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PubMed1999

Vancomycin-resistant enterococci: recent advances in genetics, epidemiology and therapeutic options.

Vancomycin-resistant enterococci (VRE) have gained much attention in the last decade. Currently, there are five known types of vancomycin resistance based on genes encoding ligase enzymes that the organisms use to produce their cell wall precursors, namely, VanA, VanB, VanC, VanD and VanE. An additional unclassified type was discovered in Australia. The basis of resistance among these phenotypes appears to be similar in that the resistant organisms produce peptidoglycan precursors that end in moieties other than D-alanyl-D-alanine, the usual target of vancomycin. The other dipeptide-like termini identified to date include D-alanyl-D-lactate and D-alanyl-D-serine, which have low affinity for glycopeptides. Recent evidence suggests that glycopeptide-producing organisms might be the remote origin of the vancomycin resistance genes. In European countries, avoparcin, a glycopeptide used in farm animals as a growth promoter, has been linked to the occurrence of VRE and occasional common strains have been identified in food products, farm animals, healthy subjects and hospitalized patients. There have been no such reports in the USA where heavy use of vancomycin and use of broad spectrum antibiotics such as cephalosporins have been identified as important risk factors for acquisition of VRE. Transmission within the same or between hospitals has been reported in many countries. Infection control measures and efforts to use antibiotics, particularly vancomycin, more appropriately have been implemented in a number of healthcare facilities with varying degrees of success. Many antibiotics, as a single agent or a combination of drugs, as well as various new antibiotics have been tested in vitro, in animal models, or used in anecdotal cases but clinical data from large comparative trials are not available to date. Because of the limited susceptibility of many VRE to other agents, efforts to control these organisms are particularly important. Copyright 1999 Harcourt Publishers LtdCopyright 1999 Harcourt Publishers Ltd.

Journal Article↗

PubMed1997

Efficacy and safety of vancomycin constant-rate infusion in the treatment of chronic Gram-positive bone and joint infections.

OBJECTIVE: To evaluate the efficacy and safety of vancomycin constant-rate infusion over 24 h in the treatment of Gram-positive bone infections, METHODS: Vancomycin (40 mg/kg/day) was administered without a loading dose to 15 patients (12 male, three female) aged 23--90 years, weighing 46--85 kg, with postoperative chronic bone and joint infections. The 24-h dose was adjusted to maintain plasma levels between 25 and 35 mg/L. Mean duration of therapy was 6.2 months (4--8.5) via a portable infusion pump. Sites of infection included hip and femur (10), tibia (three), patella (one) and vertebrae (one). Sequestrectomy (two), removal of material (7/8 prosthetic hips, 1/5 metal implants) and debridement (two) were performed at the beginning of the treatment. Involved bacteria included Staphylococcus aureus (eight, six methicillin resistant), S. epidermidis (four methicillin-resistant), Enterococcus faecalis (one), Enterococcus avium (one) and Streptococcus bovis (one). RESULTS: MIC of vancomycin ranged from 1 to 4 mg/L. The mean vancomycin bone concentration when available was 67.7plus minus38.9 microg/L. Based on a mean post-treatment follow-up of 14plus minus4 months (6--20.6), cure was achieved in 10 patients (66.6%). Failures were related to the inability to remove the infected prosthesis (one) or implants (three) and to the persistence of a deep wound abcess (one). Adverse events included pruritus (four cases), tinnitus (two), mild transient elevation of creatinine level (three) and transient neutropenia (two). Vancomycin was maintained in all the patients. CONCLUSIONS: Prolonged treatment with vancomycin constant-rate infusion is effective and safe for treatment of Gram-positive chronic bone and joint infections, providing that complete surgical débridement and prosthetic material removal are performed.

Journal Article↗

PubMed2003

Role of environmental contamination as a risk factor for acquisition of vancomycin-resistant enterococci in patients treated in a medical intensive care unit.

