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At least 19 recordsLinked to original sources
PubMed1978

Trimethoprim-sulfamethoxazole vs sulfamethoxazole for acute urinary tract infections in children.

A total of 118 children between 6 months and 10 years of age with acute urinary tract infection were treated in a random; double-blind manner with 12 mg/kg/day of trimethoprim-sulfamethoxazole (61 patients) or 50 mg/kg/day of sulfamethoxazole (57 patients) for ten days. Mean trimethoprim and sulfamethoxazole susceptibilities of Escherichia coli isolated from these patients were 1.2 and 0.6 microgram/ml, respectively. Mean serum concentrations of trimethoprim and sulfamethoxazole were 1.8 and 62 microgram/ml, respectively, one hour after the dose. Of the children who completed the ten days of prescribed medication, clinical and bacteriological cure was confirmed immediately after treatment for all but one patient in each group. Most patients in each treatment group with recurrent infections had underlying urological abnormalities. Severe hematological, renal, or hepatic toxicity requiring interruption of treatment was not encountered. No advantage of trimethoprim-sulfamethoxazole over sulfamethoxazole alone for acute urinary tract infection was demonstrated.

Acute Disease↗
PubMed2026

Genome-wide identification of conditionally essential genes for growth in the presence of sulfamethoxazole and trimethoprim in sulfamethoxazole- and trimethoprim-resistant Escherichia coli.

UNLABELLED: Resistance to sulfonamides (SULs) and trimethoprim (TMP) in Escherichia coli threatens their clinical relevance. Beyond known resistance mechanisms, little is understood about the cellular responses that enable resistant E. coli to grow under these antibiotic stresses. This study aimed to identify genes that support bacterial growth under SUL and TMP stress. Two saturated transposon mutant libraries were constructed in resistant E. coli MG1655 harboring either dfrA1 or sul2. They were grown with and without 1/2 and 1/4 minimum inhibitory concentration (MIC) of sulfamethoxazole (SMX) or TMP, and mutant depletion was assessed via transposon-directed insertion-site sequencing. At 1/2 MIC, 36 and 89 genes were identified as conditionally essential during SMX and TMP exposure, while 5 and 2 genes were classified as conditionally essential at 1/4 MIC. Genes identified as conditionally essential at 1/4 MIC were also important at 1/2 MIC. Conditionally essential genes belonged to lipopolysaccharide biosynthesis, peptidoglycan metabolism, energy production, membrane integrity, phosphate metabolism, and stress responses, highlighting the role of these factors in maintaining cell stability under SMX and TMP stress. Validation with 10 conditionally essential genes (apaH, mtn, surA, waaO, nlpI, prc, wzxE, fadR, degP, and tpiA) showed that deletion mutants indeed exhibited growth defects and two- to eightfold reductions in MIC under antibiotic stresses compared to their parent strains. This study highlights cellular responses to SMX and TMP under antibiotic stress, and it has identified a list of genes whose products may serve as potential helper drug targets to resensitize resistant E. coli to SMX and TMP treatments. IMPORTANCE: Sulfonamides (SULs) and trimethoprim (TMP) are broad-spectrum antimicrobials. They are commonly used to treat infections in both humans and animals. Resistance against SUL and TMP is widespread in pathogenic bacteria, and there is a need to overcome this problem. One possibility is to target the cellular mechanism by which the resistant bacteria adapt to growth in the presence of the antimicrobials. In this study, we identify the genes, besides the resistance genes, which enable resistant Escherichia coli to grow in the presence of SUL and TMP. We further show that knocking out many of these genes attenuates the resistant E. coli for growth during SUL and/or TMP stress, irrespective of which SUL- or TMP-resistant gene the bacteria carry. The gene products of these genes may serve as potential helper drug targets to resensitize resistant E. coli to sulfamethoxazole and TMP treatments.

Escherichia coli↗
PubMed1975

Comparison of trimethoprim-sulfamethoxazole with sulfamethoxazole in urinary tract infections of children.

The effect of trimethorpim-sulfamethoxazole was compared with that of sulfamethoxazole alone in 26 children with urinary tract infection, randomly assigned according to a double-blind procedure to two equally sized groups. TMX-SMX was found to be superior in rendering the urine culture negative for the 3 months after the start of treatment. Also, over 12-month follow-up period there were fewer recurrences in the patients who received TMP-SMX but here the difference between the two groups did not reach statistical significance.

