Immunologic and biochemical alterations in severe falciparum malaria: relation to neurological symptoms and outcome.

The relation between the immune response and the clinical features of severe falciparum malaria was studied in Burundian adults with (n = 31) and without (n = 17) cerebral involvement. At the time of admission, mean values for age, temperature, and blood levels of hemoglobin, creatinine, bilirubin, and glucose were similar in the two groups. Plasma levels of tumor necrosis factor alpha, interferon gamma, interleukin 10 (IL-10), and soluble intercellular adhesion molecule 1 were similarly elevated in the two groups. Mean parasite counts and mean plasma levels of soluble E-selectin were higher in severe noncerebral malaria than in cerebral malaria and were correlated with each other. After adjustment for parasitemia, levels of soluble E-selectin remained higher in noncerebral malaria. All seven patients who died had cerebral disease. These patients had higher levels of creatinine, bilirubin, IL-10, and soluble E-selectin than did patients with nonfatal cerebral malaria. After adjustment for creatinine and bilirubin levels, IL-10 and soluble E-selectin concentrations were similar in fatal and nonfatal cases of cerebral infection. In these African adults, none of the immunologic variables investigated was specific to cerebral malaria or to a fatal outcome.

Prognostic indicators in adult cerebral malaria: a study in Burundi, an area of high prevalence of HIV infection.

We examined the possible risk factors for poor prognostic in cerebral malaria in 31 adults from Burundi, an area of high prevalence rate of HIV-1 infection. Depth of coma, temperature, vomiting, seizures, parasite load, or anaemia did not modify the outcome. High levels of creatinine, bilirubin, and/or lactates were indicators of poor prognostic. HIV-1 infection did not affect the clinical or biological presentation of cerebral malaria, and did not appear to influence the outcome.

PIP: This article reports the findings of a study conducted to identify the relationship between HIV infection and cerebral malaria in Burundi. Study subjects were selected from hospital patients diagnosed with cerebral malaria. The Glasgow scale was used for unconscious patients as a measurement for admission into this study. Parasite density was determined with Giemsa-stained thick blood smears. HIV-1 testing was done by enzyme-linked immunosorbent assay (ELISA) techniques and positives were confirmed by Western blot. All patients received 10 mg of quinine per kg of body weight as an initial dose by intravenous infusion. This regimen was followed by a daily dose of 25 mg/kg body weight via intravenous infusion. If after 2 days the patient could take treatment orally, it was switched. This treatment regimen lasted 5-7 days total. Statistical analysis was performed using the Mann-Whitney U test, the Fisher exact test, and the Chi-square test. Of the 31 study patients, 22 were male and 9 were female. 7 (22.6%) died within the first 96 hours. The surviving 24 patients had a mean coma recovery time of 33.7 +or- 25.8 hours. No neurological damage was noted. The mean Glasgow score was 8.3 +or- 2.7 for the whole group of 31 patients. The mean malaria parasitemia was 11,920 (95% CI: 643-221,018) parasites/mcl of blood. Plasma levels of creatinine were higher in fatal cases than in patients who survived (307.2 +or- 261.8 mcmol/L vs. 135.1 +or- 55.3 mcmol/L). Of the 31 patients, 12 (38.7%) had antibodies to HIV-1. No relationship between positive HIV-1 and cerebral malaria was found, and no patient showed any clinical symptoms of acquired immunodeficiency syndrome.