BACKGROUND: Colonization pressure, proximity to another case, exposure to a nurse who cares for another case, enteral feeding, and the use of sucralfate, vancomycin hydrochloride, cephalosporins, or antibiotics are among the defined risk factors for acquisition of vancomycin-resistant enterococci (VRE) in the intensive care unit (ICU) setting. However, the role of rooms with contaminated environmental surfaces has not been well delineated. METHODS: Retrospective case-control study conducted on patients admitted to the medical ICU (MICU) of a tertiary-care, university-affiliated medical center during a 9-month period. Patients who acquired VRE (cases) were matched with 2 randomly selected control subjects who did not acquire VRE and had been in the MICU for at least the same number of days. RESULTS: Thirty cases were matched with 60 appropriate controls. Cases were more likely to have been in the hospital for longer than 7 days before MICU admission (P =.009); to have occupied a specific room with persisting contaminated surfaces (P =.06); to have had a central venous catheter (P =.05); to have received vancomycin (P =.02), cephalosporins (P =.03), and quinolones (P =.006) before MICU admission; and to have received vancomycin (P =.02) and metronidazole sodium phosphate (P =.03) after MICU admission. Multivariate analysis showed that a hospital stay of longer than 1 week before MICU admission (P =.04), use of vancomycin before or after MICU admission (P =.03), use of quinolones before MICU admission (P =.03), and placement in a contaminated room (P =.02) were the best predictors of VRE acquisition. CONCLUSIONS: Among all other factors associated with VRE transmission, VRE acquisition may depend on room contamination, even after extensive cleaning. This study underscores the need for better cleaning and the role of the environment in transmission of VRE.

Aged↗

PubMed2004

Method of detecting beta-lactam antibiotic induced vancomycin resistant MRSA (BIVR).

Despite the fact that the combination of vancomycin and a beta-lactam antibiotic are known to act synergistically on vancomycin-susceptible Staphylococcus aureus (VSSA), some MRSA have emerged showing antagonism to the combination of vancomycin and a beta-lactam antibiotic. These MRSA are called beta-lactam antibiotic-induced vancomycin resistant MRSA (BIVR). A method based on this antagonistic phenomenon has been devised to detect BIVR strains. The method inhibits the VSSA strain but allows the BIVR strain to grow. Forty-six commercially available beta-lactam antibiotics induced the vancomycin-resistance. Using this detection method, 717 MRSA clinical isolates obtained from eight institutes throughout Japan were thus screened and 6.3% of these were detected as BIVR when judged at 48 h.

Drug Antagonism↗

PubMed2006

Vancomycin-susceptible dairy and clinical enterococcal isolates carry vanA and vanB genes.

A total of 109 enterococcal isolates from dairy food products and from human and dog infections, isolated in Portugal, and 26 type and reference strains of the genus Enterococcus were screened for vancomycin resistance. MIC values, both for vancomycin and teicoplanin, were determined. The genetic relatedness of isolates carrying either vanA and/or vanB was determined using Pulsed Field Gel Electrophoresis. For vanA carrying isolates, transposon Tn1546 was partially mapped using PCR. None of the 59 dairy isolates was resistant to vancomycin. Among the 50 clinical isolates, only one, carrying vanB, behaved as resistant, with a MIC value of 256 microg/mL. The type and reference strains used were susceptible both to vancomycin and teicoplanin. vanA was found in 37% of the dairy isolates and 40% of the clinical isolates. vanB was only detected in 18% of the clinical, both human and dog, isolates. PCR partial mapping of Tn1546 revealed 23 different patterns among 42 isolates. Some patterns were shared between dairy and clinical isolates. Using Pulsed Field Gel Electrophoresis six groups of isolates were found to be genetically undistinguishable and grouping was found to be geographically and location specific/related. No genetic relatedness was found between isolates from dairy, human and veterinary sources. These results show that an incomplete and/or unfunctional Tn1546 element may explain the absence of resistant behaviour in the studied isolates, even when vanA gene is present. Moreover, the work reported shows that both clinical (human and animal) and dairy isolates have been in contact with VanA genotype of resistance and suggest that dissemination of vanA gene has been through transposable elements, like Tn1546, and not by clonal dissemination of a resistant strain. Therefore, a national strategy should be implemented to survey both vancomycin resistance and its genetic dissemination.

