# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 4795 | 0 | 1.0000 | 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 |
| 4797 | 1 | 0.9999 | 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 |
| 4796 | 2 | 0.9999 | 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 |
| 4793 | 3 | 0.9999 | Methicillin-Resistant Staphylococcus aureus in the Oral Cavity: Implications for Antibiotic Prophylaxis and Surveillance. The oral cavity harbors a multitude of commensal flora, which may constitute a repository of antibiotic resistance determinants. In the oral cavity, bacteria form biofilms, and this facilitates the acquisition of antibiotic resistance genes through horizontal gene transfer. Recent reports indicate high methicillin-resistant Staphylococcus aureus (MRSA) carriage rates in the oral cavity. Establishment of MRSA in the mouth could be enhanced by the wide usage of antibiotic prophylaxis among at-risk dental procedure candidates. These changes in MRSA epidemiology have important implications for MRSA preventive strategies, clinical practice, as well as the methodological approaches to carriage studies of the organism. | 2020 | 33402829 |
| 4792 | 4 | 0.9999 | Antibiotic resistance in the staphylococci. There has been much interest in the media, international as well as national, on the potential for the development of "superbugs' by which is usually meant pathogenic bacteria resistant to all available antibiotics. Two of the genera most often thought to fall into this category are the staphylococci (MRSA or Methicillin Resistant Staphylococcus aureus) and the enterococci (VRE or Vancomycin Resistant Enterococci) and although this article concentrates on the staphylococci the two share much in the way of transmissible genes. | 1997 | 9161125 |
| 4794 | 5 | 0.9999 | Resistance to antibiotics used in dermatological practice. The increased prevalence of bacterial resistance is one of the major problems of medicine today. Antibiotic resistance can be defined as the situation where the minimal inhibitory concentration is greater than the concentration obtainable in vivo. Resistance genes are easily transferred among bacteria, especially bacteria on skin and mucous membranes. In dermatological patients the most important resistance problems are found among staphylococci, Propionibacterium acnes and, to some extent, streptococci. Staphylococcus aureus strains have developed worldwide resistance to penicillin due to betalactamase production in > 90% of cases, and methicillin resistance is now a major problem with resistance levels of > 50% in certain areas of the world. These resistant strains are often multiresistant, and include resistance to erythromycin and tetracycline, with resistance to quinolone developing rapidly. Group A streptococci are still susceptible to penicillin, but increasing problems with erythromycin and tetracycline have been reported. After treatment with both systemic and oral antibiotics, P. acnes develops resistance in more than 50% of cases, and it is estimated that one in four acne patients harbours strains resistant to tetracycline, erythromycin, and clindamycin. To limit the development of antibiotic resistance, it is necessary to establish an antibiotic policy (prescription rules, reimbursement strategy, development of both national and local guidelines, and limitations on non-medical use). Clinicians also need access to rapid diagnostic methods, including resistance testing. This may provide further data for surveillance systems, reporting both antibiotic consumption and resistance levels. The involvement of clinical doctors in teaching and research in this area is probably the most important aspect, along with their involvement in the formulation of national and local guidelines. In the future we may consider it more important to ensure that future patients can be offered antibiotic treatment, rather than focusing on the patient presenting today. | 1998 | 9990406 |
| 4754 | 6 | 0.9999 | Enterococci and streptococci. Besides Staphylococcus aureus, other Gram-positive bacteria have become multidrug-resistant and cause therapeutic problems, particularly amongst hospitalised patients. The acquisition of vancomycin resistance by strains of Enterococcus faecium and Enterococcus faecalis is of particular concern and has resulted in treatment failures. Some of the infections caused by these bacteria do respond to treatment with new antibiotics that have been released in the last few years, however more options are required as not all enterococci are inherently susceptible and resistance is beginning to emerge amongst those that were susceptible. Resistance to commonly used antibiotics is also emerging in Streptococcus spp., particularly to the tetracyclines and macrolides. In both genera, multiresistant strains spread between patients and between hospitals. In the laboratory, these bacteria show considerable susceptibility to tigecycline, with little propensity to develop resistance, indicating that tigecycline could assume an important role in controlling infections caused by these Gram-positive bacteria. | 2007 | 17659211 |
