We conducted a prospective, randomized study to compare the efficacy of oral fusidic acid, oral metronidazole, oral vancomycin, and oral teicoplanin for the treatment of Clostridium difficile-associated diarrhea. Treatment resulted in clinical cure for 94% of the patients who were treated with vancomycin, 96% of those treated with teicoplanin, 93% of those treated with fusidic acid, and 94% of those treated with metronidazole. Clinical symptoms recurred in 16% of patients treated with vancomycin, 7% of those treated with teicoplanin, 28% of those treated with fusidic acid, and 16% of those treated with metronidazole. There was asymptomatic carriage of C. difficile toxin in 13% of patients treated with vancomycin, 4% of those treated with teicoplanin, 24% of those treated with fusidic acid, and 16% of those treated with metronidazole. No adverse effects related to therapy with vancomycin or teicoplanin were observed. Considering the costs of treatment, our findings suggest that metronidazole is the drug of choice for C. difficile-associated diarrhea and that glycopeptides should be reserved for patients who cannot tolerate metronidazole or who do not respond to treatment with this drug.

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Apart from cellular immunity and immunopathology, various cytokines have been implicated in malaria-associated immunosuppression. In this study, serum levels of transforming growth factor-beta (TGF-beta) were determined with an enzyme-linked immunosorbent assay in 37 patients with acute Plasmodium falciparum malaria prior to, during, and after therapy and in 17 healthy controls in Bangkok, Thailand. Patients were treated with artesunate and mefloquine. TGF-beta serum levels were found decreased prior to treatment (14 +/- 11 pg/ml versus 63 +/- 15 pg/ml in healthy controls; P < 0.05). The serum concentrations of TGF-beta increased after initiation of treatment and were within normal range on day 21. Serum levels of both tumor necrosis factor-alpha (TNF-alpha) and soluble TNF-receptor 55 kDa were inversely correlated to serum levels of TGF-beta (r = -0.667 and r = -0.592, n = 37; respectively, P < 0.05 for both). No correlation between parasitemia and serum levels of TGF-beta could be found. The results are compatible with a decreased production and release, an enhanced clearance or utilization, or tissue accumulation of TGF-beta in acute P. falciparum malaria.