Anti-Bacterial Agents↗

PubMed2000

Vancomycin resistance emerging in a clonal outbreak caused by ampicillin-resistant Enterococcus faecium.

OBJECTIVES: To describe the first nosocomial outbreak of ampicillin-resistant Enterococcus faecium (ARE) in Norway, where a few vancomycin-resistant strains have also been identified. METHODS: All cases of ARE and vancomycin-resistant Enterococcus faecium (VRE) diagnosed by the medical microbiological laboratories in a region inhabited by approximately 1 million people were registered. Isolates obtained during the period 1 January 1995 to 31 December 1996 were characterized by pulsed field-gel electrophoresis and the clinical data were recorded. RESULTS: One hundred and forty-nine patients (64 males, 85 females, mean age 70.5 years) were infected with ARE. Isolates from 115 cases were genomically related to the outbreak strain. Infections included bacteremia (14), wound infections (31), urinary tract infections (97) and other infections (seven). Most had a severe underlying disease and 93% of the patients had received antibiotics for a mean time of 23 days. Twenty-four patients (16.1%) died during hospitalization. Four infections were caused by a vanB-type VRE that was genomically related to the ARE outbreak strain. The prescription rate for vancomycin was low, but an increase in vancomycin use paralleled the appearance of VRE. The highest monthly incidence rate was 2.5 per 1000 patient admissions in July 1996 declining to 0.5 in December 1996. CONCLUSIONS: The first nosocomial outbreak caused by ARE was observed in 1995 in Norway and is still ongoing. One year after the onset, VRE occurred in wards which had a relatively high consumption of vancomycin.

Aged↗

PubMed2000

Isolation and characterization of vancomycin-tolerant Streptococcus pneumoniae from the cerebrospinal fluid of a patient who developed recrudescent meningitis.

The emergence of tolerance to vancomycin has recently been reported in Streptococcus pneumoniae, the most common cause of bacterial meningitis. A vancomycin- and cephalosporin-tolerant strain of S. pneumoniae, the Tupelo strain, was isolated from the cerebrospinal fluid of a patient who then developed recrudescence of meningitis despite treatment with vancomycin and a third-generation cephalosporin. The Tupelo strain evidenced no lysis in the exponential or stationary phase of growth when exposed to vancomycin and only minimal loss of viability. Further characterization revealed normal autolysin expression, localization, and triggering by detergents, indicating that the defect leading to tolerance in the Tupelo strain is in the control pathway for triggering of autolysis. Because tolerance is a precursor phenotype to resistance and may lead to clinical failure of antibiotic therapy, these observations may have important implications for vancomycin use in infections caused by S. pneumoniae.

Bacteriolysis↗

PubMed2000

Vancomycin-intermediate and -resistant Staphylococcus aureus: what the infectious disease specialist needs to know.

Ever since the first strain of Staphylococcus aureus with reduced susceptibility to vancomycin and teicoplanin was reported from Japan, there has been a lot of confusion regarding the laboratory and clinical approach to patients with infections due to S. aureus with reduced susceptibility to vancomycin. To date, 6 clinical infections with vancomycin-intermediate S. aureus (VISA) have been reported in the United States. Intermediate resistance appears to develop from preexisting strains of methicillin-resistant S. aureus in the presence of vancomycin, and all but 1 infection occurred in patients with exposure to dialysis for renal insufficiency. Detection of VISA is difficult in the laboratory, and special inquiries about susceptibility testing methods may be needed. These VISA-infected patients had underlying illnesses, and their infections did not appear to respond well to conventional treatment. Prevention strategies have been outlined. Without continued vigilance in enforcing infection-control measures, improved use of antimicrobials, and coordination of efforts among public health authorities, increasing levels of vancomycin resistance in S. aureus are likely to be encountered.

