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PubMed2003

Antianaerobic antibiotic therapy promotes overgrowth of antibiotic-resistant, gram-negative bacilli and vancomycin-resistant enterococci in the stool of colonized patients.

BACKGROUND AND OBJECTIVE: Antianaerobic antibiotic therapy promotes persistent high-density growth of vancomycin-resistant enterococci (VRE) in the stool of colonized patients. We tested the hypothesis that antibiotic regimens with potent antianaerobic activity promote overgrowth of coexisting antibiotic-resistant, gram-negative bacilli in the stool of VRE-colonized patients. DESIGN: Eight-month prospective study examining the effect of antibiotic therapy on the stool density of gram-negative bacilli resistant to ceftazidime, ciprofloxacin, or piperacillin/tazobactam. SETTING: A Department of Veterans Affairs medical center including an acute care hospital and nursing home. PATIENTS: All VRE-colonized patients with at least 3 stool samples available for analysis. RESULTS: One-hundred forty stool samples were obtained from 37 study patients. Forty-nine (61%) of 80 stool samples obtained during therapy with an antianaerobic regimen were positive for an antibiotic-resistant, gram-negative bacillus, where-as only 14 (23%) of 60 samples obtained 4 or more weeks after completion of such therapy were positive (P < .001). Twenty-four (65%) of the 37 patients had one or more stool cultures positive for a gram-negative bacillus resistant to ciprofloxacin, ceftazidime, or piperacillin/tazobactam. The density of these organisms was higher during therapy with antianaerobic regimens than in the absence of such therapy for at least 2 weeks (mean +/- standard deviation, 5.6 +/- 1.4 and 3.9 +/- 0.71 log10 organisms/g; P < .001). CONCLUSION: Limiting the use of antianaerobic antibiotics in VRE-colonized patients may reduce the density of colonization with coexisting antibiotic-resistant, gram-negative bacilli.

Adult↗

PubMed2005

Use of a multiplex molecular beacon platform for rapid detection of methicillin and vancomycin resistance in Staphylococcus aureus.

Drug resistance, particularly vancomycin and methicillin resistance, in Staphylococcus aureus continues to emerge as a significant public health threat in both the hospital and community settings. In addition to the limited treatment options, S. aureus strains acquire and express numerous virulence factors that continue to increase its ability to cause a wide spectrum of human disease. As a result, empirical treatment decisions are confounded and there is a heightened need for a diagnostic test (or assay) to rapidly identify antibiotic resistance and specific virulence determinants and indicate the appropriate treatment. To that end we developed a platform using multiplex molecular beacon probes with real-time PCR for the rapid detection of drug resistance-determining genes and virulence factors in S. aureus. In this study, we demonstrate the specificity and sensitivity of our platform for detection of the genes conferring methicillin (mecA) and vancomycin (vanA) resistance as well as a gene encoding the virulence factor Panton-Valentine leucocidin (lukF) in S. aureus isolates.

Anti-Bacterial Agents↗

PubMedDate not supplied

Proficiency of clinical laboratories in and near Monterrey, Mexico, to detect vancomycin-resistant enterococci.

Early detection of vancomycin-resistant enterococci is important for preventing its spread among hospitalized patients. We surveyed the ability of eight hospital laboratories in and near Monterrey, Mexico, to detect vancomycin resistance in Enterococcus spp. and found that although laboratories can reliably detect high-level vancomycin resistance, many have difficulty detecting low-level resistance.

Anti-Bacterial Agents↗

PubMed2006

Successful therapy of experimental endocarditis caused by vancomycin-resistant Staphylococcus aureus with a combination of vancomycin and beta-lactam antibiotics.

