Structural Retinal Analysis in Toxoplasmic Retinochoroiditis: OCT Follow-Up with Three-Dimensional Reconstruction

Abstract

Background: Ocular toxoplasmosis remains the leading cause of posterior uveitis worldwide. Optical coherence tomography (OCT) provides valuable insights into the structural alterations associated with this condition. The present study aimed to characterize the vitreous, retinal, and choroidal morphological changes observed during both the active and scarred stages of ocular toxoplasmosis using OCT imaging. A secondary objective was to evaluate the added value of three-dimensional reconstruction in the assessment of retinal lesions. Methods: A retrospective study was conducted on 12 eyes belonging to 12 patients diagnosed with toxoplasmosis retinochoroiditis (TRC). Optical coherence tomography (OCT) scans centered on the active lesions were qualitatively analyzed at baseline and follow-up. Additionally, a ResUNet model was trained to generate a full volumetric reconstruction of the retinochoroidal lesions in selected cases. Results: Twelve eyes were analyzed at a mean of 16.2 days from symptom onset. The mean follow-up duration was 144 days (range: 12-490 days). OCT imaging revealed characteristic alterations in the retina, choroid, and vitreous body, which were documented both at baseline and at follow-up. Representative cases were selected for three-dimensional reconstruction to illustrate the extent of retinal architectural involvement. Conclusions: OCT analysis refines our understanding of the structural damage associated with ocular toxoplasmosis, while three-dimensional reconstruction enhances our ability to visualize and interpret these alterations on a larger scale.

Keywords: optical coherence tomography; three-dimensional reconstruction; toxoplasmic retinal choroiditis.

Figure 1

Original—true B-scan image; Original Stripped—synthetic stripped image for training; Reconstructed—result after inference.

Figure 2

Original B-scan and filtered B-scan.

Figure 3

Color fundus photography (CFP) at the time of diagnosis. (A) Marked vitritis producing the classic appearance of a headlight in the fog. (B) An active white toxoplasmic retinochoroiditis lesion is visible adjacent to a retinal choroidal pigmented scar. (C) Optic nerve involvement is seen, vasculitis and a macular star. (D) Active macular lesion adjacent to a retinal choroidal atrophic scar.

Figure 4

OCT scan at the time of diagnosis. (A) Intraretinal hyperreflectivities (circle) in the ONL, close to the TRC lesion. (B) Retinal hyperreflectivity (vertical bracket), increased thickness, RPE bowing (ellipse), and choroidal hyporeflectivity (horizontal bracket). (C) Posterior hyaloid hyperreflectivities (arrows). (D) ILM deposits (arrows). (E) RPE bumps (rectangle) and RPE bowing. (F) ILM deposits (circle), hyperreflective vitreous dots (square/rectangle), and subretinal fluid (arrow). (G) Subretinal hyperreflective dots (circle) and intraretinal fluid (arrow). (H) Increased RPE thickness (arrow). (I) “Hairy appearance” (arrow). (J) Hyperreflective dots above the blood vessels (arrows). (K) Hyperreflective dots around a retinal blood vessel (circle). (L) Hyperreflective dots around choroidal vessels (arrows).

Figure 5

(A1) CFP at baseline, 10 days after symptom onset: white chorioretinal foveal lesion. (A2) OCT scan: parafoveal increased retinal thickness, with macular hole, increased RPE thickness, RPE bowing. (A3) Three-dimensional reconstruction showing increased retinal thickness around the fovea, with vitreous cells, thickened choroid, and RPE. (A4) Cross-section of the 3D model; increased retinal thickness is visualized at the edge of the fovea; dispersed vitreous cells. (B1) CFP 12 days from baseline, with retinal lesion starting to fade. (B2) OCT of the same horizontal slab as A2 showing decreased retinal thickness, multiple hyporreflective spaces, and almost flat RPE line. (B3) Large area surrounding the fovea of decreased retinal thickness showing irregular retinal surface. (B4) Section through the lesion showing altered retinal thickness with gliotic hyperreflective retinal tissue and less RPE bowing (see Supplementary Video S1).

Figure 6

(A) OCT at baseline showing increased and hyperreflective retinal lesion, with a hyporeflective space. (B) OCT at 6 months showing decreased retinal thickness, hyperreflective gliotic tissue, discontinuity of RPE, EZ, ELM, and choroidal hypertransmission. (C) Three-dimensional reconstruction at baseline showing perifoveal increased retinal thickness, with vitreous cells and attached posterior hyaloid. (D) Three-dimensional reconstruction at 6 months showing enlarged foveal depression, disappearance of vitreous cells, and posterior vitreous detachment. (E) Cross-section of the 3D model at baseline showing increased perifoveal retinal thickness, choroidal shadowing, dispersed vitreous cells, and intraretinal hyporeflective spaces. (F) Cross-section of the 3D model at 6 months showing enlarged foveal depression with discontinuity of RPE, EZ, and ELM; the retinal vessels are prominent on the surface of the retina (see Supplementary Video S2).

Figure 7

(A) CFP 35 days after onset showing TRC along the vascular arcade. (B) OCT scan at baseline showing retinal hyperreflectivity with increased choroidal thickness underneath, thickened posterior hyaloid with hyperreflective cells in the vitreous and on the hyaloid, and thickened and partially detached ILM with hypereflective cells. (C) OCT scan after 35 days: decreased retinal thickness around the lesion was noted, as well as decreased choroidal thickness and hyporeflectivity, and increased detachment of posterior hyaloid. (D) Three-dimensional reconstruction at baseline: numerous vitreous cells are depicted; attached posterior hyaloid, RPE bumps, and ONL hyperreflectivities are observed. (E) Three-dimensional reconstruction after 35 days: partially attached posterior hyaloid with persistent vitreous cells. (F) Cross-section of the 3D model at baseline showing increased choroidal thickness, adhesion between ILM and posterior hyaloid, and focal adhesion of hyaloid on the retinal surface. (G) Cross-section of the 3D model after 35 days, showing increased hyperreflective retinal lesion, with disorganized retina around it, decreased choroidal thickness, and increased PVD. (H) Three-dimensional colored reconstruction at baseline and (I) after 35 days, better highlighting the distribution of hyperreflective dots: on the external face of ILM, between ILM and posterior hyaloid face, attached to the posterior hyaloid externa land internal face, and in the vitreous (see Supplementary Video S3).

Figure 8

(A) CFP at baseline highlighting a large chorioretinal scar and an active perifoveal TRC. (B–D) OCT scans at baseline, at 10 days, and at 24 months, showing the transformation of an active foveal lesion into a chorioretinal scar. (E,F) Three-dimensional reconstruction of the entire retinal volume showing the dynamic transformation of the retinal architecture from an increased foveal thickness into a chorioretinal scar, together with increased choroidal transmission and the progression of the PVD. (G) Cross-section of the 3D model through the fovea depicting the transition from increased retinal thickness and hyperreflectivity to atrophy and gliotic tissue (see Supplementary Video S4).

Figure 9

(A) CFP at baseline (left side) and at the 11-month follow-up (right side). (B) OCT scan at baseline: because the orientation of the images is different, the reconstruction could not be performed. (C) OCT scan at the 11-month follow-up, showing extensive chorioretinal damage, with merging of the old scar with the new one. (D) Three-dimensional reconstruction of the entire volume at baseline showing extremely irregular retinal surface and incomplete PVD. (E) Cross-section of the 3D model, depicting chorioretinal atrophy, gliotic tissue, RPE atrophy, and increased choroidal transmission (see Supplementary Video S5).