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PubMed2003

Newborn hearing screening: tobramycin and vancomycin are not risk factors for hearing loss.

OBJECTIVE: To investigate the chance of detecting hearing loss with neonatal hearing screening in relation to exposure to tobramycin and vancomycin. STUDY DESIGN: Automated auditory brainstem response (A-ABR) hearing screening was performed in all neonates with at least one risk factor. Data on drug administration were abstracted from patient files. Exposure to these drugs was related to the result of hearing screening. In patients failing hearing screening, exposure to ototoxic medication was assessed in the light of other risk factors for hearing loss. RESULTS: Six hundred twenty-five patients were analyzed; 45 neonates failed hearing screening. Tobramycin, vancomycin, and furosemide were used in 508, 130, and 174 patients, respectively. Exposure to vancomycin, tobramycin, or furosemide or a combination, defined in terms of treatment duration, total dose, or serum concentrations of antibiotics, was not related to failure to pass A-ABR screening. Ototoxic medication was not the most probable risk factor in any of the patients with serum concentrations outside the therapeutic range. CONCLUSIONS: Routine therapeutic drug monitoring of vancomycin and tobramycin in neonates for ototoxicity reasons is not helpful in detecting patients at risk for clinically important hearing loss in the 2- to 4-kHz range. A longer period of audiometric follow-up is needed to determine any long-term effects.

Anti-Bacterial Agents↗

PubMed1997

D-Alanyl-D-lactate and D-alanyl-D-alanine synthesis by D-alanyl-D-alanine ligase from vancomycin-resistant Leuconostoc mesenteroides. Effects of a phenylalanine 261 to tyrosine mutation.

The Gram-positive bacterium Leuconostoc mesenteroides, ATCC 8293, is intrinsically resistant to the antibiotic vancomycin. This phenotype correlates with substitution of D-Ala-D-lactate (D-Ala-D-Lac) termini for D-Ala-D-Ala termini in peptidoglycan intermediates in which the depsipeptide has much lower affinity than the dipeptide for vancomycin binding. Overproduction of the L. mesenteroides D-Ala-D-Ala ligase (LmDdl) 2 in E. coli and its purification to approximately 90% homogeneity allow demonstration that the LmDdl2 does have both depsipeptide and dipeptide ligase activity. Recently, we reported that mutation of an active site tyrosine (Tyr), Tyr216, to phenylalanine (Phe) in the E. coli DdlB leads to gain of D-Ala-D-Lac depsipeptide ligase activity in that enzyme. The vancomycin-resistant LmDdl2 has a Phe at the equivalent site, Phe261. To test the prediction that a Tyr residue predicts dipeptide ligase while an Phe residue predicts both depsipeptide and dipeptide ligase activity, the F261Y mutant protein of LmDdl2 was constructed and purified to approximately 90% purity. F216Y LmDdl2 showed complete loss of the ability to couple D-Lac but retained D-Ala-D-Ala dipeptide ligase activity. The Tyr-->Phe substitution on the active site omega-loop in D-Ala-D-Ala ligases is thus a molecular indicator of both the ability to make D-Ala-D-Lac and intrinsic resistance to the vancomycin class of glycopeptide antibiotics.

Alanine↗

PubMed2004

Two episodes of vancomycin-resistant Enterococcus faecium outbreaks caused by two genetically different clones in a newborn intensive care unit.

