# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 4752 | 0 | 1.0000 | Antibiotic resistance in gram-positive bacteria: epidemiological aspects. The emergence and spread of antibiotic resistance in gram-positive bacterial pathogens has become an increasing problem. There has been a dramatic increase in the prevalence of methicillin-resistant Staphylococcus aureus (MRSA), coagulase-negative staphylococci and enterococci. This is mainly due to the clonal dissemination of certain epidemic multiply-resistant strains, for example, those of MRSA and S. pneumoniae, as well as to the spread of resistance genes as exemplified by those causing glycopeptide resistance in enterococci. | 1999 | 10511391 |
| 4754 | 1 | 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 | 2 | 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 |
| 4797 | 3 | 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 |
| 4798 | 4 | 0.9999 | 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 |
| 2506 | 5 | 0.9999 | High-level gentamicin resistance in Enterococcus: microbiology, genetic basis, and epidemiology. Antibiotic resistance is an ever-increasing problem in enterococci. These bacteria are remarkable in their ability to acquire and disseminate antibiotic resistance genes by a variety of routes. Since first described in 1979, high-level resistance to gentamicin (MIC, greater than 2,000 micrograms/mL) has spread worldwide and has been responsible for serious infections. Resistance is plasmid-mediated and due to aminoglycoside-modifying enzymes. High-level gentamicin resistance indicates that there will be no synergistic bactericidal activity with penicillin-gentamicin combinations. The epidemiology of nosocomial enterococcal infections is remarkably similar to that of nosocomial infections caused by methicillin-resistant staphylococci and by multidrug-resistant gram-negative bacilli. The most likely way these resistant bacteria are spread among hospital patients is via transient carriage on the hands of hospital personnel. Patient-to-patient and interhospital transmission of strains has been reported recently. However, clonal dissemination is not the cause of the increased frequency of resistant strains, since gentamicin resistance appears in a variety of different conjugative and nonconjugative plasmids in Enterococcus. | 1990 | 2117300 |
| 4751 | 6 | 0.9999 | Emerging antibiotic-resistant bacteria. Their treatment in total joint arthroplasty. Successful treatment of an infected total joint arthroplasty can be achieved in approximately 90% of cases. This outcome may be jeopardized by the emergence of antibiotic resistance in bacteria common to these infections. Staphylococci are the most frequently isolated bacteria in total joint infections, and the prevalence of antibiotic resistance in these organisms among all nosocomial and community-acquired infections has been increasing. As many as 46.7% of Staphylococcus aureus strains and 85.7% of coagulase-negative staphylococci strains are methicillin-resistant. Enterococci also are commonly isolated from infected total joint arthroplasties. The prevalence of vancomycin-resistant enterococci among all enterococci strains is estimated at 23%. As the prevalence of these resistant bacteria continues to increase among all infections, it is anticipated that they will be encountered more regularly in total joint infections. Knowledge of the mechanisms of resistance of these bacteria and currently available and newly developed antimicrobials is key to preventing the expansion of antimicrobial resistance and ensuring the future successful treatment of total joint infections. | 1999 | 10611866 |
| 4796 | 7 | 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 | 8 | 0.9998 | 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 | 9 | 0.9998 | 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 |
| 4594 | 10 | 0.9998 | Linezolid resistance genes and genetic elements enhancing their dissemination in enterococci and streptococci. Linezolid is considered a last resort drug in treatment of severe infections caused by Gram-positive pathogens, resistant to other antibiotics, such as vancomycin-resistant enterococci (VRE), methicillin-resistant staphylococci and multidrug resistant pneumococci. Although the vast majority of Gram-positive pathogenic bacteria remain susceptible to linezolid, resistant isolates of enterococci, staphylococci and streptococci have been reported worldwide. In these bacteria, apart from mutations, affecting mostly the 23S rRNA genes, acquisition of such genes as cfr, cfr(B), optrA and poxtA, often associated with mobile genetic elements (MGE), plays an important role for resistance. The purpose of this paper is to provide an overview on diversity and epidemiology of MGE carrying linezolid-resistance genes among clinically-relevant Gram-positive pathogens such as enterococci and streptococci. | 2018 | 30253132 |