Administration, Oral↗
PubMed1975

A comparison of trimethorprim-sulfamethoxazole with sulfamethoxazole alone in infections localized to the kidneys.

Ninety patients with urinary tract infections were treated in a randomized double-blind study with either a combination of trimethoprim and sulfamethoxazole (TMP-SMX) or sulfamethoxazole alone (SMX). Thirty of 42 patients treated with TMP-SMX were cured by the time of follow-up compared with 26 of 48 treated with SMX alone. Of the 29 patients infected with SMX-resistent organisms, the combination TMP-SMX cured 12 of 17, whereas SMX alone cured 2 of 12. Of the 61 patients infected with SMX-sensitive organisms, TMP-SMX cured 18 of 25; SMX alone cured 24 of 36. In 50 women the infection was found localized to The upper urinary tract by the use of the Fairley bladder washout technique. TMPsmx cured 16 or 24 of these patients with proved upper tract infections and SMX alone cured 11 of 26. Although none of these differences were significant, TMP-SMX appears to be an effective drug combination for the therapy of proved upper tract infection and is also effective in eradicating sulfonamide-resistant organisms.

Administration, Oral↗
PubMed1978

In vitro susceptibility of Haemophilus influenzae to sulfamethoxazole-trimethoprim and cefaclor, cephalexin, and cephradine.

Sulfamethoxazole-trimethoprim and three oral cephalosporins, cefaclor, cephalexin, and cephradine, were evaluated in vitro as possible alternatives to chloramphenicol in the treatment of non-central nervous system infections due to ampicillin-resistant Haemophilus influenzae. Sixty-four isolates of H. influenzae, including 31 beta-lactamase-positive strains, were tested by the agar dilution method. All strains were inhibited by 0.78/0.039 mug sulfamethoxazole-trimethoprim per ml and by 0.78 mug of chloramphenicol per ml. At 6.25 mug/ml, 100, 11, and 3% of all strains were inhibited by cefaclor, cephalexin, and cephradine, respectively. Thus, on the basis of drug concentrations presumably achievable in serum, 100% of strains were susceptible to sulfamethoxazole-trimethoprim, chloramphenicol, and cefaclor. However, a considerable inoculum effect was noted with both beta-lactamase-positive and -negative strains, when tested with sulfamethoxazole-trimethoprim; the minimal inhibitory concentrations of cefaclor were only slightly affected. Also, synergistic effects of sulfamethoxazole-trimethoprim, sulfamethoxazole-erythromycin, and sulfamethoxazole-cefaclor were seen when combinations were tested against both beta-lactamase-positive and -negative strains, as determined by minimal inhibitory concentrations measured by the broth dilution method and by killing curve analyses. These results support further evaluation of these combinations and of cefaclor alone for the treatment of non-central nervous system infections due to H. influenzae.

Cephalosporins↗
PubMed1979

Comparison of sulfamethoxazole alone and combined with trimethoprim in urinary tract infections.

In a double blind, randomized study, sulfamethoxazole was compared alone and in combination with trimethoprim as commonly used in therapeutic regimes for the treatment of uncomplicated acute urinary tract infections in out-patients. The cure of sulfamethoxazole alone was 92.2%, and for sulfamethoxazole plus trimethoprim 97.6%. The rate of side-effects for the former was 5%, for the latter 21.8%. If the failure rate plus the rate of occurrence of rash, which necessitated discontinuing the drug, are combined, it appears that 8.8% of the patients were at a disadvantage receiving sulfamethoxazole compared to 9.7% for the combination of sulfamethoxazole plus trimethoprim. When considering the cure rate and rate of side-effects together, therefore, the position of sulfamethoxazole alone as a suitable drug in this type of infection is defended.

Adult↗
PubMed1979

Rapid assay for determination of trimethoprim and sulfamethoxazole levels in serum by spectrofluorometry.

A rapid spectrofluorometric method for determining the levels of both trimethoprim and sulfamethoxazole from the same specimen of serum is described. The method involves stepwise extraction of the specimen first with chloroform at an alkaline pH (pH 9.0) for trimethoprim followed by n-butyl chloride at an acidic pH (pH 2.0) for sulfamethoxazole. To quantitate trimethoprim, the chloroform layer was subjected to fluorometry by exciting the specimen at 295 nm and measuring the relative intensity at 330 nm. To determine sulfamethoxazole levels, the n-butyl chloride layer was subjected to fluorometry by exciting the specimen at 285 nm and measuring the relative intensity at 330 nm. Relative intensities were linear (r greater than 0.99) over the concentration ranges of 0.5 to 40 microgram/ml for trimethoprim and 1 to 400 microgram/ml for sulfamethoxazole. Values obtained by this spectrofluorometric procedure were in excellent agreement with those obtained by a conventional fluorometric assay for trimethoprim and a colorimetric assay for sulfamethoxazole. Elevated levels of endogenous metabolic products and numerous other drugs, including a number of antimicrobial agents, did not interfere with the method. Although salicylates interfere with the determination of sulfamethoxazole, an appropriate correction can be made. This method can also be used to determine the drug levels in cerebrospinal fluid.