In 2001 two outbreak episodes (January-March and June-July) caused by vancomycin-resistant E. faecium (VRE) of the VanA-type were observed at a neonatal intensive care unit (NICU) of a university hospital in south-west Germany. To identify the initial source and the route of transmission environmental samples were examined as well as stool samples from patients and the staff. VRE was not found in environmental samples. However, stool samples from 24 hospitalised children tested positive and bacterial clonality was assessed by Sma1-based macro restriction analysis. Furthermore, esp gene and vancomycin resistance gene carriage were examined as well as bacteriocin production. PCR analysis showed that all 24 isolates carried vanA gene cluster, encoding resistance to vancomycin and teicoplanin. However, five of the vanA-positive isolates were resistant to vancomycin but not to teicoplanin. Only these five isolates produced bacteriocin, but in none of the isolates esp gene was detected. PFGE revealed that both outbreaks were caused by two different clones. The patient initiating the first episode, was identified whereas the origin of the second episode remained unknown. From one of the 40 staff stool samples VRE was isolated. This strain was related to the clone of the summer outbreak. In conclusion there were two independent episodes of self limiting VRE outbreaks and transmission on the ward is highly probable.

Bacterial Proteins↗

PubMed2006

Formulation and testing of vancomycin loaded albumin microspheres prepared by spray-drying.

Microparticles are widely employed as carriers of biologically active compounds with many possible applications. For targeted drug delivery and sustained release purposes, biopolymers (i.e. polysaccharides and proteins) have been proposed. In this study, microsphere formulations of vancomycin were prepared by the spray-drying method. Bovine serum albumin (BSA) was used as a polymer matrix and was cross-linked with glutaraldehyde after microsphere preparation. The product yield obtained from the spray-drying method was approximately 75%. The mean particle size was 5 +/- 1.6 microm, with the majority of particles between 4 and 8 microm. The extent of cross-linking affected the release of vancomycin from microspheres. Moreover, both rate and extent of vancomycin release from microspheres decreased with increasing glutaraldehyde concentration. Encapsulation of vancomycin did not alter the bioactivity of the drug and it was more effective in killing Staphylococcus aureus than the solution form.

Aerosols↗

PubMed1999

Clinical and molecular biological analysis of a nosocomial outbreak of vancomycin-resistant enterococci in a neonatal intensive care unit.

Vancomycin-resistant enterococci (VRE) have emerged as important nosocomial pathogens since 1988. We report here an outbreak of VRE between April 1997 and May 1997 in our neonatal intensive care unit (NICU). All isolates from four patients were identified as Enterococcus faecium positive and were resistant to vancomycin and teicoplanin. All of the patients with VRE were isolated for at least 5 d after admission to the unit and the positive cultures lasted between 13 and 31 d. There were no cases of sepsis or mortality in the patients with VRE. Two cases had previously received vancomycin therapy. All isolates were shown to have the vanA gene and had the same band pattern on repetitive PCR. After the four episodes, all equipment used to care for the patients were decontaminated and the staff engaged in therapy used disposable gloves and gowns. There were no more episodes. However, the NICU is no longer a safety area with regards to vancomycin-resistant enterococcal infection.

Anti-Bacterial Agents↗

PubMed1995

Vancomycin pharmacokinetics in spinal cord injured patients: a comparison with age-matched, able-bodied controls.

To compare the pharmacokinetics of vancomycin in chronic spinal cord injured patients and hospitalized, age-matched, able-bodied controls, we evaluated 14 spinal cord injured patients and 14 controls. Pharmacokinetic parameters of total body clearance (CL), distribution volume (V), elimination rate constant (k) and elimination half-life (t1/2) were calculated from two steady-state vancomycin serum concentrations by the method of Sawchuk and Zaske. Demographic data such as age, ideal body weight (IBW), total body weight (TBW) and serum creatinine at start of therapy (SCr), pharmacokinetic parameters and predicted dosages to achieve specific peak (30 mcg/ml) and through concentrations (5-10 mcg/ml) were calculated for both groups. Statistical comparisons were made using a two sample, Student's t-test. Demographic data between groups differed only in mean serum creatinine (p = 0.04). There were no statistically significant differences in mean pharmacokinetic parameters of CL and V or mean predicted dosages. Mean elimination rate constant was significantly smaller and mean elimination half-life was significantly longer in spinal cord injured patients (p = 0.02 and p = 0.04, respectively). The longer dosing interval predicted in spinal cord injured patients trended toward statistical significance (p = 0.10). We conclude that with chronic spinal cord injury, 1) the elimination half-life of vancomycin is increased and these patients may require longer dosing intervals and 2) distribution volume and predicted vancomycin doses are unaltered compared with controls.

