# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 4898 | 0 | 1.0000 | Antibiotics and bacterial resistance. A few elements of genetic basis for this relationship. In the preantibiotic era, many people died of bacterial infections caused by such pathogens as Staphylococcus aureus and Streptococcus pyogenes, Streptococcus pneumoniae and Mycobacterium tuberculosis. Antibiotics have reduced the mortality from infectious diseases but not the prevalence of these diseases. It was not long after the clinical introduction of the first antibiotics in the 1950s that the first reports of bacterial resistance began to appear. Use, and often abuse or misuse, of antimicrobial agents has encouraged the evolution of bacteria toward resistance, resulting often in therapeutic failure. In the beginning, new antibiotics have always appeared in plenty of time to provide new cures for diseases caused by resistant bacterial pathogens. Also, some clinically important groups of bacteria showed no signs of major increases in resistance. For example, S. pneumoniae strains remained susceptible to penicillin long after other bacteria had become resistant to it. Recent developments of bacteria resistance to antibiotics are indeed disquieting. | 1995 | 8993117 |
| 4318 | 1 | 0.9999 | Emerging problems of antibiotic resistance in community medicine. Emergence of antimicrobial resistance in bacteria associated with community acquired infections has made the choice of empirical therapy more difficult and more expensive. The problems due to possible spread of MRSA to the community, emergence of penicillin resistance in S. pneumoniae, ampicillin resistance in H. influenzae, and multiresistance among common enteric pathogens are highlighted. Bacteria have a remarkable ability to develop resistance to many of the newly synthesized antimicrobial agents but the appropriate use of antibiotics will delay and in many cases prevent the emergence of resistance. | 1996 | 10879217 |
| 9798 | 2 | 0.9999 | Fight Against Antimicrobial Resistance: We Always Need New Antibacterials but for Right Bacteria. Antimicrobial resistance in bacteria is frightening, especially resistance in Gram-negative Bacteria (GNB). In 2017, the World Health Organization (WHO) published a list of 12 bacteria that represent a threat to human health, and among these, a majority of GNB. Antibiotic resistance is a complex and relatively old phenomenon that is the consequence of several factors. The first factor is the vertiginous drop in research and development of new antibacterials. In fact, many companies simply stop this R&D activity. The finding is simple: there are enough antibiotics to treat the different types of infection that clinicians face. The second factor is the appearance and spread of resistant or even multidrug-resistant bacteria. For a long time, this situation remained rather confidential, almost anecdotal. It was not until the end of the 1980s that awareness emerged. It was the time of Vancomycin-Resistance Enterococci (VRE), and the threat of Vancomycin-Resistant MRSA (Methicillin-Resistant Staphylococcus aureus). After this, there has been renewed interest but only in anti-Gram positive antibacterials. Today, the threat is GNB, and we have no new molecules with innovative mechanism of action to fight effectively against these bugs. However, the war against antimicrobial resistance is not lost. We must continue the fight, which requires a better knowledge of the mechanisms of action of anti-infectious agents and concomitantly the mechanisms of resistance of infectious agents. | 2019 | 31470632 |
| 4294 | 3 | 0.9998 | Anaerobic infections: update on treatment considerations. Anaerobic bacteria are the predominant indigenous flora of humans and, as a result, play an important role in infections, some of which are serious with a high mortality rate. These opportunistic pathogens are frequently missed in cultures of clinical samples because of shortcomings in collection and transport procedures as well as lack of isolation and susceptibility testing of anaerobes in many clinical microbiology laboratories. Correlation of clinical failures with known antibacterial resistance of anaerobic bacteria is seldom possible. Changes in resistance over time, and the discovery and characterization of resistance determinants in anaerobic bacteria, has increased recognition of problems in empirical treatment and has even resulted in changes in treatment guidelines. This review discusses the role of anaerobic bacteria in the normal flora of humans, their involvement in different mixed infections, developments in antibacterial resistance of the most frequent anaerobic pathogens and possible new treatment options. | 2010 | 20426496 |
