses [16]. of the optic nerve and posterior retina and is primarily a clinical diagnosis with ancillary serological testing to identify the associated underlying cause. Neuroretinitis commonly presents with rapid, unilateral vision loss, optic disc edema and the delayed development of a macular star, which may be due to increased permeability and leakage of the optic disc vasculature [17]. However, prior to the macular star developing, or in rare cases where it never develops, the diagnosis of neuroretinitis may be difficult and may require multimodal imaging to detect [17]. Despite hypothesized changes in the optic nerve and peripapillary retinal vasculature, neuroretinitis is rarely associated with the development of a BRAO [18]. Although a variety of infectious agents are associated with neuroretinitis, most cases are associated with B. henselae and toxoplasma associated neuroretinitis is rare [17,19,20]. Exam findings that may support toxoplasma neuroretinitis include the presence of moderate to severe vitritis and an adjacent retinochoroidal scar [10].

Retinal vascular disease secondary to ocular toxoplasmosis is uncommon and is characterized by venular or arteriolar sheathing in the same quadrant as the retinochoroiditis [10,20]. However, the development of a BRAO is a rare complication of active or resolved ocular toxoplasmosis lesions and has been described in only a few case reports [21-23]. While the pathogenesis is not fully elucidated, several hypotheses have been made regarding the development of BRAO in the setting of both active and resolved ocular toxoplasmosis. During disease activity, the occlusion may result from an acute necrotizing reaction from the retinitis, causing vasoconstriction of the affected arteriole thereby diminishing blood flow and leading to thrombosis of the vessel [21,24]. Other potential factors may include increased blood viscosity and local arteriole inflammatory changes [21]. However, segmental retinal periarteritis (Kyrieleis plaques) is not likely to contribute to the development of BRAOs in active toxoplasmosis as a more recent imaging study found inflammation is confined to the vascular endothelium and felt to be insufficient to cause thrombosis [25]. The development of a BRAO after disease quiescence can also be seen as a delayed complication of ocular toxoplasmosis and is hypothesized to result from compression of the involved artery from the evolving chorioretinal scar [22].Taken together, an active, necrotizing lesion surrounding and leading to infarction of the affected vessel would be most consistent with our case, and while difficult to fully visualize, the only discernable Kyrieleis plaques were distal to the BRAO origin and no scar had developed yet.

To our knowledge, this is the first case of neuroretinitis with an active, full thickness retinochoroidal lesion and concurrent BRAO associated with ocular toxoplasmosis. This case highlights the diagnostic complexity and overlapping manifestations of inflammatory and vascular pathologies and their associated impact on ocular health. Documenting such rare manifestations is helpful in expanding the clinical spectrum of ocular toxoplasmosis and offers practical guidance for clinicians managing patients with similar findings.

Toxoplasmosis should be considered in cases of combined neuroretinitis and retinal artery occlusions, especially in the presence of intraocular inflammation. Unfortunately, with an isolated case report, recommendations on treatment and long-term prognosis are not possible.

Patient Consent

The patient has given both written and verbal consent to publish case details.

CDC was supported by the National Institutes of Health K08 award EY034892. The funding organization had no role in the design or conduction of the study. This work was also supported in part by an Unrestricted Grant from Research to Prevent Blindness, New York, NY, to the Department of Ophthalmology & Visual Sciences, University of Utah.

