Detection of Toxoplasmal Antigen and Antibody in Ocular Fluids in Experimental Ocular Toxoplasmosis

Rollins, David F.; Tabbara, Khalid F.; O’Connor, G. Richard; Araujo, Fausto G.; Remington, Jack S.

doi:10.1001/archopht.1983.01040010455024

Cited by 18 publications

(5 citation statements)

References 12 publications

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“…A comparable situation may be envisaged when the suprachoroidal route of infection is adopted [27], and may similarly account for the failure to induce ocular toxoplasmosis in primed rabbits reported by several groups [19, 26, 28]. The detection of circulating antigen both prior to and shortly after the development of ocular lesions (when manifested) in rabbits supports this contention [29]. Hogan et al [30] were the first to explore the possibility of inducing ocular toxoplasmosis by injecting parasites intravitreally into guinea pigs, and Kaufman [31] later adopted this model to study therapeutic modalities.…”

Section: Discussionsupporting

confidence: 40%

Experimental Ocular Toxoplasmosis in Naive and Primed Rabbits

Garweg

Kuenzli²,

Boehnke³

1998

Ophthalmologica

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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.

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Section: Discussionsupporting

confidence: 40%

Experimental Ocular Toxoplasmosis in Naive and Primed Rabbits

Garweg

Kuenzli²,

Boehnke³

1998

Ophthalmologica

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“…Whereas Frenkel has been a proponent of the theory that toxoplasmic chorioretinitis in older children and adults is a hypersensitivity phenomenon [277], O'Connor and colleagues concluded that both the acute and the recurrent forms of necrotizing chorioretinitis are due to multiplication of T. gondii tachyzoites in the retina and that release of antigen into the retina of previously sensitized persons does not result in recurrence of the inflammatory response. T. gondii antigen and antibody have been detected in ocular fluids in experimental ocular toxoplasmosis [278]. The rapid resolution of inflammation that occurs with antimicrobial treatment in infants, children, and adults with congenital toxoplasmosis [279] suggests that parasite replication and the resulting destruction of retinal tissue causes the eye disease.…”

Section: Special Problems Concerning Pathogenesis In the Eye And Braincontrasting

confidence: 40%

Toxoplasmosis

Remington¹,

McLeod²,

Wilson³

et al. 2011

Infectious Diseases of the Fetus and Newborn

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“…In experimental animals we have found that antitoxoplasma antibodies and toxoplasma antigens may be detected in the vitreous specimens of rabbits with toxoplasmic retinochoroiditis [10]. The antigen is detected at the height of activity of the disease and antibodies are found in the vitreous of all infected eyes at six weeks after the onset of the disease.…”

Section: Experimental Toxoplasmosismentioning

confidence: 40%

Ocular toxoplasmosis

Tabbara¹

1990

Int Ophthalmol

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Toxoplasmosis is a common infection of man and animals. The disease is widespread in nature and has a worldwide distribution. The infection is caused by the organism Toxoplasma gondii which was first isolated by Nicolle and Manceaux in Tunis from a North African rodent. The disease can be congenital or acquired with a variety of clinical manifestations that may range from a subclinical course to a generalized infection with fatal outcome. The ocular manifestations of the disease include sudden onset of floaters with blurring of vision. Toxoplasmosis causes a localized necrotizing retinitis with inflammation of the subjacent choroid. The retina sustains the primary injury and the major damage.

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Detection of Toxoplasmal Antigen and Antibody in Ocular Fluids in Experimental Ocular Toxoplasmosis

Cited by 18 publications

References 12 publications

Experimental Ocular Toxoplasmosis in Naive and Primed Rabbits

Experimental Ocular Toxoplasmosis in Naive and Primed Rabbits

Toxoplasmosis

Ocular toxoplasmosis

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