Ozone-Resistant Bacteria, an Inconvenient Hazard in Water Reclamation: Resistance Mechanism, Propagating Capacity, and Potential Risks. - Related Documents




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906101.0000Ozone-Resistant Bacteria, an Inconvenient Hazard in Water Reclamation: Resistance Mechanism, Propagating Capacity, and Potential Risks. Resistant bacteria have always been of research interest worldwide. In the urban water system, the increased disinfectant usage gives more chances for undesirable disinfection-resistant bacteria. As the strongest oxidative disinfectant in large-scale water treatment, ozone might select ozone-resistant bacteria (ORB), which, however, have rarely been reported and are inexplicit for their resistant mechanisms and physiological characteristics. In this study, six strains of ORB were screened from a water reclamation plant in Beijing. Three of them (O7, CR19, and O4) were more resistant to ozone than all previously reported ORB or even spores. The ozone consumption capacity of extracellular polymeric substances and cell walls was proved to be the main sources of bacterial ozone resistance, rather than intracellular antioxidant enzymes. The transcriptome results elucidated that strong ORB possessed a combined antioxidant mechanism consisting of the enhanced transcription of protein synthesis, protein export, and polysaccharide export genes (LptF, LptB, NodJ, LivK, LviG, MetQ, MetN, and GltU). This study confirmed the existence of ORB in urban water systems and brought doubts to the idea of a traditional control strategy against chlorine-resistant bacteria. A salient "trade-off" effect between the ozone resistance and propagation ability indicated the weakness and potential control approaches of ORB.202439344972
898110.9988Response mechanisms of different antibiotic-resistant bacteria with different resistance action targets to the stress from photocatalytic oxidation. The stress response of antibiotic-resistant bacteria (ARB) and the spread of antibiotic resistance genes (ARGs) pose a serious threat to the aquatic environment and human beings. This study mainly explored the effect of the heterogeneous photocatalytic oxidation (UVA-TiO(2) system) on the stress response mechanism of ARB with different antibiotic resistance action targets, including the cell wall, proteins, DNA, RNA, folate and the cell membrane. Results indicate that the stress response mechanism of tetracycline- and sulfamethoxazole-resistant E. coli DH5α, which targets the synthesis of protein and folate, could rapidly induce global regulators by the overexpression of relative antibiotic resistance action target genes. Different stress response systems were mediated via cross-protection mechanism, causing stronger tolerance to an adverse environment than other ARB. Moreover, the photocatalytic inactivation mechanism of bacterial cells and a graded response of cellular stress mechanism caused differences in the intensity of the stress mechanism of antibiotic resistance action targets. E. coli DH5α resistant to cefotaxime and polymyxin, targeting synthesis of the cell wall and cell membrane, respectively, could confer greater advantages to bacterial survival and higher conjugative transfer frequency than E. coli DH5α resistant to nalidixic acid and rifampicin, which target the synthesis of DNA and RNA, respectively. This new perspective provides detailed information on the practical application of photocatalytic oxidation for inactivating ARB and hampering the spreading of ARGs in the aquatic environment.202235453030
898820.9988Experimental evolution of UV resistance in a phage. The dsDNA bacteriophage T7 was subjected to 30 cycles of lethal ultraviolet light (UV) exposure to select increased resistance to UV. The exposure effected a 0.9999 kill of the ancestral population, and survival of the ending population was nearly 50-fold improved. At the end point, a 2.1 kb deletion of early genes and three substitutions in structural-genes were the only changes observed at high frequency throughout the 40 kb genome; no changes were observed in genes affecting DNA metabolism. The deletion accounted for only a two-fold improvement in survival. One possible explanation of its benefit is that it represents an error catastrophe, whereby the genome experiences a reduced mutation rate. The mechanism of benefit provided by the three structural-gene mutations remains unknown. The results offer some hope of artificially evolving greater protection against sunlight damage in applications of phage therapy to plants, but the response of T7 is weak compared to that observed in bacteria selected to resist ionizing radiation. Because of the weak response, mathematical analysis of the selection process was performed to determine how the protocol might have been modified to achieve a greater response, but the greatest protection may well come from evolving phages to bind materials that block the UV.201830013847
