Journal articles: 'Rifampicin‐resistant Mutants'

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Al- Khafaji, K. A., and A. N. Al- Thwami. "Identification of differences in virulence factors production from mutant isolates of clinical Vibrio cholerae S." Journal of Biotechnology Research Center 5, no. 1 (January 1, 2011): 61–73. http://dx.doi.org/10.24126/jobrc.2011.5.1.149.

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Antibiotic resistant mutants for rifampicin, streptomycin and klindamycin were isolated from the clinical isolate of Vibrio choleraeS mutated by chemical mutagens. Mutation frequency of V. cholerae S depends on the treatment time and the highest viable count of antibiotic resistant were for Rifampicin after treatment with Acridine orange, Ethedium bromide, Nitrosoguanidine, 5-Florouracil, 2-Bromouracil and cyclophosphamide. One thousand mutant isolates were examined for morphological differences in colony surface, color and diameter. The treatment with AO, NTG, 5-FU, and 2-BU gave opaque to orange color larger diameter about 5-7 mm of Rifampicin resistant mutant isolates at TSA and 25% of these mutant appeared as wrinkled surface. Klindamycin resistant mutants of V. cholerae S were appeared as similar to the wild type while, Streptomycin resistant mutants of appeared as pin- point white smooth colonies on TSA. No differences were seen for oxidase, string test and fermentation pattern for sucrose and lactose. Toxin CoregulatedPili production was differed from high level order designated as +++ to mild ++ and low level designated as + after mutation with 5-FU and 2-BU. However, 15% of rifampicin resistant mutant isolates gave no agglutination phenomena. No proteases activity detected even after 48 hour of incubation; the production of lipases enzyme did not affected; while, mutator isolates produced high level of β- haemolysins about 2.5 fold. About 90% of cyclophosphamide- rifampicin mutant showed homogenized culture with no auto agglutination but high level of proteases. While, only 10% of cyclophosphamide - rifampicin mutants gave slightly auto agglutination and didn’t produce proteases enzyme. The production of both TCP and CT were increased from rough pigment producing mutant isolates comparing with yellow and smooth mutants.

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Ostash, B. O., Yu Misaki, B. S. Dolya, Ya I. Kharaton, T. Busche, A. M. Luzhetskyy, J. Kalinowski, K. Ochi, and V. O. Fedorenko. "Generation and initial characterization of a collection of spontaneous Streptomyces albus J1074 mutants resistant to rifampicin." Faktori eksperimental'noi evolucii organizmiv 27 (September 1, 2020): 139–43. http://dx.doi.org/10.7124/feeo.v27.1316.

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Aim. Streptomyces albus J1074 is one of the most popular streptomycete chassis for heterologous expression of natural product (NP) biosynthetic gene clusters (BGCs). There is keen interest in further improvement of the strain to provide increased yields of corresponding NPs. Introduction of certain types of antibiotic resistance mutations is a proven way to improve Streptomyces strains. For example, selection for increased resistance to rifampicin is known to lead to increased antibiotic activity. Here we used available lineages of antibiotic-resistant mutants of S. albus to raise rifampicin-resistant variants (Rifr) and to study their properties. Methods. Microbiological and molecular genetic approaches were combined to generate Rifr mutants and to study their properties. Results. By plating S. albus onto GYM agar supplemented with 10 mcg/mL of rifampicin, we isolated 85 stable Rifr colonies, whose resistance level was within 10-200 mcg/mL range. Sequencing revealed wide spectrum of missense mutations within rpoB gene. Bioassays demonstrated dramatically increased endogenous antibiotic activity of certain Rifr mutants. Conclusions. Selection for rifampicin resistance is a viable way to increase the yields of NPs in S. albus. Keywords: Streptomyces albus J1074, antibiotic resistance, rifampicin.

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Jin, Ding Jun, William A. Walter, and Carol A. Gross. "Characterization of the termination phenotypes of rifampicin-resistant mutants." Journal of Molecular Biology 202, no. 2 (July 1988): 245–53. http://dx.doi.org/10.1016/0022-2836(88)90455-x.

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Lee, D. H., R. J. Miles, and J. R. M. Inal. "Antibiotic sensitivity and mutation rates to antibiotic resistance inMycoplasma mycoidesssp.mycoides." Epidemiology and Infection 98, no. 3 (June 1987): 361–68. http://dx.doi.org/10.1017/s0950268800062129.

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SUMMARYThe antibiotic resistance ofMycoplasma mycoidesssp.mycoidesstrain T1was investigated. This strain was resistant to high levels ( > 100 μg ml−1) of rifampicin and nalidixic acid. It was sensitive to streptomycin, spectinomycin and novobiocin; however, single step mutants with high levels of resistance ( > 100 μg ml−1) were readily isolated. With erythromycin and tylosin for which the minimum inhibitory concentration (MIC) for the parent strain was < 0·1 μg ml−1, mutants resistant to > 100 μg ml−1were obtained in two and three steps respectively. The MIC of tetracycline in single step resistant mutants (0·6 μg ml−1) was tenfold higher than the parent strain, but could not be increased further. There was only a twofold increase in resistance to chloramphenicol in single step mutants. The frequency of resistant mutants varied with the antibiotic and was between 4× 10minuss;6and 2× 10−8. The mutation rate to antibiotic resistance to streptomycin, spectinomycin, novobiocin, erythromycin and tylosin was between 3× 10−8and 5× 10−9per cell per generation. There was a fivefold decrease in mutation rate to resistance to 60 μg ml−1streptomycin compared to that to 20 μg ml−1.

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Bhatnagar, N., E. Getachew, S. Straley, J. Williams, M. Meltzer, and A. Fortier. "Reduced Virulence Of Rifampicin-Resistant Mutants Of Francisella Tularensis [X]." Journal of Infectious Diseases 170, no. 4 (October 1, 1994): 841–47. http://dx.doi.org/10.1093/infdis/170.4.841.

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Do, Thi Thuy, Jerónimo Rodríguez-Beltran, Esmeralda Cebrián-Sastre, Alexandro Rodríguez-Rojas, Alfredo Castañeda-García, and Jesús Blázquez. "Inactivation of a New Potassium Channel Increases Rifampicin Resistance and Induces Collateral Sensitivity to Hydrophilic Antibiotics in Mycobacterium smegmatis." Antibiotics 11, no. 4 (April 12, 2022): 509. http://dx.doi.org/10.3390/antibiotics11040509.

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Rifampicin is a critical first-line antibiotic for treating mycobacterial infections such as tuberculosis, one of the most serious infectious diseases worldwide. Rifampicin resistance in mycobacteria is mainly caused by mutations in the rpoB gene; however, some rifampicin-resistant strains showed no rpoB mutations. Therefore, alternative mechanisms must explain this resistance in mycobacteria. In this work, a library of 11,000 Mycobacterium smegmatis mc2 155 insertion mutants was explored to search and characterize new rifampicin-resistance determinants. A transposon insertion in the MSMEG_1945 gene modified the growth rate, pH homeostasis and membrane potential in M. smegmatis, producing rifampicin resistance and collateral susceptibility to other antitubercular drugs such as isoniazid, ethionamide and aminoglycosides. Our data suggest that the M. smegmatis MSMEG_1945 protein is an ion channel, dubbed MchK, essential for maintaining the cellular ionic balance and membrane potential, modulating susceptibility to antimycobacterial agents. The functions of this new gene point once again to potassium homeostasis impairment as a proxy to resistance to rifampicin. This study increases the known repertoire of mycobacterial ion channels involved in drug susceptibility/resistance to antimycobacterial drugs and suggests novel intervention opportunities, highlighting ion channels as druggable pathways.

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Severinov, K., M. Soushko, A. Goldfarb, and V. Nikiforov. "Rifampicin region revisited. New rifampicin-resistant and streptolydigin-resistant mutants in the beta subunit of Escherichia coli RNA polymerase." Journal of Biological Chemistry 268, no. 20 (July 1993): 14820–25. http://dx.doi.org/10.1016/s0021-9258(18)82407-3.

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Rodriguez, Carlos Hernan, Alejandra De Ambrosio, Milena Bajuk, Mariela Spinozzi, Marcela Nastro, Karina Bombicino, Marcela Radice, Gabriel Gutkind, Carlos Vay, and Angela Famiglietti. "In vitro antimicrobials activity against endemic Acinetobacter baumannii multiresistant clones." Journal of Infection in Developing Countries 4, no. 03 (February 3, 2010): 164–67. http://dx.doi.org/10.3855/jidc.604.

