# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 3745 | 0 | 1.0000 | Antimicrobial resistance in methicillin-resistant staphylococcus aureus. In the medical community, antibiotics are revered as a miracle because they stop diseases brought on by pathogenic bacteria. Antibiotics have become the cornerstone of contemporary medical advancements ever since penicillin was discovered. Antibiotic resistance developed among germs quickly, placing a strain in the medical field. Methicillin-resistant Staphylococcus aureus (MRSA), Since 1961, has emerged as the major general antimicrobial resistant bacteria (AMR) worldwide. MRSA can easily transmit across the hospital system and has mostly gained resistance to medications called beta-lactamases. This enzyme destroys the cell wall of beta-lactam antibiotics resulting in resistance against that respective antibiotic. Daptomycin, linezolid and vancomycin were previously used to treat MRSA infections. However, due to mutations and Single nucleotide polymorphisms (SNPs) in Open reading frames (ORFs) and SCCmec machinery of respective antibody, MRSA developed resistance against those antibiotics. The MRSA strains (USA300, CC398, CC130 etc.), when their pan-genomes were analyzed were found the genes involved in invoking resistance against the antibiotics as well as the epidemiology of that respective strain. PENC (penicillin plus potassium clavulanate) is the new antibiotic showing potential in treatment of MRSA though it is itself resistant against penicillin alone. In this review, our main focus is on mechanism of development of AMR in MRSA, how different ORFs are involved in evoking resistance in MRSA and what is the core-genome of different antimicrobial resistant MRSA. | 2023 | 36936699 |
| 4796 | 1 | 0.9996 | 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 |
| 4790 | 2 | 0.9995 | Combating vancomycin resistance in bacteria: targeting the D-ala-D-ala dipeptidase VanX. In the past 20 years, vancomycin and other glycopeptide antibiotics have been administered to patients with Streptococcal and Staphylococcal infections that were resistant to all other antibiotics or to patients who were allergic to penicillins and cephalosporins. After extensive use of vancomycin and other glycopeptide antibiotics in humans, several strains of Enterococcus have developed high-level vancomycin resistance (collectively called VRE, vancomycin-resistant Enterococcus), and this resistance phenotype has spread to other organisms. The spread of vancomycin resistance to other pathogens and, potentially, to bacterial strains on the CDC's bioterrorism watch list is a major biomedical concern. Bacteria most often become resistant to vancomycin by acquiring a transposon containing genes that encode for a number of proteins, five of which are essential for the high-level resistance phenotype. The five essential gene products are called VanR, VanS, VanH, VanA, and VanX. Previous studies have shown that the inactivation of VanX results in an organism that is sensitive to vancomycin and that VanX is an excellent inhibitor target. In this review the known inhibitors and structural and mechanistic properties of VanX will be discussed. These data will be used to offer suggestions for novel, rationally-designed or -redesigned inhibitors, which could potentially be used in combination with existing glycopeptide antibiotics as a treatment for vancomycin-resistant bacterial infections. | 2006 | 16789876 |
| 4798 | 3 | 0.9995 | 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 |
| 4797 | 4 | 0.9995 | 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 |
| 9798 | 5 | 0.9995 | 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 |
| 4795 | 6 | 0.9995 | 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 |
| 4754 | 7 | 0.9994 | 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 |
| 4792 | 8 | 0.9994 | 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 |
| 4753 | 9 | 0.9994 | 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 |
| 4752 | 10 | 0.9994 | 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 |
| 4748 | 11 | 0.9994 | Bacteria antibiotic resistance: New challenges and opportunities for implant-associated orthopedic infections. There has been a dramatic increase in the emergence of antibiotic-resistant bacterial strains, which has made antibiotic choices for infection control increasingly limited and more expensive. In the U.S. alone, antibiotic-resistant bacteria cause at least 2 million infections and 23,000 deaths a year resulting in a $55-70 billion per year economic impact. Antibiotics are critical to the success of surgical procedures including orthopedic prosthetic surgeries, and antibiotic resistance is occurring in nearly all bacteria that infect people, including the most common bacteria that cause orthopedic infections, such as Staphylococcus aureus (S. aureus). Most clinical cases of orthopedic surgeries have shown that patients infected with antibiotic-resistant bacteria, such as methicillin-resistant S. aureus (MRSA), are associated with increased morbidity and mortality. This paper reviews the severity of antibiotic resistance at the global scale, the consequences of antibiotic resistance, and the pathways bacteria used to develop antibiotic resistance. It highlights the opportunities and challenges in limiting antibiotic resistance through approaches like the development of novel, non-drug approaches to reduce bacteria functions related to orthopedic implant-associated infections. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:22-32, 2018. | 2018 | 28722231 |