830630.9988A glucose-mediated antibiotic resistance metabolic flux from glycolysis, the pyruvate cycle, and glutamate metabolism to purine metabolism. INTRODUCTION: Bacterial metabolic environment influences antibiotic killing efficacy. Thus, a full understanding for the metabolic resistance mechanisms is especially important to combat antibiotic-resistant bacteria. METHODS: Isobaric tags for relative and absolute quantification-based proteomics approach was employed to compare proteomes between ceftazidime-resistant and -sensitive Edwarsiella tarda LTB4 (LTB4-R(CAZ) and LTB4-S, respectively). RESULTS: This analysis suggested the possibility that the ceftazidime resistance mediated by depressed glucose is implemented through an inefficient metabolic flux from glycolysis, the pyruvate cycle, glutamate metabolism to purine metabolism. The inefficient flux was demonstrated by the reduced expression of genes and the decreased activity of enzymes in the four metabolic pathways. However, supplement upstream glucose and downstream guanosine separately restored ceftazidime killing, which not only supports the conclusion that the inefficient metabolic flux is responsible for the resistance, but also provides an effective approach to reverse the resistance. In addition, the present study showed that ceftazidime is bound to pts promoter in E. tarda. DISCUSSION: Our study highlights the way in fully understanding metabolic resistance mechanisms and establishing metabolites-based metabolic reprogramming to combat antibiotic resistance.202337915850
834540.9987Antibiotic Resistance via Bacterial Cell Shape-Shifting. Bacteria have evolved to develop multiple strategies for antibiotic resistance by effectively reducing intracellular antibiotic concentrations or antibiotic binding affinities, but the role of cell morphology in antibiotic resistance remains poorly understood. By analyzing cell morphological data for different bacterial species under antibiotic stress, we find that bacteria increase or decrease the cell surface-to-volume ratio depending on the antibiotic target. Using quantitative modeling, we show that by reducing the surface-to-volume ratio, bacteria can effectively reduce the intracellular antibiotic concentration by decreasing antibiotic influx. The model further predicts that bacteria can increase the surface-to-volume ratio to induce the dilution of membrane-targeting antibiotics, in agreement with experimental data. Using a whole-cell model for the regulation of cell shape and growth by antibiotics, we predict shape transformations that bacteria can utilize to increase their fitness in the presence of antibiotics. We conclude by discussing additional pathways for antibiotic resistance that may act in synergy with shape-induced resistance.202235616332
897450.9987Escherichia coli Bacteria Develop Adaptive Resistance to Antibacterial ZnO Nanoparticles. Antibacterial agents based on nanoparticles (NPs) have many important applications, e.g., for the textile industry, surface disinfection, wound dressing, water treatment, and food preservation. Because of their prevalent use it is important to understand whether bacteria could develop resistance to such antibacterial NPs similarly to the resistance that bacteria are known to develop to antibiotics. Here, it is reported that Escherichia coli (E. coli) develops adaptive resistance to antibacterial ZnO NPs after several days' exposure to the NPs. But, in contrast to antibiotics-resistance, the observed resistance to ZnO NPs is not stable-after several days without exposure to the NPs, the bacteria regain their sensitivity to the NPs' antibacterial properties. Based on the analyses it is suggested that the observed resistance is caused by changes in the shape of the bacteria and the expressions of membrane proteins. The findings provide insights into the response of bacteria to antibacterial NPs, which is important to elucidate for designing and evaluating the risk of applications based on antibacterial NPs.201833103858
897560.9987Targeting bacterial biofilm-related genes with nanoparticle-based strategies. Persistent infection caused by biofilm is an urgent in medicine that should be tackled by new alternative strategies. Low efficiency of classical treatments and antibiotic resistance are the main concerns of the persistent infection due to biofilm formation which increases the risk of morbidity and mortality. The gene expression patterns in biofilm cells differed from those in planktonic cells. One of the promising approaches against biofilms is nanoparticle (NP)-based therapy in which NPs with multiple mechanisms hinder the resistance of bacterial cells in planktonic or biofilm forms. For instance, NPs such as silver (Ag), zinc oxide (ZnO), titanium dioxide (TiO(2)), copper oxide (Cu), and iron oxide (Fe(3)O(4)) through the different strategies interfere with gene expression of bacteria associated with biofilm. The NPs can penetrate into the biofilm structure and affect the expression of efflux pump, quorum-sensing, and adhesion-related genes, which lead to inhibit the biofilm formation or development. Therefore, understanding and targeting of the genes and molecular basis of bacterial biofilm by NPs point to therapeutic targets that make possible control of biofilm infections. In parallel, the possible impact of NPs on the environment and their cytotoxicity should be avoided through controlled exposure and safety assessments. This study focuses on the biofilm-related genes that are potential targets for the inhibition of bacterial biofilms with highly effective NPs, especially metal or metal oxide NPs.202438841057