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Background: Multidrug-resistant strains of Acinetobacter baumannii have been reported increasingly around the world. The administration of an association of antibiotics has been proposed to create an active combination and to prevent the emergence of resistance. Methodology: The activity of colistin, rifampicin, gentamicin, imipenem and their associations was evaluated by means of killing curves in fourteen isolates belonging to three endemic PFGE types, in a university hospital of Buenos Aires city. The 14 isolates were selected on the basis of different mechanisms responsible for resistance to carbapenems and different susceptibility to colistin. Results: The mechanism responsible for the resistance to imipenem was the production of OXA-23 and OXA-58 carbapenemases. Heteroresistance to colistin was observed in six isolates. The associations colistin-rifampicin and colistin-imipenem were synergistic in heteroresistant isolates and prevented the development of colistin-resistant mutants. The association imipenem-gentamicin was bactericidal in gentamicin susceptible isolates, whereas the association imipenem-rifampicin was always indifferent. Conclusion: The antimicrobial activity and the presence of synergy are related to the antimicrobials' susceptibilities irrespective of the PFGE type or the OXA-carbapenemase produced.

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von Freiesleben, Ulrik, Knud V. Rasmussen, Tove Atlung, and Flemming G. Hansen. "Rifampicin-resistant initiation of chromosome replication from oriC in ihf mutants." Molecular Microbiology 37, no. 5 (September 2000): 1087–93. http://dx.doi.org/10.1046/j.1365-2958.2000.02060.x.

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Silvia, Sophia, Samantha A. Donahue, Erin E. Killeavy, Gerwald Jogl, and Steven T. Gregory. "A Survey of Spontaneous Antibiotic-Resistant Mutants of the Halophilic, Thermophilic Bacterium Rhodothermus marinus." Antibiotics 10, no. 11 (November 11, 2021): 1384. http://dx.doi.org/10.3390/antibiotics10111384.

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Rhodothermus marinus is a halophilic extreme thermophile, with potential as a model organism for studies of the structural basis of antibiotic resistance. In order to facilitate genetic studies of this organism, we have surveyed the antibiotic sensitivity spectrum of R. marinus and identified spontaneous antibiotic-resistant mutants. R. marinus is naturally insensitive to aminoglycosides, aminocylitols and tuberactinomycins that target the 30S ribosomal subunit, but is sensitive to all 50S ribosomal subunit-targeting antibiotics examined, including macrolides, lincosamides, streptogramin B, chloramphenicol, and thiostrepton. It is also sensitive to kirromycin and fusidic acid, which target protein synthesis factors. It is sensitive to rifampicin (RNA polymerase inhibitor) and to the fluoroquinolones ofloxacin and ciprofloxacin (DNA gyrase inhibitors), but insensitive to nalidixic acid. Drug-resistant mutants were identified using rifampicin, thiostrepton, erythromycin, spiramycin, tylosin, lincomycin, and chloramphenicol. The majority of these were found to have mutations that are similar or identical to those previously found in other species, while several novel mutations were identified. This study provides potential selectable markers for genetic manipulations and demonstrates the feasibility of using R. marinus as a model system for studies of ribosome and RNA polymerase structure, function, and evolution.

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Amusengeri, Arnold, Asifullah Khan, and Özlem Tastan Bishop. "The Structural Basis of Mycobacterium tuberculosis RpoB Drug-Resistant Clinical Mutations on Rifampicin Drug Binding." Molecules 27, no. 3 (January 28, 2022): 885. http://dx.doi.org/10.3390/molecules27030885.

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Tuberculosis (TB), caused by the Mycobacterium tuberculosis infection, continues to be a leading cause of morbidity and mortality in developing countries. Resistance to the first-line anti-TB drugs, isoniazid (INH) and rifampicin (RIF), is a major drawback to effective TB treatment. Genetic mutations in the β-subunit of the DNA-directed RNA polymerase (rpoB) are reported to be a major reason of RIF resistance. However, the structural basis and mechanisms of these resistant mutations are insufficiently understood. In the present study, thirty drug-resistant mutants of rpoB were initially modeled and screened against RIF via a comparative molecular docking analysis with the wild-type (WT) model. These analyses prioritized six mutants (Asp441Val, Ser456Trp, Ser456Gln, Arg454Gln, His451Gly, and His451Pro) that showed adverse binding affinities, molecular interactions, and RIF binding hinderance properties, with respect to the WT. These mutant models were subsequently analyzed by molecular dynamics (MD) simulations. One-hundred nanosecond all-atom MD simulations, binding free energy calculations, and a dynamic residue network analysis (DRN) were employed to exhaustively assess the impact of mutations on RIF binding dynamics. Considering the global structural motions and protein–ligand binding affinities, the Asp441Val, Ser456Gln, and His454Pro mutations generally yielded detrimental effects on RIF binding. Locally, we found that the electrostatic contributions to binding, particularly by Arg454 and Glu487, might be adjusted to counteract resistance. The DRN analysis revealed that all mutations mostly distorted the communication values of the critical hubs and may, therefore, confer conformational changes in rpoB to perturb RIF binding. In principle, the approach combined fundamental molecular modeling tools for robust “global” and “local” level analyses of structural dynamics, making it well suited for investigating other similar drug resistance cases.

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Widanarni, D. Meha, Sri Nuryati, Sukenda, and A. Suwanto. "Pathogenicity Assay of Vibrio harveyi in Tiger Shrimp Larvae Employing Rifampicin-Resistant as A Molecular Marker." Jurnal Akuakultur Indonesia 3, no. 3 (December 1, 2007): 23. http://dx.doi.org/10.19027/jai.3.23-27.

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Rifampicin-resistant marker was employed as a reporter to assay pathogenicity of Vibrio harveyi in shrimp larvae. V. harveyi M. G3 and G7 that difference not schizotyping as shown by Pulsed-Filed Gel Electrophoresis (PFGE) used in this study. Spontaneous mutation was conducted to generate V. harveyi resistant to rifampicin. Two groups of shrimp post-larvae (PL5) were immersed for 30 min in 106 CFU/ml of mutants and wild type of V. harveyi, respectively; and then placed in a 2 liter shrimp rearing tank for five days. A control group was immersed in sterile seawater. Growth curve analysis and pathogenicity assay of V. harveyi showed that each of the V. harveyi mutant exhibited almost identical profiles to that of the wild type parental strain and did not show alteration in their pathogenicity. Sample from dead shrimp larvae showed that the dead shrimp larvae were infected by V. harveyi RfR, indicated that rifampicin-resistant marker effective as a reporter to assay pathogenicity of Vibrio harveyi in shrimp larvae. Key words: shrimp larvae, Vibrio harveyi, rifampicin-resistant, molecular marker

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Dolya, Borys, Olena Hryhorieva, Khrystyna Sorochynska, Maria Lopatniuk, Iryna Ostash, Vasylyna-Marta Tseduliak, Eva Baggesgaard Sterndorff, et al. "Properties of Multidrug-Resistant Mutants Derived from Heterologous Expression Chassis Strain Streptomyces albidoflavus J1074." Microorganisms 11, no. 5 (April 30, 2023): 1176. http://dx.doi.org/10.3390/microorganisms11051176.

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Streptomyces albidoflavus J1074 is a popular platform to discover novel natural products via the expression of heterologous biosynthetic gene clusters (BGCs). There is keen interest in improving the ability of this platform to overexpress BGCs and, consequently, enable the purification of specialized metabolites. Mutations within gene rpoB for the β-subunit of RNA polymerase are known to increase rifampicin resistance and augment the metabolic capabilities of streptomycetes. Yet, the effects of rpoB mutations on J1074 remained unstudied, and we decided to address this issue. A target collection of strains that we studied carried spontaneous rpoB mutations introduced in the background of the other drug resistance mutations. The antibiotic resistance spectra, growth, and specialized metabolism of the resulting mutants were interrogated using a set of microbiological and analytical approaches. We isolated 14 different rpoB mutants showing various degrees of rifampicin resistance; one of them (S433W) was isolated for the first time in actinomycetes. The rpoB mutations had a major effect on antibiotic production by J1074, as evident from bioassays and LC-MS data. Our data support the idea that rpoB mutations are useful tools to enhance the ability of J1074 to produce specialized metabolites.

