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Agar Dilution Method (agar + dilution_method)
Selected AbstractsComposition and antimicrobial activity of the volatile oil of Artemisia kopetdaghensis Krasch., M.Pop.FLAVOUR AND FRAGRANCE JOURNAL, Issue 6 2006& Linecz ex Poljak from Iran Abstract Artemisia kopetdaghensis Krasch., M.Pop. & Linecz ex Poljak (Asteraceae) is a common perennial herb growing wild in north-eastern parts of Iran. The essential oil of A. kopetdaghensis was isolated by hydrodistillation in 2.14% (v/w) yield. The chemical composition of the essential oil was examined by GC and GC,MS. Thirty-three compounds were identified, representing 86.8% of the total oil. The major constituents were methyleugenol (24.4%), geranial (13.6%), davanone (11.1%), camphor (9.8%) and neral (7.4%). Minimum inhibitory concentration was determined, using the agar dilution method, against eight bacteria and two fungal strains. The essential oil showed a moderate antimicrobial activity. Copyright © 2006 John Wiley & Sons, Ltd. [source] The Bifidogenic Growth Stimulator Inhibits the Growth and Respiration of Helicobacter pyloriHELICOBACTER, Issue 5 2010Kumiko Nagata Abstract Background:, Triple therapy with amoxicillin, clarithromycin, and a proton-pump inhibitor is a common therapeutic strategy for the eradication of Helicobacter pylori (H. pylori). However, frequent appearance of clarithromycin-resistant strains is a therapeutic challenge. While various quinones are known to specifically inhibit the growth of H. pylori, the quinone 1,4-dihydroxy-2-naphthoic acid (DHNA) produced by Propionibacterium has strong stimulating effect on Bifidobacterium. We were interested to see whether DHNA could inhibit the growth of H. pylori in in vitro or in vivo experimental setting. Materials and Methods:, The minimum inhibitory concentration (MIC) of DHNA was determined by the agar dilution method. The inhibitory action of DHNA on the respiratory activity was measured by using an oxygen electrode. Germ-free mice infected with H. pylori were given DHNA in free drinking water containing 100 ,g/mL for 7 days. Results:, DHNA inhibited H. pylori growth at low MIC values, 1.6,3.2 ,g/mL. Likewise, DHNA inhibited clinical isolates of H. pylori, resistant to clarithromycin. However, DHNA did not inhibit other Gram negative or anaerobic bacteria in the normal flora of the human intestine. Both H. pylori cellular respiration and adenosine 5,-triphosphate (ATP) generation were dose-dependently inhibited by DHNA. Similarly, the culture filtrates of propionibacterial strains inhibited the growth of H. pylori, and oral administration of DHNA could eradicate H. pylori in the infected germ-free mice. Conclusions:, The bifidogenic growth stimulator DHNA specifically inhibited the growth of H. pylori including clarithromycin-resistant strains in vitro and its colonization activity in vivo. The bactericidal activity of DHNA was via inhibition of cellular respiration. These actions of DHNA may have clinical relevance in the eradication of H. pylori. [source] The HOMER Study: The Effect of Increasing the Dose of Metronidazole When Given with Omeprazole and Amoxicillin to Cure Helicobacter pylori InfectionHELICOBACTER, Issue 4 2000Karna Dev Bardhan Background.Helicobacter pylori eradication with omeprazole, amoxycillin, and metronidazole is both effective and inexpensive. However, eradication rates with different dosages and dosing vary, and data on the impact of resistance are sparse. In this study, three different dosages of omeprazole, amoxycillin, and metronidazole were compared, and the influence of metronidazole resistance on eradication was assessed. Methods. Patients (n = 394) with a positive H. pylori screening test result and endoscopy-proven duodenal ulcer in the past were enrolled into a multicenter study performed in four European countries and Canada. After baseline endoscopy, patients were randomly assigned to treatment for 1 week with either omeprazole, 20 mg twice daily, plus amoxycillin, 1,000 mg twice daily, plus metronidazole, 400 mg twice daily (low M); or omeprazole, 40 mg once daily, plus amoxycillin, 500 mg three times daily, plus metronidazole, 400 mg three times daily (medium M); or omeprazole, 20 mg twice daily, plus amoxycillin, 1,000 mg twice daily, plus metronidazole, 800 mg twice daily (high M). H. pylori status at entry was assessed by a 13C urea breath test and a culture. Eradication was defined