Vancomycin-resistant enterococci.

Review of the resistance of Enterococcus (E. faecalis and Enterococcus faecium) to vancomycin in history, epidemiology, drug resistance mechanism and management

MEDLINE, IDIS and current journal search of English articles on vancomycin-resistant enterococci (VRE) from 1982 to 1994

Studies and reports on vancomycin-resistant Enterococcus faecalis and Enterococcus faecium were evaluated. Case reports, cohorts, epidemiology, in vitro and in vivo studies were evaluated

It was reported that the minimum inhibitory concentration of vancomycin was 32 μg / mL or more

A large-scale occurrence of VRE infection has occurred due to in-hospital infection. Such occurrences require enhanced infection control procedures to limit the spread of VRE. Vancomycin resistance in Enterococcus faecalis and Enterococcus faecium is classified into phenotypes VanA and VanB. The mechanism of vancomycin resistance is caused by the production of the peptide peptide D - Ala - D - Lac which replaces D - Ala - D - Ala in the peptidoglycan pathway, thereby preventing vancomycin and D - Ala. The combination peptidoglycan cell wall vanA gene of -D-Ala is associated with a transposable factor (Tn 1546) that can be metastasized by conjugation and most data indicate that vanB has an endogenous origin. Education, aggressive infection control measures. In order to deal with the problem of VRE, it is necessary to establish a monitoring plan and properly use vancomycin.

In recent years, the prevalence rate of VRE has increased dramatically and has become a worldwide problem. Prior exposure to vancomycin and antibiotics (eg cephalosporins, anti-anaerobic agents), physical location within the hospital, immunosuppression, prolongation of hospital stay, VRE gastrointestinal colonization associated with VRE infection and colonization Several factors. Antibiotic therapy for severe VRE infection is phenotypically dependent. The best treatment for the VanA phenotype is unclear; the VanB phenotype can be treated with teicoplanin and aminoglycoside

Recently, the incidence of infectious diseases caused by Enterococcus has increased in the United States. These bacteria are resistant to treatment of vancomycin (vancomycin-resistant enterococci or VRE). In addition, vancomycin resistance, they also seem to be able to tolerate the treatment of other drugs, may also transfer resistance genes to other bacteria (necessity of study of Staphylococcus aureus including cautious use of vancomycin , Improvement of training and medical staff, etc.). The main purpose of these interventions is to spread the VRE to hospital staff, residents, visitors or the general public, so that VRE patients can visit the hospital freely and go to the hospital. Treatment services for vancomycin resistance to other bacteria and diffusion prevention

Enterococci bacteria naturally live in the intestines (Department of Health, 2006). Several Enterococcus strains develop tolerance to antibiotics known as vancomycin. These strains are called vancomycin-resistant enterococci or VRE. Antibiotic resistant strains and nonresistant strains are not relevant. When they affect the urinary tract, surgical wounds or inpatient's blood they cause serious concern. In such a case, treatment becomes difficult and even life threatening. Especially vulnerable patients are hospitalized patients with severe disease such as cancer, blood disease, kidney disease or immunodeficiency. Despite good health protection, the VRE may be infected by medical experts who treat patients and do not follow appropriate precautions. VRE can be infected by touching directly with hands and may be infected via infected surface or medical equipment (DH)