Commentary Sense and nonsense of corticosteroid administration in the treatment of ocular toxoplasmosis

There is no consensus about the use of corticosteroids for the treatment of ocular toxoplasmosis. In clinical practice, corticosteroids are usually given in combination with antiparasitic drugs to reduce the inflammatory reaction during active chorioretinitis and to minimise tissue damage. Specifically, in the case of pericentral location, this presumed eVect might help to retain central visual acuity and limit scotomas. However, the use of corticosteroids can lead to progression of the underlying infectious disease, as repeatedly demonstrated by the occurrence of fulminant ocular toxoplasmosis following both systemic and periocular administration (Fig 1). On the other hand, low dose corticosteroid monotherapy has been administered without severe side eVects. To our knowledge, a well defined study of the eVect of corticosteroid monotherapy in ocular toxoplasmosis as well as the additional value of corticosteroids as adjuvant therapy has not been performed. Thus, the use of corticosteroids for the treatment of ocular toxoplasmosis is controversial, and the timing and dosages during the course of the disease are not well defined. During an acute infection with Toxoplasma gondii, oocysts ingested by the host give rise to the extracellular forms (tachyzoites), which actively penetrate host cells and replicate; subsequently the disease enters the chronic stage when cysts are formed. The signal for formation of cysts is not known; the onset and the quality of the host immune response may be an important factor. The mechanism of chronic recurrent ocular toxoplasmosis is unknown; it is presumed that the multiplication of parasites, liberated from the cysts, causes damage to adjacent retinal tissue. The hypothesis of autoimmunity, directed against retinal S-antigen, has not been proved unequivocally. 11 In fact, the interaction between T gondii and the competent immune system does not lead to parasite elimination, but to a reduction in parasite load and changes in morphology and surface antigen expression.