# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 4235 | 0 | 1.0000 | Molecular mechanisms of antibacterial multidrug resistance. Treatment of infections is compromised worldwide by the emergence of bacteria that are resistant to multiple antibiotics. Although classically attributed to chromosomal mutations, resistance is most commonly associated with extrachromosomal elements acquired from other bacteria in the environment. These include different types of mobile DNA segments, such as plasmids, transposons, and integrons. However, intrinsic mechanisms not commonly specified by mobile elements-such as efflux pumps that expel multiple kinds of antibiotics-are now recognized as major contributors to multidrug resistance in bacteria. Once established, multidrug-resistant organisms persist and spread worldwide, causing clinical failures in the treatment of infections and public health crises. | 2007 | 17382878 |
| 4240 | 1 | 0.9999 | Genetics of antimicrobial resistance. Antimicrobial resistant strains of bacteria are an increasing threat to animal and human health. Resistance mechanisms to circumvent the toxic action of antimicrobials have been identified and described for all known antimicrobials currently available for clinical use in human and veterinary medicine. Acquired bacterial antibiotic resistance can result from the mutation of normal cellular genes, the acquisition of foreign resistance genes, or a combination of these two mechanisms. The most common resistance mechanisms employed by bacteria include enzymatic degradation or alteration of the antimicrobial, mutation in the antimicrobial target site, decreased cell wall permeability to antimicrobials, and active efflux of the antimicrobial across the cell membrane. The spread of mobile genetic elements such as plasmids, transposons, and integrons has greatly contributed to the rapid dissemination of antimicrobial resistance among several bacterial genera of human and veterinary importance. Antimicrobial resistance genes have been shown to accumulate on mobile elements, leading to a situation where multidrug resistance phenotypes can be transferred to a susceptible recipient via a single genetic event. The increasing prevalence of antimicrobial resistant bacterial pathogens has severe implications for the future treatment and prevention of infectious diseases in both animals and humans. The versatility with which bacteria adapt to their environment and exchange DNA between different genera highlights the need to implement effective antimicrobial stewardship and infection control programs in both human and veterinary medicine. | 2006 | 17127523 |
| 4046 | 2 | 0.9999 | Horizontal Gene Transfer and Its Association with Antibiotic Resistance in the Genus Aeromonas spp. The evolution of multidrug resistant bacteria to the most diverse antimicrobials known so far pose a serious problem to global public health. Currently, microorganisms that develop resistant phenotypes to multiple drugs are associated with high morbidity and mortality. This resistance is encoded by a group of genes termed 'bacterial resistome', divided in intrinsic and extrinsic resistome. The first one refers to the resistance displayed on an organism without previous exposure to an antibiotic not involving horizontal genetic transfer, and it can be acquired via mutations. The latter, on the contrary, is acquired exclusively via horizontal genetic transfer involving mobile genetic elements that constitute the 'bacterial mobilome'. This transfer is mediated by three different mechanisms: transduction, transformation, and conjugation. Recently, a problem of public health due to implications in the emergence of multi-drug resistance in Aeromonas spp. strains in water environments has been described. This is derived from the genetic material transfer via conjugation events. This is important, since bacteria that have acquired antibiotic resistance in natural environments can cause infections derived from their ingestion or direct contact with open wounds or mucosal tissue, which in turn, by their resistant nature, makes their eradication complex. Implications of the emergence of resistance in Aeromonas spp. by horizontal gene transfer on public health are discussed. | 2019 | 31540466 |
| 9908 | 3 | 0.9999 | Insights on the Horizontal Gene Transfer of Carbapenemase Determinants in the Opportunistic Pathogen Acinetobacter baumannii. Horizontal gene transfer (HGT) is a driving force to the evolution of bacteria. The fast emergence of antimicrobial resistance reflects the ability of genetic adaptation of pathogens. Acinetobacter baumannii has emerged in the last few decades as an important opportunistic nosocomial pathogen, in part due to its high capacity of acquiring resistance to diverse antibiotic families, including to the so-called last line drugs such as carbapenems. The rampant selective pressure and genetic exchange of resistance genes hinder the effective treatment of resistant infections. A. baumannii uses all the resistance mechanisms to