| 4595 | 11 | 0.9998 | Transfer of mupirocin resistance from Staphylococcus haemolyticus clinical strains to Staphylococcus aureus through conjugative and mobilizable plasmids. Coagulase-negative staphylococci are thought to act as reservoirs of antibiotic resistance genes that can be transferred to Staphylococcus aureus, thus hindering the combat of this bacterium. In this work, we analyzed the presence of plasmids conferring resistance to the antibiotic mupirocin-widely used to treat and prevent S. aureus infections in hospital environments-in nosocomial S. haemolyticus strains. About 12% of the 75 strains tested were resistant to mupirocin, and this phenotype was correlated with the presence of plasmids. These plasmids were shown to be diverse, being either conjugative or mobilizable, and capable of transferring mupirocin resistance to S. aureus Our findings reinforce that S. haemolyticus, historically and mistakenly considered as a less important pathogen, is a reservoir of resistance genes which can be transferred to other bacteria, such as S. aureus, emphasizing the necessity of more effective strategies to detect and combat this emergent opportunistic pathogen. | 2016 | 27190144 |
| 4795 | 12 | 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 |
| 4593 | 13 | 0.9998 | Origin, evolution and dissemination of antibiotic resistance genes. Comparison of resistance genes from different sources support the hypothesis that the antibiotic-producing microorganisms are the source of resistant determinants present in clinical isolates. There is also evidence that Gram-positive cocci (staphylococci and streptococci) can serve as a reservoir of resistance genes for Gram-negative bacteria. | 1987 | 2856426 |
| 4750 | 14 | 0.9998 | A Review of Detection Methods for Vancomycin-Resistant Enterococci (VRE) Genes: From Conventional Approaches to Potentially Electrochemical DNA Biosensors. Vancomycin-resistant Enterococci (VRE) genes are bacteria strains generated from Gram-positive bacteria and resistant to one of the glycopeptides antibiotics, commonly, vancomycin. VRE genes have been identified worldwide and exhibit considerable phenotypic and genotypic variations. There are six identified phenotypes of vancomycin-resistant genes: VanA, VanB, VanC, VanD, VanE, and VanG. The VanA and VanB strains are often found in the clinical laboratory because they are very resistant to vancomycin. VanA bacteria can pose significant issues for hospitalized patients due to their ability to spread to other Gram-positive infections, which changes their genetic material to increase their resistance to the antibiotics used during treatment. This review summarizes the established methods for detecting VRE strains utilizing traditional, immunoassay, and molecular approaches and then focuses on potential electrochemical DNA biosensors to be developed. However, from the literature search, no information was reported on developing electrochemical biosensors for detecting VRE genes; only the electrochemical detection of vancomycin-susceptible bacteria was reported. Thus, strategies to create robust, selective, and miniaturized electrochemical DNA biosensor platforms to detect VRE genes are also discussed. | 2023 | 36832060 |
| 4857 | 15 | 0.9998 | The emergence of bacterial resistance and its influence on empiric therapy. The discovery of antimicrobial agents had a major impact on the rate of survival from infections. However, the changing patterns of antimicrobial resistance caused a demand for new antibacterial agents. Within a few years of the introduction of penicillin, the majority of staphylococci were resistant to that drug. In the 1960s the production of the semisynthetic penicillins provided an answer to the problem of staphylococcal resistance. In the early 1960s most Escherichia coli were susceptible to the new beta-lactam antibiotic ampicillin; by the end of that decade, plasmid-mediated beta-lactamase resistance was found in 30%-50% of hospital-acquired E. coli. Use of certain agents resulted in the selection of bacteria, such as Klebsiella, that are intrinsically resistant to ampicillin. The original cephalosporins were stable to beta-lactamase, but the use of these agents was in part responsible for the appearance of infections due to Enterobacter species, Citrobacter species, and Pseudomonas aeruginosa. These bacteria, as well as Serratia, were resistant to many of the available beta-lactam agents. Aminoglycosides initially provided excellent activity against most of the facultative gram-negative bacteria. However, the widespread dissemination of the genes that cause production of the aminoglycoside-inactivating enzymes altered the use of those agents. Clearly, the evolution of bacterial resistance has altered the prescribing patterns for antimicrobial agents. Knowledge that beta-lactam resistance to ampicillin or cephalothin is prevalent is causing physicians to select as empiric therapy either a combination of two or more agents or agents to which resistance is uncommon. The new cephalosporins offer a broad spectrum of anti-bacterial activity coupled with low toxicity. However, physicians must closely follow the changing ecology of bacteria when these agents are used, because cephalosporins can also select bacteria resistant to themselves and thereby abolish their value as empiric therapy. | 1983 | 6342103 |
