# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 9110 | 0 | 0.9920 | Bacterial resistance to antibiotics: the role of biofilms. Bacteria adhere to natural and synthetic, medically important surfaces within an extracellular polymer generically termed the glycocalyx. This quasi-structure is a biofilm. The enhanced antibiotic resistance of biofilm bacteria, relative to floating (planktonic) bacteria, encourages the establishment of chronic bacterial infections. Resistance mechanisms include the hinderance of antibiotic diffusion by the glycocalyx, the physiology of the bacteria and the environment conditions of the niche in which the biofilm resides. | 1991 | 1763187 |
| 9108 | 1 | 0.9919 | Learning from losers. Bacteria can overcome environmental challenges by killing nearby bacteria and incorporating their DNA. | 2017 | 29148975 |
| 755 | 2 | 0.9917 | Pervasive gene deregulation underlies adaptation and maladaptation in trimethoprim-resistant E. coli. Bacteria employ a number of mechanisms to adapt to antibiotics. Mutations in transcriptional regulators alter the expression levels of genes that can change the susceptibility of bacteria to antibiotics. Two-component signaling proteins are a major class of signaling molecule used by bacteria to regulate transcription. In previous work, we found that mutations in MgrB, a feedback regulator of the PhoQP two-component system, conferred trimethoprim tolerance to Escherichia coli. Here, we elucidate how mutations in MgrB have a domino-like effect on the gene regulatory network of E. coli. As a result, pervasive perturbation of gene regulation ensues. Depending on the environmental context, this pervasive deregulation is either adaptive or maladaptive. Our study sheds light on how deregulation of gene expression can be beneficial for bacteria when challenged with antibiotics, and why regulators like MgrB may have evolved in the first place. | 2023 | 38032208 |
| 489 | 3 | 0.9917 | Symbiotic interactions between free-living amoeba and harboured mercury-resistant bacteria. A co-culture of environmental Acanthamoeba sp. associated to Hg-sensitive, narrow or broad-spectrum Hg-resistant Aeromonas sp. strains was exposed to HgCl(2) and phenylmercuric acetate. Amoebic growth depended on the Hg-resistance determinants of harboured bacteria. This laboratory model helped in understanding the mechanisms of Hg-resistance observed in amoeba isolated in river waters after a mercuric pollution. Amoeba acquired Hg-resistance by using symbiotic resistant bacteria. | 1993 | 23195537 |
| 8238 | 4 | 0.9916 | Resistance to enediyne antitumor antibiotics by CalC self-sacrifice. Antibiotic self-resistance mechanisms, which include drug elimination, drug modification, target modification, and drug sequestration, contribute substantially to the growing problem of antibiotic resistance among pathogenic bacteria. Enediynes are among the most potent naturally occurring antibiotics, yet the mechanism of resistance to these toxins has remained a mystery. We characterize an enediyne self-resistance protein that reveals a self-sacrificing paradigm for resistance to highly reactive antibiotics, and thus another opportunity for nonpathogenic or pathogenic bacteria to evade extremely potent small molecules. | 2003 | 12970566 |
| 2498 | 5 | 0.9915 | Emerging carbapenemases: a global perspective. The celestial rise in antibiotic resistance among Gram-negative bacteria has challenged both the scientific and pharmaceutical sectors. The hallmark of this general increase is the unbridled dissemination of carbapenem resistance genes, namely KPC, OXA and metallo-β-lactamase variants. In particular, the media attention given to the NDM-1 metallo-β-lactamase has highlighted the global consequences of human behaviour on spreading antibiotic resistance. | 2010 | 21129630 |
| 8326 | 6 | 0.9915 | The force awakens: The dark side of mechanosensing in bacterial pathogens. For many bacteria, the ability to sense physical stimuli such as contact with a surface or a potential host cell is vital for survival and proliferation. This ability, and subsequent attachment, confers a wide range of benefits to bacteria and many species have evolved to take advantage of this. Despite the impressive diversity of bacterial pathogens and their virulence factors, mechanosensory mechanisms are often conserved. These include sensing impedance of flagellar rotation and resistance to type IV pili retraction. There are additional mechanisms that rely on the use of specific membrane-bound adhesins to sense either surface proximity or shear forces. This review aims to examine these mechanosensors, and how they are used by pathogenic bacteria to sense physical features in their environment. We will explore how these sensors generate and transmit signals which can trigger modulation of virulence-associated gene expression in some of the most common bacterial pathogens: Pseudomonas aeruginosa, Proteus mirabilis, Escherichia coli and Vibrio species. | 2021 | 33279672 |