| 4797 | 4 | 0.9998 | Antibiotic resistance among clinically important gram-positive bacteria in the UK. The resistance of bacteria to antibiotics, particularly those used for first-line therapy, is an increasing cause for concern. In the UK, the prevalence of resistance to methicillin and mupirocin in Staphylococcus aureus, and to penicillin and macrolides in Streptococcus pneumoniae, appear to be increasing. There has also been an increase in the number of hospitals where glycopeptide-resistant enterococci are known to have been isolated. The increases in methicillin-resistant S. aureus and glycopeptide-resistant enterococci are due, in part, to the inter-hospital spread of epidemic strains. Although new quinolones and streptogramins with activity against Gram-positive bacteria (including strains resistant to currently available agents) are under development, there is no reason to believe that resistance to these agents will not emerge. The control of resistance in Gram-positive bacteria will require a multi-faceted approach, including continued and improved surveillance, a reduction in the unnecessary use of antibiotics, and the application of other strategies such as vaccination. | 1998 | 9777517 |
| 4316 | 5 | 0.9998 | Why do antimicrobial agents become ineffectual? Antibiotic resistance has evolved over the past 50 years from a merely microbiological curiosity to a serious medical problem in hospitals all over the world. Resistance has been reported in almost all species of gram-positive and -negative bacteria to various classes of antibiotics including recently developed ones. Bacteria acquire resistance by reducing permeability and intracellular accumulation, by alteration of targets of antibiotic action, and by enzymatic modification of antibiotics. Inappropriate use of an antibiotic selects resistant strains much more frequently. Once resistant bacteria has emerged, the resistance can be transferred to other bacteria by various mechanisms, resulting in multiresistant strains. MRSA is one of the typical multiresistant nosocomial pathogens. A study of the PFGE pattern of endonuclease-digested chromosomal DNA showed that MRSA of a few clones were disseminated among newborns in the NICU of a Japanese hospital. In this regard, it is important to choose appropriate antibiotics and then after some time, to change to other classes to reduce the selection of resistant strains. Since the development of epoch-making new antibiotics is not expected in the near future, it has become very important to use existing antibiotics prudently based on mechanisms of antibiotic action and bacterial resistance. Control of nosocomial infection is also very important to reduce further spread of resistant bacteria. | 1998 | 10097676 |
| 4317 | 6 | 0.9998 | Development and spread of bacterial resistance to antimicrobial agents: an overview. Resistance to antimicrobial agents is emerging in a wide variety of nosocomial and community-acquired pathogens. The emergence and spread of multiply resistant organisms represent the convergence of a variety of factors that include mutations in common resistance genes that extend their spectrum of activity, the exchange of genetic information among microorganisms, the evolution of selective pressures in hospitals and communities that facilitate the development and spread of resistant organisms, the proliferation and spread of multiply resistant clones of bacteria, and the inability of some laboratory testing methods to detect emerging resistance phenotypes. Twenty years ago, bacteria that were resistant to antimicrobial agents were easy to detect in the laboratory because the concentration of drug required to inhibit their growth was usually quite high and distinctly different from that of susceptible strains. Newer mechanisms of resistance, however, often result in much more subtle shifts in bacterial population distributions. Perhaps the most difficult phenotypes to detect, as shown in several proficiency testing surveys, are decreased susceptibility to beta-lactams in pneumococci and decreased susceptibility to vancomycin in staphylococci. In summary, emerging resistance has required adaptations and modifications of laboratory diagnostic techniques, empiric anti-infective therapy for such diseases as bacterial meningitis, and infection control measures in health care facilities of all kinds. Judicious use is imperative if we are to preserve our arsenal of antimicrobial agents into the next decade. | 2001 | 11524705 |
| 4242 | 7 | 0.9998 | The basis of antibiotic resistance in bacteria. The ability of bacteria to resist the inhibitory and lethal actions of antibiotics is a major clinical problem, and has been observed with every antimicrobial agent. In this article, the major mechanisms of antibiotic resistance are reviewed, and the clinical relevance of such resistance in selected bacteria is discussed. | 1990 | 2192071 |
