784 Am. J. Trop. Med. Hyg., 59(5), 1998, pp. 784–786 Copyright  1998 by The American Society of Tropical Medicine and Hygiene REACTIVATION OF CHAGAS’ DISEASE IN A HUMAN IMMUNODEFICIENCY VIRUS– INFECTED PATIENT LEADING TO SEVERE HEART DISEASE WITH A LATE POSITIVE DIRECT MICROSCOPIC EXAMINATION OF THE BLOOD ANA MARLI C. SARTORI, MARTA H. LOPES, LUIZ A. BENVENUTI, BRUNO CARAMELLI, ANDRE ´ IA O. DI PIETRO, ELIZABETH V. NUNES, LORENA P. RAMIREZ, AND MARIA APARECIDA SHIKANAI-YASUDA AIDS Clinic, Department of Infectious and Parasitic Diseases, Heart Institute, and Laboratory of Medical Investigation (Parasitology), Sa ˜o Paulo University School of Medicine, Sa ˜o Paulo, Brazil; Instituto Adolfo Lutz, Sa ˜o Paulo, Brazil; Center for the Study of the Polymorphism in Microorganisms, Unite ´ Mixte de Recherche, Centre National de la Recherche Scientifique, Institut de Recherche pour le Developpement en Cooperation, Montpellier, France Abstract. We report a human immunodeficiency virus (HIV)–infected man with chronic Chagas’ disease who developed a congestive heart failure that could not be clinically controlled. Endomyocardial biopsy revealed severe myocarditis and the xenodiagnosis result was positive, but Trypanosoma cruzi by direct microscopic examination of the blood was found only four months after the symptoms had started. Treatment with benznidazole was effective in reducing parasitemia, stabilizing the clinical status, and controlling tissue damage related to the parasite. Although the finding of T. cruzi trypomastigotes by direct microscopic examination of the blood has been considered the mark of Chagas’ reactivation in immunocompromised patients with chronic disease, in this case it was a late finding. Since 1990 there have been reports of reactivation of chronic Chagas’ disease in patients infected with human im- munodeficiency virus (HIV). 1–6 In these patients, Trypano- soma cruzi most commonly affects the central nervous sys- tem (CNS) with expansive lesions or meningoencephalitis. 1–4 When the CNS is affected, the diagnosis of trypanosomiasis reactivation is clear because in immunocompetent patients with chronic Chagas’ disease CNS involvement is not ob- served. 7 Cardiopathy during Chagas’ disease reactivation in HIV- infected patients has also been reported, usually associated with major CNS involvement. 1,3,4 Heart disease as the main clinical manifestation of T. cruzi reactivation in HIV-infected patients has rarely been described. 5 In these cases, it is very difficult to make a differential diagnosis between Chagas’ disease reactivation and severe chronic chagasic cardiopathy since the clinical manifestations are similar. Trypanosoma cruzi trypomastigotes observed by direct microscopic ex- amination of the blood characterizes the acute phase of the disease and have been used to confirm Chagas’ disease re- activation. 5 This is because during the chronic phase of the disease in immunocompetent patients, parasitemia can only be demonstrated by indirect methods (xenodiagnosis [in this procedure, insect vectors are fed blood from suspected pa- tients and between 30 and 90 days after the blood meal, parasites are detected microscopically in the feces or intes- tines of the bugs], blood culture, or inoculation into exper- imental animals). We have previously reported a case series of 18 patients with chronic Chagas’ disease and HIV infection, in which three cases of trypanosomiasis reactivation with cardiac manifestation occurred. 6 In this paper, we report the follow- up of one patient who presented with severe heart disease caused by Chagas’ diseases reactivation. Treatment with benznidazole was effective in reducing parasitemia and con- trolling tissue damage. CASE REPORT A 36-year-old man had lived his first five years in an endemic area for vectorial transmission of Chagas’ disease in Brazil and then moved to the city of Sa ˜o Paulo, a non- endemic area where he had been living for 31 years. He was an intravenous drug user, had had sex with men, and had had an asymptomatic HIV infection since September 1988. In October 1994, his chest radiographs showed no abnor- malities (Figure 1). On February 4, 1995 he was admitted to the Infectious Diseases Clinic of the Hospital das Clinicas, a large teaching hospital affiliated with the University of Sa ˜o Paulo. During the previous eight months he had presented weight loss, mal- aise and thrush; during the last two months he developed congestive heart failure, which rapidly evolved to functional class IV. 8 This could not be clinically controlled and led to his hospitalization. On physical examination, he showed signs of congestive heart failure. Chest radiographs showed a significant global heart en- largement (Figure 2). A two-dimensional echocardiogram showed severe dysfunction and dilation of all cavities (end diastolic left ventricular diameter = 6.7 cm; end diastolic left ventricular volume = 301 ml; end systolic left ventric- ular diameter = 5.9 cm; end systolic left ventricular volume = 205 ml, left ventricular ejection fraction = 31%). An elec- trocardiogram (ECG) showed a right-bundle-branch block, left anterior-fascicular hemiblock, and isolated atrial and polymorphic ventricular extrasystoles. Test results for anti- HIV antibodies (ELISA and Western blot) were positive. His CD4 lymphocyte count was 826 cells/mm 3 (20.7% of the total lymphocytes) and his CD8 lymphocyte count was 2,266 cells/mm 3 (56.8% of the total lymphocytes). Chagas’ disease serologic test results were positive (indirect hemagglutina- tion titer  1:160 and indirect immunofluorescence titer = 1:160), and serologic results were negative for IgM antibod- ies to T. cruzi. Trypanosoma cruzi parasitemia was detected by xenodiagnosis and the proportion of positive bugs (64.1%) showed high parasitemia. However, at this time the blood cultures for T. cruzi (using 1 ml of blood on liver infusion tryptose medium) and the direct microscopic ex- amination for trypomastigote forms of the parasite in the blood were negative. An endomyocardial biopsy was per- formed. The histologic examination of the endomyocardial fragments demonstrated a severe confluent lymphocytic in-