861870.9987Insights into the microbial degradation and resistance mechanisms of glyphosate. Glyphosate, as one of the broad-spectrum herbicides for controlling annual and perennial weeds, is widely distributed in various environments and seriously threatens the safety of human beings and ecology. Glyphosate is currently degraded by abiotic and biotic methods, such as adsorption, photolysis, ozone oxidation, and microbial degradation. Of these, microbial degradation has become the most promising method to treat glyphosate because of its high efficiency and environmental protection. Microorganisms are capable of using glyphosate as a phosphorus, nitrogen, or carbon source and subsequently degrade glyphosate into harmless products by cleaving C-N and C-P bonds, in which enzymes and functional genes related to glyphosate degradation play an indispensable role. There have been many studies on the abiotic and biotic treatment technologies, microbial degradation pathways and intermediate products of glyphosate, but the related enzymes and functional genes involved in the glyphosate degradation pathways have not been further discussed. There is little information on the resistance mechanisms of bacteria and fungi to glyphosate, and previous investigations of resistance mechanisms have mainly focused on how bacteria resist glyphosate damage. Therefore, this review explores the microorganisms, enzymes and functional genes related to the microbial degradation of glyphosate and discusses the pathways of microbial degradation and the resistance mechanisms of microorganisms to glyphosate. This review is expected to provide reference for the application and improvement of the microbial degradation of glyphosate in microbial remediation.202236049517
649780.9986Problems of conventional disinfection and new sterilization methods for antibiotic resistance control. The problem of bacterial antibiotic resistance has attracted considerable research attention, and the effects of water treatment on antibiotic resistant bacteria (ARB) and antibiotic resistance genes (ARGs) are being increasingly investigated. As an indispensable part of the water treatment process, disinfection plays an important role in controlling antibiotic resistance. At present, there were many studies on the effects of conventional and new sterilization methods on ARB and ARGs. However, there is a lack of literature relating to the limitations of conventional methods and analysis of new techniques. Therefore, this review focuses on analyzing the deficiencies of conventional disinfection and the development of new methods for antibiotic resistance control to guide future research. Firstly, we analyzed the effects and drawbacks of conventional disinfection methods, such as chlorine (Cl), ultraviolet (UV) and ozone on antibiotic resistance control. Secondly, we discuss the research progress and shortcomings of new sterilization methods in antibiotic resistance. Finally, we propose suggestions for future research directions. There is an urgent need for new effective and low-cost sterilization methods. Disinfection via UV and chlorine in combination, UV/chlorine showed greater potential for controlling ARGs.202032957272
834290.9986Inflammatory immunity and bacteriological perspectives: A new direction for copper treatment of sepsis. Copper is an essential trace element for all aerobic organisms because of its unique biological functions. In recent years, researchers have discovered that copper can induce cell death through various regulatory mechanisms, thereby inducing inflammation. Efforts have also been made to alter the chemical structure of copper to achieve either anticancer or anti-inflammatory effects. The copper ion can exhibit bactericidal effects by interfering with the integrity of the cell membrane and promoting oxidative stress. Sepsis is a systemic inflammatory response caused by infection. Some studies have revealed that copper is involved in the pathophysiological process of sepsis and is closely related to its prognosis. During the infection of sepsis, the body may enhance the antimicrobial effect by increasing the release of copper. However, to avoid copper poisoning, all organisms have evolved copper resistance genes. Therefore, further analysis of the complex relationship between copper and bacteria may provide new ideas and research directions for the treatment of sepsis.202438692229
