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Enterococcus | Johns Hopkins ABX Guide
Beta-lactamase—producing enterococci are occasionally problematic, particularly when large numbers of organisms are present in tissues eg, in endocarditis vegetation. However, only a few genes controlled directly by CroR have been identified thus far.
The second pump is EfrAB, an ABC-type transporter that enhances resistance to a variety of structurally unrelated compounds, including quinolones, when expressed in E. They are pregnancy category B. You can learn more about how we ensure our content is accurate and current by reading our cost policy. Enterococcal disease, epidemiology, and implications for treatment.
However, australia of these newly licensed agents quinupristin-dalfopristin, linezolid, daptomycin, tigecycline has been entirely free of resistance. Absence of bioactive metabolites of augmentin and amoxycillin in man. High-molecular-weight PBPs are often categorized as Class A bifunctional, exhibiting both transglycosylase and transpeptidase activities and Page B monofunctional, exhibiting transpeptidase activity but lacking augmentin activity.
However, none of these newly licensed agents quinupristin-dalfopristin, linezolid, daptomycin, tigecycline has been entirely free of resistance.
Gene products that specify the production of modified peptidoglycan precursors include VanH dehydrogenase that converts pyruvate to lactate look here VanA ligase that forms D-Ala-D-Llac augmentin.
As more strains become sequenced, it is clear that the enterococcal genome is quite plastic, with enterococcus elements liberally sprinkled throughout and implicated in a australia of genome rearrangements and transfers.
Clinical management of non-faecium non-faecalis vancomycin-resistant enterococci infection. Enterococcal infections often develop augmentin people with health conditions, particularly those that require Internet treatment. Although the mechanism of conjugative transfer was not established in cost study, a plausible mechanism could involve mobilization mediated by co-integrated enterococcal conjugative plasmids, as recently described in E.
Overview of genetic mechanisms of glycopeptide resistance Nine distinct gene clusters conferring glycopeptide resistance have been described in enterococci. These determinants differ from each other both genetically and phenotypically, based on their physical location encoded on a mobile genetic element or in the core genome ; the specific glycopeptides to which they confer resistance often distinguished operationally as providing resistance to both vancomycin and teicoplanin, or providing resistance to vancomycin but not teicoplanin ; the level of resistance they confer; whether resistance is inducible or constitutively expressed; and the type of peptidoglycan precursor that is produced by their gene products.
The Van gene clusters encode several functions: i a regulatory module, namely a two-component signal transduction system that is responsible for sensing the presence of glycopeptides and activating expression of the resistance genes in inducible Van types; ii enzymes that produce the modified peptidoglycan precursors, including enzymatic machinery that is required to produce the appropriate substitute D-Lac or D-Ser , and a ligase that fuses D-Ala to either D-Lac or D-Ser to make the corresponding dipeptide that can be incorporated into peptidoglycan precursors via the normal biosynthetic machinery of the cell; and iii D,D-carboxypeptidases that eliminate any of the normal unmodified peptidoglycan precursor synthesized by the natural biosynthetic machinery of the cell, thereby ensuring that nearly all precursors reaching the cell surface are of the modified variety.
The VanA and VanB types are the most common among clinical isolates and have been studied in the greatest detail.
The VanA determinant Figure 1 confers a high level of resistance to vancomycin and teicoplanin. VanA is typically encoded on Tn or related transposons, and includes seven open reading frames transcribed from two separate promoters. The regulatory apparatus is encoded by the VanR response regulator and VanS sensor kinase two-component system, which are transcribed from a common promoter, while the remaining genes are transcribed from a second promoter.
Gene products that specify the production of modified peptidoglycan precursors include VanH dehydrogenase that converts pyruvate to lactate and VanA ligase that forms D-Ala-D-Llac dipeptide. Figure 1. Regulation of vancomycin resistance gene clusters.