| 4753 | 7 | 0.9999 | Vancomycin-resistant enterococci. Enterococci, a part of normal gut flora, are not particularly pathogenic organisms in humans. For example, they do not cause respiratory tract infections. The most frequent enterococcal infections are urinary tract infections. Despite their lack of pathogenicity, enterococci have emerged as significant nosocomial pathogens in the United States and elsewhere. Enterococci are formidable pathogens because of their resistance to antimicrobial agents. Enterococci are intrinsically resistant to beta-lactam agents and aminoglycosides and were the first bacteria to acquire vancomycin resistance. Infection control measures have been far from effective at preventing the dissemination of vancomycin-resistant enterococci in the hospital. Therapy for infections due to vancomycin-resistant enterococci presents real challenges. Most isolates remain susceptible to nitrofurantoin, but this agent is useful only for urinary tract infections. The greatest threat posed by vancomycin-resistant enterococci is the potential to transfer their resistance genes to more pathogenic gram-positive bacteria, which could produce truly frightening pathogens. | 1998 | 9597252 |
| 4317 | 8 | 0.9999 | 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 |
| 4422 | 9 | 0.9999 | 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 |
| 4318 | 10 | 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 |
| 4800 | 11 | 0.9999 | Human infections caused by glycopeptide-resistant Enterococcus spp: are they a zoonosis? Following the detection of glycopeptide-resistant enterococci (GRE) in 1986 and their subsequent global dissemination during the 1990s, many studies have attempted to identify the reservoirs and lines of resistance transmission as a basis for intervention. The eradication of reservoirs and the prevention of GRE spread is of major importance for two reasons: (i) the emergence of high-level glycopeptide resistance in invasive enterococcal clinical isolates that are already multiresistant, has left clinicians with therapeutic options that are only at the experimental stage; and (ii) the resistance genes may spread to more virulent bacterial species such as Staphylococcus aureus, Streptococcus pneumoniae and Clostridium difficile. VanA-type strains, resistant to high levels of both vancomycin and teicoplanin, are the most commonly encountered enterococci with acquired glycopeptide resistance in humans. A widespread VanA-type GRE reservoir was detected early in farm animals that were exposed to the glycopeptide growth-promoter avoparcin. Numerous studies have provided indirect evidence for the transfer of VanA-type GRE and their resistance determinants from animal reservoirs to humans. The data collected have expanded our understanding of the promiscuous nature of antibiotic resistance, and have provided the groundwork for logical decision-making with the objective of deterring the dissemination of resistant bacteria and of their resistance genes. | 2001 | 11688531 |
| 4858 | 12 | 0.9999 | Successful interventions for gram-negative resistance to extended-spectrum beta-lactam antiobiotics. Antibiotic resistance among nosocomial pathogens in this country's hospitals adds significantly to patient morbidity and mortality, and the cost of health care. Optimism for identifying antimicrobial agents that would "solve the problem" of resistance has been replaced by a much more guarded and realistic view of the battle between humans and pathogenic microorganisms. Efforts now are more appropriately directed toward limiting, rather than completely eliminating, resistance, generally by either infection control or antibiotic control measures, and sometime combinations of the two. Methicillin-oxacillin resistance in Staphylococcus aureus (MRSA) results from the expression of an acquired penicillin-binding protein (PBP 2a) that is not transferable in vitro. In most hospitals, even those with high percentages of MRSA, relatively few resistant clones are identified, suggesting transmission of individual strains throughout the hospital population. Because person-to-person spread is so important in transmission of MRSA, strategies aimed at preventing transmission of the resistant strains are remarkably effective when strictly enforced. Ceftazidime resistance in Enterobacteriaceae results from point mutations within genes that encode widely prevalent and often transferable plasmid-mediated enzymes. In addition, mutations of these genes that allow hydrolysis of cephalosporins usually result in decreased activity against other drugs, including the penicillins and beta-lactamase inhibitors. Effective measures to control ceftazidime-resistant Enterobacteriaceae have as their cornerstone limiting administration of antibiotics that select for the emergence and spread of these mutations, especially ceftazidime. The importance of infection-control techniques in limiting the prevalence of ceftazidime-resistant Enterobacteriaceae is less well established. Methods that are informed by a detailed understanding of the molecular mechanisms of resistance and resistance spread offer the best hope for limiting dissemination of antibiotic-resistant bacteria in a cost-effective manner. | 1999 | 10456609 |