| 9811 | 7 | 0.9914 | "Infectious Supercarelessness" in Discussing Antibiotic-Resistant Bacteria. Many bacterial pathogens are exhibiting resistance to increasing numbers of antibiotics making it much more challenging to treat the infections caused by these microbes. In many reports in the media and perhaps even in discussions among physicians and biomedical scientists, these bacteria are frequently referred to as "bugs" with the prefix "super" appended. This terminology has a high potential to elicit unjustified inferences and fails to highlight the broader evolutionary context. Understanding the full range of biological and evolutionary factors that influence the spread and outcomes of infections is critical to formulating effective individual therapies and public health interventions. Therefore, more accurate terminology should be used to refer these multidrug-resistant bacteria. | 2016 | 28174759 |
| 4137 | 8 | 0.9914 | The Prehistory of Antibiotic Resistance. Antibiotic resistance is a global problem that is reaching crisis levels. The global collection of resistance genes in clinical and environmental samples is the antibiotic "resistome," and is subject to the selective pressure of human activity. The origin of many modern resistance genes in pathogens is likely environmental bacteria, including antibiotic producing organisms that have existed for millennia. Recent work has uncovered resistance in ancient permafrost, isolated caves, and in human specimens preserved for hundreds of years. Together with bioinformatic analyses on modern-day sequences, these studies predict an ancient origin of resistance that long precedes the use of antibiotics in the clinic. Understanding the history of antibiotic resistance is important in predicting its future evolution. | 2016 | 27252395 |
| 9107 | 9 | 0.9914 | A versatile pH-responsive peptide based dynamic biointerface for tracking bacteria killing and infection resistance. Herein we reported a versatile dynamic biointerface based on pH-responsive peptide self-assembly and disassembly to capture the bacteria to avoid bacteria further infected tissue around that can release peptides from the surface in a slightly acidic environment to kill the bacteria with the specificity. The exposed biointerface still presented infection resistance. | 2021 | 34350905 |
| 9924 | 10 | 0.9914 | Molecular mechanisms of fluoroquinolone resistance. Fluoroquinolones have a broad spectrum of activity for complicated urinary tract infections, gastrointestinal infections, respiratory tract infections, sexually transmitted diseases, and chronic osteomyelitis. Since fluoroquinolones are excellent antibiotics for a number of clinical indications, their consumption has increased rapidly, both in human medicine and in food animals. Resistance to fluoroquinolones is chromosomal mediated, involving mutations either in the target genes including DNA gyrase (gyrA or gyrB) and topoisomerase IV (parC or parE), or in the regulatory factors controlling bacterial permeability or the efflux capacity of the bacteria. This review focuses on mechanisms of fluoroquinolone resistance, including known and proposed molecular mechanisms. This review also discuses the clinical impact of fluoroquinolone-resistant bacteria. | 2003 | 12741725 |
| 4135 | 11 | 0.9913 | Bacterial monopolists: the bundling and dissemination of antimicrobial resistance genes in gram-positive bacteria. Antibiotic resistance is the unavoidable result of our placing selective pressure on the microbial community. Advances in molecular biology techniques in the past 2 decades have allowed us to greatly improve our understanding of the mechanisms by which resistance emerges and disseminates among human pathogenic bacteria. Gram-positive bacteria employ a diverse array of elements, including plasmids, transposons, insertion sequences, and bacteriophages, to disseminate resistance. An understanding of these mechanisms and their prevalence can improve our ability to treat clinical infections in hospitalized patients, as well as to predict and control the spread of resistant bacteria in the nosocomial environment. | 2000 | 11017827 |