The VanS or VanSB sensor kinases are anchored in the cytoplasmic membrane by two transmembrane segments TM that flank the predicted more The VanB locus Figure 1 confers moderate to high-level resistance to vancomycin, but is not induced by teicoplanin. The genetic organization of VanB is similar to that of VanA, in that it contains two distinct promoters transcribing seven open reading frames, but there are some significant differences.
However VanB lacks a homolog of VanZ, and instead encodes a protein named VanW, whose role in resistance is not fully understood.
The VanS sensor kinase is thought to recognize a poorly defined stimulus that signals the presence of vancomycin in the environment. VanS thereby becomes activated and autophosphorylates a conserved histidine residue on the cytoplasmic side of the protein. As a result, the phosphatase activity of VanS is critical to maintain the signaling pathway in the off state in the absence of an inducing antibiotic.
In fact, constitutively resistant mutants that carry lesions in VanS can be isolated from patients during glycopeptide therapy. For example, examination of successive isolates of E. Although both VanA and VanB rely on two-component signaling systems to control Van expression, it is clear that there are important differences between these regulatory systems. For example, the VanS and VanSB sensor kinases exhibit relatively little sequence identity in the N-terminal portion that serves as the site of stimulus recognition.
Given the distinct architecture of these two sensor kinases, it seems plausible that they recognize and respond to different molecular signals to trigger kinase activation and expression of the resistance genes. In fact, this predicted difference in ligand binding—and consequently, in the inducibility of the signaling system—underlies the difference in teicoplanin susceptibility of enterococci that contain VanA vs.
Although the molecular identity of the actual inducing signal s remain unclear, the VanA resistance genes are induced by the presence of both vancomycin and teicoplanin thereby conferring resistance to both , but the VanB resistance genes are only induced by vancomycin—hence, VanB strains remain susceptible to teicoplanin.
Of note, VanSB can acquire mutations of various types that lead to constitutive expression of the resistance genes or to inducibility by teicoplanin, thereby altering the phenotype of such mutants carrying the VanB locus. Regulation by host factors? Some evidence suggests that one or more sensor kinases encoded in the genome of the enterococcal host can contribute to the regulation of the Van resistance genes. Similarly, the VanE cluster in E.
Such findings suggest that enterococci encode endogenous two-component signaling systems whose natural function is to monitor the integrity of the cell wall for perturbations, and activate appropriate adaptive responses to ensure cell wall maintenance; and further, that the glycopeptide resistance gene cassettes have managed to exploit these endogenous systems to assist in the regulation of glycopeptide resistance.
Other host factors may also play a role in regulation of Van expression. For example, expression of the VanE vancomycin resistance genes may be influenced by the alteration of DNA supercoiling in E.
The expanding Van alphabet While the VanA- and VanB-type vancomycin resistance clusters continue to be the predominant forms that account for vancomycin resistance in hospitals, new Van resistance gene clusters have been recently described, which brings the number of known gene clusters capable of conferring Van resistance to nine. Fitness cost of vancomycin resistance Despite the complex mechanism that underlies glycopeptide resistance, resistant enterococci have disseminated worldwide, suggesting that resistance imposes little or no biological cost to the bacteria.
The investigators found that expression of vancomycin resistance imposed a significant fitness cost, both when expression is induced by the antibiotic and when expression is constitutive due to mutation of the regulatory apparatus. However, uninduced vancomycin resistance did not impose a measurable fitness cost.
Alternative mechanism of glycopeptide resistance A novel mechanism of glycopeptide resistance has been described in laboratory-selected vancomycin-resistant mutants of E. This mechanism is unrelated to that encoded by the Van gene clusters namely, those with production of peptidoglycan precursors containing D-Lac or D-Ser substitutions. The investigators selected highly resistant mutants in vitro and performed extensive analysis of peptidoglycan structure in the mutants.
Their analysis revealed that the beta-lactam insensitive L,D-transpeptidase pathway discussed in more detail below, under Ampicillin resistance was activated. This alternative transpeptidase named Ldtfm is capable of crosslinking enterococcal peptidoglycan using the L-Lys found at the 3rd position of the peptide stem rather than the D-Ala found at position 4, as is typical of most PBPs.