| 2507 | 16 | 0.9998 | Epidemiology of resistance to diaminopyrimidines. Resistance to trimethoprim emerged in Enterobacteriaceae and later in other Gram-negative and Gram-positive bacteria within two years of the clinical introduction of the drug. Resistance is borne in many different replicons often present in multiply-resistant epidemic bacteria. The incidence of trimethoprim resistance is highly variable, depending upon methodology, type of patients, local epidemiology: this can be illustrated by the high variation of trimethoprim resistance among Salmonella, Shigella or MRSA in various countries and by the incidence of resistance in penicillin-resistant Streptococcus pneumoniae. | 1993 | 8195837 |
| 4799 | 17 | 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 |
| 4747 | 18 | 0.9998 | Linezolid versus vancomycin in vitro activity against methicillin-resistant Staphylococcus aureus biofilms. Most microorganisms as well as bacteria live in a community under natural conditions. Bacteria adopted to biofilm mode of life more than 3 billion years ago to survive extreme, harsh environments. They become harmful when they acquire resistance to antibiotics and overcome the standard therapies, which is most commonly found in hospitals. Therefore, many studies have been published regarding antimicrobial resistance (AMR). Staphylococcus aureus is a dangerous pathogen, ubiquitously prevalent as a commensal and opportunistic microorganism in human populations. Methicillin-resistant Staphylococcus aureus (MRSA) is considered one of the major medical problems worldwide since they are frequent colonizers of implanted medical devices causing a variety of hospital-acquired infections. For many years, vancomycin has been the drug of choice for MRSA whereas linezolid is considered the last resort drug. This comparative, cross-sectional study investigated the effects of linezolid on biofilm formation in vitro compared to vancomycin across 85 MRSA isolates. To our knowledge, this is the first study to report high levels of linezolid resistance in MRSA in Iraq. In this brief report, 5 MRSA strains showed resistance to linezolid, with minimum inhibitory concentration (MIC) values of 256 μg/ml. The exact same isolates exhibited vancomycin resistance with MIC values of 1024 μg/ml. All linezolid-resistant MRSA (LR-MRSA) strains demonstrated biofilm formation ability. Additionally, linezolid inhibited the expression of adhesion-related genes cna and clfB. The authors concluded that linezolid exerts a comparable effect to vancomycin in biofilm treatment. | 2025 | 39947358 |
| 4817 | 19 | 0.9998 | Relationship Between Biofilm Formation and Antimicrobial Resistance in Gram-Negative Bacteria. Gram-negative microorganisms are a significant cause of infection in both community and nosocomial settings. The increase, emergence, and spread of antimicrobial resistance among bacteria are the most important health problems worldwide. One of the mechanisms of resistance used by bacteria is biofilm formation, which is also a mechanism of virulence. This study analyzed the possible relationship between antimicrobial resistance and biofilm formation among isolates of three Gram-negative bacteria species. Several relationships were found between the ability to form biofilm and antimicrobial resistance, being different for each species. Indeed, gentamicin and ceftazidime resistance was related to biofilm formation in Escherichia coli, piperacillin/tazobactam, and colistin in Klebsiella pneumoniae, and ciprofloxacin in Pseudomonas aeruginosa. However, no relationship was observed between global resistance or multidrug-resistance and biofilm formation. In addition, compared with other reported data, the isolates in the present study showed higher rates of antimicrobial resistance. In conclusion, the acquisition of specific antimicrobial resistance can compromise or enhance biofilm formation in several species of Gram-negative bacteria. However, multidrug-resistant isolates do not show a trend to being greater biofilm producers than non-multiresistant isolates. | 2019 | 30142035 |