| 4257 | 8 | 0.9998 | Antibiotic resistance in bacteria. Antibiotic resistance in bacteria has emerged as a medical catastrophe. This results from the speed at which bacteria multiply and are spread, and the ease with which they can change their genetic material or acquire new genes. They exert biochemical resistance by preventing entry of the drug, by rapidly extruding the drug, or by enzymatically inactivating the drug or altering its molecular target. The presence of antibiotics in the internal environments of human beings and animals provides a selective pressure for any resistant organisms to become predominant. Examples of antibiotic resistance in several important human pathogens are Streptococcus pneumoniae, enterococci, staphylococci, enteric bacilli, Haemophilus influenzae, Neisseria gonorrhoeae, Neisseria meningitidis, and Mycobacterium tuberculosis. | 1995 | 7631202 |
| 4796 | 9 | 0.9998 | The specter of glycopeptide resistance: current trends and future considerations. Two glycopeptide antibiotics, vancomycin and teicoplanin, are currently available for clinical use in various parts of the world, whereas a third, avoparcin, is available for use in agricultural applications and in veterinary medicine in some countries. Because of their outstanding activity against a broad spectrum of gram-positive bacteria, vancomycin and teicoplanin have often been considered the drugs of "last resort" for serious infections due to drug-resistant gram-positive pathogens. Glycopeptides had been in clinical use for almost 30 years before high-level resistance, first reported in enterococcal species, emerged. More recently, there have been disturbing reports of low- and intermediate-level resistance to vancomycin in strains of Staphylococcus aureus. A review of earlier reports reveals, however, that S. aureus strains with reduced susceptibility to glycopeptides were first identified >40 years ago. Such strains may occur in nature or may have developed low-level mutational resistance in response to the selection pressure of glycopeptide therapy. Of considerably greater concern is the possibility that vancomycin resistance genes found in enterococci may be transferred to more virulent organisms such as staphylococci or Streptococcus pneumoniae. | 1998 | 9684651 |
| 4062 | 10 | 0.9998 | Antibiotic resistance mechanisms in bacteria of oral and upper respiratory origin. Over the past 20 years, antibiotic resistance has increased in virtually every species of bacteria examined. In this paper, the main mechanisms of antibiotic resistance currently known for antibiotics used for treatment of disease caused by oral and upper respiratory bacteria will be reviewed, with an emphasis on the most commonly used antibiotics. The possible role that mercury, which is released from silver amalgams, plays in the oral/respiratory bacterial ecology is also discussed, as it relates to possible selection of antibiotic resistant bacteria. | 1998 | 9573495 |
| 4293 | 11 | 0.9998 | Resistance to ocular antibiotics: an overview. The introduction of new antibiotic compounds into therapy initiates the development of resistance by the target bacteria. Resistance increases the risk of treatment failure with potentially serious consequences. Local application of antibacterial compounds to the eyes may lead to bacterial resistance in bacterial isolates from the eyes. The incidence of resistant strains of common pathogens is probably increasing. As compounds can be absorbed into the systemic circulation following ocular administration, the subsequent low concentrations in the blood could provide the selective pressure for the survival of resistant bacteria in the body. Despite this possibility, there are no reports of systemic resistance in bacteria following ocular administration of antibacterial compounds. All health-care professionals should be concerned about this possibility and continue to use these important compounds with respect. | 2007 | 17535364 |
| 4309 | 12 | 0.9998 | The Characterization of Enterococcus Genus: Resistance Mechanisms and Inflammatory Bowel Disease. The constantly growing bacterial resistance against antibiotics is recently causing serious problems in the field of human and veterinary medicine as well as in agriculture. The mechanisms of resistance formation and its preventions are not well explored in most bacterial genera. The aim of this review is to analyse recent literature data on the principles of antibiotic resistance formation in bacteria of the Enterococcus genus. Furthermore, the habitat of the Enterococcus genus, its pathogenicity and pathogenicity factors, its epidemiology, genetic and molecular aspects of antibiotic resistance, and the relationship between these bacteria and bowel diseases are discussed. So-called VREfm - vancomycin resistant Enterococcus faecium and its currently rapidly growing resistance as well as the significance of these bacteria in nosocomial diseases is described. | 2020 | 32292819 |