The investigators found that a cryptic D,D-carboxypeptidase was activated in the glycopeptide-resistant mutants, whose activity resulted in production of peptidoglycan peptide stem precursors that are tetrapeptides lacking the terminal D-Ala , rather than pentapeptides.
Such precursors are not substrates for binding by glycopeptide antibiotics, but can be cross-linked by the Ldtfm transpeptidase. However, it remains unknown whether this mechanism of glycopeptide resistance is relevant in clinical isolates. Daptomycin resistance Daptomycin is a lipopeptide antibiotic with potent in vitro bactericidal activity against Gram-positive bacteria.
The mechanism of antimicrobial action for daptomycin has not been unequivocally established, but is thought to involve calcium-dependent insertion into the cytoplasmic membrane followed by membrane depolarization, release of intracellular potassium ions, and rapid cell death Alborn, Jr. Because its mechanism of action is distinct from those of other antibiotics, daptomycin is useful for treatment of infections that are caused by multidrug-resistant Gram-positive strains.
Daptomycin resistance has been observed in clinical isolates following daptomycin therapy, typically as a result of mutations in chromosomal genes. Daptomycin-nonsusceptible clinical E. The investigators determined that these strains did not carry mutations in homologs of genes known to confer nonsusceptibility to daptomycin in S. However, the genes responsible for resistance were not identified. Recent studies have begun to explore the genetic basis of daptomycin resistance in enterococci Arias, et al.
The genomes of a pair of E. In that study, unique-sequence polymorphisms were found in cls, gdpD both thought to be involved in phospholipid metabolism and liaF, but no polymorphisms were found in homologs of the genes identified in daptomycin-resistant S.
Follow up analysis with in vitro selection for daptomycin-resistant variants of the original susceptible strain led to the identification of mutations in liaF and gdpD. Importantly, the daptomycin-resistant phenotype was determined to be a consequence of the identified mutations, as site-directed mutagenesis to recapitulate these mutations in an otherwise daptomycin-susceptible host conferred enhanced daptomycin resistance, demonstrating that mutations in these genes confer resistance.
Similarly, in a clinical strain pair of E. Changes in cls, liaF, liaS, or liaR were also identified in other daptomycin-resistant clinical isolates of enterococci, which suggests that such mutations play a key role in the development of daptomycin resistance in vivo. Development of daptomycin resistance appeared to be associated with profound ultrastructural changes in the cell envelope and septal apparatus, although it remains unclear if these changes are functionally important for resistance or merely an incidental consequence of the mutations.
LiaF is part of the three-component LiaFSR regulatory system, which is known to coordinate the response of the cell envelope to antibiotics and antimicrobial peptides in some Gram-positive bacteria, which suggests that perturbations in the activity of this signaling system may alter envelope properties in a such a way that daptomycin can no longer interact with, or insert into, the membrane efficiently.
In parallel studies, Palmer and coworkers systematically selected daptomycin-resistant variants of E. Whole-genome sequence comparison identified mutations in seven genes, including cls, rpoN, and additional genes whose cellular functions in other contexts have not been established.
Transfer of the cls mutant allele to a susceptible E. Time-resolved analysis of the emergence of mutations during daptomycin exposure revealed that cls mutations appeared early in multiple independent selections, which highlights its importance.
Additional daptomycin-resistant mutants were obtained that lacked such cls mutation, which shows that alternative paths to daptomycin resistance also exist. Collectively, the results from these two studies suggest that, while the underlying mechanisms are genetically distinct from those identified in S.
Aminoglycoside resistance Aminoglycosides act by binding to the 16S rRNA of the 30S ribosomal subunit and interfering with protein synthesis. Enterococci generally exhibit a moderate level of intrinsic aminoglycoside resistance that has been attributed to poor uptake of antibiotics.
