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At least 19 recordsLinked to original sources
PubMed2002

[Growth of rifampin-dependent Mycobacterium tuberculosis in conditions without rifampin].

OBJECTIVE: To study the growth of rifampin-dependent Mycobacterium tuberculosis in conditions without rifampin. METHODS: A typical rifampin-dependent strain was identified and a single colony growing in the optimal concentration of rifampin was selected and inoculated (10(-4) mg/ml) to L-J and 12B liquid media, cultured at 37 degrees C. The bacterial growth and characteristics were studied. RESULTS: In the L-J medium containing rifampin, bacterial growth was observed in two weeks, but in the medium without rifampin tiny colonies were not observed until three weeks. In the 12B media with and without rifampin, bacterial growth was evident on day 9 and day 13 respectively. Thick and larger colonies and cauliflower-like growth were observed in media containing rifampin, but smaller colonies and fried egg-like growth were observed in media without rifampin. Microscopic study showed thick and heavily stained bacteria in media containing rifampin, but small and lightly stained bacteria in media without rifampin. Transmission electron microscopy demonstrated that bacteria growing in the presence of rifampin had complete cell walls, but those growing in the absence of rifampin had abnormal cell walls. CONCLUSION: Rifampin-dependent Mycobacterium tuberculosis may be changed into bacterial L-forms in media without rifampin.

Antibiotics, Antitubercular↗
PubMed1980

Treatment of experimental staphylococcal infections: effect of rifampin alone and in combination on development of rifampin resistance.

Rifampin is a potentially useful anti-staphylococcal agent, but resistance develops frequently when the drug is used alone. The efficacy of rifampin, trimethoprim, and a penicillin alone or in combination was examined in mice with acute or subacute infections. Mice were infected intraperitoneally with penicillin-susceptible Staphylococcus aureus. Survival after penicillin therapy was only 9.1% in contrast to survival after rifampin therapy which was 68% (P less than 0.001). No rifampin-resistant S. aureus were isolated from peritoneal fluid or heart blood samples from dead animals in these short-term experiments. Rifampin was ineffective (survival, 4.8%) for infections instituted with rifampin-resistant strains. Long-term experiments were conducted after intravenous injection of 4 x 10(8) S. aureus. Forty percent of the animals survived after methicillin therapy; 77% survived after rifampin therapy (P less than 0.001). However, 40% of those animals that died after rifampin therapy died with rifampin-resistant organisms. No animal dying in groups treated with a combination of rifampin and trimethoprim (85% survival) or rifampin and methicillin (79% survival) died with rifampin-resistant organisms. Thus, rifampin combined with a penicillin or trimethoprim was effective in preventing the development of rifampin-resistant strains.

Acute Disease↗
PubMed1993

Quinolones in treatment of human brucellosis: comparative trial of ofloxacin-rifampin versus doxycycline-rifampin.

Quinolones have been reported to be active against Brucella species in vitro. In this prospective randomized study, the efficacy and safety of the combination of ofloxacin plus rifampin were compared with the efficacy and safety of doxycycline plus rifampin, both combinations administered for a 6-week period in treatment of brucellosis. Sixty-one patients were enrolled in the study, and 49 had blood or bone marrow cultures positive for Brucella melitensis. Thirty patients received 200 mg of doxycycline plus 600 mg of rifampin once daily, and 31 patients were treated with 400 mg of ofloxacin plus 600 mg of rifampin once daily for 6 weeks. Nine patients in each group had complications of the disease. There was one therapeutic failure in the ofloxacin-rifampin treatment group, and one patient from each group relapsed (3.3% of those in the doxycycline-rifampin treatment group versus 3.2% of those in the ofloxacin-rifampin treatment group). Gastric discomfort was the major side effect observed in 13 patients (43.3%) who received doxycycline plus rifampin, whereas only 2 patients (6.5%) treated with ofloxacin plus rifampin complained of gastric irritation. These results suggest that the combination of ofloxacin plus rifampin administered for 6 weeks is as effective as doxycycline plus rifampin given for the same period, regardless of the presence of complications of the disease.

Adolescent↗
PubMed1991

Rifampin resistance of Legionella pneumophila is not increased during therapy for experimental Legionnaires disease: study of rifampin resistance using a guinea pig model of Legionnaires disease.