| 4315 | 13 | 0.9998 | Problems and dilemmas of antimicrobial resistance. An important obstacle to the long-term efficacy of an antimicrobial agent is the appearance and spread of resistance to the agent. The fact that many antimicrobials are produced by microorganisms in nature may provide long-term selective pressure for the emergence of resistance in antibiotic-producing as well as -nonproducing organisms. Indeed, the rapidity with which many resistances have appeared after the introduction of a new antibiotic suggests that these resistance genes were already present somewhere in nature prior to clinical use. In the hospital setting, the most recent worrisome resistance traits to emerge include plasmid-mediated resistance to imipenem and to third-generation cephalosporins among nosocomial gram-negative bacteria, and the acquisition of resistance to vancomycin by enterococci. Methicillin-resistant staphylococci continue to be a problem and are increasingly resistant to numerous other agents such as rifampin and the newer fluoroquinolones. The most important resistances seen in community-acquired organisms include beta-lactam resistance in pneumococci and combined ampicillin and chloramphenicol resistance in Haemophilus influenzae. Shigellae resistant to essentially all commonly used oral agents are also a problem, particularly in developing countries. No end is in sight to the problem of antimicrobial resistance, and thus new strategies to prevent infections and control resistant organisms continue to be necessary. | 1992 | 1480504 |
| 4795 | 14 | 0.9998 | Epidemiology and mechanisms of glycopeptide resistance in enterococci. PURPOSE OF REVIEW: This review updates epidemiologic trends and our understanding of glycopeptide resistance in enterococci. RECENT FINDINGS: Colonization and infection rates with vancomycin resistant enterococci continue to increase throughout the world while factors contributing to this rise continue to be defined. While no interventions exist to eradicate colonization, infection control procedures are cost effective and decrease the prevalence of vancomycin resistant enterococcal colonization and infection. New molecular methods show great promise in strengthening our ability to detect colonization with these bacteria. Furthermore, our understanding of the origin of vancomycin resistant enterococci continues to grow. Paenibacillus species found in soil have been found to carry homologues of vanA-associated glycopeptide resistance genes found in enterococci. Also, additional evidence supports previous data that VanB-associated resistance may have been horizontally transferred from gastrointestinal tract bacteria to enterococci. Finally, glycopeptide resistance has been transferred to methicillin-resistant Staphylococcus aureus in clinical practice on several occasions. SUMMARY: The prevalence of vancomycin resistant enterococci will likely continue to increase. Implementation of infection control strategies, in conjunction with deployment of advanced technologies for detection of vancomycin resistant enterococci, may curb this rise. The emergence of vancomycin resistant S. aureus is of concern. | 2005 | 16258324 |
| 4422 | 15 | 0.9998 | Diversity among multidrug-resistant enterococci. Enterococci are associated with both community- and hospital-acquired infections. Even though they do not cause severe systemic inflammatory responses, such as septic shock, enterococci present a therapeutic challenge because of their resistance to a vast array of antimicrobial drugs, including cell-wall active agents, all commercially available aminoglycosides, penicillin and ampicillin, and vancomycin. The combination of the latter two occurs disproportionately in strains resistant to many other antimicrobial drugs. The propensity of enterococci to acquire resistance may relate to their ability to participate in various forms of conjugation, which can result in the spread of genes as part of conjugative transposons, pheromone-responsive plasmids, or broad host-range plasmids. Enterococcal hardiness likely adds to resistance by facilitating survival in the environment (and thus enhancing potential spread from person to person) of a multidrug-resistant clone. The combination of these attributes within the genus Enterococcus suggests that these bacteria and their resistance to antimicrobial drugs will continue to pose a challenge. | 1998 | 9452397 |