VRS1 is the first isolated strain of vancomycin-resistant Staphylococcus aureus (VRSA) found to carry the vanA gene complex previously described in Enterococcus. Under vancomycin pressure, VRS1 makes aberrant cell walls consisting of stem tetrapeptide and depsipeptide that lack the terminal D-Ala-D-Ala residues targeted by vancomycin. Previous data have suggested that this aberrant cell wall is not cross-linked by PBP2a, the enzyme responsible for cell wall transpeptidation in the presence of beta-lactam antibiotics. We examined the efficacy of treating VRS1 with a combination of vancomycin and beta-lactam antibiotics in vitro and in vivo. We found that the MIC of oxacillin for VRS1 decreased from >256 microg/ml to <1 microg/ml in the presence of vancomycin. Using the rabbit model of endocarditis, we treated VRS1-infected rabbits with nafcillin alone, vancomycin alone, or a combination of nafcillin and vancomycin. Treatment with nafcillin in combination with vancomycin cleared bloodstream infections within 24 h and sterilized 12/13 spleens (92%), as well as 8/13 kidneys (62%), following 3 days of treatment. Mean aortic valve vegetation counts were reduced 3.48 log(10) CFU/g with the combination therapy (compared to untreated controls) and were significantly lower than with either vancomycin or nafcillin given alone. VRS1 was extremely virulent in this model, as no untreated rabbits survived the 3-day trial. Treatment of clinical infections due to VRSA with the combination of vancomycin and beta-lactams may be an option, based on these results.

Animals↗

PubMed2003

Carriage of methicillin-resistant Staphylococcus aureus, ceftazidime-resistant Gram-negative bacilli, and vancomycin-resistant enterococci before and after intensive care unit admission.

OBJECTIVE: To measure patients' risk for acquiring antibiotic-resistant microorganisms associated with intensive care unit admission. DESIGN: Prospective, observational study. SETTING: Ten public hospitals including one university medical center. PATIENTS: Consecutive patients admitted to ten intensive care units. INTERVENTIONS: Serial patient surveillance cultures were screened for vancomycin-resistant enterococci, methicillin-resistant Staphylococcus aureus (MRSA), ceftazidime-resistant Gram-negative bacilli (CR-GNB), Acute Physiology and Chronic Health Evaluation II score, and antibiotic and medical device exposures. MEASUREMENTS AND MAIN RESULTS: A total of 1,697 patient admissions in ten intensive care units were enrolled. The overall carriage rate of antibiotic-resistant bacteria at intensive care unit entry was 12.1% for MRSA, 14% for CR-GNB and 4.7% for both. At discharge from the intensive care unit, new carriage of MRSA, CR-GNB, and both was found in 11.1%, 14.2%, and 2.4% of the patients, respectively. The acquisition rates in the individual units correlated highly and positively with proportion of patients with carriage at intensive care unit entry for both MRSA (n = 10, Pearson's r =.89, p < 0.001) and CR-GNB (n = 10, Pearson's r =.92, p < 0.001). By logistic regression, severity of illness (odds ratio, 1.4), length of stay (odds ratio, 1.7), use of penicillins (odds ratio, 1.9), and number of antibiotics (odds ratio, 1.2) and medical devices (odds ratio, 1.2) were independently associated with intensive care unit acquisition of MRSA. In comparison, variables independently associated with intensive care unit acquisition of CR-GNB were Acute Physiology and Chronic Health Evaluation II score (odds ratio, 1.5), number of antibiotics (odds ratio, 1.1), and artificial airway (odds ratio, 1.5). CONCLUSIONS: These data suggest that hospitalization in the intensive care unit introduces significant risk to patients in terms of transmission of MRSA and/or CR-GNB. This risk seems to be influenced strongly by the proportion of patients with colonization at intensive care unit admission and is associated with severity of illness, length of stay, and exposures to antibiotics and medical devices.

Aged↗

PubMed2002

The prevalence and mechanisms of vancomycin resistance in Staphylococcus aureus.