Isolates of Legionella pneumophila serogroup 1, obtained from guinea pigs with experimentally induced Legionnaires disease, were tested for rifampin resistance. Thirteen isolates were from animals treated with rifampin alone, four isolates were from animals treated with saline, and three isolates each were from animals treated with erythromycin or erythromycin plus rifampin; all of these isolates were derived from the same parent strain, F889. Most of the isolates were obtained from rifampin-treated animals that survived infection but had persistence of bacteria in their lungs at necropsy. No differences in rifampin agar dilution MICs were detected for the 23 isolates and parent strain that were tested. None of the 13 isolates from animals treated with rifampin alone had a high number of resistant organisms detected by using a rifampin gradient plate assay. Thirteen isolates plus the parent strain were tested by using a quantitative method of determining resistance frequency. Considerable heterogeneity among isolates was observed, but there was no evidence of increased resistance for any treatment group. The range of rifampin resistance frequencies was 10(-7) to 10(-8). No evidence for rifampin-induced resistance of L. pneumophila was found in this study.

Animals↗
PubMed2005

Relapse and acquired rifampin resistance in HIV-infected patients with tuberculosis treated with rifampin- or rifabutin-based regimens in New York City, 1997-2000.

BACKGROUND: The relationship between rifamycin use and either relapse or treatment failure with acquired rifampin resistance (ARR) among human immunodeficiency virus (HIV)-infected patients with tuberculosis (TB) is not well understood. METHODS: We conducted a retrospective cohort study of HIV-infected and HIV-uninfected persons with rifampin-susceptible TB, (1) to compare relapse rates, ARR, and treatment failure, according to HIV serostatus; and (2) to examine whether and how use of rifamycin was associated with clinical outcomes of interest among HIV-infected patients with TB. RESULTS: HIV-infected patients were more likely to have ARR than were HIV-uninfected patients (0.9% vs. 0.1%; P = .007), and the association remained significant in multivariate analysis (adjusted odds ratio [OR], 5.5; 95% confidence interval [CI], 1.4-21.5). Among HIV-infected patients with TB, none of 57 patients treated with rifabutin-based regimens alone had ARR, and only 1 of 395 patients treated with rifabutin given in combination with a rifampin-based regimen had ARR, whereas 6 of 355 patients treated with a rifampin-based regimen alone had relapse and ARR. HIV-infected patients treated with rifampin-based regimens alone had a higher risk for relapse and development of rifampin resistance if intermittent dosing of rifampin was started during the intensive phase of treatment, compared with patients who did not receive intermittent dosing (hazard ratio [HR] for relapse, 6.7 [95% CI, 1.1-40.1]; HR for ARR, 6.4 [95% CI, 1.1-38.4]). This association remained when confined to patients with a CD4+ T lymphocyte count of < 100 lymphocytes/mm3. Intermittent dosing started only after the intensive phase of treatment did not increase the risks of relapse and ARR among HIV-infected patients with TB. CONCLUSION: The risk for ARR among HIV-infected persons with TB did not depend on the rifamycin used but, rather, on the rifampin dosing schedule in the intensive phase of treatment.

AIDS-Related Opportunistic Infections↗
PubMed1985

Prosthetic valve endocarditis caused by Staphylococcus epidermidis. Development of rifampin resistance during vancomycin and rifampin therapy.

Development of rifampin-resistant Staphylococcus epidermidis was documented in three patients receiving vancomycin and rifampin therapy for prosthetic valve endocarditis. The minimum inhibitory concentrations and minimum bactericidal concentrations of rifampin for the original three isolates were 0.4 micrograms/mL or less. Organisms cultured during relapse or prosthetic valve replacement had minimum inhibitory concentrations of rifampin that were 12.5, 50, and greater than 100 micrograms/mL, respectively. Surgical intervention was necessary in all patients. One died, and one required a second prosthetic valve placement. The patients were treated with vancomycin plus aminoglycoside following identification of rifampin resistance. These observations suggest that vancomycin and rifampin may not be adequate therapy for prosthetic valve endocarditis caused by S epidermidis.

Drug Resistance, Microbial↗
PubMed2000

Trials of daily, long-term minocycline and rifampin or clarithromycin and rifampin in the treatment of borderline lepromatous and lepromatous leprosy.

Daily, long-term treatment with minocycline 100 mg and rifampin 600 mg was initiated in 24 previously untreated borderline lepromatous (BL) and lepromatous (LL) patients for a total of 646 patient-months, averaging 26.9 months per patient. The same regimen was started in 12 BL and LL patients having a bacteriologic relapse for a total of 379 patient-months, averaging 32.5 months per patient, and in 12 patients judged to be at high risk for relapse for a total of 354 patient-months, averaging 29.5 months per patient. Daily, long-term treatment with clarithromycin 500 mg and rifampin 600 mg was initiated in 8 previously untreated BL and LL patients for a total of 174 patient-months, averaging 21.8 months per patient. The results in these 56 patients were compared to those obtained in 34 previously untreated BL and LL patients who were treated concurrently receiving daily, long-term dapsone 100 mg and rifampin 600 mg. No evidence of dangerous drug reactions or bone marrow, kidney or liver toxicity was seen in any of these five patient groups. Drug intolerance in 10 of the 90 patients studied necessitated discontinuing the chosen regimen, 4 from rifampin, 3 from dapsone, 2 from minocycline and 1 of undetermined attribution. The use of either minocycline or clarithromycin in conjunction with rifampin appears to pose no great risk when used long term.