survive against carbapenems but production of carbapenemases are the major mechanism, which may act in synergy with others. A. baumannii appears to use all the mechanisms of gene dissemination. Beyond conjugation, the mostly reported recent studies point to natural transformation, transduction and outer membrane vesicles-mediated transfer as mechanisms that may play a role in carbapenemase determinants spread. Understanding the genetic mobilization of carbapenemase genes is paramount in preventing their dissemination. Here we review the carbapenemases found in A. baumannii and present an overview of the current knowledge of contributions of the various HGT mechanisms to the molecular epidemiology of carbapenem resistance in this relevant opportunistic pathogen. | 2016 | 27681923 |
| 4241 | 4 | 0.9999 | Mechanisms of antimicrobial resistance and implications for epidemiology. The development of antibacterial agents has provided a means of treating bacterial diseases which were, previously, often fatal in both man and animal and thus represents one of the major advances of the 20th century. However, the efficacy of these agents is increasingly being compromised by the development of bacterial resistance to the drugs currently available for therapeutic use. Bacterial resistance can be combated in two ways. New drugs to which bacteria are susceptible can be developed and policies to contain the development and spread of resistance can be implemented. Both strategies require an understanding of the mechanisms of drug resistance, its epidemiology and the role of environmental factors in promoting resistance. Over the past thirty years our knowledge of bacterial resistance has increased dramatically mainly due to new technology that has become available. Bacteria are able to resist antibacterials by a variety of mechanisms: for example, altering the target to decrease susceptibility to the antibacterial, inactivating or destroying the drug, reducing drug transport into the cell or metabolic bypass. These drug resistance determinants are mediated via one of two distinct genetic mechanisms, a mutation in the bacterial chromosome or by a transmissible element; either a plasmid or a transposon. Significant differences exist between these two types of drug resistance as transmissible resistance, which is mainly plasmid-mediated, permits intraspecies and even interspecies transfer to occur. In contrast, chromosomal resistance can only be passed on to progeny. Transmissible antibacterial resistance is the major cause of concern as it can lead to the rapid spread of antibacterial resistance and has proven difficult, if not impossible, to eradicate. Furthermore, plasmids and transposons can code for multiple antibiotic resistance as well as virulence genes. Antibacterials for which transferable resistance has been identified include most commonly used antibacterials such as beta-lactams, aminoglycosides, macrolides, sulphonamides, tetracyclines, chloramphenicol and trimethoprim. One notable exception is the 4-quinolones for which plasmid-mediated resistance has yet to be identified. | 1993 | 8212509 |
| 4152 | 5 | 0.9999 | Quinolone resistance: much more than predicted. Since quinolones are synthetic antibiotics, it was predicted that mutations in target genes would be the only mechanism through which resistance could be acquired, because there will not be quinolone-resistance genes in nature. Contrary to this prediction, a variety of elements ranging from efflux pumps, target-protecting proteins, and even quinolone-modifying enzymes have been shown to contribute to quinolone resistance. The finding of some of these elements in plasmids indicates that quinolone resistance can be transferable. As a result, there has been a developing interest on the reservoirs for quinolone-resistance genes and on the potential risks associated with the use of these antibiotics in non-clinical environments. As a matter of fact, plasmid-encoded, quinolone-resistance qnr genes originated in the chromosome of aquatic bacteria. Thus the use of quinolones in fish-farming might constitute a risk for the emergence of resistance. Failure to predict the development of quinolone resistance reinforces the need of taking into consideration the wide plasticity of biological systems for future predictions. This plasticity allows pathogens to deal with toxic compounds, including those with a synthetic origin as quinolones. | 2011 | 21687414 |
| 4425 | 6 | 0.9999 | Multidrug resistance in bacteria. Large amounts of antibiotics used for human therapy, as well as for farm animals and even for fish in aquaculture, resulted in the selection of pathogenic bacteria resistant to multiple drugs. Multidrug resistance in bacteria may be generated by one of two mechanisms. First, these bacteria may accumulate multiple genes, each coding for resistance to a single drug, within a single cell. This accumulation occurs typically on resistance (R) plasmids. Second, multidrug resistance may also occur by the increased expression of genes that code for multidrug efflux pumps, extruding a wide range of drugs. This review discusses our current knowledge on the molecular mechanisms involved in both types of resistance. | 2009 | 19231985 |
