Can the route of Toxoplasma gondii infection affect the ophthalmic outcomes?

Abstract

Ocular toxoplasmosis is the most common cause of retinochoroiditis worldwide in humans. Some studies highlighted the idea that ocular lesions differ according to the route of infection but none of them mimicked the natural route. The current study aimed to investigate the ophthalmic outcomes in congenital and oral routes of infection with Toxoplasma in experimental animals. Mice were divided into three groups; group I: congenital infection, group II: acquired oral infection and group III: non-infected. We used Me49 chronic low-virulence T. gondii strain. We found that retina is the most affected part in both modes of infections. However, the retinal changes are different and more pronounced in case of congenital infection. The congenitally infected mice showed retinal lesions e.g. total detachment of retinal pigment epithelium from the photoreceptor layer and irregular arrangement of retinal layers. More severe damage was observed in mice infected early in pregnancy. While the postnatal orally infected mice showed fewer changes. In conclusion, the routes of Toxoplasma infection affect the ophthalmic outcomes and this may be the case in human disease. Although both are vision threatening, it seems that the prognosis of postnatal acquired ocular toxoplasmosis is better than that of congenital disease.

Murine Model of Primary Acquired Ocular Toxoplasmosis: Fluorescein Angiography and Multiplex Immune Mediator Profiles in the Aqueous Humor

“…54 Additionally, because the immune mechanisms between intraperitoneal infection and peroral infection are different, 58 the associated pathologic outcomes are different as well. Some congenital OT models were investigated pathologically, 56,59 and the peroral infection route was reported to cause fewer ocular pathologic changes compared with congenital infection. 59 Thus the route of infection might affect the pathologic outcome.…”

“…Some congenital OT models were investigated pathologically, 56,59 and the peroral infection route was reported to cause fewer ocular pathologic changes compared with congenital infection. 59 Thus the route of infection might affect the pathologic outcome. Moreover, differences in parasite factors (such as the pathogenicity of T. gondii strains 48,60 and primary parasite load), host factors (such as mouse strain), or clinical stage factors (such as congenital or acquired, primary or recurrent, and acute or chronic) might influence the pathologic findings.…”

Implications of TORCH Diseases in Retinal Development—Special Focus on Congenital Toxoplasmosis

“…Alterations in the profile of the structures of retinal layers, such as detachment of the pigmented epithelium from the ONL and irregularities in the placement of retinal layers, have been described in the literature in congenitally infected mice, where ocular abnormalities were more evident than in acquired infection (Ashour et al, 2018). However, the literature lacks studies systematically describing whether the damage found in congenital OT is derived from alterations that occur during the proliferation and differentiation of retinal progenitor cells during development.…”

Maternal Toxoplasma gondii infection affects proliferation, differentiation and cell cycle regulation of retinal neural progenitor cells in mouse embryo

“…These changes were noticed in congenitally T. gondii-infected mice, where more extensive eye damage was noted as compared to acquired OT (Ashour et al, 2018). Moreover, congenital T. gondii infection in mice caused structural damage to the retina of infected offspring, including reduced number of cells in the Outer Nuclear Layer (ONL), mild alteration of Müller glial markers and disorganization of nuclear layers (Lahmar et al, 2010(Lahmar et al, , 2014Ashour et al, 2018). Despite the severity of congenital ocular toxoplasmosis and the efforts to establish experimental models to recapitulate the human disease in the laboratory settings, very few studies have successfully detected the parasite (either tachyzoites or cysts) in the retinal tissue per se (Lee et al, 1983;Hay et al, 1984;Lahmar et al, 2010;Dukaczewska et al, 2015).…”