Humans↗
PubMed1978

Therapy of gonorrhea. Comparison of trimethoprim-sulfamethoxazole and ampicillin.

Eighty-nine men with gonococcal urethritis were randomly treated with trimethoprim-sulfamethoxazole, four tablets (trimethoprin, 320 mg, and sulfamethoxazole, 1,600 mg) twice daily for two days, or ampicillin, 3.5 g, plus probenecid, 1 g, in a single dose. Forty-one (95.3%) of 43 patients who received trimethoprin-sulfamethosazole and 41 (97.6%) of 42 given ampicillin were cured. Neither drug caused major side effects. All isolates of Neisseria gonorrhoeae were susceptible in vitro to trimethoprim-sulfame-thoxazole, and all but one were inhibited by ampicillin. The ampicillin-resistant strain (minimum inhibitory concentration, 4 micrograms/ml) produced penicillinase and was reovered from a patient who responded to treatment with trimethoprim-sulfamethoxazole. There was no significant correlation between the minimum inhibitory concentrations of trimethoprim-sulfamethoxazole and ampicillin. It is concluded that trimethoprim-sulfamethoxazole is as efficacious and safe as ampicillin in the therapy of gonococcal urethritis.

Ampicillin↗
PubMed1975

Comparison of trimethoprim-sulfamethoxazole and amoxicillin in therapy of chloramphenicol-resistant and chloramphenicol-sensitive typhoid fever.

The efficacy of orally administered trimethoprim-sulfamethoxazole was compared with that of oral amoxicillin in therapy of typhoid fever due to both epidemic chloramphenicol-resistant and endemic chloramphenicol-sensitive Salmonella typhi. Both drug regimens were effective and of comparable value in treatment of chloramphenicol-resistant infections, as measured by duration of fever (124 hr and 115 hr, respectively) and duration of bacteremia (1.0 and 0.4 days, respectively). Trimethoprim-sulfamethoxazole therapy of infections due to chloramphenicol-sensitive S. typhi resulted in more rapid lysis of fever than did amoxicillin therapy. Trimethoprim and sulfamethoxazole were not synergistic in vitro against the chloramphenicol-resistant strain of S. typhi, and the role of sulfamethoxazole in treatment of such infections appears to be minimal. Oral administration of trimethoprim-sulfamethoxazole is effective therapy of chloramphenicol-resistant, and probably of ampicillin-amoxicillin-resistant, typhoid fever.

Adolescent↗
PubMed1979

Limited effect of trimethoprim-sulfamethoxazole prophylaxis on Pneumocystis carinii.

Trimethoprim-sulfamethoxazole has been proven effective in the treatment and prevention of Pneumocystis carinii pneumonitis in lower animals and humans. How effective the drug combination is in eradicating P. carinii from the host is not known. The immunosuppressed rat model was used to determine whether or not trimethoprim-sulfamethoxazole effectively eradicated the organism. Animals treated with trimethoprim-sulfamethoxazole for as long as 6 weeks were then placed in individual isolator cages, immunosuppressed with prednisone for 12 weeks, and sacrificed. P. carinii was found in the lungs of at least 90% of the drug-treated as well as untreated control groups. The data indicate that trimethoprim-sulfamethoxazole has a limited rather than a lethal effect on P. carinii and that protection is afforded only during the period of trimethoprim-sulfamethoxazole administration.

Animals↗
PubMed1979

Drug therapy reviews: trimethoprim-sulfamethoxazole.