| 9906 | 7 | 0.9999 | Multi-resistant Gram-negative bacilli: from epidemics to endemics. PURPOSE OF REVIEW: Infections due to multi-drug resistant Gram-negative bacilli represent a worrying situation for the management of hospitalized patients. In addition, these bacteria are increasingly involved in epidemics throughout the world. This review focuses on recent data that may help to understand the emergence and dissemination of multi-drug resistant bacilli and the current trend from epidemic to endemic situations. RECENT FINDINGS: Well-established clones enhance their resistance phenotype by the acquisition of new resistant genes, via gene capture genetic units (plasmids, transposons or integrons), thus facilitating the co-selective process under different antimicrobial selective pressures and therefore the long-term persistence of organisms in selective environments. Not only resistant bacterial clones are selected, but also their genetic structures carrying resistance genes. Therefore, current epidemiology of multi-drug resistant bacilli is not only focused on bacterial clones but also on any kind of resistance gene capture units. In this scenario a multiclonal population structure of bacterial organisms corresponds to a collection of different strains sharing resistance genes carried by horizontally transferred genetic structures. As different strains tend to prefer different environments, this concept helps understand why the epidemiology of multi-drug resistant Gram-negative bacilli is moving from epidemics to endemics. SUMMARY: The emergence and spread of multi-drug resistant bacilli in the nosocomial setting should be understood in terms of a complex interplay of bacterial clonality, resistance genes and genetic structures promoting rapid dissemination of antimicrobial resistance. Intervention strategies in the forthcoming scenario should identify existing epidemic and/or endemic situations involving clonal organisms or resistance genes carried by epidemic gene capture units. | 2003 | 12861084 |
| 4423 | 8 | 0.9998 | Inactivation of antibiotics and the dissemination of resistance genes. The emergence of multidrug-resistant bacteria is a phenomenon of concern to the clinician and the pharmaceutical industry, as it is the major cause of failure in the treatment of infectious diseases. The most common mechanism of resistance in pathogenic bacteria to antibiotics of the aminoglycoside, beta-lactam (penicillins and cephalosporins), and chloramphenicol types involves the enzymic inactivation of the antibiotic by hydrolysis or by formation of inactive derivatives. Such resistance determinants most probably were acquired by pathogenic bacteria from a pool of resistance genes in other microbial genera, including antibiotic-producing organisms. The resistance gene sequences were subsequently integrated by site-specific recombination into several classes of naturally occurring gene expression cassettes (typically "integrons") and disseminated within the microbial population by a variety of gene transfer mechanisms. Although bacterial conjugation once was believed to be restricted in host range, it now appears that this mechanism of transfer permits genetic exchange between many different bacterial genera in nature. | 1994 | 8153624 |
| 4325 | 9 | 0.9998 | Research Updates of Plasmid-Mediated Aminoglycoside Resistance 16S rRNA Methyltransferase. With the wide spread of multidrug-resistant bacteria, a variety of aminoglycosides have been used in clinical practice as one of the effective options for antimicrobial combinations. However, in recent years, the emergence of high-level resistance against pan-aminoglycosides has worsened the status of antimicrobial resistance, so the production of 16S rRNA methyltransferase (16S-RMTase) should not be ignored as one of the most important resistance mechanisms. What is more, on account of transferable plasmids, the horizontal transfer of resistance genes between pathogens becomes easier and more widespread, which brings challenges to the treatment of infectious diseases and infection control of drug-resistant bacteria. In this review, we will make a presentation on the prevalence and genetic environment of 16S-RMTase encoding genes that lead to high-level resistance to aminoglycosides. | 2022 | 35884160 |
