Herein, we report a patient with foveal toxoplasmic retinochoroiditis that showed anatomical reorganization of the fovea with intravitreal and oral antibiotics and corticosteroid. Response to treatment and control of infection and inflammation was associated with the reformation of the foveal pit and restoration of the layered structure of the tissue. While macular toxoplasmic retinochoroiditis are usually associated with scar formation and severe visual reduction, our patient’s visual acuity was well recovered, most probably due to foveal reorganization.
Different modes of foveal regeneration were proposed in spontaneous or surgical closure of macular hole (MH): 1) regular regeneration resulted in the formation of a fovea which contained a foveola and photoreceptors in the center; 2) irregular regeneration resulted in the formation of a fovea which did not contain a foveola and central photoreceptors and was filled by a tissue formed by Müller and retinal pigment epithelial cells . Because the fovea is free of astrocytes , the closure is likely mediated by Müller cells. Concentric contraction of the Müller cell processes envelops the photoreceptor cells in the outer nuclear layer and at the external limiting membrane and result in the centripetal movement of photoreceptor cells . The irregular regeneration was mediated by proliferation of Müller and retinal pigment epithelial cells [6, 7]. It was suggested that closure of small MHs and the subsequent reconstruction of the normal foveal structure are mediated by active mechanisms of Müller cells, without cell proliferation, that resemble those involved in ontogenetic foveal development . We believe that reorganization of fovea in our patient may be related to Müller cells, like what happens in MH repair.
Histopathologic findings in an eye with active toxoplasmic retinochoroiditis show cell infiltration and edema, initially in the internal retina and then in the vitreous and choroid. As a result of the infiltration, there is a disorganization of the retinal layers [8, 9]. This hystopathological feature can be correlated to the spectral domain optical coherence tomography (SD-OCT) findings of hyper-reflectivity and increased thickness of retina at the lesion site . Some of the SD-OCT findings in reactivation of ocular toxoplasmosis have been described previously which included increased reflectivity in the inner retina, shadowing of the outer retina layers, thickened and detached posterior hyaloid with irregular hyperreflective formations [11,12,13]. Alwassia A. et al.  described the progression of retinitis in a case with acute ocular toxoplasmosis using SD-OCT. In this patient, the development of cystic spaces in the area of previous hyperreflectivity possibly represents the progression from retinitis to liquefactive necrosis as a result of inflammation. The retina in this case began a healing process as the gap within the retina caused by necrosis became smaller. Our patient also initially underwent cavitary changes, similar to the evolution of a MH, possibly due to a liquefactive necrosis. MH formation has been previously described as a complication of ocular toxoplasmosis [15,16,17,18]. Its pathogenesis in association with toxoplasmic retinochoroiditis is controversial, although vitreomacular traction caused by inflammation of the vitreous, changes in the posterior hyaloid membrane and posterior vitreous detachment [15, 16] and/or retinochoroidal ischemia based on the presence of retinochoroidal hypoperfusion  have been speculated. Tanaka R. et al.  presented a case of ocular toxoplasmosis with the development of a giant MH during treatment for posterior uveitis which was not closed despite vitrectomy. In another report, Doshi S. et al.  presented a young male with the diagnosis of left eye toxoplasma retinochoroiditis who was treated with oral co-trimoxazole and prednisolone and a single dose of intravitreal clindamycin along with dexamethasone. After 1 week, the vision dropped with the fundus showing resolving retinitis and a full thickness MH confirmed on OCT scan. One week following the occurrence of the MH, though the vision remained stable, there was spontaneous closure of the MH. They hypothesized that a limited separation of the posterior hyaloid that there was above the fovea after the intravitreal injection may be the reason for development of the MH. The strong vitreoretinal adhesion at the site of active retinitis might have prevented this hyaloid detachment from progressing, further causing its collapse and formation of a scaffold over which the MH closed. Fortunately, in our patient the healing process began with fluid absorption and the changes did not progress to the MH formation.
In conclusion, we believe that although toxoplasmic retinochoroiditis lesions often heal with atrophy and scar, early treatment may prevent scar formation and allows retinal layer reorganization.