PURPOSE: To describe the presentation and clinical course of septic shock due to Toxoplasma gondii in patients infected with the human immunodeficiency virus (HIV). PATIENTS AND METHODS: From April 1988 to February 1992, nine HIV-infected patients were admitted because of predominant septic shock (7 patients) or developed septic shock in the ICU (2 patients). The recent CD4+ cell count ranged from 2 to 84 x 10(6)/L. RESULTS: The main clinical features were (1) a history of fever for longer than 15 days, with a recent increase to more than 39.5 degrees C; (2) a recent history of dyspnea (< 15 days, 8 cases; < 7 days, 3 cases); and (3) recent onset of thrombocytopenia (6 of 9 cases). All patients were in shock (hyperkinetic profile in 6 of 7; hypokinetic in 1 of 7), and 8 of 9 were in respiratory distress (ratio of PaO2 over fractional concentration of oxygen in the inspired gas of 117 +/- 23; range, 88 to 155). Chest roentgenograms revealed diffuse alveolar infiltrates in six of nine cases. The serum lactate dehydrogenase (LDH) activity was 6,510 +/- 5,080 IU/L (range, 1,010 to 15,450 IU/L). Serologic tests for T gondii were negative in two cases. Toxoplasma gondii was isolated from lung (9/9), bone marrow (5/7), or blood (2/2). One, 3, and 2 patients had brain, ocular, and myocardial involvement, respectively. No other microbial pathogens were isolated. Seven patients died, 5 less than 3 days after admission. CONCLUSION: Disseminated toxoplasmosis can cause septic shock in HIV-infected patients. In two cases, the disease was probably a primary infection. The association of high fever, acute dyspnea, recent onset of thrombocytopenia, and a very high level of LDH activity is suggestive of disseminated toxoplasmosis.
PURPOSE: To describe the presentation and clinical course of septic shock due to Toxoplasma gondii in patients infected with the human immunodeficiency virus (HIV). PATIENTS AND METHODS: From April 1988 to February 1992, nine HIV-infectedpatients were admitted because of predominant septic shock (7 patients) or developed septic shock in the ICU (2 patients). The recent CD4+ cell count ranged from 2 to 84 x 10(6)/L. RESULTS: The main clinical features were (1) a history of fever for longer than 15 days, with a recent increase to more than 39.5 degrees C; (2) a recent history of dyspnea (< 15 days, 8 cases; < 7 days, 3 cases); and (3) recent onset of thrombocytopenia (6 of 9 cases). All patients were in shock (hyperkinetic profile in 6 of 7; hypokinetic in 1 of 7), and 8 of 9 were in respiratory distress (ratio of PaO2 over fractional concentration of oxygen in the inspired gas of 117 +/- 23; range, 88 to 155). Chest roentgenograms revealed diffuse alveolar infiltrates in six of nine cases. The serum lactate dehydrogenase (LDH) activity was 6,510 +/- 5,080 IU/L (range, 1,010 to 15,450 IU/L). Serologic tests for T gondii were negative in two cases. Toxoplasma gondii was isolated from lung (9/9), bone marrow (5/7), or blood (2/2). One, 3, and 2 patients had brain, ocular, and myocardial involvement, respectively. No other microbial pathogens were isolated. Seven patients died, 5 less than 3 days after admission. CONCLUSION: Disseminated toxoplasmosis can cause septic shock in HIV-infectedpatients. In two cases, the disease was probably a primary infection. The association of high fever, acute dyspnea, recent onset of thrombocytopenia, and a very high level of LDH activity is suggestive of disseminated toxoplasmosis.
Authors: Ricardo Garcia Pastorello; Anderson da Costa Lino Costa; Marcio Valente Yamada Sawamura; Antonio Carlos Nicodemo; Amaro Nunes Duarte-Neto Journal: Autops Case Rep Date: 2018-03-16