9162100.9986Joint effects of antibiotics and quorum sensing inhibitors on resistance development in bacteria. Quorum sensing inhibitors (QSIs) are promising alternatives to antibiotics. While QSIs have great application potential in a variety of fields, their joint effects with antibiotics on bacteria, especially on antibiotic resistance mutations, remain largely unexplored. Herein, we report the joint effects of four commonly used antibiotics and two QSIs on bacterial growth and resistance mutations in E. coli. It was found that QSIs presented antagonistic or additive effects with antibiotics on bacterial growth, and more importantly, QSIs exhibited an attenuating effect on antibiotic-induced resistance mutations. Further analysis demonstrated that antibiotics might enhance resistance mutations by promoting the expressions of rpoS, lexA and recA, while QSIs attenuated the mutations by promoting the expressions of mutS and uvrD. The present research provides a comprehensive understanding of the joint effects of antibiotics and QSIs on bacteria, which may benefit the risk assessment of their combined exposure.202134060581
6503110.9986The role of operating parameters and oxidative damage mechanisms of advanced chemical oxidation processes in the combat against antibiotic-resistant bacteria and resistance genes present in urban wastewater. An upsurge in the study of antibiotic resistance in the environment has been observed in the last decade. Nowadays, it is becoming increasingly clear that urban wastewater is a key source of antibiotic resistance determinants, i.e. antibiotic-resistant bacteria and antibiotic resistance genes (ARB&ARGs). Urban wastewater reuse has arisen as an important component of water resources management in the European Union and worldwide to address prolonged water scarcity issues. Especially, biological wastewater treatment processes (i.e. conventional activated sludge), which are widely applied in urban wastewater treatment plants, have been shown to provide an ideal environment for the evolution and spread of antibiotic resistance. The ability of advanced chemical oxidation processes (AOPs), e.g. light-driven oxidation in the presence of H(2)O(2), ozonation, homogeneous and heterogeneous photocatalysis, to inactivate ARB and remove ARGs in wastewater effluents has not been yet evaluated through a systematic and integrated approach. Consequently, this review seeks to provide an extensive and critical appraisal on the assessment of the efficiency of these processes in inactivating ARB and removing ARGs in wastewater effluents, based on recent available scientific literature. It tries to elucidate how the key operating conditions may affect the process efficiency, while pinpointing potential areas for further research and major knowledge gaps which need to be addressed. Also, this review aims at shedding light on the main oxidative damage pathways involved in the inactivation of ARB and removal of ARGs by these processes. In general, the lack and/or heterogeneity of the available scientific data, as well as the different methodological approaches applied in the various studies, make difficult the accurate evaluation of the efficiency of the processes applied. Besides the operating conditions, the variable behavior observed by the various examined genetic constituents of the microbial community, may be directed by the process distinct oxidative damage mechanisms in place during the application of each treatment technology. For example, it was shown in various studies that the majority of cellular damage by advanced chemical oxidation may be on cell wall and membrane structures of the targeted bacteria, leaving the internal components of the cells relatively intact/able to repair damage. As a result, further in-depth mechanistic studies are required, to establish the optimum operating conditions under which oxidative mechanisms target internal cell components such as genetic material and ribosomal structures more intensively, thus conferring permanent damage and/or death and preventing potential post-treatment re-growth.201829153875
8963120.9986Photodynamic therapy on mRNA levels in bacteria. Antimicrobial photodynamic therapy (aPDT) has shown efficacy in inactivating different bacterial species by photosensitizer-induced free radical production. Despite aPDT is considered unable to cause resistant strains, enzymatic pathways for detoxification of reactive oxygen species and transmembrane photosensitizer efflux systems could cause resistance to aPDT. Resistance mechanisms can be evaluated by measurement of mRNA from by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Thus, the aim of this study was to access the mRNA level data obtained by RT-qPCR in bacterial cells submitted to photodynamic therapy. Studies performed on mRNA levels in bacteria after PDT were assessed on MEDLINE/Pubmed. The mRNA levels from genes related to various functions have been successfully evaluated in both Gram-positive and -negative bacteria after aPDT by RT-qPCR. Such an approach has improved the understanding of aPDT-induced effects, and reinforced the effectiveness of aPDT on bacteria, which can cause infections in different human tissues.202439214913
