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PubMed2002

Vancomycin resistance in staphylococci.

Vancomycin resistance has been reported in clinical isolates of both coagulase-negative staphylococci and Staphylococcus aureus. The emerging threat of widespread vancomycin resistance poses a serious public health concern given the fact that vancomycin has long been the preferred treatment of antibiotic-resistant gram-positive organisms. Though major efforts are now being focused on improving our understanding of vancomycin resistance, there is much that remains unknown at this time. This article reviews the major epidemiologic, microbiologic, and clinical characteristics of vancomycin resistance in both coagulase-negative staphylococci and S. aureus. The review begins with a discussion of issues common to both coagulase-negative staphylococci and S. aureus, such as definitions, laboratory detection of vancomycin resistance, and infection control issues related to vancomycin-resistant staphylococci. The rest of the article is then devoted to a discussion of issues unique to each organism, including epidemiology, risk factors for infection, mechanisms of resistance, and management options.

Anti-Bacterial Agents↗

PubMed2006

Multihospital surveillance of nosocomial methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococcus, and Clostridium difficile: analysis of a 4-year data-sharing project, 1999-2002.

BACKGROUND: This study sought to establish a benchmark of resistant organism rates among a cohort of regional hospitals. METHODS: The Centers for Disease Control and Prevention (CDC) definitions were used to standardize the methodology for obtaining rates per 1000 patient days of nosocomial infection and colonization with methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus (VRE), and nosocomial infection with Clostridium difficile (CDIF). Only newly acquired nosocomial cases were counted. Data were reported as individual hospital control charts and as cohorted aggregate data. VHA East Coast Infection Control Professionals from 32 hospitals in New Jersey and Pennsylvania were involved. RESULTS: Benchmarks were established with pooled mean rates for each cohort. During the observational period, a statistically significant downward trend was observed for VRE and MRSA (P = .02 and .0007, respectively), and an upward trend was observed for CDIF (P = .0256). CONCLUSION: Benchmarks were established to compare nosocomial MRSA, VRE, and CDIF rates. Although significant changes in rates were observed, no attempt was made to establish a causal relationship between infection control practices and observed rates. However, a secondary gain was achieved through sharing best practices.

Benchmarking↗

PubMedDate not supplied

Medicare reimbursement for home infusion therapy: a contributor to the development of community acquired vancomycin-resistant enterococci?

Vancomycin is a bacteriocidal antibiotic widely used to treat gram-positive infections, including methicillin-resistant Staphylococcus aureus. During the past 5 years, there have been increasingly frequent reports of infections caused by enterococci species resistant to vancomycin. Until recently, this was a phenomenon limited almost exclusively to the hospital. Presently, there are reports of vancomycin-resistant enterococci developing in the outpatient and home care population. The intent of this article is to present one possible explanation for this trend in the hope that further research will be stimulated.

Community-Acquired Infections↗

PubMed2000

Evidence of delays in transferring patients with methicillin-resistant Staphylococcus aureus or vancomycin-resistant Enterococcus to long-term-care facilities.

This retrospective case-control study examined whether there was a difference in length of time awaiting long-term-care placement for patients identified as having methicillin-resistant Staphylococcus aureus or vancomycin-resistant Enterococcus compared to controls. Thirty-nine patients with methicillin-resistant Staphylococcus aureus or vancomycin-resistant Enterococcus waited for placement an average of 61 days longer than controls (P<.0002). The average number of requests for placement was 2.5 compared to 1.7 for controls (P=.015).

Aged↗

PubMed2001

Vancomycin-resistant Enterococcus faecium meningitis successfully managed with linezolid: case report and review of the literature.

Enterococci cause serious illness in immunocompromised patients and severely ill, hospitalized patients. Resistance to vancomycin has increased in frequency during the past few years. Limited therapeutic options are available for vancomycin-resistant enterococcal infections and the optimum therapy has not been established. We report a case of nosocomial vancomycin-resistant Enterococcus faecium meningitis in the setting of hyperinfection with Strongyloides stercoralis that was successfully treated with linezolid. We also review the previously reported cases of vancomycin-resistant E. faecium meningitis.

