Experimental Ocular Toxoplasmosis in Naive and Primed Rabbits

Abstract

Purpose: Investigations of the course of ocular toxoplasmosis and the influence of a host’s immunological status in an animal model would contribute to our understanding of the pathophysiology underlying this condition. In the current study, these aspects are addressed using naive and primed rabbits infected transvitreally with the non-cyst-forming BK strain of Toxoplasma gondii. Materials and Methods: Of 45 latex agglutination test-negative rabbits, 27 were infected subcutaneously with 5,000 Toxoplasma tachyzoites, and the ensuing infection treated by systemic administration of clindamycin for 20 days. Four of these rabbits died from generalized infection. The remaining 23 primed rabbits were then inoculated periretinally with a further 5,000 Toxoplasma tachyzoites, administered via the transvitreal route; the 18 naive rabbits were treated likewise. Results: All 18 naive and 21 of the 23 primed rabbits developed toxoplasmic retinochoroiditis. As regarded progression of the disease, dissemination of the condition (p = 0.0001), degree of vitreal infiltration (p = 0.0001) and incidence of retinal detachment (p < 0.05) were all more pronounced in the naive group. Despite treatment, 4 of the 18 (22%) naive rabbits died from generalized infection, as did 4 of the 27 (15%) subcutaneously infected ones (prior to periretinal infection). In the primed (secondarily infected) animal group, only moderate signs of systemic infection were manifested, and there were no fatalities. Conclusion: The high incidence (> 90%) of retinochoroiditis achieved even in primed animals, by introducing Toxoplasma tachyzoites via the transvitreal route, may reflect the maintenance of an intact uveovascular barrier during the early stages of the disease. The pattern of infection, in being restricted primarily to the retina, mimics the situation evinced in humans. Regarding propagation of the disease, the condition manifested in naive rabbits resembles that occurring in immunodeficient patients, whereas that evoked in primed animals corresponds to recurrence of infection in immunocompetent patients.

Anti-retinal autoantibodies in experimental ocular and systemic toxoplasmosis

“…Experimental ocular toxoplasmosis was induced either as a primary disease in infection-naïve rabbits or as a secondary one in infection-immunized animals by the intraocular injection of tachyzoites of the highly virulent BK strain of Toxoplasma gondii, as previously described [30]. Twelve 4-month-old seronegative Dutch belt rabbits of both sexes, weighing 3.5 to 5 kg, were used in this study.…”

“…By drawing on an experimental rabbit model of systemic and primary and secondary ocular toxoplasmosis [30], we wished to investigate the onset and development of the humoral response to the retinal S-antigen, using an established autoantibody ELISA technique [31][32][33]. A comparison between primary ocular and systemic toxoplasmosis will reveal whether any cross-reactivity exists between toxoplasmal and retinal antigens, and that between primary and secondary OT will disclose whether a correlation exists between the levels of anti-retinal antibodies and the degree of ocular tissue destruction.…”

Experimental Models of Ocular Toxoplasmosis

“…The infection is described as a dissemination of retinochorioiditis, vitreal infiltration, and retinal detachment [30]. First affecting retina before choroid, differing from Felidae model.…”

The antibody response in experimental ocular toxoplasmosis

“…85-23, revised 1985) and to the ARVO guidelines for animal research under the surveillance of the local Public Veterinary Health Authorities. Experimental ocular toxoplasmosis was induced in infection-naïve rabbits or secondarily induced by intraocular reinfection in systemically infection-immunized animals as previously reported [19], using the same strain of Toxoplasma gondii tachyzoites.…”