6745130.9986Decreased Antibiotic Susceptibility in Pseudomonas aeruginosa Surviving UV Irradition. Given its excellent performance against the pathogens, UV disinfection has been applied broadly in different fields. However, only limited studies have comprehensively investigated the response of bacteria surviving UV irradiation to the environmental antibiotic stress. Here, we investigated the antibiotic susceptibility of Pseudomonas aeruginosa suffering from the UV irradiation. Our results revealed that UV exposure may decrease the susceptibility to tetracycline, ciprofloxacin, and polymyxin B in the survival P. aeruginosa. Mechanistically, UV exposure causes oxidative stress in P. aeruginosa and consequently induces dysregulation of genes contributed to the related antibiotic resistance genes. These results revealed that the insufficient ultraviolet radiation dose may result in the decreased antibiotic susceptibility in the pathogens, thus posing potential threats to the environment and human health.202133613479
4277140.9986Exposure to phages has little impact on the evolution of bacterial antibiotic resistance on drug concentration gradients. The use of phages for treating bacterial pathogens has recently been advocated as an alternative to antibiotic therapy. Here, we test a hypothesis that bacteria treated with phages may show more limited evolution of antibiotic resistance as the fitness costs of resistance to phages may add to those of antibiotic resistance, further reducing the growth performance of antibiotic-resistant bacteria. We did this by studying the evolution of phage-exposed and phage-free Pseudomonas fluorescens cultures on concentration gradients of single drugs, including cefotaxime, chloramphenicol, and kanamycin. During drug treatment, the level of bacterial antibiotic resistance increased through time and was not affected by the phage treatment. Exposure to phages did not cause slower growth in antibiotic-resistant bacteria, although it did so in antibiotic-susceptible bacteria. We observed significant reversion of antibiotic resistance after drug use being terminated, and the rate of reversion was not affected by the phage treatment. The results suggest that the fitness costs caused by resistance to phages are unlikely to be an important constraint on the evolution of bacterial antibiotic resistance in heterogeneous drug environments. Further studies are needed for the interaction of fitness costs of antibiotic resistance with other factors.201424665341
9374150.9986Mathematical modelling of antibiotic interaction on evolution of antibiotic resistance: an analytical approach. BACKGROUND: The emergence and spread of antibiotic-resistant pathogens have led to the exploration of antibiotic combinations to enhance clinical effectiveness and counter resistance development. Synergistic and antagonistic interactions between antibiotics can intensify or diminish the combined therapy's impact. Moreover, these interactions can evolve as bacteria transition from wildtype to mutant (resistant) strains. Experimental studies have shown that the antagonistically interacting antibiotics against wildtype bacteria slow down the evolution of resistance. Interestingly, other studies have shown that antibiotics that interact antagonistically against mutants accelerate resistance. However, it is unclear if the beneficial effect of antagonism in the wildtype bacteria is more critical than the detrimental effect of antagonism in the mutants. This study aims to illuminate the importance of antibiotic interactions against wildtype bacteria and mutants on the deacceleration of antimicrobial resistance. METHODS: To address this, we developed and analyzed a mathematical model that explores the population dynamics of wildtype and mutant bacteria under the influence of interacting antibiotics. The model investigates the relationship between synergistic and antagonistic antibiotic interactions with respect to the growth rate of mutant bacteria acquiring resistance. Stability analysis was conducted for equilibrium points representing bacteria-free conditions, all-mutant scenarios, and coexistence of both types. Numerical simulations corroborated the analytical findings, illustrating the temporal dynamics of wildtype and mutant bacteria under different combination therapies. RESULTS: Our analysis provides analytical clarification and numerical validation that antibiotic interactions against wildtype bacteria exert a more significant effect on reducing the rate of resistance development than interactions against mutants. Specifically, our findings highlight the crucial role of antagonistic antibiotic interactions against wildtype bacteria in slowing the growth rate of resistant mutants. In contrast, antagonistic interactions against mutants only marginally affect resistance evolution and may even accelerate it. CONCLUSION: Our results emphasize the importance of considering the nature of antibiotic interactions against wildtype bacteria rather than mutants when aiming to slow down the acquisition of antibiotic resistance.202438426146
