[Enterococci resistant to glycopeptides]

Vincent Cattoir1, Roland Leclercq

  • 1Centre national de référence de la résistance aux antibiotiques, Laboratoire associé entérocoques, service de microbiologie, CHU de Caen, avenue Côte de Nacre, Caen, France.

Medecine Sciences : M/S
|November 26, 2010
PubMed

Insights

Multidrug-resistant Enterococcus faecium causes infections and is resistant to glycopeptide antibiotics. Hospital-adapted strains (CC17) are spreading, necessitating surveillance and control measures.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Genetics

Context:

  • Enterococci cause significant community- and hospital-acquired infections.
  • Glycopeptide antibiotics (vancomycin, teicoplanin) target bacterial cell wall synthesis.
  • Enterococcus faecium exhibits increasing multidrug resistance, including to glycopeptides.

Purpose:

  • To investigate the mechanisms and spread of glycopeptide-resistant Enterococcus faecium.
  • To identify characteristics of hospital-adapted strains contributing to outbreaks.

Summary:

  • Glycopeptide resistance in Enterococcus faecium arises from acquiring genes that alter cell wall precursors.
  • Hospital outbreaks are linked to a specific hospital-adapted clonal complex (CC17) of E. faecium.
  • CC17 strains display high-level resistance to ampicillin and fluoroquinolones and possess virulence factors.

Impact:

  • Effective control of enterococcal outbreaks requires understanding resistance mechanisms and strain epidemiology.
  • Surveillance of spreading hospital-adapted clonal strains is crucial for infection control.
  • New therapeutic antibiotics are available, but strain monitoring remains essential.

Related Concept Videos

Inhibitors of Gram-positive Cell Wall Synthesis01:23

Inhibitors of Gram-positive Cell Wall Synthesis

Bacterial cell walls are typically rigid structures composed mainly of peptidoglycan, a mesh-like polymer that provides mechanical strength and maintains cell shape. The synthesis of peptidoglycan is a crucial process in bacterial growth and serves as a primary target for many antibiotics.Mechanism of Action of Beta-Lactam AntibioticsBeta-lactam antibiotics, such as penicillin, inhibit peptidoglycan synthesis in actively growing cells. These antibiotics share a characteristic four-membered...
Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Development of Antibiotic Resistance01:30

Development of Antibiotic Resistance

Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
Inhibitors of Bacterial Protein Synthesis01:25

Inhibitors of Bacterial Protein Synthesis

Aminoglycosides constitute a highly potent class of bactericidal antibiotics that exert their antimicrobial effects by targeting the bacterial ribosome, specifically disrupting protein synthesis. These polycationic molecules consist of amino-modified sugars linked via glycosidic bonds to an aminocyclitol core such as 2-deoxystreptamine or streptamine. Their strong positive charges facilitate tight binding to the negatively charged phosphate backbone of ribosomal RNA (rRNA), primarily at the 16S...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...