Anti-Bacterial Agents↗

PubMed2003

Coexistence of vancomycin-resistant enterococci and Staphylococcus aureus in the intestinal tracts of hospitalized patients.

The potential for transfer of vancomycin-resistance genes from enterococci to Staphylococcus aureus exists when these organisms share an ecologic niche. We performed an 8-month prospective study to determine the frequency at which S. aureus and vancomycin-resistant enterococci (VRE) coexist in the intestinal tracts of VRE-colonized patients and evaluated whether antianaerobic antibiotic therapy promoted increased density of S. aureus colonization. Of 37 patients colonized with vancomycin-resistant Enterococcus faecium, 23 (62%) had S. aureus recovered from stool specimens and 20 (87%) had methicillin-resistant strains. There was no significant difference in the mean density (+/- standard deviation) of S. aureus during versus > or =1 month after discontinuation of antianaerobic antibiotic therapy (5.1+/-1.5 vs. 4.7+/-1.6 log10 colony-forming units per gram of stool; P=.34). No S. aureus isolates were resistant to vancomycin. S. aureus and VRE often coexist in the intestinal tract, providing a potential reservoir for the emergence of vancomycin-resistant S. aureus isolates.

Aged↗

PubMed2006

Vancomycin: a history.

Vancomycin became available for clinical use >50 years ago but was soon discarded in favor of other antibiotics that were deemed to be more efficacious and less toxic. The advent of pseudomembranous enterocolitis, coupled with the spread of methicillin-resistant Staphylococcus aureus, led to a resurgence in the use of vancomycin. Almost immediately, concerns arose with regard to its therapeutic utility. In addition, resistance to vancomycin developed, first in enterococci and later in staphylococci. Several types of resistance have now been identified, each with a unique effect on infections treated with vancomycin. Recent studies have rekindled interest in the best way to administer the antibiotic. The findings of future studies may result in a return to measuring levels of vancomycin in serum, to assure a successful therapeutic outcome.

Anti-Bacterial Agents↗

PubMed2006

Adaptation of methicillin-resistant Staphylococcus aureus in the face of vancomycin therapy.

For the past 2 decades, vancomycin has served as the cornerstone of therapy against serious methicillin-resistant Staphylococcus aureus infections. This role is increasingly challenged by questions of efficacy, including reduced efficacy against infections caused by glycopeptide-intermediate S. aureus strains. In an evaluation of clinical glycopeptide-intermediate S. aureus isolates and serial, clinical methicillin-resistant S. aureus isolates obtained from patients receiving vancomycin for the treatment of bacteremia, we found that loss of function of the accessory gene regulator operon may confer a survival advantage to S. aureus under vancomycin selection pressure, particularly in strains with the accessory gene regulator group II genotype. Other advantages in a nosocomial setting may include enhancement of biofilm formation and promotion of physiologic changes supporting colonization. We conclude that loss of accessory gene regulator function in methicillin-resistant S. aureus might, in part, explain the decreased efficacy of vancomycin in the therapy of methicillin-resistant S. aureus bacteremia, thus highlighting the need to reevaluate the criteria of susceptibility to vancomycin.

Adaptation, Biological↗

PubMed2003

Association between antecedent intravenous antimicrobial exposure and isolation of vancomycin-resistant enterococci.