Anti-Bacterial Agents↗
PubMed2006

Comparison between doxycycline-rifampin-amikacin and doxycycline-rifampin regimens in the treatment of brucellosis.

BACKGROUND: Combination drug therapy of brucellosis leads to recovery of symptoms, shortening of symptomatic interval, and decrease in morbidity rate, but single drug therapy is associated with more relapse episodes and a higher rate of drug resistance. Different drug combinations have been evaluated in the treatment of brucellosis. Considering the failure of treatment and relatively high rate of relapse of the disease with the World Health Organization's (WHO) recommended therapeutic regimen, we evaluated a new regimen that we assumed would increase the success of treatment and decrease the rate of relapse. In this study we compare the standard regimen of the WHO, doxycycline-rifampin (DR), to triple therapy with doxycycline-rifampin-amikacin (ADR). METHODS: Two hundred and twenty-eight consecutive patients with brucellosis, who attended Hamedan Sina Hospital between 1999 and 2001, whether seen as outpatients or as inpatients, were enrolled in the study. The participants were randomly allocated to the DR group (receiving doxycycline 100 mg twice a day and rifampin 10 mg/kg body weight/day every morning, both taken orally for eight weeks) or the ADR group (receiving doxycycline 100 mg twice a day and rifampin 10 mg/kg body weight/day every morning, both taken orally for eight weeks, plus 7.5 mg/kg amikacin intramuscularly twice a day for seven days). The patients were checked for the relief of symptoms, drug side-effects, and relapse of disease during the treatment and follow-up. RESULTS: Of the 228 patients enrolled, eight were withdrawn - four patients from the DR group and four from the ADR group. Of the remaining 220 participants (110 in the ADR group and 110 in the DR group), 107 were male (48.6%) and 113 were female (51.4%). Mean age was 35.7+/-17 years in the ADR group and 37+/-18.4 years in the DR group (p=0.5). In the DR group, 97 (88.2%) and in the ADR group, 106 (96.4%) of the patients had relief of symptoms (a significant difference by Chi-square test (p=0.04)). After completion of treatment, and at the sixth month follow-up, nine (9.3%) patients in the DR group and six (5.7%) in the ADR group experienced a relapse of the disease, with no significant difference (p=0.4). Mild side-effects were found in only 10 patients, and none required discontinuation of the therapeutic regimen. Of these patients, four were from DR group and six from ADR group; no significant difference was observed (p=0.7). CONCLUSIONS: Given the fact that the ADR regimen had a higher efficacy and more rapid action in terms of relief of symptoms compared to the DR regimen, and that no significant difference in drug side-effects and disease relapse existed in the patients of either group, adding amikacin to the DR standard treatment regimen seems beneficial.

Adolescent↗
PubMed1996

Comparative antimycobacterial activities of rifampin, rifapentine, and KRM-1648 against a collection of rifampin-resistant Mycobacterium tuberculosis isolates with known rpoB mutations.

A collection of 24 rifampin-resistant clinical isolates of Mycobacterium tuberculosis with characterized RNA polymerase beta-subunit (rpoB) gene mutations was tested against the antimycobacterial agents rifampin, rifapentine, and KRM-1648 to correlate levels of resistance with specific rpoB genotypes. The results indicate that KRM-1648 is more active in vitro than rifampin and rifapentine, and its ability to overcome rifampin resistance in strains with four different genetic alterations may prove to be useful in understanding structure-function relationships.

Antibiotics, Antitubercular↗
PubMed2005

Different rifampin sensitivities of Escherichia coli and Mycobacterium tuberculosis RNA polymerases are not explained by the difference in the beta-subunit rifampin regions I and II.

Mycobacterium tuberculosis RNA polymerase is 1,000-fold more sensitive to rifampin than Escherichia coli RNA polymerase. Chimeric E. coli RNA polymerase in which the beta-subunit segment encompassing rifampin regions I and II (amino acids [aa] 463 through 590) was replaced with the corresponding region from M. tuberculosis (aa 382 through 509) did not show an increased sensitivity to the antibiotic. Thus, the difference in amino acid sequence between the rifampin regions I and II of the two species does not account for the difference in rifampin sensitivity of the two polymerases.

Amino Acid Sequence↗
PubMed1986

Rifampin-induced release of hydrazine from isoniazid. A possible cause of hepatitis during treatment of tuberculosis with regimens containing isoniazid and rifampin.