The mechanism of action, antimicrobial spectrum, pharmacokinetic properties, drug interactions, adverse reactions and therapeutic uses of trimethoprim-sulfamethoxazole, a combination enzyme-specific inhibitor of bacterial folate synthesis, are reviewed. Trimethoprim-sulfamethoxazole currently is approved by the FDA for the therapy of established recurrent bacterial urinary tract infections, pneumocystosis, otitis media in children and shigellosis. Claimed advantages of the drug are synergistic activity, bactericidal activity and ability to decrease the rate of emergence of resistance to the individual components. Trimethoprim-sulfamethoxazole is the drug of choice for treatment of pneumocystosis and an acceptable oral therapy for recurrent urinary tract infections caused by susceptible bacteria. In children with otitis media, it is used as an alternative to ampicillin and amoxicillin and is preferred when these patients are penicillin-sensitive or when the infection is caused by beta-lactamase-producing Haemophilus influenzae. Hematologic reactions (anemia, thrombocytopenia, granulocytopenia, agranulocytosis) to trimethoprim-sulfamethoxazole occur rarely. Gastrointestinal intolerance and skin eruptions are the most prevalent adverse reactions. Most untoward reactions to trimethoprim-sulfamethoxazole develop within two weeks of onset of therapy, and their incidence compares favorably with that of standard agents administered for the same indications.

Acute Disease↗
PubMed1976

Trimethoprim-sulfamethoxazole therapy for shigellosis.

Twenty-eight infants and children hospitalized for severe shigellosis were treated orally either with ampicillin trihydrate (100 mg/kg/day administered in divided doses every six hours) or with trimethoprim-sulfamethoxazole (trimethoprim, 10 mg; sulfamethoxazole, 50 mg/kg/day in divided doses every 12 hours) for five days. Four patients with ampicillin-resistant shigellae continued to have diarrhea and positive stool cultures during therapy. Patients with susceptible shigellae treated with ampicillin and all patients treated with trimethoprim-sulfamethoxazole responsed promptly and comparably within an average of 1.6 and 1.7 days, respectively, until stool cultures were negative, and 3.1 and 2.9 days, respectively, until diarrhea stopped. Patients with ampicillin-resistant shigellae responded to treatment with trimethoprim-sulfamethoxazole. It is concluded that trimethoprim-sulfamethoxazole is the best currently available drug for treatment of shigellosis in areas where multiple antibiotic resistance of shigellae is common.

Age Factors↗
PubMed1979

[Sulfamethoxazole concentration in the homogenate of the human embryo].

The investigations on the extent of placental drug transfer has conventionally been based on determining drug concentration in cord blood at delivery. There is, however, data that levels in cord blood at delivery may provide misleading information on the extent of drug transfer in utero. It is due to the fact that not every drug reaches the fetus in pharmacologically active form. Hence, the evaluation of placental drug transfer requires determination of free drug concentration in fetal tissues. Seven women with indications for interruption of pregnancy for social reasons have taken Biseptol 480--Polfa (400 mg sulfamethoxazole and 80 mg trimethoprim) for 4-5 days before the operation. Each woman received 1,92 g of drug (4 tablets) a day in two divided doses. In the tissues obtained during abortion, the concentration of sulfamethoxazole was estimated by the modified method of Bratton and Marchall . The obtained results show that in the first trimester of gestation sulfamethoxazole crosses human placental barrier; it is detectable in embryo in a great amount. This fact indicates that administration of Biseptol to the pregnant mother may be harmful for the embryo. Our investigations have not permitted yet on for the statement that there is the correlation between the sulfamethoxazole concentration and week of gestation during the first trimester.

Biological Transport↗
PubMed1976

Prostatic tissue and fluid concentrations of trimethoprim and sulfamethoxazole: experimental and clinical studies.

The concentrations of trimethoprim and sulfamethoxazole were determined in prostatic fluid and tissue of the dog after constant intravenous infusion. Concentrations of trimethoprim in both prostatic fluid and tissue exceeded the simultaneous serum concentrations, whereas the sulfamethoxazole prostatic fluid and tissue concentrations were much lower than the simultaneous serum concentrations. Prostatic tissue obtained from patients undergoing transurethral resection of the prostate also contained trimethoprim in higher but sulfamethoxazole in lower concentrations than the simultaneous serum concentrations after oral administration of these drugs preoperatively. In a patient with urinary diversion, trimethoprim was found in prostatic fluid in concentrations as high as forty-four times the simultaneous serum concentrations whereas sulfamethoxazole was found in concentrations representing only a fraction of the simultaneous serum concentrations. These findings lend support to the use of trimethoprim in the treatment of bacterial prostatitis.

Animals↗
PubMed1977

Prophylactic efficacy of nitrofurantoin macrocrystals and trimethoprim-sulfamethoxazole in urinary infections. Biologic effects on the vaginal and rectal flora.

