Molecular structure of trimethoprimTetrahydrofolate synthesis pathway
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Trimethoprim

Trimethoprim is a bacteriostatic antibiotic mainly used in the prophylaxis and treatment of urinary tract infections (cystitis). It belongs to the class of chemotherapeutic agents known as dihydrofolate reductase inhibitors. Trimethoprim was formerly marketed by GlaxoWellcome under trade names including Proloprim®, Monotrim® and Triprim®; but these trade names have been licensed to various generic pharmaceutical manufacturers. more...

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Mechanism of action

Trimethoprim acts by interfering with the action of bacterial dihydrofolate reductase, inhibiting synthesis of tetrahydrofolic acid. Folic acid is an essential precursor in the de novo synthesis of the DNA nucleosides thymidine and uridine. Bacteria are unable to take up folic acid from the environment (i.e. the infection host) thus are dependent on their own de novo synthesis - inhibition of the enzyme starves the bacteria of two bases necessary for DNA replication and transcription.

Co-trimoxazole

Trimethoprim is commonly used in combination with sulfamethoxazole, a sulfonamide antibiotic, which inhibits the an earlier step in the folate synthesis pathway (see diagram above). This combination, known as co-trimoxazole, results in a synergistic antibacterial effect by inhibiting successive steps in folate synthesis. Its use has been declining due to reports of sulfamethoxazole bone marrow toxicity.

Clinical indications

Trimethoprim, used as monotherapy, is indicated for the prophylaxis and treatment of urinary tract infections (cystitis). Co-trimoxazole, owing to its greater efficacy, is indicated for a wider range of infections. For example, it is used as prophylaxis in patients at risk for Pneumocystis jiroveci pneumonia (e.g. AIDS patients and those with some hematological malignancies), as therapy in Whipple's disease and certain other infections.

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POST - ANTIFUNGAL EFFECT OF AZOLES AND SULFAMETHOXAZOLE-TRIMETHOPRIM IN EXPERIMENTAL PARACOCCIDIOIDOMYCOSIS
From Revista do Instituto de Medicina Tropical de Sao Paulo, 10/1/05 by Lourenço, D S

Lourenço, D. S.1; Vitali, L. H.2; Afonso, A. O.3; Malta, M. H. B.4; Martinez, R.5

1,3,4 Faculdade de Medicina de Ribeirão Preto - USP - Clínica Médico; 25 FMRP-USP - Internal Medicine

Introduction - The dugs prescribed for treatment of paracoccidioidomycosis are frequently interrupted by patients with poor socioeconomic level or alcoholics. In this study, the efficacy and post-antifungal effect of ketoconazole, fluconazole, itraconazole and sulfamethoxazole-trimethoprim was tested comparatively against experimental infection of female Wistar rats with Paracoccidioides brasiliensis. Methods - The animals were treated for one to four weeks by gavage with 4 to 16mg/Kg of ketoconazole (K), 4 to 16mg/Kg of fluconazole (F), 2 to 8mg/Kg of itraconazole (I), and 10 to 100mg/Kg weight/day of sulfamethoxazole-trimethoprim (ST). Results - Itraconazole and fluconazole were more effective in reducing the fungal burden in respect to control group. The amount of yeast in the lungs was reduced 24, 45, 661, and 4 times, respectively, for K, I, F and ST. In the spleen the reduction of fungal burden obtained with the same drugs was. 2, 2, 5 and 2 times, respectively. The survival 61 day after inoculation of P. brasiliensis was 27% for untreated animals and 27%, 67%. 82%. and 17% for the rats treated with K, F, I, and ST, respectively. The post-antifungal effect on the animals that received 6 or 12 doses of the drugs, followed three weeks of interruption of treatment, showed that K, in the lung, and F, in the spleen, provided greater inhibition of the return of fungal multiplication. Discussion- It is concluded, for the model and experimental design used, that itraconazole and fluconazole had a stronger action, immediate and post-treatment, on the control of infection with P. brasilienxis. Financial support: FAEPA Foundation, Hospital das Clinicas da FMRP-USP.

Copyright Instituto de Medicina Tropical de Sao Paulo Oct 2005
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