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Malshetty, Vidyasagar, Krishna Kurthkoti, Arnab China, Bratati Mallick, Subburaj Yamunadevi, Pau Biak Sang, Narayanaswamy Srinivasan, Valakunja Nagaraja, and Umesh Varshney. "Novel insertion and deletion mutants of RpoB that render Mycobacterium smegmatis RNA polymerase resistant to rifampicin-mediated inhibition of transcription." Microbiology 156, no. 5 (May 1, 2010): 1565–73. http://dx.doi.org/10.1099/mic.0.036970-0.

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The startling increase in the occurrence of rifampicin (Rif) resistance in the clinical isolates of Mycobacterium tuberculosis worldwide is posing a serious concern to tuberculosis management. The majority of Rif resistance in bacteria arises from mutations in the RpoB subunit of the RNA polymerase. We isolated M. smegmatis strains harbouring either an insertion (6 aa) or a deletion (10 aa) in their RpoB proteins. Although these strains showed a compromised fitness for growth in 7H9 Middlebrook medium, their resistance to Rif was remarkably high. The attenuated growth of the strains correlated with decreased specific activities of the RNA polymerases from the mutants. While the RNA polymerases from the parent or a mutant strain (harbouring a frequently occurring mutation, H442Y, in RpoB) were susceptible to Rif-mediated inhibition of transcription from calf thymus DNA, those from the insertion and deletion mutants were essentially refractory to such inhibition. Three-dimensional structure modelling revealed that the RpoB amino acids that interact with Rif are either deleted or unable to interact with Rif due to their unsuitable spatial positioning in these mutants. We discuss possible uses of the RpoB mutants in studying transcriptional regulation in mycobacteria and as potential targets for drug design.

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Vilchèze, Catherine, Travis Hartman, Brian Weinrick, Paras Jain, Torin R. Weisbrod, Lawrence W. Leung, Joel S. Freundlich, and William R. Jacobs. "Enhanced respiration prevents drug tolerance and drug resistance in Mycobacterium tuberculosis." Proceedings of the National Academy of Sciences 114, no. 17 (April 10, 2017): 4495–500. http://dx.doi.org/10.1073/pnas.1704376114.

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Persistence, manifested as drug tolerance, represents a significant obstacle to global tuberculosis control. The bactericidal drugs isoniazid and rifampicin kill greater than 99% of exponentially growing Mycobacterium tuberculosis (Mtb) cells, but the remaining cells are persisters, cells with decreased metabolic rate, refractory to killing by these drugs, and able to generate drug-resistant mutants. We discovered that the combination of cysteine or other small thiols with either isoniazid or rifampicin prevents the formation of drug-tolerant and drug-resistant cells in Mtb cultures. This effect was concentration- and time-dependent, relying on increased oxygen consumption that triggered enhanced production of reactive oxygen species. In infected murine macrophages, the addition of N-acetylcysteine to isoniazid treatment potentiated the killing of Mtb. Furthermore, we demonstrate that the addition of small thiols to Mtb drug treatment shifted the menaquinol/menaquinone balance toward a reduced state that stimulates Mtb respiration and converts persister cells to metabolically active cells. This prevention of both persister cell formation and drug resistance leads ultimately to mycobacterial cell death. Strategies to enhance respiration and initiate oxidative damage should improve tuberculosis chemotherapies.

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Monama, Mokgerwa Zacharia, Fisayo Olotu, and Özlem Tastan Bishop. "Investigation of Multi-Subunit Mycobacterium tuberculosis DNA-Directed RNA Polymerase and Its Rifampicin Resistant Mutants." International Journal of Molecular Sciences 24, no. 4 (February 7, 2023): 3313. http://dx.doi.org/10.3390/ijms24043313.

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Emerging Mycobacterium tuberculosis (Mtb) resistant strains have continued to limit the efficacies of existing antitubercular therapies. More specifically, mutations in the RNA replicative machinery of Mtb, RNA polymerase (RNAP), have been widely linked to rifampicin (RIF) resistance, which has led to therapeutic failures in many clinical cases. Moreover, elusive details on the underlying mechanisms of RIF-resistance caused by Mtb-RNAP mutations have hampered the development of new and efficient drugs that are able to overcome this challenge. Therefore, in this study we attempt to resolve the molecular and structural events associated with RIF-resistance in nine clinically reported missense Mtb RNAP mutations. Our study, for the first time, investigated the multi-subunit Mtb RNAP complex and findings revealed that the mutations commonly disrupted structural–dynamical attributes that may be essential for the protein’s catalytic functions, particularly at the βfork loop 2, β’zinc-binding domain, the β’ trigger loop and β’jaw, which in line with previous experimental reports, are essential for RNAP processivity. Complementarily, the mutations considerably perturbed the RIF-BP, which led to alterations in the active orientation of RIF needed to obstruct RNA extension. Consequentially, essential interactions with RIF were lost due to the mutation-induced repositioning with corresponding reductions in the binding affinity of the drug observed in majority of the mutants. We believe these findings will significantly aid future efforts in the discovery of new treatment options with the potential to overcome antitubercular resistance.

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Tóth, I., Márta Csík, and L. Emçdy. "Spontaneous antibiotic resistance mutation associated pleiotropic changes in Escherichia coli O157:H7." Acta Veterinaria Hungarica 51, no. 1 (January 1, 2003): 29–44. http://dx.doi.org/10.1556/avet.51.2003.1.3.

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Besides the well-known O157:H7 clone causing enterohaemorrhagic colitis and haemolytic uraemic syndrome in Europe, Japan and North America, the number of Escherichia coli isolates with non-motile (NM) phenotype has considerably increased. We supposed that spontaneous antibiotic resistance mutation could cause this phenotypic change. To model our hypothesis we isolated rifampicin- (Rif) and ampicillin- (Amp) resistant mutants from E. coli O157:H7 prototype strains 7785 and EDL933. Among Rif r mutants we could isolate strains with no or reduced motility, while the Ampr mutants became hypermotile. The biochemical profile of the mutants had not changed but phage sensitivity and generation time of the mutants were altered. Among the representative strains we did not find polymorphism with Southern blot analysis and no polymorphism was found in the fliC gene of the mutants. The described characteristics have proven to be stable. In a mice virulence assay by intravenous infections the virulence of the derivatives was also found to be changed. In summary, we found that the antibiotic-resistant phenotype in E. coli O157:H7 was coexpressed with several other phenotypic changes including motility and virulence. It can be assumed that expression of the involved phenotypes may be under the influence of a common regulatory cascade. Further work is needed to identify the components and mechanism of this regulatory system.

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Safi, Hassan, Robert D. Fleischmann, Scott N. Peterson, Marcus B. Jones, Behnam Jarrahi, and David Alland. "Allelic Exchange and Mutant Selection Demonstrate that Common Clinical embCAB Gene Mutations Only Modestly Increase Resistance to Ethambutol in Mycobacterium tuberculosis." Antimicrobial Agents and Chemotherapy 54, no. 1 (October 12, 2009): 103–8. http://dx.doi.org/10.1128/aac.01288-09.

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ABSTRACT Mutations within codon 306 of the Mycobacterium tuberculosis embB gene modestly increase ethambutol (EMB) MICs. To identify other causes of EMB resistance and to identify causes of high-level resistance, we generated EMB-resistant M. tuberculosis isolates in vitro and performed allelic exchange studies of embB codon 406 (embB406) and embB497 mutations. In vitro selection produced mutations already identified clinically in embB306, embB397, embB497, embB1024, and embC13, which result in EMB MICs of 8 or 14 μg/ml, 5 μg/ml, 12 μg/ml, 3 μg/ml, and 4 μg/ml, respectively, and mutations at embB320, embB324, and embB445, which have not been identified in clinical M. tuberculosis isolates and which result in EMB MICs of 8 μg/ml, 8 μg/ml, and 2 to 8 μg/ml, respectively. To definitively identify the effect of the common clinical embB497 and embB406 mutations on EMB susceptibility, we created a series of isogenic mutants, exchanging the wild-type embB497 CAG codon in EMB-susceptible M. tuberculosis strain 210 for the embB497 CGG codon and the wild-type embB406 GGC codon for either the embB406 GCC, embB406 TGC, embB406 TCC, or embB406 GAC codon. These new mutants showed 6-fold and 3- to 3.5-fold increases in the EMB MICs, respectively. In contrast to the embB306 mutants, the isogenic embB497 and embB406 mutants did not have preferential growth in the presence of isoniazid or rifampin (rifampicin) at their MICs. These results demonstrate that individual embCAB mutations confer low to moderate increases in EMB MICs. Discrepancies between the EMB MICs of laboratory mutants and clinical M. tuberculosis strains with identical mutations suggest that clinical EMB resistance is multigenic and that high-level EMB resistance requires mutations in currently unknown loci.