| 8325 | 12 | 0.9913 | The Effects of Airflow on the Mechanosensitive Channels of Escherichia coli MG1655 and the Impact of Survival Mechanisms Triggered. Understanding how bacteria respond to ventilated environments is a crucial concept, especially when considering accurate airflow modeling and detection limits. To properly design facilities for aseptic conditions, we must minimize the parameters for pathogenic bacteria to thrive. Identifying how pathogenic bacteria continue to survive, particularly due to their multi-drug resistance characteristics, is necessary for designing sterile environments and minimizing pathogen exposure. A conserved characteristic among bacterial organisms is their ability to maintain intracellular homeostasis for survival and growth in hostile environments. Mechanosensitive (MS) channels are one of the characteristics that guide this phenomenon. Interestingly, during extreme stress, bacteria will forgo favorable homeostasis to execute fast-acting survival strategies. Physiological sensors, such as MS channels, that trigger this survival mechanism are not clearly understood, leaving a gap in how bacteria translate physical stress to an intracellular response. In this paper, we study the role of mechanosensitive ion channels that are potentially triggered by aerosolization. We hypothesize that change in antimicrobial uptake is affected by aerosolization stress. Bacteria regulate their defense mechanisms against antimicrobials, which leads to varying susceptibility. Based on this information we hypothesize that aerosolization stress affects the antimicrobial resistance defense mechanisms of Escherichia coli (E. coli). We analyzed the culturability of knockout E. coli strains with different numbers of mechanosensitive channels and compared antibiotic susceptibility under stressed and unstressed airflow conditions. As a result of this study, we can identify how the defensive mechanisms of resistant bacteria are triggered for their survival in built environments. By changing ventilation airflow velocity and observing the change in antibiotic responses, we show how pathogenic bacteria respond to ventilated environments via mechanosensitive ion channels. | 2023 | 37764080 |
| 9932 | 13 | 0.9913 | Beta-lactam resistance mechanisms in gram-negative bacteria. Beta-lactam antibiotics are commonly used to treat a variety of bacterial infections. Gram-negative bacteria have evolved several resistance mechanisms including altered permeability and beta-lactamase production. New trends in resistance are emerging amongst clinical isolates which may reflect the choice of beta-lactam employed. | 1986 | 2856616 |
| 4438 | 14 | 0.9913 | Penicillin binding proteins, beta-lactams, and lactamases: offensives, attacks, and defensive countermeasures. A strong outer covering of peptidoglycan (the sacculus) is essential for most bacteria. Beta-lactams have evolved billions of years ago and can block saccular growth of the organism. This led to the evolution of beta-lactamases and resistant penicillin binding proteins (PBPs). With the introduction of lactam antibiotics by the pharmaceutical industry, resistance genes in nature were laterally transferred to antibiotic-treated disease-causing organisms and additional modification of beta-lactamase genes and of the regulatory genes of the mecA region took place. However, it can be concluded that very little of either type of resistance mechanisms represents new basic evolution against the penicillin type antibiotics. In the last 60 years the resistant bacteria in the main arose by movement of genes from other organisms, from minor genetic changes, and from alteration of the regulation of synthesis. | 2000 | 11192022 |
| 9700 | 15 | 0.9913 | Predation and selection for antibiotic resistance in natural environments. Genes encoding resistance to antibiotics appear, like the antibiotics themselves, to be ancient, originating long before the rise of the era of anthropogenic antibiotics. However, detailed understanding of the specific biological advantages of antibiotic resistance in natural environments is still lacking, thus limiting our efforts to prevent environmental influx of resistance genes. Here, we propose that antibiotic-resistant cells not only evade predation from antibiotic producers but also take advantage of nutrients released from cells that are killed by the antibiotic-producing bacteria. Thus, predation is potentially an important mechanism for driving antibiotic resistance during slow or stationary phase of growth when nutrients are deprived. This adds to explain the ancient nature and widespread occurrence of antibiotic resistance in natural environments unaffected by anthropogenic antibiotics. In particular, we suggest that nutrient-poor environments including indoor environments, for example, clean rooms and intensive care units may serve as a reservoir and source for antibiotic-producing as well as antibiotic-resistant bacteria. | 2016 | 26989434 |