| 4336 | 13 | 0.9998 | Antibiotic Resistance in Bacteria-A Review. A global problem of multi-drug resistance (MDR) among bacteria is the cause of hundreds of thousands of deaths every year. In response to the significant increase of MDR bacteria, legislative measures have widely been taken to limit or eliminate the use of antibiotics, including in the form of feed additives for livestock, but also in metaphylaxis and its treatment, which was the subject of EU Regulation in 2019/6. Numerous studies have documented that bacteria use both phenotypis and gentic strategies enabling a natural defence against antibiotics and the induction of mechanisms in increasing resistance to the used antibacterial chemicals. The mechanisms presented in this review developed by the bacteria have a significant impact on reducing the ability to combat bacterial infections in humans and animals. Moreover, the high prevalence of multi-resistant strains in the environment and the ease of transmission of drug-resistance genes between the different bacterial species including commensal flora and pathogenic like foodborne pathogens (E. coli, Campylobacter spp., Enterococcus spp., Salmonella spp., Listeria spp., Staphylococcus spp.) favor the rapid spread of multi-resistance among bacteria in humans and animals. Given the global threat posed by the widespread phenomenon of multi-drug resistance among bacteria which are dangerous for humans and animals, the subject of this study is the presentation of the mechanisms of resistance in most frequent bacteria called as "foodborne pathoges" isolated from human and animals. In order to present the significance of the global problem related to multi-drug resistance among selected pathogens, especially those danger to humans, the publication also presents statistical data on the percentage range of occurrence of drug resistance among selected bacteria in various regions of the world. In addition to the phenotypic characteristics of pathogen resistance, this review also presents detailed information on the detection of drug resistance genes for specific groups of antibiotics. It should be emphasized that the manuscript also presents the results of own research i.e., Campylobacter spp., E. coli or Enetrococcus spp. This subject and the presentation of data on the risks of drug resistance among bacteria will contribute to initiating research in implementing the prevention of drug resistance and the development of alternatives for antimicrobials methods of controlling bacteria. | 2022 | 36009947 |
| 4799 | 14 | 0.9998 | Glycopeptide-resistant enterococci: a decade of experience. Since their first description in 1988, glycopeptide-resistant enterococci (GRE) have emerged as a significant cause of nosocomial infections and colonisations, particularly in Europe and the USA. Two major genetically distinct forms of acquired resistance, designated VanA and VanB, are recognised, although intrinsic resistance occurs in some enterococcal species (VanC) and a third form of acquired resistance (VanD) has been reported recently. The biochemical basis of each resistance mechanism is similar; the resistant enterococci produce modified peptidoglycan precursors that show decreased binding affinity for glycopeptide antibiotics. Although VanA resistance is detected readily in the clinical laboratory, the variable levels of vancomycin resistance associated with the other phenotypes makes detection less reliable. Under-reporting of VanB resistance as a result of a lower detection rate may account, in part, for the difference in the numbers of enterococci displaying VanA and VanB resistance referred to the PHLS Laboratory of Hospital Infection. Since 1987, GRE have been referred from >1100 patients in almost 100 hospitals, but 88% of these isolates displayed the VanA phenotype. It is possible that, in addition to the problems of detection, there may be a real difference in the prevalence of VanA and VanB resistance reflecting different epidemiologies. Our present understanding of the genetic and biochemical basis of these acquired forms of glycopeptide resistance has been gained mainly in the last 5 years. However, these relatively new enterococcal resistances appear still to be evolving; there have now been reports of transferable VanB resistance associated with either large chromosomally borne transposons or plasmids, genetic linkage of glycopeptide resistance and genes conferring high-level resistance to aminoglycoside antibiotics, epidemic strains of