8987160.9986Alternating antibiotic treatments constrain evolutionary paths to multidrug resistance. Alternating antibiotic therapy, in which pairs of drugs are cycled during treatment, has been suggested as a means to inhibit the evolution of de novo resistance while avoiding the toxicity associated with more traditional combination therapy. However, it remains unclear under which conditions and by what means such alternating treatments impede the evolution of resistance. Here, we tracked multistep evolution of resistance in replicate populations of Staphylococcus aureus during 22 d of continuously increasing single-, mixed-, and alternating-drug treatment. In all three tested drug pairs, the alternating treatment reduced the overall rate of resistance by slowing the acquisition of resistance to one of the two component drugs, sometimes as effectively as mixed treatment. This slower rate of evolution is reflected in the genome-wide mutational profiles; under alternating treatments, bacteria acquire mutations in different genes than under corresponding single-drug treatments. To test whether this observed constraint on adaptive paths reflects trade-offs in which resistance to one drug is accompanied by sensitivity to a second drug, we profiled many single-step mutants for cross-resistance. Indeed, the average cross-resistance of single-step mutants can help predict whether or not evolution was slower in alternating drugs. Together, these results show that despite the complex evolutionary landscape of multidrug resistance, alternating-drug therapy can slow evolution by constraining the mutational paths toward resistance.201425246554
8343170.9986Bacterial Stress Responses as Potential Targets in Overcoming Antibiotic Resistance. Bacteria can be adapted to adverse and detrimental conditions that induce general and specific responses to DNA damage as well as acid, heat, cold, starvation, oxidative, envelope, and osmotic stresses. The stress-triggered regulatory systems are involved in bacterial survival processes, such as adaptation, physiological changes, virulence potential, and antibiotic resistance. Antibiotic susceptibility to several antibiotics is reduced due to the activation of stress responses in cellular physiology by the stimulation of resistance mechanisms, the promotion of a resistant lifestyle (biofilm or persistence), and/or the induction of resistance mutations. Hence, the activation of bacterial stress responses poses a serious threat to the efficacy and clinical success of antibiotic therapy. Bacterial stress responses can be potential targets for therapeutic alternatives to antibiotics. An understanding of the regulation of stress response in association with antibiotic resistance provides useful information for the discovery of novel antimicrobial adjuvants and the development of effective therapeutic strategies to control antibiotic resistance in bacteria. Therefore, this review discusses bacterial stress responses linked to antibiotic resistance in Gram-negative bacteria and also provides information on novel therapies targeting bacterial stress responses that have been identified as potential candidates for the effective control of Gram-negative antibiotic-resistant bacteria.202235889104
9427180.9986Polysaccharides' Structures and Functions in Biofilm Architecture of Antimicrobial-Resistant (AMR) Pathogens. Bacteria and fungi have developed resistance to the existing therapies such as antibiotics and antifungal drugs, and multiple mechanisms are mediating this resistance. Among these, the formation of an extracellular matrix embedding different bacterial cells, called biofilm, is an effective strategy through which bacterial and fungal cells are establishing a relationship in a unique environment. The biofilm provides them the possibility to transfer genes conferring resistance, to prevent them from desiccation and to impede the penetration of antibiotics or antifungal drugs. Biofilms are formed of several constituents including extracellular DNA, proteins and polysaccharides. Depending on the bacteria, different polysaccharides form the biofilm matrix in different microorganisms, some of them involved in the first stage of cells' attachment to surfaces and to each other, and some responsible for giving the biofilm structure resistance and stability. In this review, we describe the structure and the role of different polysaccharides in bacterial and fungal biofilms, we revise the analytical methods to characterize them quantitatively and qualitatively and finally we provide an overview of potential new antimicrobial therapies able to inhibit biofilm formation by targeting exopolysaccharides.202336835442
8333190.9986Role of Extracellular DNA in Bacterial Response to SOS-Inducing Drugs. The SOS response is a conserved stress response pathway that is triggered by DNA damage in the bacterial cell. Activation of this pathway can, in turn, cause the rapid appearance of new mutations, sometimes called hypermutation. We compared the ability of various SOS-inducing drugs to trigger the expression of RecA, cause hypermutation, and produce elongation of bacteria. During this study, we discovered that these SOS phenotypes were accompanied by the release of large amounts of DNA into the extracellular medium. The release of DNA was accompanied by a form of bacterial aggregation in which the bacteria became tightly enmeshed in DNA. We hypothesize that DNA release triggered by SOS-inducing drugs could promote the horizontal transfer of antibiotic resistance genes by transformation or by conjugation.202337107011