Acetamides↗

PubMed1999

Costs of treating infections caused by methicillin-resistant staphylococci and vancomycin-resistant enterococci.

Infection with methicillin-resistant Staphylococcus aureus (MRSA) or vancomycin-resistant Enterococcus faecium (VREF) increases the risk of mortality and results in prolonged hospitalization and high utilization of costly treatment modalities. Measures to prevent the spread of MRSA (and possibly VREF) include patient isolation and decontamination, hygiene measures, ward closure, and screening of patients and staff for carriage. In seriously ill patients, the increased use of vancomycin for the treatment of MRSA can lead to the emergence of VREF colonization/infection. Quinupristin/dalfopristin is effective in the treatment of MRSA infections, including nosocomial pneumonia, skin and soft tissue infection, and septicaemia. In the treatment of nosocomial pneumonia, clinical success rates were equivalent between quinupristin/dalfopristin and vancomycin. In the context of a hospital policy which emphasizes effective hygiene measures and the prudent use of antibacterials, quinupristin/dalfopristin is an effective antimicrobial that can help to control the high costs associated with multiresistant MRSA and VREF infections.

Enterococcus faecium↗

PubMed2006

Emergence of linezolid resistance in the vancomycin-resistant Enterococcus faecium multilocus sequence typing C1 epidemic lineage.

A relatively high rate of vancomycin-resistant Enterococcus faecium not susceptible to linezolid was observed in intensive care unit patients. Linezolid-resistant isolates carried the G2576T mutation in the 23S rRNA gene, belonged to different clones, and shared the same allelic profile, which clusters in the C1 multilocus sequence typing epidemic lineage.

Acetamides↗

PubMed2000

Occurrence of the vancomycin-resistant genes vanA, vanB, vanCl, vanC2 and vanC3 in Enterococcus strains isolated from poultry and pork.

It is suspected that the use of avoparcin as a feeding antibiotic for the fat stock contributes to development of cross-resistance against vancomycin and teicoplanin. After isolating enterococci strains from poultry and pork meat by cultivation on citrate azide Tween carbonate agar (CATC) and screening the vancomycin resistance on Columbia colistin nalidixic acid agar (CNA, supplemented with 5% sheepblood and 5 mg vancomycin/l) the polymerase chain reaction (PCR) was used for the detection of the vancomycin resistance genes vanA ('high level'), vanB ('moderate high level'), vanC1, vanC2 and vanC3 ('low level'). Out of 1643 E.-isolates from 115 poultry and 50 pork samples, 420 isolates could be identified as vancomycin resistant, 202 isolates of which carry the vanA, one isolate both the vanA and the vanC1, 38 isolates the vanC1, 14 isolates the vanC2, nine isolates both the vanC1 and the vanC3 gene and 156 isolates carry no gene. The vanB gene was not found in these isolates. Comparing vanA-positive food isolates with those from different human sources by means of the pulsed field gel electrophoresis (PFGE) it could clearly be demonstrated that they do not show homological fingerprints according to the source of origin. It is therefore unlikely that there is a close genetic relationship between isolates from animal foodstuff and humans.

Animals↗

PubMed1989

In vitro susceptibility studies of vancomycin-resistant Enterococcus faecalis.

Vancomycin resistance exhibited by Enterococcus faecalis isolates V583, V586, and V587 is described. The vancomycin MICs ranged from 32 to 64 micrograms/ml. Although resistant to vancomycin, the isolates were susceptible to teicoplanin (MIC, less than or equal to 0.5 micrograms/ml). Such a glycopeptide susceptibility profile has not been previously described for E. faecalis. Time kill studies showed that vancomycin resistance adversely affected the synergistic activity that vancomycin and aminoglycoside combinations usually demonstrate against enterococci. However, the ability to detect vancomycin resistance varied with the susceptibility testing method used. Whereas broth microdilution, broth macrodilution, and agar dilution methods detected resistance, disk-agar diffusion and the AutoMicrobic system Gram-Positive GPS-A susceptibility card (Vitek Systems Inc., Hazelwood, Mo.) did not. To detect vancomycin resistance reliably and establish the incidence of such E. faecalis isolates, adjustments in some susceptibility testing methods may be necessary.