| 4430 | 16 | 0.9913 | βLactam Resistance Mediated by Changes in Penicillin-Binding Proteins. The widespread use, or perhaps overuse, of penicillin during the past 50 yr has driven the evolution of resistance to penicilling in numerous different species of bacteria.Typically, resistance has arisen as a result of the acquisition of β-lactamases that inactivate the antibiotic (see Chapter 25 . Alternatively, in some Gram-negative bacteria, resistance may have arisen by a reduction in the ability of the antibiotic to access its target. However, in a number of clinically important Gram-negative and Gram-positive bacteria, resistance has arisen by alteration of the targets for penicillin and other β-lactam antibiotics, namely, the penicillin-binding proteins (PBPs). | 1998 | 21390765 |
| 4836 | 17 | 0.9913 | Genes and spectrum: the theoretical limits. Antibiotic resistance can result either from mutations within a chromosomal gene or from mobile genes imported from outside. In the last 15 years, some of these mobile genes have shown a propensity to adapt to successive antibiotic challenges, the most versatile being the class A beta-lactamases. The TEM and SHV beta-lactamase nuclei, usually after one initial critical mutation, allow a series of successive mutations that increase the spectrum to hydrolyze most cephalosporins. The class C beta-lactamases also show some versatility; while it migrates from the chromosome, subtle changes can occur in the gene to broaden the spectrum. Trimethoprim resistance has shown less adaptability in gram-negative bacteria, but in gram-positive organisms the plasmid has captured the chromosomal dihydrofolate reductase of Staphylococcus epidermidis, and a minimal number of changes have occurred that decrease the binding of trimethroprim. Other resistance mechanisms appear less adaptable, relying rather on the importation of new genes to cope with new challenges. | 1998 | 9710668 |
| 4839 | 18 | 0.9913 | beta-Lactamases: protein evolution in real time. The evolution and spread of bacteria resistant to beta-lactam antibiotics has progressed at an alarming rate. Bacteria may acquire resistance to a given drug by mutation of pre-existing genes or by the acquisition of new genes from other bacteria. One ongoing example of these mechanisms is the evolution of new variants of the TEM and SHV beta-lactamases with altered substrate specificity. | 1998 | 9746943 |
| 9121 | 19 | 0.9913 | The role of efflux pumps ın antıbıotıc resıstance of gram negatıve rods. Antibiotic resistance is an important public health problem today, causing increased morbidity and mortality. Resistance to antibiotics in bacteria can develop by various mechanisms such as a change in the target site of the drug, a change in the outer membrane permeability, enzymatic defusing of the drug and efflux of the antimicrobial compound. Some bacteria have the potential to develop resistance to more than one drug by using several mechanisms together. One of the important resistance mechanisms of bacteria is active efflux pumps (EPs). EPs are pump proteins found in all cell types, located in the cell membrane. They are responsible for the excretion of various intracellular and extracellular substances (antibiotics, etc.) out of the cell. There is much research on various antimicrobials that cause antibiotic resistance in Gram negative rods, but studies on EPs are relatively few. Due to the concern that antibiotics will be insufficient in the treatment of diseases, a good understanding of EPs and the discovery of new EP inhibitors will shed light on the future of humanity. In this review, the structure of bacterial EPs in Gram negative bacteria, the role of EPs in multidrug resistance, the importance of EP inhibitors in the fight against antibiotic resistance and the phenotypic and genotypic detection methods of EPs are discussed. | 2023 | 37060362 |