1. Holland GN. Ocular toxoplasmosis: a global reassessment. Part I: epidemiology and course of disease. Am J Ophthalmol. 2003; 136: 973-988.
2. Conrady CD, Besirli CG, Baumal CR, Kovach JL, Etzel JD, Tsui JC, et al. Ocular Toxoplasmosis after Exposure to Wild Game. Ocul Immunol Inflamm. 2021: 1-6.
3. Maenz M, Schlüter D, Liesenfeld O, Schares G, Gross U, Pleyer U. Ocular toxoplasmosis past, present and new aspects of an old disease. Prog Retin Eye Res. 2014; 39: 77-106.
4. Smith JR, Ashander LM, Arruda SL, Cordeiro CA, Lie S, Rochet E, et al. Pathogenesis of ocular toxoplasmosis. Prog Retin Eye Res. 2021; 81: 100882.
5. Glasner PD, Silveira C, Kruszon-Moran D, Martins MC, Junior MB, Silveira S, et al. An Unusually High Prevalence of Ocular Toxoplasmosis in Southern Brazil. Am J Ophthalmol. 1992; 114: 136-144.
6. Johnson MW, Greven CM, Jaffe GJ, Sudhalkar H, Vine AK. Atypical, Severe Toxoplasmic Retinochoroiditis in Elderly Patients. Ophthalmology. 1997; 104: 48-57.
7. Cifuentes-González C, Rojas-Carabali W, Pérez ÁO, Carvalho E, Valenzuela F, Miguel L, et al. Risk factors for recurrences and visual impairment in patients with ocular toxoplasmosis: A systematic review and meta-analysis. PLOS ONE. 2023; 18: e0283845.
8. de-la-Torre A, Gómez-Marín J. Disease of the Year 2019: Ocular Toxoplasmosis in HIV-infected Patients. Ocul Immunol Inflamm. 2020; 28: 1031-1039.
9. de-la-Torre A, Mejía-Salgado G, Eraghi AT, Pleyer U. Age and ocular toxoplasmosis: a narrative review. FEMS Microbes. 2025; 6: xtaf002.
10. Smith JR, Cunningham ETJr. Atypical presentations of ocular toxoplasmosis. Current Opinion in Ophthalmology. 2002; 13.
11. de Souza EC, Casella AMB. Clinical and Tomographic Features of Macular Punctate Outer Retinal Toxoplasmosis. Arch Ophthalmol. 2009; 127: 1390-1394.
12. Conrady CD, Pradeep T, Yu Y, Johnson MW, VanderBeek BL. Association of Proton Pump Inhibitor/Histamine-2 Blocker Use and Ocular Toxoplasmosis: Findings from a Large US National Database. Ophthalmology Retina. 2023; 7: 261-265.
13. Khandwala NS, Miller JML, Hyde RA, Conrady CD, Rao RC, Besirli CG. The Diagnostic Conundrum of Retinitis and a Pigmented Scar. Case Rep Ophthalmol. 2021; 12: 164-168.
14. Ather M, Lyden E, Zhan Y, Haliyur R, Sinha A, Patel S, et al. Pathogen-associated visual outcomes following post-procedure endophthalmitis. Am J Ophthalmol. 2026; 283: 72-80.
15. Conrady CD, Feistmann JA, Roller AB, Boldt HC, Shakoor A. HEMORRHAGIC VASCULITIS AND RETINOPATHY HERALDING AS AN EARLY SIGN OF BACTERIAL ENDOPHTHALMITIS AFTER INTRAVITREAL INJECTION. Retin Cases Brief Rep. 2019; 13: 329-332.
16. Kharel (Sitaula) R, Janani MK, Madhavan HN, Biswas J. Outcome of polymerase chain reaction (PCR) analysis in 100 suspected cases of infectious uveitis. J Ophthalmic Inflamm Infect. 2018; 8: 2.
17. Purvin V, Sundaram S, Kawasaki A. Neuroretinitis: Review of the Literature and New Observations. J Neuro-Ophthalmol. 2011; 31.
18. Gray AV, Reed JB, Wendel RT, Morse LS. Bartonella henselae infection associated with peripapillary angioma, branch retinal artery occlusion, and severe vision loss. Am J Ophthalmol. 1999; 127: 223-224.
19. Hsu C, Uwaydat SH, Chacko JG. Toxoplasma Neuroretinitis. Case Rep Ophthalmol. 2022; 13: 751-755.
20. Miserocchi E, Modorati G, Rama P. Atypical toxoplasmosis masquerading late occurrence of typical findings. Eur J Ophthalmol. 2009; 19: 1091-1093.
21. Braunstein RA, Gass JDM. Branch Artery Obstruction Caused by Acute Toxoplasmosis. Arch Ophthalmol. 1980; 98: 512-513.
22. Iyer P, Ashkenazy N, Liu J, Laura D, Marquez MA, Albini TA. Monitoring Delayed Toxoplasmosis-Related Branch Retinal Artery Occlusion Using Widefield en face Optical Coherence Tomography and Multimodal Imaging. Case Rep Ophthalmol. 2023; 14: 369-375.
23. Aggio FB, Novelli FJ de, Rosa EL, Nobrega MJ. Combined branch retinal vein and artery occlusion in toxoplasmosis. Arquivos Brasileiros de Oftalmologia. 2016; 79.
24. Neiweem AE, Jusufbegovic D. Branch Retinal Artery Occlusion Associated with Toxoplasma Retinitis. Korean J Ophthalmol. 2020; 34: 341-342.
25. Pichi F, Veronese C, Lembo A, Mantovani A, Herbort CP, Morara M, et al. New appraisals of Kyrieleis plaques: a multimodal imaging study. Br J Ophthalmol. 2017; 101: 316.