June 1988
Volume 29, Issue 6
Free
Articles  |   June 1988
Ocular toxoplasmosis in immunosuppressed nonhuman primates.
Author Affiliations
  • G N Holland
    Francis I. Proctor Foundation for Research in Ophthalmology, University of California, San Francisco.
  • G R O'Connor
    Francis I. Proctor Foundation for Research in Ophthalmology, University of California, San Francisco.
  • R F Diaz
    Francis I. Proctor Foundation for Research in Ophthalmology, University of California, San Francisco.
  • P Minasi
    Francis I. Proctor Foundation for Research in Ophthalmology, University of California, San Francisco.
  • W M Wara
    Francis I. Proctor Foundation for Research in Ophthalmology, University of California, San Francisco.
Investigative Ophthalmology & Visual Science June 1988, Vol.29, 835-842. doi:
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    • Get Citation

      G N Holland, G R O'Connor, R F Diaz, P Minasi, W M Wara; Ocular toxoplasmosis in immunosuppressed nonhuman primates.. Invest. Ophthalmol. Vis. Sci. 1988;29(6):835-842.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

To investigate the role of cellular immunodeficiency in recurrent toxoplasmic retinochoroiditis, six Cynomolgus monkeys (Macaca fascicularis) with healed toxoplasmic lesions of the retina were immunosuppressed by total lymphoid irradiation. Three months prior to irradiation 30,000 Toxoplasma gondii organisms of the Beverley strain had been inoculated onto the macula of eye in each monkey via a pars plana approach. Toxoplasmic retinochoroiditis developed in each animal, and lesions were allowed to heal without treatment. During total lymphoid irradiation animals received 2000 centigrays (cGy) over a 7-week period. Irradiation resulted in an immediate drop in total lymphocyte counts and decreased ability to stimulate lymphocytes by phytohemagglutinin. Weekly ophthalmoscopic examinations following irradiation failed to show evidence of recurrent ocular disease despite persistent immunodeficiency. Four months after irradiation live organisms were reinoculated onto the nasal retina of the same eye in each animal. Retinochoroidal lesions identical to those seen in primary disease developed in five of six animals. Toxoplasma organisms therefore were able to proliferate in ocular tissue following the administration of immunosuppressive therapy. This study fails to support the hypothesis that cellular immunodeficiency alone will initiate recurrent toxoplasmic retinochoroiditis. Results suggest that reactivation of disease from encysted organisms involves factors other than suppression of Toxoplasma proliferation. If reactivation occurs by other mechanisms, however, cellular immunodeficiency then may allow development of extensive disease.

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