| 8839 | 12 | 0.9994 | Bacteriophage infection drives loss of β-lactam resistance in methicillin-resistant Staphylococcus aureus. Bacteriophage (phage) therapy is a promising means to combat drug-resistant bacterial pathogens. Infection by phage can select for mutations in bacterial populations that confer resistance against phage infection. However, resistance against phage can yield evolutionary trade-offs of biomedical relevance. Here, we report the discovery that infection by certain staphylococcal phages sensitizes different strains of methicillin-resistant Staphylococcus aureus (MRSA) to β-lactams, a class of antibiotics against which MRSA is typically resistant. MRSA cells that survive infection by these phages display significant reductions in minimal inhibitory concentration against different β-lactams compared to uninfected bacteria. Transcriptomic profiling reveals that these evolved MRSA strains possess highly modulated transcriptional profiles, where numerous genes involved in S. aureus virulence are downregulated. Phage-treated MRSA exhibited attenuated virulence phenotypes in the form of reduced hemolysis and clumping. Despite sharing similar phenotypes, whole-sequencing analysis revealed that the different MRSA strains evolved unique genetic profiles during infection. These results suggest complex evolutionary trajectories in MRSA during phage predation and open up new possibilities to reduce drug resistance and virulence in MRSA infections. | 2025 | 40637714 |
| 9802 | 13 | 0.9994 | Transient comparison of techniques to counter multi-drug resistant bacteria: prime modules in curation of bacterial infections. Multidrug-resistant organisms are bacteria that are no longer controlled or killed by specific drugs. One of two methods causes bacteria multidrug resistance (MDR); first, these bacteria may disguise multiple cell genes coding for drug resistance to a single treatment on resistance (R) plasmids. Second, increased expression of genes coding for multidrug efflux pumps, which extrude many drugs, can cause MDR. Antibiotic resistance is a big issue since some bacteria may withstand almost all antibiotics. These bacteria can cause serious sickness, making them a public health threat. Methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Enterococcus (VRE), Multidrug resistant Mycobacterium tuberculosis (TB), and CRE are gut bacteria that resist antibiotics. Antimicrobial resistance is rising worldwide, increasing clinical and community morbidity and mortality. Superbugs have made antibiotic resistance in some environmental niches even harder to control. This study introduces new medicinal plants, gene-editing methods, nanomaterials, and bacterial vaccines that will fight MDR bacteria in the future. | 2023 | 39816650 |
| 4800 | 14 | 0.9994 | 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 |
| 4799 | 15 | 0.9994 | 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 |
| 4858 | 16 | 0.9994 | 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 |
| 4897 | 17 | 0.9994 | 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 |
| 4794 | 18 | 0.9994 | 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 |
| 4434 | 19 | 0.9994 | Battle against Vancomycin-Resistant Bacteria: Recent Developments in Chemical Strategies. Vancomycin, a natural glycopeptide antibiotic, was used as the antibiotic of last resort for the treatment of multidrug-resistant Gram-positive bacterial infections. However, almost 30 years after its use, resistance to vancomycin was first reported in 1986 in France. This became a major health concern, and alternative treatment strategies were urgently needed. New classes of molecules, including semisynthetic antibacterial compounds and newer generations of the previously used antibiotics, were developed. Semisynthetic derivatives of vancomycin with enhanced binding affinity, membrane disruption ability, and lipid binding properties have exhibited promising results against both Gram-positive and Gram-negative bacteria. Various successful approaches developed to overcome the acquired resistance in Gram-positive bacteria, intrinsic resistance in Gram-negative bacteria, and other forms of noninherited resistance to vancomycin have been discussed in this Perspective. | 2019 | 30404451 |