glycopeptide-resistant Enterococcus faecium isolated from multiple patients in numerous hospitals, and of glycopeptide dependence (mutant enterococci that actually require these agents for growth). The gene clusters responsible for VanA and VanB resistance are located on transposable elements, and both transposition and plasmid transfer have resulted in the dissemination of these resistance genes into diverse strains of several species of enterococci. Despite extensive research, knowledge of the origins of these resistances remains poor. There is little homology between the resistance genes and DNA from either intrinsically resistant gram-positive genera or from the soil bacteria that produce glycopeptides, which argues against direct transfer to enterococci from these sources. However, recent data suggest a more distant, evolutionary relationship with genes found in glycopeptide-producing bacteria. In Europe, VanA resistance occurs in enterococci isolated in the community, from sewage, animal faeces and raw meat. This reservoir suggests that VanA may not have evolved in hospitals, and its existence has been attributed, controversially, to use of the glycopeptide avoparcin as a growth promoter, especially in pigs and poultry. However, as avoparcin has never been licensed for use in the USA and, to date, VanB resistance has not been confirmed in non-human enterococci, it is clear that the epidemiology of acquired glycopeptide resistance in enterococci is complex, with many factors contributing to its evolution and global dissemination. | 1998 | 9788808 |
| 4316 | 15 | 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 |
| 4798 | 16 | 0.9998 | Acquired vancomycin resistance in clinically relevant pathogens. Acquired resistance to vancomycin is an increasing problem in pathogenic bacteria. It is best studied and most prevalent among Enterococcus and still remains rare in other pathogenic bacteria. Different genotypes of vancomycin resistance, vanA-G, have been described. The different van gene clusters consist of up to nine genes encoding proteins of different functions; their interplay leads to an alternative cell wall precursor less susceptible to glycopeptide binding. Variants of vanA and vanB types are found worldwide, with vanA predominating; their reservoir is Enterococcus faecium. Within this species a subpopulation of hospital-adapted types exists that acquired van gene clusters and which is responsible for outbreaks of vancomycin-resistant enterococci all over the world. Acquisition of vanA by methicillin-resistant Staphylococcus aureus (MRSA) is worrisome and seven cases have been described. Nonsusceptibility to glycopeptides also occurs independently from van genes and is a growing therapeutic challenge, especially in MRSA. | 2008 | 18811239 |
| 4392 | 17 | 0.9998 | The Neglected Contribution of Streptomycin to the Tuberculosis Drug Resistance Problem. The airborne pathogen Mycobacterium tuberculosis is responsible for a present major public health problem worsened by the emergence of drug resistance. M. tuberculosis has acquired and developed streptomycin (STR) resistance mechanisms that have been maintained and transmitted in the population over the last decades. Indeed, STR resistant mutations are frequently identified across the main M. tuberculosis lineages that cause tuberculosis outbreaks worldwide. The spread of STR resistance is likely related to the low impact of the most frequent underlying mutations on the fitness of the bacteria. The withdrawal of STR from the first-line treatment of tuberculosis potentially lowered the importance of studying STR resistance. However, the prevalence of STR resistance remains very high, could be underestimated by current genotypic methods, and was found in outbreaks of multi-drug (MDR) and extensively drug (XDR) strains in different geographic regions. Therefore, the contribution of STR resistance to the problem of tuberculosis drug resistance should not be neglected. Here, we review the impact of STR resistance and detail well-known and novel candidate STR resistance mechanisms, genes, and mutations. In addition, we aim to provide insights into the possible role of STR resistance in the development of multi-drug resistant tuberculosis. | 2021 | 34946952 |
| 4312 | 18 | 0.9998 | Genes and mutations conferring antimicrobial resistance in Salmonella: an update. Resistance to various classes of antimicrobial agents has been encountered in many bacteria of medical and veterinary relevance. Particular attention has been paid to zoonotic bacteria such as Salmonella. Over the years, various studies have reported the presence of genes and mutations conferring resistance to antimicrobial agents in Salmonella isolates. This review is intended to provide an update on what is currently known about the genetic basis of antimicrobial resistance in Salmonella. | 2006 | 16716631 |
| 9798 | 19 | 0.9998 | 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 |