as two negative 13C-urea breath test results 4 and 8 weeks after therapy. Susceptibility testing using the agar dilution method was performed at entry and in patients with persistent infection after therapy. Results. The eradication rates, in terms of intention to treat (ITT) (population n = 379) (and 95% confidence interval [CI]) were as follows: low M 76% (68%, 84%), medium M 76% (68%, 84%), and high M 83% (75%, 89%). By per-protocol analysis (population n = 348), the corresponding eradication rates were: low M 81%, medium M 80%, and high M 85%. No H. pylori strains were found to be resistant to amoxycillin. Prestudy resistance of H. pylori strains to metronidazole was found in 72 of 348 (21%) of the cultures at entry (range, 10%,39% in the five countries). The overall eradication rate in prestudy metronidazole-susceptible strains was 232 of 266 (87%) and, for resistant strains, it was 41 of 70 (57%; p < .001). Within each group, the results were as follows (susceptible/resistant): low M, 85%/54%; medium M, 86%/50%; and high M, 90%/75%. There were no statistically significant differences among the treatment groups. 23 strains susceptible to metronidazole before treatment were recultured after therapy failed; 20 of these had now developed resistance. Conclusions.H. pylori eradication rates were similar (approximately 80%) with all three regimens. Metronidazole resistance reduced efficacy; increasing the dose of metronidazole appeared not to overcome the problem or significantly improve the outcome. Treatment failure was generally associated with either prestudy or acquired metronidazole resistance. These findings are of importance when attempting H. pylori eradication in communities with high levels of metronidazole resistance. [source] Inhibitory effects of aspirin and indometacin on the growth of Helicobacter pylori in vitroJOURNAL OF DIGESTIVE DISEASES, Issue 4 2002Wei Hong WANG OBJECTIVE: The interactions between non-steroidal anti-inflammatory drugs and Helicobacter pylori have not been sufficiently documented to date. The aim of this study was to investigate the possible effects of aspirin and indometacin on the growth of H. pylori and to determine the effects of aspirin on the susceptibility of H. pylori to some antimicrobials. METHODS: Kinetic studies were performed by inoculating strains of H. pylori in brucella broth with different concentrations of aspirin and indometacin. Growth of bacteria in the broth was assessed spectrophotometrically and by viable colony counts after incubation for 24 and 48 h. Bacterial morphology was determined by Gram stain under light microscopy. The minimal inhibitory concentration (MIC) of aspirin and indometacin was determined by the standard agar dilution method. The MIC of amoxicillin, clarithromycin and metronidazole was measured in the presence and absence of aspirin by the E -test method. RESULTS: Kinetic studies revealed that aspirin and indometacin inhibited the growth of H. pylori in a dose-dependent manner. The bactericidal activity of these agents was expressed by cell lysis. Aspirin at 400 µg/mL produced an almost 2-log decrease in the number of CFU/mL at 48 h. Similar inhibitory effects were obtained when 100 µg/mL indometacin was tested. The MIC at which 90% of H. pylori was inhibited was 512 µg/mL and 128 µg/mL for aspirin and indometacin, respectively. Increased susceptibility of H. pylori to amoxicillin, clarithromycin and metronidazole was found in the presence of aspirin. CONCLUSIONS: Aspirin and indometacin could significantly inhibit the growth of H. pylori when incubated in brucella broth in vitro. A subinhibitory concentration of aspirin enhanced the susceptibility of H. pylori to some antimicrobial agents. [source] Furazolidone-based triple ,rescue therapy' vs. quadruple ,rescue therapy' for the eradication of Helicobacter pylori resistant to metronidazole,ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2002V. Isakov Summary Background : The optimal treatment of patients with Helicobacter pylori resistant to metronidazole has not been established. Aim : To compare the efficacy of quadruple and furazolidone-based triple therapy in the eradication of H. pylori resistant to metronidazole. Methods : Duodenal ulcer patients (n = 70) in whom initial eradication therapy failed and who harboured H. pylori strains resistant to metronidazole were randomized to receive one of the following 7-day regimens: colloidal bismuth