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Liu, Liping, Hanne Ingmer, and Martin Vestergaard. "Genome-Wide Identification of Resveratrol Intrinsic Resistance Determinants in Staphylococcus aureus." Antibiotics 10, no. 1 (January 16, 2021): 82. http://dx.doi.org/10.3390/antibiotics10010082.

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Resveratrol has been extensively studied due to its potential health benefits in multiple diseases, for example, cancer, obesity and cardiovascular diseases. Besides these properties, resveratrol displays inhibitory activity against a wide range of bacterial species; however, the cellular effects of resveratrol in bacteria remain incompletely understood, especially in the human pathogen, Staphylococcus aureus. In this study, we aimed to identify intrinsic resistance genes that aid S. aureus in tolerating the activity of resveratrol. We screened the Nebraska Transposon Mutant Library, consisting of 1920 mutants with inactivation of non-essential genes in S. aureus JE2, for increased susceptibly to resveratrol. On agar plates containing 0.5× the minimum inhibitory concentration (MIC), 17 transposon mutants failed to grow. Of these, four mutants showed a two-fold reduction in MIC, being the clpP protease mutant and three mutants with deficiencies in the electron transport chain (menD, hemB, aroC). The remaining 13 mutants did not show a reduction in MIC, but were confirmed by spot-assays to have increased susceptibility to resveratrol. Several genes were associated with DNA damage repair (recJ, xerC and xseA). Treatment of S. aureus JE2 with sub-inhibitory concentrations of resveratrol did not affect the expression of recJ, xerC and xseA, but increased expression of the SOS–stress response genes lexA and recA, suggesting that resveratrol interferes with DNA integrity in S. aureus. Expression of error-prone DNA polymerases are part of the SOS–stress response and we could show that sub-inhibitory concentrations of resveratrol increased overall mutation frequency as measured by formation of rifampicin resistant mutants. Our data show that DNA repair systems are important determinants aiding S. aureus to overcome the inhibitory activity of resveratrol. Activation of the SOS response by resveratrol could potentially facilitate the development of resistance towards conventional antibiotics in S. aureus.

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Al-Ani, B., M. Aboshkiwa, R. E. Glass, and G. Coleman. "The patterns of extracellular protein formation by spontaneously-occurring rifampicin-resistant mutants ofStaphylococcus aureus." FEMS Microbiology Letters 70, no. 1 (June 1990): 91–94. http://dx.doi.org/10.1111/j.1574-6968.1990.tb03782.x.

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Dixit, Anupam, and Devindra Vijay Amla. "Studies on two classes of rifampicin-resistant mutants of the nitrogen-fixing cyanobacteriumNostoc muscorum." Current Microbiology 18, no. 3 (March 1989): 157–64. http://dx.doi.org/10.1007/bf01569564.

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Olivares-Fuster, O., and C. R. Arias. "Development and characterization of rifampicin-resistant mutants from high virulent strains of Flavobacterium columnare." Journal of Fish Diseases 34, no. 5 (April 14, 2011): 385–94. http://dx.doi.org/10.1111/j.1365-2761.2011.01253.x.

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Journal, Baghdad Science. "Developing of Bacterial Mutagenic Assay System for Detection of Environmental and Food MutagensV – Using Anticancer Drug Cyclophosphamide." Baghdad Science Journal 5, no. 4 (December 7, 2008): 500–512. http://dx.doi.org/10.21123/bsj.5.4.500-512.

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G-system composed of three isolates G3 ( Bacillus),G12 ( Arthrobacter )and G27 ( Brevibacterium) was used to detect the mutagenicity of the anticancer drug, cyclophosphamide (CP) under conditions similar to that used for standard mutagen, Nitrosoguanidine (NTG). The CP effected the survival fraction of isolates after treatment for 15 mins using gradual increasing concentrations, but at less extent comparing to NTG. The mutagenic effect of CP was at higher level than that of NTG when using streptomycin as a genetic marker, but the situation was reversed when using rifampicin resistant as a report marker. The latter effect appeared upon recording the mutagen efficiency (ie., number of induced mutants/microgram of mutagen). Measuring the Relative mutability revealed that isolate G12 was highly mutable by both mutagens. The Relative mutational results showed also that isolate G12 is more sensitive, except when recording rifampicin resistance as a genetic marker, and this pattern was similar to NTG.

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Bayliss, Cathy, Bonnie Lasby, Janet M. Wood, Ran Lifshitz, and Gerry L. Brown. "Mutant derivatives of Pseudomonas putida GR12-2R3 defective in nutrient utilization or cell surface structures show reduced ability to promote canola root elongation." Canadian Journal of Microbiology 39, no. 12 (December 1, 1993): 1111–19. http://dx.doi.org/10.1139/m93-168.

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Pseudomonas putida GR12-2R3 is a rifampicin-resistant derivative of a cold-tolerant, nitrogen-fixing bacterium isolated from the roots of grasses growing in the Canadian high arctic. It colonizes canola (Brassica campestris) roots and promotes canola root and shoot growth under gnotobiotic conditions and in the field. TnphoA insertion mutagenesis was used to isolate derivatives of strain GR12-2R3 that had reduced abilities to promote canola root elongation (PRE− mutants). Within a pool of 10 290 TnphoA insertion mutants, 1.4% expressed active PhoA fusion proteins (PhoA+). Among 20 PhoA+ mutants, 6 were PRE− and 4 of those strains secreted PhoA activity into the culture medium. PhoA+ strain PG269 showed PhoA activity, 25% cell associated, that was induced by canola seed exudate. The ability of this strain to promote canola root elongation was similar to that of the parent strain. Like other pseudomonads, strain GR12-2R3 utilizes a wide range of sugars, amino acids, and other compounds as carbon and nitrogen sources. Twenty-one TnphoA insertion mutants, all PhoA−, were unable to utilize a specific nutrient. That group included strains that could not utilize arabinose (Ara−, three mutants) or glycerol and other compounds (Csu−, three mutants) as carbon source and strains that could not utilize glycine (Gut−, eight mutants), histidine (Hut−, three mutants), or proline (Put−, four mutants) as nitrogen source. One Ara− mutant, three Gut− mutants, and one Csu− mutant were PRE−. Five of the mutant strains examined in detail (two PhoA− PRE−, one PhoA− PRE+, one PhoA+ PRE−, and one PhoA+ PRE+) grew less well than strain GR12-2R3 in LB and (or) seed exudate medium. Further characterization of the TnphoA target genes in selected PRE− strains is expected to yield additional insight regarding the molecular basis for the interaction between P. putida GR12-2R3 and canola.Key words: Pseudomonas putida, plant growth promoting rhizobacterium, TnphoA.

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Qi, Qin, Macarena Toll-Riera, Karl Heilbron, Gail M. Preston, and R. Craig MacLean. "The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa." Proceedings of the Royal Society B: Biological Sciences 283, no. 1822 (January 13, 2016): 20152452. http://dx.doi.org/10.1098/rspb.2015.2452.

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Antibiotic resistance carries a fitness cost that must be overcome in order for resistance to persist over the long term. Compensatory mutations that recover the functional defects associated with resistance mutations have been argued to play a key role in overcoming the cost of resistance, but compensatory mutations are expected to be rare relative to generally beneficial mutations that increase fitness, irrespective of antibiotic resistance. Given this asymmetry, population genetics theory predicts that populations should adapt by compensatory mutations when the cost of resistance is large, whereas generally beneficial mutations should drive adaptation when the cost of resistance is small. We tested this prediction by determining the genomic mechanisms underpinning adaptation to antibiotic-free conditions in populations of the pathogenic bacterium Pseudomonas aeruginosa that carry costly antibiotic resistance mutations. Whole-genome sequencing revealed that populations founded by high-cost rifampicin-resistant mutants adapted via compensatory mutations in three genes of the RNA polymerase core enzyme, whereas populations founded by low-cost mutants adapted by generally beneficial mutations, predominantly in the quorum-sensing transcriptional regulator gene lasR . Even though the importance of compensatory evolution in maintaining resistance has been widely recognized, our study shows that the roles of general adaptation in maintaining resistance should not be underestimated and highlights the need to understand how selection at other sites in the genome influences the dynamics of resistance alleles in clinical settings.

