Given the importance of host immune mechanisms, especially CD4+ lymphocytes, in protection against T cruzi, it is not surprising that immunosuppressive therapy may lead to reactivation or progression of clinical disease, as seen in experimental models.226 In humans such reactivation may be fulminant or may have unusual manifestations such as brain abscess or panniculitis. Clinically evident reactivation is uncommon in patients undergoing immunosuppressive therapy for hematologic malignancies and collagen vascular diseases; thus, routine administration of prophylactic antiparasitic therapy is not recommended. However, corticosteroid treatment is known to increase levels of parasitemia,227 and monitoring of parasitemia during treatment may be advisable in some patients.
After renal and bone marrow transplantation in patients with chronic T cruzi infection, reactivation occurs in 20% to 25%.228 Reactivation is diagnosed more reliably by measurement of parasitemia than by serologic testing, which is frequently negative.229 In such patients, it is recommended that serologic status and parasitemia be monitored routinely and any parasitemia or change in serologic status be treated promptly before clinical disease develops.230 Recipients of organs from Tcruzi-infected donors have a relatively low rate of infection; they should also be monitored and treated as needed.
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