We examined bacterial persistence and resistance in the vaginal and fecal flora of 28 women who received a total of 253 months of daily low-dosage prophylaxis with nitrofurantoin macrocystals (100 mg per day) or trimethoprim-sulfamethoxazole (40 and 200 mg respectively). During trimethoprim-sulfamehtoxazole prophylaxis, 8.5% of monthly vaginal and 27% of monthly fecal cultures grew Escherichia coli, as compared to 36 and 96%, respectively for nitrofurantoin macrocrystals. Esch. coli resistant to nitrofurantoin occurred in two of 95 fecal cultures during therapy, and Esch. coli resistant to trimethoprim-sulfamethoxazole in 16 of 182 (8.8%) fecal cultures. In the 12 months before treatment, 92 episodes of recurrent urinary infection occurred, as compared to six during treatment (none occurred on trimethoprim-sulfamethoxazole). These results confirm the value of trimethoprim-sulfamethoxazole prophylaxis for high-risk patient with recurrent urinary infections. Prophylaxis with nitrofurantoin macrocrystals seems adequate for less severe problems of reinfection.

Adult↗
PubMed1978

Combination of pentamidine and trimethoprim-sulfamethoxazole in therapy of Pneumocystis carinii pneumonia in rats.

Treatment with either pentamidine isethionate or trimethoprim-sulfamethoxazole significantly reduces the mortality of Pneumocystis carinii pneumonia. It is not known whether a combination might act in an additive, synergistic, or antagonistic manner. We studied the interaction of these two agents in the steroid-conditioned rat model of pneumocystosis. Of animals receiving pentamidine alone, 48% died and 45% had P. carinii cysts at autopsy. Trimethoprim-sulfamethoxazole alone resulted in 21% mortality, and cysts were found in 28%. Both agents in full doses resulted in 45% deaths and cysts in 37%. Animals treated with half-dosages of pentamidine plus trimethroprim-sulfamethoxazole had mortality of 35%, and 21% had cysts. Trimethoprim alone, in two dosages, was ineffective in eradicating P. carinii cysts. The data suggest that combination therapy is no more effective than trimethoprim-sulfamethoxazole alone in the treatment of P. carinii pneumonia.

Amidines↗
PubMed1979

Racemic warfarin and trimethoprim-sulfamethoxazole interaction in humans.

Eleven normal humans were studied to evaluate the reported interaction of racemic sodium warfarin and trimethoprim-sulfamethoxazole prospectively. Single oral doses of racemic warfarin, 1.5 mg/kg of body weight, were administered with and without 320 mg of trimethoprim and 1600 mg of sulfamethoxazole orally, beginning 7 d before the warfarin and continuing daily throughout the hypoprothrombinemia. Daily plasma samples were analyzed for one-stage prothrombin activity (Quick) and for warfarin content by high-pressure liquid chromatography. Transient cutaneous reactions developed in four of 11 subjects: a morbilliform rash in three (studies discontinued) and generalized pruritus in one. A highly significant augmentation of the warfarin effect on the mean one-stage prothrombin activity (P less than 0.03) occurred with trimethoprim-sulfamethoxazole, but no significant effect was found on the warfarin half-life (P greater than 0.5). It is concluded that trimethoprim-sulfamethoxazole interacts with racemic warfarin, possibly at a receptor-site locus.

Adult↗
PubMed1975

Effect of trimethoprim-sulfamethoxazole on the renal excretion of creatinine in man.

Treatment with the chemotherapeutic combination of 160 mg. trimethoprim plus 800 mg. sulfamethoxazole twice daily increased the serum creatinine level by an average of 2 mg. per 1. in 21 patients. The effect was clearly reversible. The chemical analysis of creatinine was not affected by the addition of trimethoprim, sulfamethoxazole or their metabolites. In 2 subjects given the drug combination for 12 days renal excretion and 24-hour clearances of creatinine decreased but iothalamate 131I clearance was unchanged. Consequently, the rise in serum creatinine does not indicate any decrease in the glomerular filtration rate. The serum creatinine started to rise within 4 hours after oral administration of a single dose. The rise in serum creatinine could be produced with trimethoprim alone but not with sulfamethoxazole alone. When the plasma creatinine was raised to 100 mg. per l. in healthy subjects (by giving creatinine orally), trimethoprim increased the creatinine levels 10 times as much as at normal plasma levels. The effect was interpreted as a competitive inhibition of the mechanism for tubular secretion of creatinine through the base-secreting pathway.

Creatinine↗