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Jeon, Se-Mi, Sanghee Park, Na-Ra Lim, Noori Lee, Jihee Jung, Nackmoon Sung, and Seonghan Kim. "Molecular Analysis of Anti-Tuberculosis Drug Resistance of Mycobacterium tuberculosis Isolated in the Republic of Korea." Antibiotics 12, no. 8 (August 17, 2023): 1324. http://dx.doi.org/10.3390/antibiotics12081324.

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Rapid and accurate detection of tuberculosis (TB) drug resistance is critical for the successful treatment and control of TB. Here, we investigated resistance to anti-TB drugs and genetic variations in 215 drug-resistant Mycobacterium tuberculosis isolates in Korea. Genetic variations were observed in rpoB Ser531Leu, katG Ser315Thr, and gyrA Asp94Gly; however, the minimum inhibitory concentrations varied, which can be attributed to other resistance mechanisms. Examination of genetic relatedness among drug-resistant isolates revealed that the cluster size of resistant bacteria was less than six strains, suggesting no evidence of a large-scale epidemic caused by a specific strain. However, rpoC mutants of the rifampicin-resistant isolates were composed of five types of clusters, suggesting that these compensatory mutations advance propagation. In the present study, more than 90% of the resistance mechanisms to major anti-TB drugs were identified, and the effect of each mutation on drug resistance was estimated. With the clinical application of recent next-generation sequencing-based susceptibility testing, the present study is expected to improve the clinical utilization of genotype-based drug susceptibility testing for the diagnosis and treatment of patients with drug-resistant TB.

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Baldwin, Susan L., Sasha E. Larsen, Valerie A. Reese, Tiffany Pecor, Brian Granger, Amit Khandhar, Christopher B. Fox, Steven G. Reed, and Rhea N. Coler. "Use of GLA-nanoalum as an effective adjuvant for a therapeutic ID93 TB vaccine." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 180.21. http://dx.doi.org/10.4049/jimmunol.200.supp.180.21.

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Abstract Tuberculosis (TB) caused by the intracellular bacterium Mycobacterium tuberculosis (Mtb) reportedly killed 1.3 million people in 2016 and is the leading cause of death caused by a single infectious organism. Increasingly worrisome is the ability of Mtb to develop extensive drug resistance. According to the 2017 WHO global TB report, there were 600,000 new rifampicin-resistant cases in 2016, and almost half a million cases with multiple drug resistant (MDR) TB. The development of new host-targeted therapeutic strategies that prevent the outgrowth of resistant mutants and/or modulate the immune response to combat Mtb infection and/or reduce disease pathology is one solution to prevent the generation of antibacterial resistance and treat drug resistant (DR)-TB. Here we evaluate a novel nanoalum adjuvant formulation containing a synthetic TLR4 agonist, glucopyranosyl lipid adjuvant (GLA), with our clinical ID93 protein as an immunotherapeutic vaccine. We show that immunotherapy with ID93+GLA-nanoalum is effective against Mtb when given as an adjunct to drug treatment in a mouse TB therapy model.

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García de Salamone, Ines E., Russell K. Hynes, and Louise M. Nelson. "Cytokinin production by plant growth promoting rhizobacteria and selected mutants." Canadian Journal of Microbiology 47, no. 5 (May 1, 2001): 404–11. http://dx.doi.org/10.1139/w01-029.

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One of the proposed mechanisms by which rhizobacteria enhance plant growth is through the production of plant growth regulators. Five plant growth promoting rhizobacterial (PGPR) strains produced the cytokinin dihydrozeatin riboside (DHZR) in pure culture. Cytokinin production by Pseudomonas fluorescens G2018, a rifampicin-resistant mutant (RIF), and two TnphoA-derived mutants (CNT1, CNT2), with reduced capacity to synthesize cytokinins, was further characterized in pure culture using immunoassay and thin layer chromatography. G2018 produced higher amounts of three cytokinins, isopentenyl adenosine (IPA), trans-zeatin ribose (ZR), and DHZR than the three mutants during stationary phase. IPA was the major metabolite produced, but the proportion of ZR and DHZR accumulated by CNT1 and CNT2 increased with time. No differences were observed between strain G2018 and the mutants in the amounts of indole acetic acid synthesized, nor were gibberellins detected in supernatants of any of the strains. Addition of 105 M adenine increased cytokinin production in 96- and 168-h cultures of strain G2018 by approximately 67%. G2018 and the mutants CNT1 and CNT2 may be useful for determination of the role of cytokinin production in plant growth promotion by PGPR.Key words: cytokinins, plant growth regulation, Pseudomonas fluorescens, rhizobacteria, plant growth promoting rhizobacteria (PGPR).

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Laycock, Phillip, John Cooper, Robert Howlin, Craig Delury, Sean Aiken, and Paul Stoodley. "In Vitro Efficacy of Antibiotics Released from Calcium Sulfate Bone Void Filler Beads." Materials 11, no. 11 (November 13, 2018): 2265. http://dx.doi.org/10.3390/ma11112265.

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15 different antibiotics were individually mixed with commercially available calcium sulfate bone void filler beads. The antibiotics were: amikacin, ceftriaxone, cefuroxime, ciprofloxacin, clindamycin, colistamethate sodium, daptomycin, gentamicin, imipenem/cilastatin, meropenem, nafcillin, rifampicin, teicoplanin, tobramycin and vancomycin. The efficacy of specific released antibiotics was validated by zone of inhibition (ZOI) testing using a modified Kirby–Bauer disk diffusion method against common periprosthetic joint infection pathogens. With a subset of experiments (daptomycin, rifampin, vancomycin alone and rifampin and vancomycin in combination), we investigated how release varied over 15 days using a repeated ZOI assay. We also tested the ability of these beads to kill biofilms formed by Staphylococcus epidermidis 35984, a prolific biofilm former. The results suggested that certain antibiotics could be combined and released from calcium sulfate with retained antibacterial efficacy. The daptomycin and rifampin plus vancomycin beads showed antimicrobial efficacy for the full 15 days of testing and vancomycin in combination with rifampin prevented resistant mutants. In the biofilm killing assay, all of the antibiotic combinations showed a significant reduction in biofilm bacteria after 24 h. The exposure time was an important factor in the amount of killing, and varied among the antibiotics.

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Liu, Anne, Lillian Tran, Elinne Becket, Kim Lee, Laney Chinn, Eunice Park, Katherine Tran, and Jeffrey H. Miller. "Antibiotic Sensitivity Profiles Determined with an Escherichia coli Gene Knockout Collection: Generating an Antibiotic Bar Code." Antimicrobial Agents and Chemotherapy 54, no. 4 (January 11, 2010): 1393–403. http://dx.doi.org/10.1128/aac.00906-09.

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ABSTRACT We have defined a sensitivity profile for 22 antibiotics by extending previous work testing the entire KEIO collection of close to 4,000 single-gene knockouts in Escherichia coli for increased susceptibility to 1 of 14 different antibiotics (ciprofloxacin, rifampin [rifampicin], vancomycin, ampicillin, sulfamethoxazole, gentamicin, metronidazole, streptomycin, fusidic acid, tetracycline, chloramphenicol, nitrofurantoin, erythromycin, and triclosan). We screened one or more subinhibitory concentrations of each antibiotic, generating more than 80,000 data points and allowing a reduction of the entire collection to a set of 283 strains that display significantly increased sensitivity to at least one of the antibiotics. We used this reduced set of strains to determine a profile for eight additional antibiotics (spectinomycin, cephradine, aztreonem, colistin, neomycin, enoxacin, tobramycin, and cefoxitin). The profiles for the 22 antibiotics represent a growing catalog of sensitivity fingerprints that can be separated into two components, multidrug-resistant mutants and those mutants that confer relatively specific sensitivity to the antibiotic or type of antibiotic tested. The latter group can be represented by a set of 20 to 60 strains that can be used for the rapid typing of antibiotics by generating a virtual bar code readout of the specific sensitivities. Taken together, these data reveal the complexity of intrinsic resistance and provide additional targets for the design of codrugs (or combinations of drugs) that potentiate existing antibiotics.

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Kim, Hyung Soo, Fung Chil Choi, and Byong Kak Kim. "Studies on development of resistant strains to antibiotics and antituberculosis agents(II) isolation of rifampicin resistant mutants fromClostridium butyricum." Archives of Pharmacal Research 11, no. 3 (September 1988): 218–24. http://dx.doi.org/10.1007/bf02861312.