The emergence of Staphylococcus aureus resistant to vancomycin has caused considerable concern. Such strains are currently rare, although they have been isolated from many areas of the world. Considerable controversy surrounds strains of S. aureus displaying heterogeneous resistance to vancomycin regarding their definition and methods for detection. This has led to considerable variance in estimates of prevalence (0-1.3%-20% in Japan) and has hindered efforts to define the clinical relevance of these strains. The mechanism of resistance involves a complex reorganization of cell wall metabolism, leading to a grossly thickened cell wall with reduced peptidoglycan cross-linking. There may be many different ways in which strains achieve this endpoint. Current knowledge and theories are summarized.

Anti-Bacterial Agents↗

PubMed2005

An active surveillance study of vancomycin-resistant Enterococcus in Queen Elizabeth Hospital, Hong Kong.

OBJECTIVE: To assess the rate of faecal vancomycin-resistant Enterococcus colonisation in high-risk patients in a regional hospital. DESIGN: Prospective observational surveillance study. SETTING: Queen Elizabeth Hospital, Hong Kong. PATIENTS: From September 2001 to December 2002, stool samples from patients in the intensive care unit and patients in whom Clostridium difficile testing was requested were used for study using a broth enrichment method. MAIN OUTCOME MEASURES: Number of faecal vancomycin-resistant Enterococcus colonisation. RESULTS: A total of 2414 cultures from 1792 patients were tested for vancomycin-resistant Enterococcus using a broth enrichment method. Only one (0.06%) patient was found to harbour a vancomycin-resistant Enterococcus faecalis in the gastro-intestinal tract. Surveillance cultures from contacts of the case revealed another six with vancomycin-resistant Enterococcus faecalis. Vancomycin-resistant Enterococcus faecalis was also later reported from a clinical specimen (catheterized urine) of another patient. They were all epidemiologically linked to the index case. Mean inhibitory concentrations of vancomycin and teicoplanin were determined to be higher than 256 and 0.5 microgram/mL, respectively by E-test for all the vancomycin-resistant Enterococcus isolates. Polymerase chain reaction analysis confirmed the presence of vanB genes and the result was in line with the phenotype. Pulsed-field gel electrophoresis confirmed a monoclonal vancomycin-resistant Enterococcus outbreak. Strict infection control measures recommended by the Centers for Disease Control and Prevention were followed and the outbreak was successfully controlled. CONCLUSION: Vancomycin-resistant Enterococcus colonisation is rare, but present among high-risk patients in our hospital. A routine surveillance programme should be implemented that will enable early case detection and prompt initiation of infection control measures to prevent the emergence of an endemic situation.

Enterococcus faecalis↗

PubMed2002

An elevated mutation frequency favors development of vancomycin resistance in Staphylococcus aureus.

The emergence of intermediate vancomycin resistance, mainly in methicillin-resistant Staphylococcus aureus strains, has become a great concern. Thorough characterization of clinical and laboratory vancomycin-intermediately resistant S. aureus (VISA) strains identified multiple, resistance-associated changes most probably due to stepwise mutations. We hypothesized that an elevated mutation frequency as found, e.g., in mutator strains defective in DNA mismatch repair could allow rapid acquisition of adaptive mutations in the presence of vancomycin. We therefore subjected S. aureus RN4220 and its isogenic mutator strain, the mutS-knockout mutant RN4220DeltamutS, to a stepwise vancomycin selection procedure. Vancomycin resistance evolved much more quickly in the mutator background than in the wild type (5 versus 19 passages, respectively). In addition, a higher resistance level could be reached (MIC, 32 versus 4 micro g/ml, respectively). The susceptibility to other antibiotics with the exception of teicoplanin remained unchanged. Concomitantly with increasing vancomycin resistance, a loss of phage typeability and differences in growth behavior as well as an improved ability to regrow at high vancomycin concentrations were observed. In conclusion, an elevated mutation rate in S. aureus led to the rapid development of vancomycin resistance, indicating that a high mutation frequency could be one of the factors that favor the emergence of vancomycin resistance in S. aureus.

Adenosine Triphosphatases↗

PubMed2005

Impact of a series of interventions in vancomycin prescribing on use and prevalence of vancomycin-resistant enterococci.

