Purpose: To describe the presentation and clinical course of septic stroke due to Toxoplasma gondii in patients infected with the human immunodeficiency virus (HIV).


Purpose: To describe the presentation and clinical course of septic stroke 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 impact (7 patients) or developed septic clash in the ICU (2 patients). The novel CD4 + cell count ranged from 2 to 84 x [10sup6]/L

Results: The main clinical features were (1) a history of febrile disease for longer than 15 days, with a fresh increase to more than 395 [degrees] C; (2) a latter history of dyspnea ([less than] 15 days, 8 cases; [les than] 7 days, 3 cases); and (3) novel onset of thrombocytopenia (6 of 9 cases). All patients were in clash (hyperkinetic profile in 6 of 7; hypokinetic in 1 of 7) and 8 of 9 were in respiratory distress (ratio of [PaO.sub.2] across fractional concentration of oxygen in the inspired gas of 117 [+ or -] 23; range, 88 to 155) Chest roentgenograms revealed diffuse alveolar infiltrates in six of nine cases. The serum lactate dehydrogenase (LDH) activity was 6510 [+ or -] 5080 IU/L (range, 1010 to 15450 IU/L). Serologic ordeals for T gondii were negative in sum of two units cases. Toxoplasma gondii was isolated from lung (9/9) bone marrow (5/7) or family (2/2). One, 3, and 2 patients had brain, ocular, and myocardial involvement, respectively. No other microbial pathogens were isolated. Seven patients died, 5 les than 3 days after admission.

Conclusion: Disseminated toxoplasmosis can cause septic stroke in HIV-infected patients. In pair cases, the disease was probably a primary infection. The association of high febrile affection acute dyspnea, recent onset of thrombocytopenia, and a real high level of LDH activity is suggestive of disseminated toxoplasmosis.



Toxoplasma gondii encephalitis is the chiefly common neurologic disease in patients infected according to the human immunodeficiency virus (HIV).[1,2] It is more common in Europe than in North America, possibly because of differences in dietary habits.[1] Extraneurologic forms of toxoplasmosis are rare in this setting and generally involve the lungs[3-5] We observ 9 cases of disseminated toxoplasmosis with septic percussion in HIV-infected patients over a 4-year period and herein report the history, presentation, clinical and laboratory findings, and outcome

MATERIALS AND METHODS

Between April 1988 and February 1992 there were 515 HIV-infected patients admitted to the ICU of the Bichat-Claude Bernard Hospital, Paris, France. Eighty-six had a diagnosis of isolated toxoplasmic encephalitis. Nine had a diagnosis of shock[6] appropriate to disseminated toxoplasmosis, with or without the adult respiratory distress syndrome (ARDS).[7] common of these cases has been reported elsewhere.[5]

Septic clash was defined according to fresh criteria as follows: sepsis-induced hypotension, with systolic life-blood pressure lower than 90 mm Hg despite adequate fluid resuscitation, along with the vicinity of hypoperfusion abnormalities or organ dysfunction.[6] The ARDS corresponded to strait-laced lung injury, evaluated with the following three components: size of roentgenographic densities; gas exchange abnormalities; and value of positive end-expiratory pressure[7]

Toxoplasmosis was diagnosed through the detection of free trophozoites in the bronchoalveolar lavage (BAL) or bone marrow aspirate through direct examination with May-Grunwald-Giemsa (MGG) staining.[8,9] Toxoplasma gondii was also descryed in the blood by monocyte culture[1011] Specific IgG and IgM antibodies were ascertained by means of an enzyme-linked immunoabsorbent assay (ELISA) means with a cutoff of 10 IU/L. Samples with negative ensues in the ELISA were further examined in the Sabin-Feldman stain test and by means of a sensitive agglutination assay.[12]

The following parameters were noted: risk factors for HIV infection; HIV-related opportunistic infections and malignant neoplasms; ongoing treatment at admission; clinical and laboratory findings; hemodynamic parameters; respiratory status; and issue The results are given as means [+ or -] SD

RESULTS

History

The nine patients (Table 1) comprised five homosexual men and four women in whom the risk factors were physic abuse in three and unidentified in united Eight of the 9 patients had AIDS at the time of the diagnosis of toxoplasmosis, and the mean absolute CD4+ small room count was 29 [+ or -] 28 x [10sup6]/L Eight patients had previously disentangleed an opportunistic infection or malignant neoplasm. Seven patients were receiving prophylactic therapy against Pneumocystis carinii pneumonia (PCP) and four were receiving zidovudine. None was receiving anti-Toxoplasma prophylaxis. Six patients had serologic markers of prior T gondii infection; the other three had negative serologic experiments on admission or during the month prior to admission and also several month previously (7 14 and 18 months) pair of these three patients also had negative arises on the Sabin-Feldman dye example and the sensitive agglutination assay.

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