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We herein describe two interesting cases of ocular toxoplasmosis (OT) wherein optical coherence tomography (OCT) findings mimicked the appearance of punctate inner retinal toxoplasmosis (PIRT) lesions. The first case was that of a young man who presented with a diminution of vision in his right eye (RE) for a week. His best-corrected visual acuity (BCVA) in the RE was 20/250, while in the left eye was 20/20 for distance. Intraocular pressures in both eyes were 12 mm Hg. His RE had 2+ anterior chamber reaction, vitreous haze grade 1 and two-disc diameters of retinochoroiditis supero-temporal to the fovea. He had a normal hemogram, non-reactive HIV TriDot test, non-reactive treponema pallidum hemagglutination assay and elevated serum toxoplasma IgG (143.04) IU/mL with normal IgM. We administered trimethoprim 160 mg along with sulfamethoxazole 800 mg twice a day for 6 weeks; tapering oral steroids for 4 weeks. Intravitreal clindamycin (2 mg/0.05 mL) was given at presentation and twice later with an interval of 1 week each. He had complete resolution of the lesion with visual improvement to 20/25 at the third-month visit. During the next 2 months, his vision dropped to 20/80 in the RE; an epiretinal membrane (ERM) with a yellowish lesion at the macula was noted, on OCT the hyper-reflective inner retinal lesion corresponding with the macular pucker mimicked the appearance of PIRT (figure 1A,B). We operated the RE for pars plana vitrectomy and epiretinal membrane removal with a favourable outcome. His vision at a 5-month visit after surgery was 20/20 with a pigmented scar, straightening of the fovea contour with relative temporal retinal thinning (figure 1C,D). We describe the second case of a teenage girl presenting with a drop in vision in her RE for 8 days. She had BCVA 20/80 in her RE along with focal necrotising retinochoroiditis lesion inferotemporal to disc with multiple areas of focal retinal vasculitis in all quadrants. Her left eye had BCVA 20/20 and was normal. She was diagnosed with right eye toxoplasma retinochoroiditis clinically and administered trimethoprim 160 mg along with sulfamethoxazole 800 mg twice a day for 6 weeks and tapering oral steroids for 4 weeks. Her baseline OCT passing through an inflamed vessel mimicked the appearance of a PIRT lesion (figure 2). Her vision improved to 20/20 with the healing of retinochoroiditis with pigmentation and scarring at the third-month visit.
PIRT is an atypical presentation of OT and an under-recognised entity that was first described by Friedmann et al. It usually presents in the second decade and appears as a single or multifocal small active retinitis lesions with minimal vitritis.1 These lesions are seen to be hyper-reflective lesions in the inner retina with variable depth up to the outer plexiform layer on OCT. The significance of diagnosing a PIRT lesion lies in the risk of progression to typical lesions and/or recurrences.2 Initiation of anti-toxoplasma therapy whether or not will prevent these risks is debatable but recommended.3 ERM is a known complication seen during the resolution of toxoplasma retinochoroiditis.4 Retinal glia, especially the Muller cells, migrate due to the inflammatory response and contribute to the formation of ERM.5 However, purely glial ERMs are non-contractile. They act as a scaffold for the proliferation and migration of RPE cells and fibroblast-like cells giving rise to the contractile membrane.6 Inner retinal changes can thus be caused by the mechanical effect of ERM due to surface contraction.7 We encountered an inner retinal hyper-reflective lesion in association with ERM in our case one after the resolution of the primary retinochoroiditis lesion.
Retinal vasculitis is associated with retinochoroiditis in OT. In our second case, the OCT scan passing through an inflamed blood vessel showed an inner retinal lesion. The presence of central two dots with a blurry and partial distorted ‘figure of eight’ appearance with back shadowing helped us differentiate this from a PIRT lesion. Major retinal vessels on OCT scan are known to have a ‘figure of eight’ appearance, which presents as central hyper-reflectivity surrounded by a configuration of two columns with back shadowing on the retina posterior to it.8 In a healthy vessel, the blood flow is laminar and is arranged in a concentric cylindrical sheet of erythrocytes, with their velocity maximum at the centre line of the vessel. The relative movement of the erythrocytes affects this hyper-reflectivity. In vasculitis, due to inflammation, the blood flow is stagnant, and this affects the movement of the erythrocytes, affecting the hyper-reflectivity and thus the loss of the ‘figure of eight’ appearance.
The differentiation of inner retinal lesions from PIRT is essential not only to avoid misinterpretation and undue treatment but also to help understand the nature and evolution of the disease process. The macular pucker and inflamed blood vessels were the two mimickers of PIRT on OCT in our study.
Patient one: I experienced decrease in vision after initial treatment for infection in my eye due to toxoplasma. My retina specialist informed me about development of membrane at macula with puckering. I was suggested and underwent vitreo-retina surgery. I had significant improvement in my vision over few months. I am thankful to my ophthalmologist for my initial diagnosis, treatment and subsequent surgery keeping my vision near normal.
Patient two: I had decrease in vision in my right eye with smoke like particles in front of my eye. These smoke like haze increased over the next week. I consulted with uveitis services and was diagnosed to have infection in my eye. They informed me of toxoplasma as a suspected cause of disease and started me on oral antibiotics and steroids. It took 2–3 weeks for vision recovery while the decrease in smoke like particles took couple of months.
Inflamed blood vessels on optical coherence tomography (OCT) can appear as an inner retinal hyper-reflective lesion with loss of ‘figure of eight’ due to stagnant blood flow.
Macular pucker secondary to an epiretinal membrane, a complication of ocular toxoplasmosis, can present as an inner retinal hyper-reflective lesion on OCT.
Inflamed blood vessels and macular pucker in a case of ocular toxoplasmosis can mimic punctate inner retinal toxoplasmosis lesions on OCT.
Careful differentiation of punctate inner retinal toxoplasmosis lesions from their mimickers is essential to avoid misinterpretation and undue treatment.
Patient consent for publication
Dr Soumyava Basu, Network head, Uveitis services, L.V. Prasad Eye Institute for his constant teaching, inspiration, support and guidance.
Contributors MSS and AKP were involved in data collection, manuscript writing and review of the literature. AK and AK were involved in the concept, design and manuscript review.
Funding Hyderabad Eye Research Foundation (LVPEI-2021-107-BHR-41).
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.