BACKGROUND: In response to vancomycin-resistant bacteria, particularly vancomycin-resistant enterococci (VRE), measures have been recommended to improve on the appropriate use of vancomycin. METHODS: Intervention 1 consisted of an automatic 72-hour vancomycin stop order; Intervention 2, a standardized procedure for sampling of blood cultures; and Intervention 3, an interdisciplinary critical care team. RESULTS: After Intervention 1, inappropriate use decreased, particularly in treatment of febrile neutropenia and undocumented gram-positive infections. After Intervention 2, the baseline rate of inappropriately drawn blood cultures (IDBCs) was unchanged, and use in patients with IDBCs was comparable during both periods. Before Intervention 3, 38/55 orders continuing > 72 hours were considered inappropriate versus 24/53 (p < .025) after. After the interventions, hospitalwide vancomycin use was reduced. Yet the overall rate of VRE infection initially decreased but then increased once again over time. DISCUSSION: Despite substantial reduction in hospitalwide vancomycin use, the impact on the overall rate of VRE was inconsistent and ward dependent.

California↗

PubMed2000

Effect of antibiotic therapy on the density of vancomycin-resistant enterococci in the stool of colonized patients.

BACKGROUND: Colonization and infection with vancomycin-resistant enterococci have been associated with exposure to antibiotics that are active against anaerobes. In mice that have intestinal colonization with vancomycin-resistant enterococci, these agents promote high-density colonization, whereas antibiotics with minimal antianaerobic activity do not. METHODS: We conducted a seven-month prospective study of 51 patients who were colonized with vancomycin-resistant enterococci, as evidenced by the presence of the bacteria in stool. We examined the density of vancomycin-resistant enterococci in stool during and after therapy with antibiotic regimens and compared the effect on this density of antianaerobic agents and agents with minimal antianaerobic activity. In a subgroup of 10 patients, cultures of environmental specimens (e.g., from bedding and clothing) were obtained. RESULTS: During treatment with 40 of 42 antianaerobic-antibiotic regimens (95 percent), high-density colonization with vancomycin-resistant enterococci was maintained (mean [+/-SD] number of organisms, 7.8+/-1.5 log per gram of stool). The density of colonization decreased after these regimens were discontinued. Among patients who had not received antianaerobic antibiotics for at least one week, 10 of 13 patients who began such regimens had an increase in the number of organisms of more than 1.0 log per gram (mean increase, 2.2 log per gram), whereas among 10 patients who began regimens of antibiotics with minimal antianaerobic activity, there was a mean decrease in the number of enterococci of 0.6 log per gram (P=0.006 for the difference between groups). When the density of vancomycin-resistant enterococci in stool was at least 4 log per gram, 10 of 12 sets of cultures of environmental specimens had at least one positive sample, as compared with 1 of 9 sets from patients with a mean number of organisms in stool of less than 4 log per gram (P=0.002). CONCLUSIONS: For patients with vancomycin-resistant enterococci in stool, treatment with antianaerobic antibiotics promotes high-density colonization. Limiting the use of such agents in these patients may help decrease the spread of vancomycin-resistant enterococci.

Adult↗

PubMed2001

[Mechanisms of methicillin and vancomycin resistance in Staphylococcus aureus].

The mechanism of methicillin and vancomycin resistance in Staphylococcus aureus (MRSA) is discussed, focusing on the phenotypic expression of resistance; i.e., pre-methicillin resistance, Egle-type resistance, heterogeneous and homogeneous resistance. Acquisition of staphylococcus cassette chromosome(SCCmec) by a recipient MSSA strain in the mecA-positive, and methicillin-susceptible status(pre-MRSA status) of S. aureus. Subsequent of the mecI-gene-mediated repression of mecA gene transcription results in the heterogeneous expression of methicillin resistance. It is only with the alternation of another chromosomal locus that the heterogeneous-to-homogeneous (hetero-to-homo) conversion of methicillin resistance occurs. Acquisition of a part of vancomycin-resistance(the level of hetero-VRSA) is associated with hetero-to-homo conversion of methicillin resistance, and full expression of vancomycin resistance(MIC = 8 mg/l) is achieved by additional acceleration of cell-wall synthesis causing apparent cell-wall thickening.