| 4239 | 10 | 0.9998 | Bacterial resistance. Pathogenic bacteria remain adaptable to an increasingly hostile environment and a wider variety of more potent antibiotics. Organisms not intrinsically prepared for defense have been able to acquire resistance to newer antimicrobial agents. Chromosomal mutations alone cannot account for the rapid emergence and spread of antibiotic resistance. It has been established that plasmids and transposons are particularly important in the evolution of antibiotic-resistant bacteria. Plasmid- or transposon-mediated resistance provides the bacteria with pre-evolved genes refined to express high-level resistance. In particular, transposons can transfer these resistance determinants in diverse bacterial species, and nature provides in humans and animals large intestinal reservoirs in which such communications are facilitated. Antibiotic therapy exerts selection pressures on bacteria. Eradication or marked reduction in the populations of susceptible organisms promotes the overgrowth of intrinsically resistant strains and favors those resistant as a result of favorable chromosomal mutations or via plasmids or transposons. In our hospitals, where antibiotic consumption continues to increase, the nosocomial flora consists of many resistant bacteria, and infections acquired in the nosocomial setting are now far more severe than their community-acquired counterparts. There is convincing evidence that infection control measures must take into further consideration the contribution of the hospital worker as carrier and mediator of antibiotic resistance. | 1991 | 1649425 |
| 4149 | 11 | 0.9998 | Antibiotic resistance genes from the environment: a perspective through newly identified antibiotic resistance mechanisms in the clinical setting. Soil bacteria may contain antibiotic resistance genes responsible for different mechanisms that permit them to overcome the natural antibiotics present in the environment. This gene pool has been recently named the 'resistome', and its components can be mobilized into the microbial community affecting humans because of the participation of genetic platforms that efficiently facilitate the mobilization and maintenance of these resistance genes. Evidence for this transference has been suggested or demonstrated with newly identified widespread genes in multidrug-resistant bacteria. These resistance genes include those responsible for ribosomal methylases affecting aminoglycosides (armA, rtmB), methyltransferases affecting linezolid (cfr) or plasmid-mediated efflux pumps conferring low-level fluoroquinolone resistance (qepA), all of which are associated with antibiotic-producing bacteria. In addition, resistance genes whose ancestors have been identified in environmental isolates that are not recognized as antibiotic producers have also been recently detected. These include the qnr and the bla(CTX) genes compromising the activity of fluoroquinolones and extended-spectrum cephalosporins, respectively. The application of metagenomic tools and phylogenetic analysis will facilitate future identification of other new resistance genes and their corresponding ancestors in environmental bacteria, and will enable further exploration of the concept of the resistome as being a unique reservoir of antibiotic resistance genes and genetic elements participating in resistance gene transfer. | 2009 | 19220348 |
| 4391 | 12 | 0.9998 | 'To be, or not to be'-The dilemma of 'silent' antimicrobial resistance genes in bacteria. Antimicrobial resistance is a serious threat to public health that dramatically undermines our ability to treat bacterial infections. Microorganisms exhibit resistance to different drug classes by acquiring resistance determinants through multiple mechanisms including horizontal gene transfer. The presence of drug resistance genotypes is mostly associated with corresponding phenotypic resistance against the particular antibiotic. However, bacterial communities harbouring silent antimicrobial resistance genes-genes whose presence is not associated with a corresponding resistant phenotype do exist. Under suitable conditions, the expression pattern of such genes often revert and regain resistance and could potentially lead to therapeutic failure. We often miss the presence of silent genes, since the current experimental paradigms are focused on resistant strains. Therefore, the knowledge on the prevalence, importance and mechanism of silent antibiotic resistance genes in bacterial pathogens are very limited. Silent genes, therefore, provide an additional level of complexity in the war against drug-resistant bacteria, reminding us that not only phenotypically resistant strains but also susceptible strains should be carefully investigated. In this review, we discuss the presence of silent antimicrobial resistance genes in bacteria, their relevance and their importance in public health. | 2022 | 35882476 |