Anti-Bacterial Agents↗

PubMed2006

Antimicrobial therapy of multidrug-resistant Streptococcus pneumoniae, vancomycin-resistant enterococci, and methicillin-resistant Staphylococcus aureus.

Antibiotic resistance among pneumococci, enterococci, and staphylococci has become increasingly important in recent decades. Clinicians should be familiar with the nuances of antibiotic susceptibility testing and interpretation in selecting antibiotics for these infections. The clinical significance of penicillin-resistant Streptococcus pneumoniae, macrolide-resistant S pneumoniae, and multidrug-resistant S pneumoniae is discussed. The clinical spectrum and therapeutic approach to Enterococcus faecalis (i.e., vancomycin-sensitive enterococci) and E faecium (i.e., vancomycin-resistant enterococci) are discussed. Differences in therapeutic approach between methicillin-sensitive Staphylococcus aureus and methicillin-resistant S aureus (MRSA) infections are reviewed. Differences between in vitro susceptibility testing and in vivo effectiveness of antibiotics for hospital-acquired MRSA (HA-MRSA) are described. Finally, the clinical features of infection and therapy of HA-MRSA and community-acquired MRSA (CA-MRSA) infections are compared.

Anti-Infective Agents↗

PubMedDate not supplied

Emergence of vancomycin-resistant enterococci.

Vancomycin and ampicillin resistance in clinical Enterococcus faecium strains has developed in the past decade. Failure to adhere to strict infection control to prevent the spread of these pathogens has been well established. New data implicate the use of specific classes of antimicrobial agents in the spread of vancomycin-resistant enterococci (VRE). Extended-spectrum cephalosporins and drugs with potent activity against anaerobic bacteria may promote infection and colonization with VRE and may exert different effects on the initial establishment and persistence of high-density colonization. Control of VRE will require better understanding of the mechanisms by which different classes of drugs promote gastrointestinal colonization.

Ampicillin Resistance↗

PubMed2004

Failure to develop vancomycin-resistant Enterococcus with oral vancomycin treatment of Clostridium difficile.

OBJECTIVE: Oral vancomycin therapy has been a risk factor for turning culture positive for vancomycin-resistant Enterococcus (VRE). VRE colonization status was reviewed for all patients who received oral vancomycin and underwent prospective cultures. METHODS: Data were extracted from the medical records of all patients receiving oral vancomycin between August 1995 and February 2001 regarding history, hospital course, and perirectal VRE cultures. Hospital policy required contact isolation for patients receiving oral vancomycin until colonization with VRE was excluded. RESULTS: Twenty-six courses of oral vancomycin were given to 22 patients. VRE colonization status after completion of therapy was evaluated for 23 courses in 20 (91%) of these patients. None of these patients became VRE culture positive during a median follow-up of 18 days (range, 9 to 39 days), with a median duration of treatment of 10 days (range, 3 to 58 days), and with a median total dose of 6,500 mg (range, 1,250 to 29,000 mg). All patients received other antibiotics within 30 days prior to therapy with oral vancomycin, during therapy with oral vancomycin, or both; 95% had received anti-anaerobic therapy and 35% had received parenteral vancomycin. CONCLUSIONS: Even when other risk factors were present, no patient receiving oral vancomycin at our facility subsequently became culture positive for VRE. This suggests that oral vancomycin therapy or other antibiotic use, including anti-anaerobic therapy, may not be a significant independent risk factor for turning culture positive for VRE among patients not previously exposed to the microbe.

Administration, Oral↗

PubMed1989

High-level vancomycin-resistant enterococci causing hospital infections.

Nosocomial infection or colonization due to enterococci with high-level resistance to vancomycin (minimal inhibitory concentrations [MICs] between 64 and greater than 2000 mg/L) has occurred in 41 patients with renal disease. These vancomycin-resistant enterococci were cultured from many sources including blood. All but one strain contained one or more plasmids ranging in molecular weight from 1.0 to 40 Megadaltons (MDa). Vancomycin resistance was transferable by conjugation to a susceptible recipient strain of Enterococcus faecalis but this was not always associated with plasmid DNA. The emergence of transferable high-level vancomycin resistance in enterococci causing significant clinical infections is of particular importance since vancomycin is widely regarded as a reserve drug for the management of infections with multi-resistant Gram-positive organisms.

