[Severity of the development of hyalitis complicating giant foci of chorioretinitis].
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The pathogenesis of retinochoroidal destruction associated with infection by Toxoplasma gondii presents a perplexing problem. A murine model of congenital toxoplasmic retinochoroiditis is described in relation to the current concepts regarding the pathogenesis of the disease process in man. It would appear that in this model at least, auto-immune mechanisms may contribute to the inflammatory process.
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A case of a 17-year-old male suffering from acute bilateral disseminated subretinal inflammatory lesions, which affected the posterior pole and the retinal periphery as well, is presented. All the laboratory tests were negative except for the Sabin-Feldman dye test which showed a positive rising titer. The clinical course of the disease is described, and the differential diagnosis discussed.
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Occurrence of congenital toxoplasmosis in subsequent siblings after the birth of an affected child is discussed. Toxoplasmic retinochoroiditis was found in 3 surviving siblings. The diagnosis was made by the typical fundus lesions in children, intracranial calcification in one child, and significant positive titer for toxoplasmic antibodies in all the children and the mother, who was asymptomatic. Serology for syphilis, skin tests for histoplasmosis and tuberculosis, blood studies with sedimentation rate, and chest roentgenograms were all negative in mother and all 3 children. The view that transmission of infection from mother to the fetus may result from a chronically infested uterine wall is supported and is thought to be the probable cause in the cases reported here. After the birth of one child with congenital toxoplasmosis, the parents may be reassured about the favorable prognosis of subsequent pregnancies with some reservation. However, it appears unwise to categorically refute the repetition of congenital toxoplasmosis in siblings. It is also suggested that because of possible danger of reactivation, the healed toxoplasmic chorioretinal lesions should be properly monitored if the patient is to be given corticosteroids for any other reason.
When treating a patient with neuroleptics or tricyclic antidepressants, it is usually assumed that complaints of blurred vision can be ascribed to the anticholinergic side effects of these drugs. The authors present a patient treated with imipramine and trifluoperazine whose complaints of blurred vision led to the diagnosis of toxoplasma chorioretinitis.
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