subcitrate, 240 mg, tetracycline, 750 mg, and furazolidone, 200 mg, each given twice daily (BTF), or omeprazole, 20 mg b.d., colloidal bismuth subcitrate, 240 mg b.d., tetracycline, 500 mg q.d.s., and metronidazole, 500 mg b.d. (OBTM). H.pylori status was assessed by culture, histology and rapid urease test before treatment and 4,6 weeks after therapy. Susceptibility to metronidazole was assessed by the agar dilution method. Results : H. pylori eradication rates with intention-to-treat/per protocol analyses were: BTF, 85.7%/90.9%; OBTM, 74.2%/89.6%. Duodenal ulcers were healed in nine of 10 (90%) patients in the BTF group and in all patients (12/12) (100%) in the OBTM group (P = N.S.). A significantly lower rate of adverse events was observed in the BTF group than in the OBTM group (31.4% vs. 60%, P = 0.03), but there was no difference in terms of discontinuation of treatment (2/35 vs. 6/35, P = N.S.). Conclusions : The 1-week BTF regimen was as effective as the OBTM regimen, and produced less adverse events. Thus, it may be used in patients in whom resistance of H. pylori to metronidazole is suspected. [source] ORIGINAL ARTICLE: In vitro and in vivo effects of the Mongolian drug Amu-ru 7 on Helicobacter pylori growth and viabilityMICROBIOLOGY AND IMMUNOLOGY, Issue 9 2010Cui Lan Bai ABSTRACT Amu-ru 7, a Mongolian folk medicine, is used to treat digestive diseases such as gastritis and gastric and duodenal ulcers. We examined the effect of Amu-ru 7 on the growth and viability of Helicobacter pylori in vivo and in vitro. By the agar dilution method, the MIC of Amu-ru 7 for H. pylori strains was shown to be 100,200 ,g/mL with a MIC90 of 200 ,g/mL. Two hundred micrograms per milliliter of Amu-ru 7 exhibited potent bactericidal activity against H. pylori in the stationary phase of growth 6 hr after treatment. Amu-ru 7 inhibited the growth of both AMPC-resistant and CAM-resistant strains, and also had a combined effect with AMPC on AMPC-resistant strain 403. The Amu-ru 7 inhibited biofilm formation by H. pylori and induced morphological changes, such as bleb-like formation and shortening of the cell. Although colonization of the stomach of the Mongolian gerbil by H. pylori was not cured by treatment with Amu-ru 7, both the mean number of H. pylori colonized and the colonization rate were decreased in Amu-ru 7 treated gerbils. These results suggest the effectiveness Amu-ru 7 as an adjunct therapy for eradication therapies consisting of a PPI combined with antibiotics. [source] Evaluation of the VITEK 2 cards for identification and antimicrobial susceptibility testing of non-glucose-fermenting Gram-negative bacilliAPMIS, Issue 4 2009WEN-SHYANG HSIEH We evaluated VITEK 2 cards (NGNC and AST-GN10) for the accuracy of identification (ID) and antimicrobial susceptibility testing (AST) of non-glucose-fermenting Gram-negative bacilli (NGF-GNB). In a total of 201 strains, 190 strains (94.5%) were correctly identified, seven strains (3.5%) showed low discrimination, four strains (2.0%) had discrepancies, and no strain remained unidentified. Reference AST of amikacin, aztreonam, cefepime, cefotaxime, ceftazidime, ciprofloxacin, imipenem, levofloxacin, piperacillin-tazobactam, and trimethoprim-sulfamethoxazole was performed by the agar dilution method. Approximately 82.5% of ID and 72.9% of AST were completed within 7 and 14 h, respectively. For NGF-GNB, other than Pseudomonas aeruginosa, Acinetobacter spp., Stenotrophomonas maltophilia, and the Burkholderia cepacia group, essential agreements (EAs) were 93.6,100.0%. Severe disagreements (resistant by the reference method to susceptible by AST-GN10) were observed for amikacin (0.9%), cefepime (1.8%), cefotaxime (1.8%), imipenem (0.9%), and piperacillin-tazobactam (0.9%). One major disagreement (susceptible to resistant) was observed for ceftazidime (0.1%). For P. aeruginosa, EAs were 85.7,100%, with severe disagreements observed for cefepime (4.8%) and piperacillin-tazobactam (4.8%). For Acinetobacter spp., EAs were 86.4,100% without disagreements. The VITEK 2 cards appear to be promising for rapid ID and reliable AST for most species of NGF-GNB. [source] Enhancement of Vancomycin Activity by Phenothiazines against Vancomycin-Resistant Enterococcus Faecium in vitroBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2010Mohammad Rahbar Minimum inhibitory concentrations (MIC) of the compounds were determined by agar dilution method, and synergy between