Acute Kidney Injury↗

PubMed2001

Bactericidal activities of two daptomycin regimens against clinical strains of glycopeptide intermediate-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus faecium, and methicillin-resistant Staphylococcus aureus isolates in an in vitro pharmacodynamic model with simulated endocardial vegetations.

Daptomycin is an investigational lipopeptide antibiotic active against gram-positive organisms. The mechanism of action is unique, resulting in interference with cell membrane transport. The bactericidal activity of daptomycin was evaluated against glycopeptide-intermediate susceptible Staphylococcus aureus (GISA), vancomycin-resistant Enterococcus faecium (VREF), and methicillin-resistant S. aureus (MRSA) in an in vitro infection model with simulated endocardial vegetations. Simulated regimens of daptomycin at 6 mg/kg/day (D6) and 10 mg/kg/day (D10) were utilized. MICs and MBCs for daptomycin were determined in the absence and in the presence of albumin with the following results (MIC/MBC): for GISA-992, 0.5/1.0 and 16/16; for VREF-590, 2.0/2.0 and 32/32; and for MRSA-494, 0.25/0.25 and 1.0/4.0 microg/ml, respectively. During the first 8 h daptomycin significantly reduced the inoculum for all organisms. Daptomycin at 6 mg/kg/day and 10 mg/kg/day had log(10) CFU/g reductions of 5 and 6, 3.4 and 5, and 6.4 and 6.5 by 8 h for GISA-992, VREF-590, and MRSA-494, respectively. Against both GISA-992 and VREF-590, the D10 regimen achieved the limit of detection at 72 h, with D6 regimens showing slight regrowth. A concentration-dependent killing effect was noted to occur, with daptomycin demonstrating a more rapid and greater kill from the D10 versus the D6 regimen. The results of this study suggest that daptomycin demonstrates significant (P < 0.05) activity against gram-positive organisms in a simulated sequestered infection site.

Anti-Bacterial Agents↗

PubMed1990

Selection for vancomycin resistance in clinical isolates of Staphylococcus haemolyticus.

Killing curves were used to characterize Staphylococcus haemolyticus isolates previously reported to contain subpopulations showing increased resistance to vancomycin. Results suggested that vancomycin and teicoplanin were ineffective at a concentration of 8 micrograms/ml and growth was seen between 24 and 48 h. Conversely, the lipopeptide antibiotic daptomycin at the same concentration rapidly killed tested strains by 6 h. Various staphylococcal strains were examined to determine if vancomycin resistance could be selected in all strains of staphylococci, was specie(s) restricted, or was unique to this patient's clinical isolates. About 1 x 10(8) colony-forming units were added to melted brain-heart infusion agar plates containing 12 micrograms/ml of vancomycin. Plates were examined after 48 h for presence of resistant clones. Results indicated that selection for vancomycin resistance was restricted to S. haemolyticus strains. Further, all S. haemolyticus isolates that displayed a double zone of growth around imipenem agar diffusion discs (Impdz) contained stably resistant subpopulations. Vancomycin resistance could not be selected in imipenem-sensitive derivative clones. Impdz isolates that were recovered from geographically distinct locations displayed nearly identical SDS-PAGE protein profiles. It appears that a characteristic susceptibility pattern displayed by clinical isolates of S. haemolyticus may provide a marker for those strains that contain subpopulations having increased resistance to vancomycin.

Bacterial Proteins↗

PubMed2001

Solid- and solution-phase synthesis of vancomycin and vancomycin analogues with activity against vancomycin-resistant bacteria.

