In a randomized trial, a 4-day quinine-clindamycin regimen was compared with the standard 7-day quinine regimen for 100 Gabonese children (50 children in each group) with severe Plasmodium falciparum malaria. In each group, only one patient died. Parasite clearance and fever clearance times were significantly shorter in the quinine-clindamycin group (P ؍ 0.03 and P ؍ 0.01, respectively) than in the quinine group, and significantly more recurring fever episodes occurred in the quinine group than in the quinine-clindamycin group shortly after initial fever clearance and parasite clearance (P < 0.001).
Alveolar echinococcosis (AE) is a rare and often fatal disease characterized by a tumorlike expansion of the metacestode Echinococcus multilocularis in the liver. Because of the severe side effects of therapy with benzimidazoles, we treated a patient with recombinant interferon gamma at a dose of 250 microg over a 3-day period once a month. Disease progression was not detected during the observed period of 18 months. Following stimulation with crude Echinococcus antigen, mRNA from interleukin 5 was still detected in peripheral blood mononuclear cells by means of reverse transcriptase polymerase chain reaction analysis, and expression of interleukin 10 in T lymphocytes (as measured by fluorescence-associated cell sorting of intracellular cytokines) was elevated. These results indicate that bolus therapy with interferon gamma has some clinical effect but does not result in a change in the T helper 2 lymphocyte-dominated immune response to this parasite.
The sensitivity of Plasmodium falciparum to chloroquine, mefloquine, quinine, quinidine, halofantrine, artemisinin, and sulfadoxine/pyrimethamine was investigated in Lambarene, Gabon in 1994. The development of in vitro susceptibility has been traced from 1983 or 1992 to 1994 for chloroquine, mefloquine, halofantrine, and quinine. Standard in vitro microtests according to World Health Organization methodology were performed. Of 33 isolates tested for susceptibility to chloroquine, 31 were resistant, one was borderline, and one isolate was sensitive (mean 50% effective concentration [EC 50 ] ϭ 1.38 mol/L of blood). With mefloquine, all isolates were fully inhibited below the threshold of resistance (mean EC 50 ϭ 0.51 mol/L of blood). Of 32 isolates tested with quinine, six had borderline resistance (mean EC 50 ϭ 0.54 mol/L of blood medium mixture). Susceptibility to quinidine was higher with a mean EC 50 of 0.15 mol/L of blood medium mixture. With halofantrine, 26 of 32 isolates matured at 3 nmol/L of blood medium mixture (mean EC 50 ϭ 1.64 nmol/L of blood medium mixture), indicating a steep decrease in susceptibility in comparison with 1992. For artemisinin, the mean EC 50 was 97.92 nmol/L of blood medium mixture. Sulfadoxine/ pyrimethamine showed five of 16 resistant isolates with a mean EC 50 of 2.46 nmol/L of blood medium mixture. Whereas chloroquine resistance remained stable with a tendency to decrease, susceptibility to mefloquine and quinine was slightly decreased. A significant increase in the mean EC 50 and EC 90 in comparison with our previous data from Gabon was found for halofantrine.
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