For example, analysis of selected mutants that exhibited enhanced gentamicin resistance in vitro suggested that impaired uptake of gentamicin can contribute directly to enhanced resistance Aslangul, et al. However, some evidence suggests that other mechanisms may contribute to, or even be primarily responsible for, intrinsic resistance of some enterococci to aminoglycosides. Moderate species-specific intrinsic resistance to aminoglycosides in E.
The inactivation of efmM in E. Addition of the 5-methyl to C sterically hinders aminoglycoside binding. The physiological effects of these two factors seems to be additive, in the sense that mutation of both genes led to the largest reduction in resistance. However, it remains unclear if aminoglycoside resistance is the primary function of EfmM. The position of m5C at the junction between the ribosomal A-site and the P-site in 16S rRNA suggests that this modification might also play a more basic role in protein synthesis by influencing codon-anticodon interactions.
High-level resistance to aminoglycosides HLGR is conferred by a mechanism distinct from those described above, and importantly, abolishes the synergistic bactericidal activity of aminoglycosides in combination with cell-wall—active agents that are important in the treatment of severe enterococcal infections, such as endocarditis.
HLGR is usually acquired on a mobile element that encodes an aminoglycoside-modifying enzyme. Rifampicin has been used for decades as part of an antibiotic cocktail to treat infections caused by Mycobacterium tuberculosis, and has recently found increasing use in the treatment of staphylococcal infections associated with indwelling medical devices, such as artificial joints.
Most resistance to rifampicin results from mutations of specific sites in the gene encoding the beta subunit of the RNA polymerase, which reduces the affinity of rifampicin for the polymerase. Mutations in RpoB responsible for rifampicin resistance have been identified in numerous and diverse species of bacteria.
Additionally, enzymatic inactivation of rifampicin has been observed in a handful of cases. Presumably this is at least partially a consequence of commensal enterococci being exposed to rifampicin during treatment for non-enterococcal infections, but other as-yet-unknown factors may contribute to the occurrence of resistant enterococcal isolates as well. Spontaneous rifampicin-resistant mutants of E. Mutations were identified in the rpoB gene of all such mutants at sites known to be associated with resistance to rifampicin in other species of bacteria.
For two particular mutants, confirmation that the rpoB point mutations are indeed responsible for rifampicin resistance was obtained by expressing the mutant alleles in an otherwise rifampicin-susceptible host. One unexpected observation was that some RpoB mutations led to an alteration in cephalosporin resistance in an allele-specific manner.
In particular, the rpoB HY mutation conferred a substantially enhanced resistance to cephalosporins in multiple lineages of E. The mechanistic basis for this observation is not known, but the rpoB HY substitution may alter rates of transcription of genes that contribute to intrinsic cephalosporin resistance in enterococci.
Rifampicin resistance in some isolates of E. The molecular explanation for this effect remains unknown and authors speculate that there may be another mechanism for rifampicin resistance besides the two known mechanisms namely, mutation in the rpoB gene and rifampicin inactivation. Quinolone resistance Quinolones generally exhibit only moderate activity against enterococci.
Resistance to aminoglycosides eg, gentamicin, streptomycin , particularly with E. Vancomycin-resistant enterococci VRE may also be resistant to other glycopeptides eg, teicoplanin , aminoglycosides, and cell wall—active beta-lactams eg, penicillin G, ampicillin. When identified, infected patients are strictly isolated. Daptomycin, oritavancin, tigecycline, and eravacycline have in vitro activity against VRE and may be off-label treatment options.
Beta-lactamase—producing enterococci are occasionally problematic, particularly when large numbers of organisms are present in tissues eg, in endocarditis vegetation. My question is, have i damaged any nerves on penile glans that result in this pain? Is it permanent, do i have to live with this pain forever?
Read More All again negative except Postive for Fungus candida albican. But rash dint went away, then he said might be skin parasitic infection. In the meantime, i developed irritation in my eyes too.
Read More bad smell, white discarghe, ichness etc and I made a penile swab, but the only result was enterococcus spp.
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