Vancomycin, the prototypical member of the glycopeptide family of antibiotics, is a clinically used antibiotic employed against a variety of drug-resistant bacterial strains including methicillin-resistant Staphylococcus aureus (MRSA). The recent emergence of vancomycin resistance, viewed as a growing threat to public health, prompted us to initiate a program aimed at restoring the potency of this important antibiotic through chemical manipulation of the vancomycin structure. Herein, we describe the development of synthetic technology based on the design of a novel selenium safety catch linker, application of this technology to a solid-phase semisynthesis of vancomycin, and the solid- and solution-phase synthesis of vancomycin libraries. Biological evaluation of these compound libraries led to the identification of a number of in vitro highly potent antibacterial agents effective against vancomycin-resistant bacteria. In addition to aiding these investigations, the solid-phase chemistry described herein is expected to enhance the power of combinatorial chemistry and facilitate chemical biology and medicinal chemistry studies.

Anti-Bacterial Agents↗

PubMed2001

Outbreak of vancomycin-resistant Enterococcus faecium of the phenotype VanB in a hospital in Warsaw, Poland: probable transmission of the resistance determinants into an endemic vancomycin-susceptible strain.

The first outbreak caused by vancomycin-resistant enterococci of the VanB phenotype in Poland was analyzed. It occurred in a single ward of a Warsaw hospital which is a specialized center for the treatment of hematological disorders. Between July 1999 and February 2000, 11 patients in the ward were found to be infected and/or colonized by Enterococcus faecium that was resistant in vitro to vancomycin and susceptible to teicoplanin. PCR analysis confirmed that the vancomycin-resistant E. faecium (VREM) isolates carried the vanB gene, which is responsible for the VanB phenotype. Pulsed-field gel electrophoresis (PFGE) typing revealed that the isolates belonged to four distinct PFGE types and that one of these was clearly predominant, including isolates collected from seven different patients. The isolates contained one or more copies of the vanB gene cluster of the identical, unique DraI/PagI (BspHI) restriction fragment length polymorphism type, which resided in either the same or different plasmid molecules or chromosomal regions. All this data suggested that the outbreak was due to both clonal spread of a single strain and horizontal transfer of resistance genes among nonrelated strains, which could be mediated by plasmids and/or by vanB gene cluster-containing transposons. The comparative analysis of vancomycin-susceptible E. faecium (VSEM) isolates collected from infections in the same ward at the time of the VREM outbreak has led to identification of a widespread VSEM strain that was possibly related to the major VREM clone. It is very likely that this endemic VSEM strain has acquired vancomycin-resistance determinants and that the acquisition occurred more than once during the outbreak.

Anti-Bacterial Agents↗

PubMed1992

Vancomycin resistance in Enterococcus gallinarum.

The vancomycin resistance expressed by several strains of Enterococcus gallinarum was studied. Resistance was expressed constitutively, as demonstrated by analysis of growth and inhibition of peptidoglycan synthesis. E. gallinarum strains were moderately resistant to vancomycin (MIC, 16 micrograms/ml) but were as susceptible as vancomycin-susceptible enterococci to the glycopeptides, teicoplanin, A35512B, A47934, A4103A, and A41030E and the glycopeptide actaplanins A1, B2, and C1. Vancomycin resistance in E. gallinarum was inhibited by beta-lactam antibiotics at concentrations that saturated penicillin-binding protein 6 (PBP 6), as demonstrated by binding competition experiments. Spontaneous mutants (frequency, 10(-8)) were two- to fourfold more resistant to beta-lactam inhibition of vancomycin resistance than the parent strain. PBP binding competition experiments suggested that PBP 6 in the mutants bound less cefotaxime, while binding of penicillin and cefoxitin was unaffected. Both a bioassay method and high-performance liquid chromatography showed that E. gallinarum membranes have enzymatic activity which modifies a model pentapeptide yielding a product that is thought to be a tetrapeptide. This activity could be a D,D-carboxypeptidase. In both the parent E. gallinarum strain and its derivatives that were resistant to the synergistic drug combination, the activity was inhibited by beta-lactams at concentrations which correlated with those that inhibit vancomycin resistance and those that saturate PBP 6. These results suggest the possibility that PBP 6 may be involved in the vancomycin resistance of E. gallinarum and that the putative D,D-carboxypeptidase activity seen in E. gallinarum membranes may be attributable to PBP 6.

Anti-Bacterial Agents↗