| 4264 | 16 | 0.9998 | Mutational Evolution of Pseudomonas aeruginosa Resistance to Ribosome-Targeting Antibiotics. The present work examines the evolutionary trajectories of replicate Pseudomonas aeruginosa cultures in presence of the ribosome-targeting antibiotics tobramycin and tigecycline. It is known that large number of mutations across different genes - and therefore a large number of potential pathways - may be involved in resistance to any single antibiotic. Thus, evolution toward resistance might, to a large degree, rely on stochasticity, which might preclude the use of predictive strategies for fighting antibiotic resistance. However, the present results show that P. aeruginosa populations evolving in parallel in the presence of antibiotics (either tobramycin or tigecycline) follow a set of trajectories that present common elements. In addition, the pattern of resistance mutations involved include common elements for these two ribosome-targeting antimicrobials. This indicates that mutational evolution toward resistance (and perhaps other properties) is to a certain degree deterministic and, consequently, predictable. These findings are of interest, not just for P. aeruginosa, but in understanding the general rules involved in the evolution of antibiotic resistance also. In addition, the results indicate that bacteria can evolve toward higher levels of resistance to antibiotics against which they are considered to be intrinsically resistant, as tigecycline in the case of P. aeruginosa and that this may confer cross-resistance to other antibiotics of therapeutic value. Our results are particularly relevant in the case of patients under empiric treatment with tigecycline, which frequently suffer P. aeruginosa superinfections. | 2018 | 30405685 |
| 4263 | 17 | 0.9998 | The emergence of antibiotic resistance by mutation. The emergence of mutations in nucleic acids is one of the major factors underlying evolution, providing the working material for natural selection. Most bacteria are haploid for the vast majority of their genes and, coupled with typically short generation times, this allows mutations to emerge and accumulate rapidly, and to effect significant phenotypic changes in what is perceived to be real-time. Not least among these phenotypic changes are those associated with antibiotic resistance. Mechanisms of horizontal gene spread among bacterial strains or species are often considered to be the main mediators of antibiotic resistance. However, mutational resistance has been invaluable in studies of bacterial genetics, and also has primary clinical importance in certain bacterial species, such as Mycobacterium tuberculosis and Helicobacter pylori, or when considering resistance to particular antibiotics, especially to synthetic agents such as fluoroquinolones and oxazolidinones. In addition, mutation is essential for the continued evolution of acquired resistance genes and has, e.g., given rise to over 100 variants of the TEM family of beta-lactamases. Hypermutator strains of bacteria, which have mutations in genes affecting DNA repair and replication fidelity, have elevated mutation rates. Mutational resistance emerges de novo more readily in these hypermutable strains, and they also provide a suitable host background for the evolution of acquired resistance genes in vitro. In the clinical setting, hypermutator strains of Pseudomonas aeruginosa have been isolated from the lungs of cystic fibrosis patients, but a more general role for hypermutators in the emergence of clinically relevant antibiotic resistance in a wider variety of bacterial pathogens has not yet been proven. | 2007 | 17184282 |
| 4247 | 18 | 0.9998 | Drug resistance in tuberculosis. Drug-resistant tuberculosis remains a worldwide problem. New laboratory methods have improved our ability to more rapidly identify resistant strains, but the most effective approach is to prevent the appearance of resistance by appropriate choice of antibiotics and directly-observed therapy. Mycobacterium tuberculosis is treated with familiar and unique drugs; consequently, mechanisms of resistance have some unique features. All drug resistance thus far identified develops by mutational events rather than acquisition of resistance genes from other bacteria. An agenda is presented for countering the appearance of further drug resistance in mycobacteria. | 1997 | 9421707 |
| 4897 | 19 | 0.9998 | Rapid diagnosis of tuberculosis. Detection of drug resistance mechanisms. Tuberculosis is still a serious public health problem, with 10.8 million new cases and 1.8 million deaths worldwide in 2015. The diversity among members of the Mycobacterium tuberculosis complex, the causal agent of tuberculosis, is conducive to the design of different methods for rapid diagnosis. Mutations in the genes involved in resistance mechanisms enable the bacteria to elude the treatment. We have reviewed the methods for the rapid diagnosis of M. tuberculosis complex and the detection of susceptibility to drugs, both of which are necessary to prevent the onset of new resistance and to establish early, appropriate treatment. | 2017 | 28318570 |