The effect of daily administration of rifampin on the direct conversion of isoniazid to isonicotinic acid and hydrazine by isoniazid hydrolase was investigated in 6 slow and 8 rapid acetylators of isoniazid. The proportion of isoniazid metabolized through this direct pathway during the first 6 h was estimated from the ratio of total isonicotinic acid formed to acetylisoniazid in urine after administration of isoniazid or acetylisoniazid. In slow acetylators, this proportion was approximately 3% when isoniazid alone was administered and approximately 6% during the maximal phase of induction caused by the daily administration of rifampin in addition to isoniazid (p less than 0.001); in rapid acetylators, the proportions were considerably less (less than 1 and 2.5%, respectively), suggesting that isoniazid hydrolase was induced by rifampin. The increased formation of hydrazine, a known hepatotoxic agent in animals, could explain the substantially higher frequency of the occurrence of hepatitis in slow than in rapid acetylators among tuberculous patients treated with daily rifampin and isoniazid.

Acetylation↗
PubMed1985

Penicillin V and rifampin for the treatment of group A streptococcal pharyngitis: a randomized trial of 10 days penicillin vs 10 days penicillin with rifampin during the final 4 days of therapy.

To improve the bacteriologic and clinical cure rates of streptococcal pharyngitis, 79 children were randomly assigned to receive penicillin V alone for 10 days (39 patients) or penicillin for the same duration and rifampin during the last 4 days of penicillin therapy (40 patients). Eleven patients given penicillin had evidence of bacteriologic failure (including eight with relapse of clinical illness) on repeat cultures done 4 to 7 days after treatment, whereas there were no failures in children given combination therapy (P = 0.0015). All eight symptomatic children improved with penicillin-rifampin therapy and subsequent cultures were negative, whereas three asymptomatic children continued to harbor group A streptococci even after combination therapy. Antibody response by antistreptolysin O or antideoxyribonuclease B assay was seen in 50.6% of patients; the antibody responses in both groups were comparable. These results show that addition of rifampin to the penicillin regimen improves the clinical and bacteriologic cure rates in children with streptococcal pharyngitis.

Adolescent↗
PubMed2003

Detection of nucleotide variability in rpoB in both rifampin-sensitive and rifampin-resistant strains of Chlamydia trachomatis.

A 656-bp PCR fragment from rpoB was sequenced from five rifampin-resistant Chlamydia trachomatis variants selected in vitro from a wild-type parent with a surprising level of genetic variability in this region. Three variants (MIC, 4 microg/ml) showed Ala522-->Val in cluster I (codons 507 to 533), which harbors mutations in most rifampin-resistant bacteria. Two high-level resistance variants (MICs, 64 and 256 microg/ml) showed His526-->Tyr in cluster I with additional genetic variation, some of which resulted in amino acid substitutions. None of the latter was situated in clusters related to rifampin resistance in other bacteria.

Antibiotics, Antitubercular↗
PubMed2006

Curing Mycobacterium ulcerans infection in mice with a combination of rifampin-streptomycin or rifampin-amikacin.

The curing activities of various durations of treatment with a combination of rifampin (RIF) and either streptomycin (STR) or amikacin (AMK) in murine Mycobacterium ulcerans infection were compared in two experiments. In the first experiment, treatment was begun 1 week after infection, when the inflammatory footpad lesion had not yet occurred (preventive model), and in the second experiment, treatment was begun 6 weeks after infection, when inflammatory footpad lesions were established (curative model). In the first experiment, 4 weeks of treatment with daily RIF-STR or RIF-AMK was able to postpone the occurrence of footpad lesion by 12 weeks (RIF-STR) or 17 weeks (RIF-AMK), thus demonstrating their promising bactericidal activities, but neither treatment was able to prevent the late occurrence of footpad lesions. In the second experiment, the overall cure rates, as assessed by the lack of rebound of inflammatory lesions or remultiplication of M. ulcerans, were only 62% after 2 weeks of treatment with RIF and an aminoglycoside and 85% after 4 weeks; but the cure rate reached 100% after 8 or 12 weeks of treatment. The cure rates were slightly higher with the AMK-containing combination than with the STR-containing combination, but the difference was at the limit of significance (P=0.07). These results show that in the murine model of Buruli ulcer, 8 weeks is the optimal duration of treatment with a combination of RIF and an aminoglycoside.

Amikacin↗
PubMed2003

Rapid detection of rifampin resistance in Mycobacterium tuberculosis isolates by heteroduplex analysis and determination of rifamycin cross-resistance in rifampin-resistant isolates.

Direct heteroduplex analysis and a universal heteroduplex generator assay were performed to detect rifampin resistance rapidly in Turkish Mycobacterium tuberculosis isolates. Cross-resistance to rifapentine, rifabutin, and rifalazil was investigated. A relationship between specific mutations and resistance patterns, which can guide the choice of an appropriate therapeutic regimen for tuberculosis patients, was identified.

Antibiotics, Antitubercular↗