Vancomycin-resistant enterococci (VRE) have become important causes of nosocomial infections. This study evaluated the association between a variety of intravenous antimicrobial exposures and the isolation of VRE using two control groups: (1) a vancomycin-susceptible enterococci (VSE) group, to assess factors associated with development of VRE, and (2) a nonenterococci control group, to assess factors associated with positive cultures for enterococci without regard to vancomycin resistance. After adjusting for the effect of other antimicrobials, time at risk, and patient morbidity, compared to vancomycin-susceptible enterococci controls, exposures to imipenem (OR = 4.9, 95% CI = 1.6-14.1) and ceftazidime (OR = 2.6, 95% CI = 1.1-6.1) were significant predictors of VRE. When compared to nonenterococci controls, exposures to ampicillin (OR = 20.1, 95% CI = 1.5-263.1) and imipenem (OR = 5.1, 95% CI = 1.5-17.1) were significantly associated with VRE. Neither piperacillin nor vancomycin was associated with VRE compared to either control group. This study offers further evidence that the replacement of broad-spectrum cephalosporins by extended-spectrum penicillins, specifically piperacillin, may be effective in reducing VRE.

Adult↗

PubMed2001

A modified population analysis profile (PAP) method to detect hetero-resistance to vancomycin in Staphylococcus aureus in a UK hospital.

One hundred methicillin-resistant Staphylococcus aureus (MRSA) strains, isolated between 1983 and 1999, were tested alongside the vancomycin hetero-resistant S. aureus (hVRSA) strain Mu 3, and vancomycin-resistant S. aureus (VRSA) strain Mu 50, for their resistance to vancomycin. This was achieved using the screening method described by Hiramatsu, gradient plates, agar incorporation, standard Etest, macrodilution Etest and a modified population analysis. Using Hiramatsu's screening method, 5% of the 100 MRSA were identified as VRSA and 5% identified as hVRSA, the gradient plates identified 7% hVRSA, and the standard and macrodilution Etests identified no hVRSA. Mu 3 appeared to be vancomycin-susceptible using both the agar incorporation and standard Etest methods, but was classified as hVRSA using the macrodilution Etest. The modified population analysis reliably detected vancomycin hetero-resistance in Mu 3 and identified no hVRSAs within the 100 MRSA sample.

Hospitals↗

PubMed2001

Selective cleavage of D-Ala-D-Lac by small molecules: re-sensitizing resistant bacteria to vancomycin.

Pathogenic enterococci are becoming resistant to currently available antibiotics, including vancomycin, the drug of last resort for Gram-positive infections. Enterococci pose a significant public health threat, not least because of the risk of transferring vancomycin resistance to the ubiquitous Staphylococcus aureus. Vancomycin resistance is manifested by cell wall peptidoglycan precursors with altered termini that cannot bind the antibiotic. Small molecules with well-oriented nucleophile-electrophile assembly and complementary chirality to the peptidoglycan termini were identified as catalytic and selective cleavers of the peptidoglycan precursor depsipeptide. These molecules were tested in combination with vancomycin and were found to re-sensitize vancomycin-resistant bacteria to the antibiotic.

Alanine↗

PubMed2002

Characterization of Tn1546 in vancomycin-resistant Enterococcus faecium isolated from canine urinary tract infections: evidence of gene exchange between human and animal enterococci.

Thirty-five enterococcal isolates were recovered from dogs diagnosed with urinary tract infections at the Michigan State University Veterinary Teaching Hospital over a 2-year period (1996 to 1998). Isolated species included Enterococcus faecium (n = 13), Enterococcus faecalis (n = 7), Enterococcus gallinarum (n = 11), and Enterococcus casseliflavus (n = 4). Antimicrobial susceptibility testing revealed several different resistance phenotypes, with the majority of the enterococcal isolates exhibiting resistance to three or more antibiotics. One E. faecium isolate, CVM1869, displayed high-level resistance to vancomycin (MIC > 32 micro g/ml) and gentamicin (MIC > 2,048 micro g/ml). Molecular analysis of this isolate revealed the presence of Tn1546 (vanA), responsible for high-level vancomycin resistance, and Tn5281 carrying aac6'-aph2", conferring high-level aminoglycoside resistance. Pulsed-field gel electrophoresis analysis revealed that CVM1869 was a canine E. faecium clone that had acquired Tn1546, perhaps from a human vancomycin-resistant E. faecium. Transposons Tn5281 and Tn1546 were located on two different conjugative plasmids. Sequence analysis revealed that in Tn1546, ORF1 had an 889-bp deletion and an IS1216V insertion at the 5' end and an IS1251 insertion between vanS and vanH. To date, this particular form of Tn1546 has only been described in human clinical vancomycin-resistant enterococcus isolates unique to the United States. Additionally, this is the first report of a vancomycin-resistant E. faecium isolated from a companion animal in the United States.