| 4876 | 13 | 0.9998 | Epidemiology of mobile colistin resistance (mcr) genes in aquatic environments. Colistin is one of the last-line therapies against multidrug-resistant Gram-negative pathogens, especially carbapenemase-producing isolates, making resistance to this compound a major global public-health crisis. Until recently, colistin resistance in Gram-negative bacteria was known to arise only by chromosomal mutations. However, a plasmid-mediated colistin resistance mechanism was described in late 2015. This mechanism is encoded by different mobile colistin resistance (mcr) genes that encode phosphoethanolamine (pEtN) transferases. These enzymes catalyse the addition of a pEtN moiety to lipid A in the bacterial outer membrane leading to colistin resistance. MCR-producing Gram-negative bacteria have been largely disseminated worldwide. However, their environmental dissemination has been underestimated. Indeed, water environments act as a connecting medium between different environments, allowing them to play a crucial role in the spread of antibiotic resistance between the natural environment and humans and other animals. For a better understanding of the role of such environments as reservoirs and/or dissemination routes of mcr genes, this review discusses primarily the various water habitats contributing to the spread of antibiotic resistance. Thereafter, we provide an overview of existing knowledge regarding the global epidemiology of mcr genes in water environments. This review confirms the global distribution of mcr genes in several water environments, including wastewater from different origins, surface water and tap water, making these environments reservoirs and dissemination routes of concern for this resistance mechanism. | 2021 | 34438108 |
| 4313 | 14 | 0.9998 | Molecular epidemiology of clinically significant antibiotic resistance genes. Antimicrobials were first introduced into medical practice a little over 60 years ago and since that time resistant strains of bacteria have arisen in response to the selective pressure of their use. This review uses the paradigm of the evolution and spread of beta-lactamases and in particular beta-lactamases active against antimicrobials used to treat Gram-negative infections. The emergence and evolution particularly of CTX-M extended-spectrum beta-lactamases (ESBLs) is described together with the molecular mechanisms responsible for both primary mutation and horizontal gene transfer. Reference is also made to other significant antibiotic resistance genes, resistance mechanisms in Gram-negative bacteria, such as carbepenamases, and plasmid-mediated fluoroquinolone resistance. The pathogen Staphylococcus aureus is reviewed in detail as an example of a highly successful Gram-positive bacterial pathogen that has acquired and developed resistance to a wide range of antimicrobials. The role of selective pressures in the environment as well as the medical use of antimicrobials together with the interplay of various genetic mechanisms for horizontal gene transfer are considered in the concluding part of this review. | 2008 | 18311156 |
| 3833 | 15 | 0.9998 | Fight evolution with evolution: plasmid-dependent phages with a wide host range prevent the spread of antibiotic resistance. The emergence of pathogenic bacteria resistant to multiple antibiotics is a serious worldwide public health concern. Whenever antibiotics are applied, the genes encoding for antibiotic resistance are selected for within bacterial populations. This has led to the prevalence of conjugative plasmids that carry resistance genes and can transfer themselves between diverse bacterial groups. In this study, we investigated whether it is feasible to attempt to prevent the spread of antibiotic resistances with a lytic bacteriophage, which can replicate in a wide range of gram-negative bacteria harbouring conjugative drug resistance-conferring plasmids. The counter-selection against the plasmid was shown to be effective, reducing the frequency of multidrug-resistant bacteria that formed via horizontal transfer by several orders of magnitude. This was true also in the presence of an antibiotic against which the plasmid provided resistance. Majority of the multiresistant bacteria subjected to phage selection also lost their conjugation capability. Overall this study suggests that, while we are obligated to maintain the selection for the spread of the drug resistances, the 'fight evolution with evolution' approach could help us even out the outcome to our favour. | 2013 | 24062801 |
| 4045 | 16 | 0.9998 | Bacterial resistance to antimicrobial agents and its impact on veterinary and human medicine. BACKGROUND: Antimicrobial resistance has become a major challenge in veterinary medicine, particularly in the context of bacterial pathogens that play a role in both humans and animals. OBJECTIVES: This review serves as an update on acquired resistance mechanisms in bacterial pathogens of human and animal origin, including examples of transfer of resistant pathogens between hosts and of resistance genes between bacteria. RESULTS: Acquired resistance is based on resistance-mediating mutations or on mobile resistance genes. Although mutations are transferred vertically, mobile resistance genes are also transferred horizontally (by transformation, transduction or conjugation/mobilization), contributing to the dissemination of resistance. Mobile genes specifying any of the three major resistance mechanisms - enzymatic inactivation, reduced intracellular accumulation or modification of the cellular target sites - have been found in a variety of bacteria that may be isolated from animals. Such resistance