Ocular toxoplasmosis in the immunocompromised host.

Abstract

Disseminated toxoplasmosis is a well-known complication of immunodeficiency states, including those induced by malignancies, steroid and cytotoxic drug therapy, and AIDS. In immunodeficient patients, toxoplasmic infections of the eye are less common than toxoplasmic infections of other organs for unknown reasons. When ocular toxoplasmosis does occur in the immunodeficient host, or if immunosuppressive therapy is administered to patients with active disease, widespread tissue destruction by proliferating organisms may result. Immunodeficiency alone may not be sufficient, however, to cause reactivation of encysted organisms in retinochoroidal scars. Ocular toxoplasmosis in the immunocompromised host presents difficult problems in diagnosis and management. There may be a variety of clinical lesions, including single foci of retinochoroiditis in one or both eyes, multifocal lesions, or diffuse areas of retinal necrosis. The majority of lesions do not arise from the borders of preexisting scars, which suggests that they result from acquired infection or dissemination of organisms from nonocular sites of disease. Toxoplasma gondii may infect iris, choroid, and vitreous-tissues that are not usually infected in the immunocompetent host. Ocular lesions appear to respond to standard antiparasitic drug therapies, but continued treatment is probably necessary to prevent reactivation of disease in the most immunocompromised patients. The best treatment regimens have yet to be determined. Histopathologic studies show little retinal inflammation; therefore anti-inflammatory drugs, such as oral steroids, probably have no role in the management of infection.