Methicillin Resistance↗

PubMed2000

[Vancomycin-resistant enterococci (VRE)].

Vancomycin-resistant enterococci is a worldwide threat not only in hospitals, but also in communities. Community-acquired infections play an important role in spreading VRE because the use of avoparcin, an antimicrobial growth promoter in food animals, is strongly suggested to cause the emergence of VRE. In particular, chickens imported into Japan have been reported to be highly contaminated with VRE, and this may be a key issue in the prevalence of VRE. Nosocomial VRE infections have become a serious problem in immuno-compromised patients throughout the world, and many VREs have been isolated in Japan in the last few years; however, fortunately, nosocomial outbreaks are still rare. VRE can survive for weeks in hospital environments, which makes infection control difficult and complicated, and strains of VRE resistant to almost all antimicrobial agents are a real threat. In outbreaks of VRE, prudent antimicrobial use and prompt effective infection control are important.

Ampicillin↗

PubMed2003

Vancomycin-resistant enterococci in King Chulalongkorn Memorial Hospital: a 5-year study.

The emergence of hospital acquired infections with bacteria resistant to antimicrobials such as vancomycin resistant enterococci (VRE) has become a worldwide concern. The authors studied the prevalence and surveillance of 5 years study of VRE in King Chulalongkon Memorial Hospital and phenotype of these resistance strains. A total of enterococci 1854 isolates were collected from clinical specimens from 1995 to 1999. Screening vancomycin resistance was identified by the agar plated method and minimal inhibitory concentration (MIC) of vancomycin was determined for vancomycin-resistance strains by E-test. The results demonstated that 15 (0.81%) VRE were isolated from 1,854 specimens. Fourteen VRE were identified as Enterococcus faecium and one strain was Enterococcus faecalis. All of these strains, carrying the VanB phenotype, were susceptible to teicoplanin. Similar to other studies, most VRE strains are E. faecium. To the authors' knowledge, this is the first VRE study carried out in King Chulalongkorn Memorial Hospital. The results showed a low prevalence of VRE and surveillance of 5 years study demonstated a gradual increase of VRE. Therefore, it is important to continue periodic surveys of VRE to prevent the spread of VRE in hospitals.

Enterococcus↗

PubMed2003

Multivalent antibiotics via metal complexes: potent divalent vancomycins against vancomycin-resistant enterococci.

Dimers of vancomycin (Van), linked by a rigid metal complex, [Pt(en)(H(2)O)(2)](2+), exhibit potent activities (MIC approximately 0.8 mug/mL, approximately 720 times more potent than that of Van itself) against vancomycin-resistant enterococci (VRE). The result suggests that combining metal complexation and receptor/ligand interaction offers a useful method to construct multivalent inhibitors.

Anti-Bacterial Agents↗

PubMed1993

Vancomycin binding to cell walls of non-streptococcal vancomycin-resistant bacteria.

The availability of peptidoglycan for binding to vancomycin was investigated in intrinsically vancomycin-resistant clinical isolates of Leuconostoc mesenteroides, Lactobacillus viridescens and Pediococcus pentosaceus. Intrinsic vancomycin resistance expressed by L. mesenteroides and P. pentosaceus was the result of poor binding of vancomycin to native or SDS-treated cell walls. Pre-exposure of L. viridescens to vancomycin decreased the subsequent binding of vancomycin to the cell walls, suggesting an alternative mechanism to that found in high-level vancomycin-resistant enterococci and intrinsically-resistant L. mesenteroides and P. pentosaceus. Vancomycin binding was sensitive to substitution of larger side chains at the C-terminus. Variations of peptidoglycan peptide types found in L. mesenteroides, L. viridescens and P. pentosaceus could account for their intrinsic vancomycin resistance.