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Hansen, Flemming G. "Reinitiation kinetics in eight dnaA(Ts) mutants of Escherichia coli: rifampicin-resistant Initiation of chromosome replication." Molecular Microbiology 15, no. 1 (January 1995): 133–40. http://dx.doi.org/10.1111/j.1365-2958.1995.tb02227.x.

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Yu, Jun, Jenny Wu, Kevin P. Francis, Tony F. Purchio, and Jagath L. Kadurugamuwa. "Monitoring in vivo fitness of rifampicin-resistant Staphylococcus aureus mutants in a mouse biofilm infection model." Journal of Antimicrobial Chemotherapy 55, no. 4 (April 1, 2005): 528–34. http://dx.doi.org/10.1093/jac/dki053.

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Carata, Elisabetta, Clelia Peano, Salvatore M. Tredici, Francesco Ferrari, Adelfia Talà, Giorgio Corti, Silvio Bicciato, Gianluca De Bellis, and Pietro Alifano. "Phenotypes and gene expression profiles of Saccharopolyspora erythraea rifampicin-resistant (rif) mutants affected in erythromycin production." Microbial Cell Factories 8, no. 1 (2009): 18. http://dx.doi.org/10.1186/1475-2859-8-18.

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A. Khalaf, Ilham. "ANTIMUTAGENIC EFFECT OF CARROT (Daucus carota) ON INDUCTION OF STREPTOMYCIN AND RIFAMPICIN RESISTANT MUTANTS IN BACTERIAL SYSTEMS." Mesopotamia Journal of Agriculture 36, no. 3 (September 28, 2008): 94–104. http://dx.doi.org/10.33899/magrj.2008.26765.

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A. Khalaf, Ilham. "ANTIMUTAGENIC EFFECT OF ROCKET (Eruca sativa ) ON INDUCTION OF STREPTOMYCIN AND RIFAMPICIN RESISTANT MUTANTS IN BACTERIAL SYSTEMS." Mesopotamia Journal of Agriculture 36, no. 4 (December 28, 2008): 139–94. http://dx.doi.org/10.33899/magrj.2008.27069.

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A. Khalaf, Ilham. "ANTIMUTAGENIC EFFECT OF ROCKET (Eruca sativa ) ON INDUCTION OF STREPTOMYCIN AND RIFAMPICIN RESISTANT MUTANTS IN BACTERIAL SYSTEMS." Mesopotamia Journal of Agriculture 36, no. 4 (December 28, 2008): 139–49. http://dx.doi.org/10.33899/magrj.2008.27317.

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38

Vlková, E., M. Grmanová, V. Rada, I. Homutová, and S. Dubná. "Selection of probiotic bifidobacteria for lambs." Czech Journal of Animal Science 54, No. 12 (December 25, 2009): 552–65. http://dx.doi.org/10.17221/151/2009-cjas.

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Twenty-six bifidobacteria were isolated from faecal samples of lambs. The isolates were identified, functional properties (survival ability at low pH and bile conditions) and antimicrobial activities against potential pathogens were determined. From the isolates with suitable properties (13 strains) rifampicin-resistant mutants were prepared by gradient plate techniques. This property enabled us to differentiate the administered organism from wild strains because resistance to rifampicin is rare among bifidobacteria. Rifampicin-resistant bifidobacteria (RRBifs) were administered to 3-days-old lambs in two trials. In the first trial the strain B. ruminantium L29 was applied to 3 lambs and was detected in faecal samples at high counts (6 log CFU/g on average) for one week. In the second trial 3 lambs received a “cocktail” of 12 strains and RRBifs survived in the intestinal tract at counts of about 6 log CFU/g for 25 days. The control group without probiotic treatment consisted of 6 animals. In both treated groups RRBifs dominated among bifidobacteria after their administration. Total bifidobacterial counts (5.64–7.32 log CFU/g) were significantly higher (P < 0.05) in treated groups compared to 2.31–2.85 log CFU/g detected in the control group during the first month of lamb life. Lactobacilli counts were also significantly higher (P < 0.05) in treated groups compared to the control. The administered bifidobacteria did not affect any other monitored bacterial groups. On the basis of in vitro test results, suitable probiotic bifidobacterial strains for lambs were chosen. Some of them survived for 30 days in the gastrointestinal tract of treated lambs, but no tested strain was able to colonise the lamb’s tract permanently. The administration of bifidobacterial “cocktail” and consequent identification of the best survived strain seems to be an effective method for selection of potential probiotics.

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Gregor, A. K., B. Klubek, and E. C. Varsa. "Identification and use of actinomycetes for enhanced nodulation of soybean co-inoculated with Bradyrhizobium japonicum." Canadian Journal of Microbiology 49, no. 8 (August 1, 2003): 483–91. http://dx.doi.org/10.1139/w03-061.

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The utilization of actinomycetes as potential soybean (Glycine max (L.)) co-inoculants was evaluated. Soil samples from Carbondale and Belleville, Ill., were used to inoculate pre-germinated soybean plants to determine antibiotic sensitivity in the native Bradyrhizobium japonicum population. Sensitivity was in the order kanamycin > tetracycline > oxytetracycline > rifampicin > neomycin. Antagonism by five actinomycete cultures toward seven test strains of B. japonicum was also assessed. The ranking average inhibition (across all seven B. japonicum strains) by these actino mycetes was Streptomyces kanamyceticus = Streptomyces coeruleoprunus > Streptomyces rimosus > Streptomyces sp. > Amy colatopsis mediterranei. Ten antibiotic combinations were used to isolate antibiotic-resistant mutants of B. japonicum I-110 and 3I1B-110 via successive cycles of mutation. Eighty-one antibiotic-resistant strains were isolated and tested for symbiotic competency; nine of which were selected for further characterization in a greenhouse pot study. Few differences in nodule number were caused by these treatments. Nodule occupancy varied from 0% to 18.3% when antibiotic-resistant strains of B. japonicum were used as the sole inoculants. However, when three mutant strains of B. japonicum were co-inoculated with S. kanamyceticus, significant increases in nodule occupancy (up to 55%) occurred. Increases in shoot nitrogen composition (27.1%40.9%) were also caused by co-inoculation with S. kanamyceticus. Key words: Bradyrhizobium japonicum, Streptomyces kanamyceticus, indigenous bradyrhizobia, co-inoculation, nodule occupancy.

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Margaret, Isabel, Juan C. Crespo-Rivas, Sebastián Acosta-Jurado, Ana M. Buendía-Clavería, María T. Cubo, Antonio Gil-Serrano, Javier Moreno, et al. "Sinorhizobium fredii HH103 rkp-3 Genes Are Required for K-Antigen Polysaccharide Biosynthesis, Affect Lipopolysaccharide Structure and Are Essential for Infection of Legumes Forming Determinate Nodules." Molecular Plant-Microbe Interactions® 25, no. 6 (June 2012): 825–38. http://dx.doi.org/10.1094/mpmi-10-11-0262.

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The Sinorhizobium fredii HH103 rkp-3 region has been isolated and sequenced. Based on the similarities between the S. fredii HH103 rkpL, rkpM, rkpN, rkpO, rkpP, and rkpQ genes and their corresponding orthologues in Helicobacter pylori, we propose a possible pathway for the biosynthesis of the S. fredii HH103 K-antigen polysaccharide (KPS) repeating unit. Three rkp-3 genes (rkpM, rkpP, and rkpQ) involved in the biosynthesis of the HH103 KPS repeating unit (a derivative of the pseudaminic acid) have been mutated and analyzed. All the rkp-3 mutants failed to produce KPS and their lipopolysaccharide (LPS) profiles were altered. These mutants showed reduced motility and auto-agglutinated when early-stationary cultures were further incubated under static conditions. Glycine max, Vigna unguiculata (determinate nodule–forming legumes), and Cajanus cajan (indeterminate nodules) plants inoculated with mutants in rkpM, rkpQ, or rkpP only formed pseudonodules that did not fix nitrogen and were devoid of bacteria. In contrast, another indeterminate nodule–forming legume, Glycyrrhiza uralensis, was still able to form some nitrogen-fixing nodules with the three S. fredii HH103 rifampicin-resistant rkp-3 mutants tested. Our results suggest that the severe symbiotic impairment of the S. fredii rkp-3 mutants with soybean, V. unguiculata, and C. cajan is mainly due to the LPS alterations rather than to the incapacity to produce KPS.

