What is the pathogenesis of ocular toxoplasmosis?

Updated: Mar 08, 2019
  • Author: Murat Hökelek, MD, PhD; Chief Editor: Michael Stuart Bronze, MD  more...
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Answer

When the organism reaches the eye through the bloodstream, depending on the host's immune status, a clinical or subclinical focus of infection begins in the retina. As the host's immune system responds and the tachyzoites convert themselves into bradyzoites, the cyst forms. The cyst is extremely resistant to the host's defenses, and a chronic, latent infection ensues. If a subclinical infection is present, no funduscopic changes are observed. The cyst remains in the normal-appearing retina. Whenever the host's immune function declines for any reason, the cyst wall may rupture, releasing organisms into the retina, and the inflammatory process restarts. If an active clinical lesion is present, healing occurs as a retinochoroidal scar. The cyst often remains inactive within or adjacent to the scar. (See the image below.)

Inactive retinochoroidal scar secondary to toxopla Inactive retinochoroidal scar secondary to toxoplasmosis.

Toxoplasma parasites are rarely identified in aqueous humor samples from patients with active ocular toxoplasmosis. [10] This suggests that parasite proliferation occurs only during the early phase of infection and that the retinal damages are probably caused by subsequent inflammatory responses.

When human retinal pigment epithelium (RPE) cells are infected with Toxoplasma gondii, there is an increased production of several cytokines, including interleukin 1beta (IL-1ß), interleukin 6 (IL-6), granulocyte-macrophage colony-stimulating factor, and intercellular adhesion molecule (ICAM). [11] Patients with acquired toxoplasmic retinochoroiditis exhibit higher levels of IL-1 than asymptomatic patients. [12]


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