Amino Acid Sequence↗

PubMed2004

DD1.5k, the gene preferentially expressed in bloodstream isolates of vancomycin-resistant Enterococcus faecium.

Vancomycin-resistant Enterococcus faecium (VREFM) is becoming a threatening pathogen. We identified a gene called DD1.5K by differential display-PCR, which was preferentially expressed in the bloodstream isolates of VREFM. Due to its amino acid similarity to transfer complex protein, trsE, and tissue-specific expression, this gene may be involved in virulence of VREFM.

Adaptation, Physiological↗

PubMed1999

Quinupristin/dalfopristin: therapeutic potential for vancomycin-resistant enterococcal infections.

Vancomycin-resistant Enterococcus faecium (VREF) is an opportunistic pathogen, which causes infections among severely ill, hospitalized patients, in whom it is likely to increase the risk of progressive local or systemic disease and to worsen the prognosis. Because these organisms are often highly resistant to penicillin, ampicillin and many other antimicrobials including the glycopeptides, there are few proven therapeutic alternatives for the treatment of infection caused by VREF. Quinupristin/dalfopristin is highly active against VREF in vitro. A prolonged post-antibiotic effect, good polymorphonuclear leucocyte/macrophage penetration and slow release, and active metabolites allow this agent to be used with an 8 or 12 h dosing interval. The combined results from a Phase III non-comparative study and an emergency-use study of quinupristin/dalfopristin for the treatment of VREF infection produced a clinical response rate (cure or improvement) in 142 (73.6%) of 193 clinically evaluable patients. The baseline pathogen was eradicated or presumed eradicated from 110 of 156 (70.5%) bacteriologically evaluable patients. Fifty-two per cent of the severely ill patients in these two studies died, but no death was attributed to quinupristin/dalfopristin therapy. The most common adverse event was arthralgia (9.1%). Quinupristin/dalfopristin has demonstrated efficacy for the treatment of serious VREF infections, including those that have failed conventional therapy.

Anti-Bacterial Agents↗

PubMed1994

Modification of peptidoglycan precursors is a common feature of the low-level vancomycin-resistant VANB-type Enterococcus D366 and of the naturally glycopeptide-resistant species Lactobacillus casei, Pediococcus pentosaceus, Leuconostoc mesenteroides, and Enterococcus gallinarum.

The biochemical basis for the acquired or natural resistance of various gram-positive organisms to glycopeptides was studied by high-pressure liquid chromatographic analysis of their peptidoglycan UDP-MurNAc-peptide precursors. In all cases, resistance was correlated with partial or complete replacement of the C-terminal D-Ala-D-Ala-containing UDP-MurNAc-pentapeptide by a new precursor with a modified C terminus. Nuclear magnetic resonance analysis by sequential assignment showed that the new precursor encountered in Enterococcus faecium D366, a strain belonging to the VANB class, which expresses low-level resistance to vancomycin, was UDP-MurNAc-L-Ala-gamma-D-Glu-L-Lys-D-Ala-D-lactate, identical to that previously found in the VANA class, which expresses high-level resistance to vancomycin. High-pressure liquid chromatographic analyses, composition determinations, and digestion by R39 D,D-carboxypeptidase demonstrated the exclusive presence of the new precursor in Lactobacillus casei and Pediococcus pentosaceus, which are naturally highly resistant to glycopeptides. The low-level natural resistance of Enterococcus gallinarum to vancomycin was found to be associated with the synthesis of a new precursor identified as a UDP-MurNAc-pentapeptide containing a C-terminal D-serine. The distinction between low and high levels of resistance to glycopeptides appeared also to depend on the presence or absence of a substantial residual pool of a D-Ala-D-Ala-containing UDP-MurNAc-pentapeptide.

Amino Acid Sequence↗