phenothiazines and vancomycin was investigated using Checkerboard (microbroth dilution) technique. We found that all enterococci strains, regardless of their susceptibility to vancomycin, were inhibited by phenothiazines at concentrations varying from 8 to 256 ,g/ml, with thiethylperazine being the most potent inhibitory agent. Besides, all the phenothiazines showed partial synergy with vancomycin and could lessen MIC of vancomycin from 512 to 8 ,g/ml at their sub-inhibitory concentrations. The highest reduction in MIC was observed with chlorpromazine (32 times); however, thiethylperazine and promethazine stood next (24 times). Although resistance modification was observed at concentrations higher than those that phenothiazines reach in vivo, the potential offered by non-antibiotics justify further animal experiments as well as clinical trials to establish their clinical relevance. [source] In vitro susceptibility of the seven Malassezia species to ketoconazole, voriconazole, itraconazole and terbinafineBRITISH JOURNAL OF DERMATOLOGY, Issue 4 2000A.K. Gupta Fifty-five strains, either authentic or ex-type, of seven Malassezia species were investigated for in vitro susceptibility to various concentrations (0·03,64·0 µg/mL) of three azole drugs, ketoconazole, voriconazole and itraconazole, as well as the allylamine terbinafine, using the agar dilution method. All strains of the seven Malassezia species were susceptible to the three azole drugs at low concentrations. M. furfur, M. sympodialis, M. slooffiae, M. pachydermatis, M. globosa, M. obtusa and M. restricta were most sensitive to ketoconazole and itraconazole, with minimum inhibitory concentrations (MICs) ranging from , 0·03 to 0·125 ,g/mL. The recently introduced antifungal, voriconazole, was also very effective, with MIC80 values , 0·03 ,g/mL for 80% of strains. MICs of terbinafine against the seven Malassezia species ranged from , 0·03 to 64·0 ,g/mL. There were variations in susceptibility of the seven Malassezia species to ketoconazole, voriconazole, itraconazole and terbinafine. Strains of M. furfur, M. globosa and M. obtusa were more tolerant to terbinafine than the remaining Malassezia species; M. sympodialis was highly susceptible. M. furfur strains tested with terbinafine ranged from highly susceptible to relatively resistant. Correct identification of Malassezia species could facilitate selection of appropriate antifungal therapy. [source] Activity of telithromycin and seven other agents against 1034 pediatric Streptococcus pneumoniae isolates from ten central and eastern European centersCLINICAL MICROBIOLOGY AND INFECTION, Issue 7 2003B. Bozdogan Objective, To test the activity of telithromycin against 1034 Streptococcus pneumoniae isolates from pediatric patients in ten centers from ten central and eastern European countries during 2000,2001, and to compare it with the activities of erythromycin A, azithromycin, clarithromycin, clindamycin, and quinupristin,dalfopristin. Methods, The minimum inhibitory concentrations (MICs) of telithromycin, erythromycin A, azithromycin, clarithromycin, clindamycin, levofloxacin, quinupristin,dalfopristin and penicillin G were tested by the agar dilution method with incubation in air, and mechanisms of resistance to macrolides and quinolones were investigated. Results, Strains were isolated from sputum, tracheal aspirates, ear, eye, blood, and cerebrospinal fluid. Among S. pneumoniae strains tested, 36% had raised penicillin G MICs (, 0.12 mg/L). Susceptibilities were as follows: telithromycin, quinupristin,dalfopristin and levofloxacin, , 99%; clindamycin, 83%; and erythromycin A, azithromycin and clarithromycin, 78%. Of 230 (22.3%) erythromycin A-resistant S. pneumoniae strains, 176 (79.6%) had erm(B), 38 (16.1%) had mef(A), and 10 (4.3%) had mutations in 23S ribosomal RNA or in ribosomal protein L4. The rates of drug-resistant S. pneumoniae are high in all centers except Kaunas, Riga, and Prague. Conclusion, Telithromycin had low MICs against all strains, irrespective of macrolide, azalide or clindamycin resistance. Ribosomal methylation was the most prevalent resistance mechanism among all resistant strains, except in Sofia, where the prevalence of the efflux mechanism was higher. [source] Comparison of the E test to the reference agar dilution method for antibiotic susceptibility testing of Clostridium difficileCLINICAL MICROBIOLOGY AND INFECTION, Issue 3 2000I. Poilane [source] | ||||||||||