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Didier, Jean-Philippe, Régis Villet, Elzbieta Huggler, Daniel P. Lew, David C. Hooper, William L. Kelley, and Pierre Vaudaux. "Impact of Ciprofloxacin Exposure on Staphylococcus aureus Genomic Alterations Linked with Emergence of Rifampin Resistance." Antimicrobial Agents and Chemotherapy 55, no. 5 (February 28, 2011): 1946–52. http://dx.doi.org/10.1128/aac.01407-10.

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ABSTRACTIntensive use of antimicrobial agents in health care settings not only leads to the selection of multiresistant nosocomial isolates ofStaphylococcus aureusbut may also promote endogenous, resistance-conferring mutations in bacterial genes that encode drug targets. We evaluated the spectrum of rifampin resistance-conferring mutations in cultures of methicillin-susceptibleS. aureus(MSSA) or methicillin-resistantS. aureus(MRSA) strains exposedin vitroto sub-MICs of ciprofloxacin. Growth of ciprofloxacin-susceptible MRSA strain MRGR3 and ciprofloxacin-resistant MSSA strain RA1 (a NCTC 8325 derivative) in the presence of 1/2× or 1/4× MIC of ciprofloxacin led to higher frequencies of rifampin-resistant mutants on agar supplemented with rifampin (0.25 mg/liter) than under ciprofloxacin-free conditions. While rifampin-resistant mutants from ciprofloxacin-free cultures essentially showed single-amino-acid substitutions, a significant proportion of rifampin-resistant mutants from ciprofloxacin-exposed cultures displayed in-frame deletions or insertions in therpoBgene at several positions of the rifampin resistance cluster I. In-frame deletions or insertions were also recorded inrpoBcluster I of rifampin-resistant mutants from ciprofloxacin-exposed cultures ofmutSandmutLDNA repair mutants of ciprofloxacin-resistantS. aureusstrain RA1. Frequencies of rifampin-resistant mutants grown under ciprofloxacin-free medium were higher for mutant strains RA1mutS2and RA1mutL, but not RA1recA, than for their parent RA1. In conclusion, ciprofloxacin-mediated DNA damage inS. aureus, as exemplified by the wide diversity of deletions or insertions inrpoB, suggests the occurrence of major, quinolone-mediated disturbances in DNA fork progression and replication repair. Besides promoting antibiotic resistance, accumulation of unrepaired DNA replication errors, including insertions and deletions, may also contribute to potentially lethal mutations.

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Petrovskaya, Tatyana A., and Dmitry V. Tapalskiy. "Influence of different antibiotic groups on the development of mutational resistance to colistin among Klebsiella pneumoniae." Clinical Microbiology and Antimicrobial Chemotherapy 23, no. 2 (2021): 166–72. http://dx.doi.org/10.36488/cmac.2021.2.166-172.

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Objective. To determine the concentration of colistin, preventing the selection of colistin-resistant mutants of K. pneumoniae, and to evaluate the effect of antibiotics of different groups on the development of mutational resistance to colistin. Materials and Methods. Minimum inhibitory concentrations (MIC) of colistin were determined for 88 K. pneumoniae strains by the method of serial microdilutions in broth, and carbapenemase genes were detected. The selection of colistin-resistant subpopulations was performed on cation-adjusted MüllerHinton agar (MHA) with the addition of 16 mg/l colistin. Mutant prevention concentration (MPC) of colistin is determined on MHA containing 0, 1, 2, 4, 8, 16, 32, 64 and 128 mg/l of colistin. Also, MPCs of colistin were determined in the presence of a fixed concentration of the second antibiotic: clarithromycin (2 mg/l), azithromycin (2 mg/l), rifampicin (1 mg/l), clindamycin (0.5 mg/l), meropenem (8 mg/l), linezolid (2 mg/l), amikacin (1 mg/l), vancomycin (2 mg/l), doxycycline (2 mg/l). Results. All strains remained susceptible to colistin (colistin MIC 0.06–1.0 mg/l). Resistance to meropenem (MIC > 8 mg/l) was detected in 48 strains (54.5%), 46 of them were carbapenemase producers: KPC – 6 strains (6.8%), OXA-48 – 26 strains (29.5%), NDM – 14 strains (15.9%). Growth of colonies on MHA with 16 mg/l of colistin was found for 96.6% of the strains. The frequency of mutational resistance occurrence ranged from 6 × 10-9 to 10-6 (median: 2 × 10-7). The mutational nature of colistin resistance was confirmed for 36.4% of the strains. The MPC values of colistin were in the range of 16–256 mg/l; (MPC50 32 mg/l, MPC90 256 mg/l) and significantly (32–1024 times) exceeded the MIC values. In the presence of 1 mg/l of rifampicin, the MPC of colistin decreased 4–64 times (MPC50 4 mg/l, MPC90 4 mg/l). In the presence of 2 mg/l of doxycycline, MPC of colistin decreased 2–64 times for all strains (MPC50 8 mg/l, MPC90 16 mg/l). The presence of linezolid (2 mg/l) and vancomycin (2 mg/l) did not significantly change MPC of colistin. Meropenem at a concentration of 8 mg/l had no significant effect on colistin MPC for carbapenemase-producing K. pneumoniae strains. None of the antibiotics lowered the MPC50 of colistin to its clinically achievable serum concentrations. Conclusions. A high frequency of formation of mutational resistance to colistin in K. pneumoniae was revealed. The MPC values of colistin are outside the range of clinically achievable serum concentrations and may decrease in the presence of other antibiotics.

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Firsov, Alexander A., Maria V. Golikova, Elena N. Strukova, Yury A. Portnoy, Svetlana A. Dovzhenko, Mikhail B. Kobrin, and Stephen H. Zinner. "Pharmacokinetically-based prediction of the effects of antibiotic combinations on resistant Staphylococcus aureus mutants: in vitro model studies with linezolid and rifampicin." Journal of Chemotherapy 29, no. 4 (October 17, 2016): 220–26. http://dx.doi.org/10.1080/1120009x.2016.1245174.

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Sakthivel, N., and T. W. Mew. "Efficacy of bacteriocinogenic strains of Xanthomonas oryzae pv. oryzae on the incidence of bacterial blight disease of rice (Oryza sativa L.)." Canadian Journal of Microbiology 37, no. 10 (October 1, 1991): 764–68. http://dx.doi.org/10.1139/m91-131.

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A total of 144 isolates of Xanthomonas oryzae pv. oryzae were screened for bacteriocin production against 30 indicator strains of X. oryzae pv. oryzae. Forty isolates showed broad-spectrum inhibitory activity against 20–27 indicators, presumably because of the production of bacteriocin compounds. The selected isolates were screened for bacteriocin production at 29 °C and tested for virulence on rice differentials. Since all of the isolates were pathogenic, nonpathogenic bacteria were generated through N-methyl-N-nitro-N-nitrosoguanidine mutagenesis and by repeated subculturing. Epiphytic colonization and survival of pathogens and of nonpathogenic bacteriocin producers on rice plants were monitored, using mutants resistant to streptomycin and rifampicin. An improved method of pathogen inoculation was developed and used to evaluate biological control. Treatment with nonpathogenic bacteriocin-producing bacteria resulted in reductions of bacterial blight incidence up to 31–99% in greenhouse tests and 11–73% in the screenhouse. Bacterial leaf streak severity was reduced 4–20% in the greenhouse and disease incidence was reduced 20–39% in the screenhouse. Key words: bacteriocin, biological control, Xanthomonas oryzae pv. oryzae, mutagenesis, rice.

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Chellini, Paula R., Eduardo B. Lages, Pedro H. C. Franco, Fernando H. A. Nogueira, Isabela C. César, and Gerson A. Pianetti. "Development and Validation of an HPLC Method for Simultaneous Determination of Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol Hydrochloride in Pharmaceutical Formulations." Journal of AOAC INTERNATIONAL 98, no. 5 (September 1, 2015): 1234–39. http://dx.doi.org/10.5740/jaoacint.14-237.