Animals↗

PubMed2001

Vancomycin resistance reversal in enterococci by flavonoids.

The development of clinical vancomycin-resistant strains of enterococci (VRE) is a major cause for concern. Here we show that a combination of galangin or 3,7-dihydroxyflavone with vancomycin may be used to sensitize resistant strains of Enterococcus faecalis and Enterococcus faecium to the level of vancomycin-sensitive strains. Minimum inhibitory concentrations (MICs) and viable counts were determined in Iso-sensitest broth using a microtitre method. MICs of vancomycin against 67% of resistant clinical isolates and a type strain of enterococci were lowered from > 250 microg mL(-1) to < 4 microg mL(-1) in the presence of galangin (12.5 microg mL(-1)) or 3,7-dihydroxyflavone (6.25 microg mL(-1)). Viable counts for type culture E. faecalis ATCC 51299 showed the flavonoids alone significantly lowered numbers of colony forming units (CFUs). CFUs were maintained at low levels (< 10(3) CFU mL(-1)) for 24 h by vancomycin/flavone combinations. This combinational action in reversing vancomycin resistance of enterococci highlights novel drug targets and has importance in the design of new therapeutic regimes against resistant pathogens.

Anti-Bacterial Agents↗

PubMed2003

Vancomycin resistance: occurrence, mechanisms and strategies to combat it.

Vancomycin has long been considered the antibiotic of last resort against serious and multi-drug-resistant infections caused by Gram-positive bacteria. However, vancomycin resistance has emerged, first in enterococci and, more recently, in Staphylococcus aureus. Here, the authors attempt to review the prevalence and the mechanisms of such resistance. Furthermore, they focus on strategies that have been developed or are under current investigation to overcome infections caused by vancomycin-resistant strains. Among these are glycopeptide derivatives with higher potency than vancomycin, small molecules that resensitise bacteria to the antibiotic and novel non-glycopeptide antibiotics. These agents are targeted to interfere with protein and/or peptidoglycan (PG) synthesis and integrity or with membrane permeability. Whilst most of these agents are still in clinical or preclinical development, some have entered the clinic and currently represent the only option for treating vancomycin-resistant enterococci (VRE).

Anti-Bacterial Agents↗

PubMedDate not supplied

Increasing resistance to vancomycin and other glycopeptides in Staphylococcus aureus.

Strains of Staphylococcus aureus with reduced susceptibility to glycopeptides have been reported from Japan, the United States, Europe, and the Far East. Although isolates with homogeneous resistance to vancomycin (MICs = 8 microg/mL) continue to be rare, there are increasing reports of strains showing heteroresistance, often with vancomycin MICs in the 1-4 microg/mL range. Most isolates with reduced susceptibility to vancomycin appear to have developed from preexisting methicillin-resistant S. aureus infections. Many of the isolates with reduced susceptibility to glycopeptides have been associated with therapeutic failures with vancomycin. Although nosocomial spread of the vancomycin-intermediate S. aureus (VISA) strains has not been observed in U.S. hospitals, spread of VISA strains has apparently occurred in Japan. Broth microdilution tests held a full 24 hours are optimal for detecting resistance in the laboratory; however, methods for detecting heteroresistant strains are still in flux. Disk-diffusion tests, including the Stokes method, do not detect VISA strains. The Centers for Disease Control and Prevention and other groups have issued recommendations regarding appropriate infection control procedures for patients infected with these strains.

Anti-Bacterial Agents↗