genes are associated with plasmids, transposons, gene cassettes, integrative and conjugative elements or other mobile elements. Bacteria, including zoonotic pathogens, can be exchanged between animals and humans mainly via direct contact, but also via dust, aerosols or foods. Proof of the direction of transfer of resistant bacteria can be difficult and depends on the location of resistance genes or mutations in the chromosomal DNA or on a mobile element. CONCLUSION: The wide variety in resistance and resistance transfer mechanisms will continue to ensure the success of bacterial pathogens in the future. Our strategies to counteract resistance and preserve the efficacy of antimicrobial agents need to be equally diverse and resourceful. | 2017 | 27581211 |
| 4234 | 17 | 0.9998 | Progress on mechanisms of antibiotic resistance in Clostridioides difficile. Clostridioides difficile (CD) is one of the most common pathogens causing health-care-associated infectious diarrhea and is listed by the U.S. Centers for Disease Control and Prevention as an urgent antibiotic resistance (AR) threat. Many resistance genes can be transferred between different CD strains present in the clinical setting, community, and environment. The antimicrobial resistance (AMR) of CD continues to evolve with the emergence and acquisition of new drug resistance mechanisms. CD has developed diverse drug resistance mechanisms, such as drug alteration, modification of the target site, and extrusion of drugs via efflux pumps. Researches have provided comprehensive knowledge about resistance mechanisms of macrolides and quinolones in CD. However, the mechanisms of resistance for metronidazole, vancomycin, and other therapeutic antibiotics against Clostridioides difficile infection (CDI) are only beginning to be elucidated. Some previously unfound mechanisms, such as plasmid-mediated drug resistance in CD, may also play an important role. In this review, we summarize the research progress on drug resistance mechanisms of CD with antimicrobial drugs already used clinically, such as metronidazole, vancomycin, and fidaxomicin, thereby providing the references for the clinical treatment and prevention of CDI, as well as the development of new antibacterial drugs and detection kits for drug resistant bacteria. | 2023 | 38764268 |
| 4150 | 18 | 0.9998 | The worldwide emergence of plasmid-mediated quinolone resistance. Fluoroquinolone resistance is emerging in gram-negative pathogens worldwide. The traditional understanding that quinolone resistance is acquired only through mutation and transmitted only vertically does not entirely account for the relative ease with which resistance develops in exquisitely susceptible organisms, or for the very strong association between resistance to quinolones and to other agents. The recent discovery of plasmid-mediated horizontally transferable genes encoding quinolone resistance might shed light on these phenomena. The Qnr proteins, capable of protecting DNA gyrase from quinolones, have homologues in water-dwelling bacteria, and seem to have been in circulation for some time, having achieved global distribution in a variety of plasmid environments and bacterial genera. AAC(6')-Ib-cr, a variant aminoglycoside acetyltransferase capable of modifying ciprofloxacin and reducing its activity, seems to have emerged more recently, but might be even more prevalent than the Qnr proteins. Both mechanisms provide low-level quinolone resistance that facilitates the emergence of higher-level resistance in the presence of quinolones at therapeutic levels. Much remains to be understood about these genes, but their insidious promotion of substantial resistance, their horizontal spread, and their co-selection with other resistance elements indicate that a more cautious approach to quinolone use and a reconsideration of clinical breakpoints are needed. | 2006 | 17008172 |
| 4140 | 19 | 0.9998 | Use of antimicrobials in veterinary medicine and mechanisms of resistance. This review deals with the application of antimicrobial agents in veterinary medicine and food animal production and the possible consequences arising from the widespread and multipurpose use of antimicrobials. The various mechanisms that bacteria have developed to escape the inhibitory effects of the antimicrobials most frequently used in the veterinary field are reported in detail. Resistance of bacteria to tetracyclines, macrolide-lincosamide-streptogramin antibiotics, beta-lactam antibiotics, aminoglycosides, sulfonamides, trimethoprim, fluoroquinolones and chloramphenicol/florfenicol is described with regard to enzymatic inactivation, decreased intracellular drug accumulation and modification/protection/replacement of the target sites. In addition, basic information is given about mobile genetic elements which carry the respective resistance genes, such as plasmids, transposons, and gene cassettes/integrons, and their ways of spreading via conjugation, mobilisation, transduction, and transformation. | 2001 | 11432414 |