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Abstract Tuberculosis treatment consists of a fixed dose combination of rifampicin (RIF), isoniazid (INH), pyrazinamide (PYZ), and ethambutol hydrochloride (EMB). The combined treatment using various drugs is necessary for patient curing, without recrudescence, and for prevention of drug-resistant mutants, which may occur during treatment. An HPLC-diode array detector (DAD) method for the simultaneous determination of RIF, INH, PYZ, and EMB in fixed dose combination tablets was developed and validated. Chromatographic experiments were performed on an Agilent 1200 HPLC system, and the separation was carried out on a Purospher STAR RP18e (250 × 4.6 mm id, 5 μm, Merck) analytical column. Gradient elution was carried out with a mobile phase of 20 mM monobasic sodium phosphate buffer with 0.2% triethylamine (pH 7.0) and acetonitrile at a flow rate of 1.5 mL/min. The total run time was 12 min, and the re-equilibration time was 5 min. EMB detection was performed at 210 nm, and RIF, INH, and PYZ were detected at 238 nm, using a DAD. The method proved to be specific, linear (r2 > 0.99), precise (RSD <2%), accurate, and robust and may be applied to the QC analysis of pharmaceutical formulations.

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Therrien, Dustin A., Kranti Konganti, Jason J. Gill, Brian W. Davis, Andrew E. Hillhouse, Jordyn Michalik, H. Russell Cross, Gary C. Smith, Thomas M. Taylor, and Penny K. Riggs. "Complete Whole Genome Sequences of Escherichia coli Surrogate Strains and Comparison of Sequence Methods with Application to the Food Industry." Microorganisms 9, no. 3 (March 16, 2021): 608. http://dx.doi.org/10.3390/microorganisms9030608.

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In 2013, the U.S. Department of Agriculture Food Safety and Inspection Service (USDA-FSIS) began transitioning to whole genome sequencing (WGS) for foodborne disease outbreak- and recall-associated isolate identification of select bacterial species. While WGS offers greater precision, certain hurdles must be overcome before widespread application within the food industry is plausible. Challenges include diversity of sequencing platform outputs and lack of standardized bioinformatics workflows for data analyses. We sequenced DNA from USDA-FSIS approved, non-pathogenic E. coli surrogates and a derivative group of rifampicin-resistant mutants (rifR) via both Oxford Nanopore MinION and Illumina MiSeq platforms to generate and annotate complete genomes. Genome sequences from each clone were assembled separately so long-read, short-read, and combined sequence assemblies could be directly compared. The combined sequence data approach provides more accurate completed genomes. The genomes from these isolates were verified to lack functional key E. coli elements commonly associated with pathogenesis. Genetic alterations known to confer rifR were also identified. As the food industry adopts WGS within its food safety programs, these data provide completed genomes for commonly used surrogate strains, with a direct comparison of sequence platforms and assembly strategies relevant to research/testing workflows applicable for both processors and regulators.

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Abadi, F. J., P. E. Carter, P. Cash, and T. H. Pennington. "Rifampin resistance in Neisseria meningitidis due to alterations in membrane permeability." Antimicrobial Agents and Chemotherapy 40, no. 3 (March 1996): 646–51. http://dx.doi.org/10.1128/aac.40.3.646.

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Rifampin-resistant (Rifr) Neisseria meningitidis strains are known to have single point mutations in the central conserved regions of the rpoB gene. We have demonstrated two distinct resistance phenotypes in strains with identical mutations in this region, an intermediate level of resistance in Rifr clinical isolates and a high level of resistance in mutants selected in vitro. The possible role of membrane permeability in the latter was investigated by measuring MICs in the presence of Tween 80; values for high-level-resistance mutants were reduced to intermediate levels, whereas those for intermediate-level-resistance strains were unaffected. The highly resistant mutants were also found to have increased resistance to Triton X-100 and gentian violet. Sequencing of the meningococcal mtrR gene and its promoter region (which determine resistance to hydrophobic agents in Neisseria gonorrhoeae) from susceptible or intermediate strains and highly resistant mutants generated from them showed no mutation within this region. Two-dimensional gel electrophoresis of two parent and Rif mutant strains showed identical shifts in the pI of one protein, indicating that differences between the parent and the highly Rifr mutant are not confined to the rpoB gene. These results indicate that both permeability and rpoB mutations play a role in determining the resistance of N. meningitidis to rifampin.

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Mariam, Deneke H., Yohannes Mengistu, Sven E. Hoffner, and Dan I. Andersson. "Effect of rpoB Mutations Conferring Rifampin Resistance on Fitness of Mycobacterium tuberculosis." Antimicrobial Agents and Chemotherapy 48, no. 4 (April 2004): 1289–94. http://dx.doi.org/10.1128/aac.48.4.1289-1294.2004.

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ABSTRACT Rifampin is a major drug used in the treatment of tuberculosis infections, and increasing rifampin resistance represents a worldwide clinical problem. Resistance to rifampin is caused by mutations in the rpoB gene, encoding the β-subunit of RNA polymerase. We examined the effect of three different rpoB mutations on the fitness of Mycobacterium tuberculosis. Rifampin-resistant mutants were isolated from a virulent clinical isolate of M. tuberculosis (strain Harlingen) in vitro at a mutation frequency of 2.3 × 10−8. Mutations in the rpoB gene were identified, and the growth rates of three defined mutants were measured by competition with the susceptible parent strain in laboratory medium and by single cultures in a macrophage cell line and in laboratory medium. All of the mutants showed a decreased growth rate in the three assays. The relative fitness of the mutants varied between 0.29 and 0.96 (that of the susceptible strain was set to 1.0) depending on the specific mutant and assay system. Unexpectedly, the relative fitness ranking of the mutants differed between the different assays. In conclusion, rifampin resistance is associated with a cost that is conditional.

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Malik, Muhammad, Kalyan Chavda, Xilin Zhao, Nirali Shah, Syed Hussain, Natalia Kurepina, Barry N. Kreiswirth, Robert J. Kerns, and Karl Drlica. "Induction of Mycobacterial Resistance to Quinolone Class Antimicrobials." Antimicrobial Agents and Chemotherapy 56, no. 7 (May 7, 2012): 3879–87. http://dx.doi.org/10.1128/aac.00474-12.

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ABSTRACTAn agar plate assay was developed for detecting the induction of drug-resistant mycobacterial mutants during exposure to inhibitors of DNA gyrase. WhenMycobacterium smegmatison drug-containing agar, resistant colonies arose over a period of 2 weeks. ArecAdeficiency reduced mutant recovery, consistent with involvement of the SOS response in mutant induction. The C-8-methoxy compounds gatifloxacin and moxifloxacin allowed the recovery of fewer resistant mutants than either ciprofloxacin or levofloxacin when present at the same multiple of the MIC; a quinolone-like 8-methoxy-quinazoline-2,4-dione was more effective at restricting the emergence of resistant mutants than its cognate fluoroquinolone. Thus, the structure of fluoroquinolone-like compounds affects mutant recovery. A spontaneous mutator mutant ofM. smegmatis, obtained by growth in medium containing both isoniazid and rifampin, increased mutant induction during exposure to ciprofloxacin. Moreover, the mutator increased the size of spontaneous resistant mutant subpopulations, as detected by population analysis. Induction of ciprofloxacin resistance was also observed withMycobacterium tuberculosisH37Rv. When measured with clinical isolates, no difference in mutant recovery was observed between multidrug-resistant (MDR) and pansusceptible isolates. This finding is consistent with at least some MDR isolates ofM. tuberculosislacking mutators detectable by the agar plate assay. Collectively, the data indicate that the use of fluoroquinolones against tuberculosis may induce resistance and that the choice of quinolone may be important for restricting the recovery of induced mutants.

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Vogler, Amy J., Joseph D. Busch, Stephanie Percy-Fine, Christine Tipton-Hunton, Kimothy L. Smith, and Paul Keim. "Molecular Analysis of Rifampin Resistance in Bacillus anthracis and Bacillus cereus." Antimicrobial Agents and Chemotherapy 46, no. 2 (February 2002): 511–13. http://dx.doi.org/10.1128/aac.46.2.511-513.2002.

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ABSTRACT Rifampin-resistant mutants were selected from UV-light-treated Bacillus cereus (20 mutants) and attenuated B. anthracis (23 mutants). In addition, spontaneous rifampin-resistant mutants were also isolated in attenuated B. anthracis (22 mutants). The rifampin resistance clusters of the rpoB gene were sequenced for all 65 mutants. Mutations associated with resistance were consistent with those from other bacteria, though two novel changes were observed. The spontaneous rate of resistance was estimated at 1.57 × 10−9 mutations/generation by a Luria-Delbrück fluctuation test.

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Journal articles on the topic 'Rifampicin‐resistant Mutants'

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