Adult↗

PubMed2006

Mechanical effects of the use of vancomycin and meropenem in acrylic bone cement.

BACKGROUND: The increasing resistance of certain bacteria to antibiotics commonly used in bone cements has led to a demand for alternative antibacterial agents. The antibiotics added to bone cements may, however, have detrimental effects on the mechanical properties of the cement. MATERIAL AND METHODS: We evaluated the mechanical effects of adding vancomycin and meropenem to bone cement by compression, bending and fatigue tests. RESULTS: Addition of vancomycin at a concentration of up to 2.5% (w/w) had no effect on the compressive strength. Bending and fatigue strength were negatively affected by vancomycin but not by meropenem. INTERPRETATION: A cement containing 1.25% vancomycin and 1.25% meropenem might be an interesting compromise between the introduction of antibacterial properties and preservation of the mechanical properties. With this concentration of additives the compressive strength and the fatigue strength remain unchanged, while the bending strength (-14%) and the bending modulus (-9%) are only slightly reduced and remain above the limits set by the ISO5833 standard.

Anti-Bacterial Agents↗

PubMed1999

An outbreak of vancomycin-dependent Enterococcus faecium in a bone marrow transplant unit.

Outbreaks of vancomycin-resistant enterococci (VRE) are well described. The presence of mutants of VRE, such as vancomycin-dependent enterococci (VDE), in individual patients has been documented, but their potential to spread nosocomially has not been known. We present the first cluster of patients who acquired VDE nosocomially. Five bone marrow transplantation patients were infected or colonized by a genotypically indistinguishable multiantibiotic-resistant strain of Enterococcus faecium. Vancomycin dependence in 3 of the 5 isolates was demonstrated. All cluster patients had received protracted prophylactic treatment with vancomycin (mean, 22.6 days), and specimens from >/=2 body sites were repeatedly culture-positive for the outbreak strain. The outbreak was controlled with aggressive infection control strategies, and prophylactic antibiotic policies were revised. Awareness of the potential for nosocomial spread of multiantibiotic-resistant VDE is vital for the care of immunocompromised patients, especially those receiving prophylactic antibiotics.

Adult↗

PubMed2000

Vancomycin-induced neutropenia resolves after substitution with teicoplanin.

Neutropenia is an uncommon adverse effect associated with prolonged vancomycin therapy. Neutrophil counts normally recover after discontinuation of vancomycin in this situation, but treatment options are needed for those patients who require ongoing antibiotic therapy. We describe a case of vancomycin-induced neutropenia in which the neutropenia resolved after vancomycin was replaced by the structurally related compound teicoplanin.

Adult↗

PubMed2000

The search for a better treatment for recurrent Clostridium difficile disease: use of high-dose vancomycin combined with Saccharomyces boulardii.

Recurrent Clostridium difficile disease (CDD) is a difficult clinical problem because antibiotic therapy often does not prevent further recurrences. In a previous study, the biotherapeutic agent Saccharomyces boulardii was used in combination with standard antibiotics and was found to be effective in reducing subsequent recurrences of CDD. In an effort to further refine a standard regimen, we tested patients receiving a regimen of a standard antibiotic for 10 days and then added either S. boulardii (1 g/day for 28 days) or placebo. A significant decrease in recurrences was observed only in patients treated with high-dose vancomycin (2 g/day) and S. boulardii (16.7%), compared with those who received high-dose vancomycin and placebo (50%; P=.05). No serious adverse reactions were observed in these patients. Comparison of data from this trial with data from previous studies indicates that recurrent CDD may respond to a short course of high-dose vancomycin or to longer courses of low-dose vancomycin when either is combined with S. boulardii.

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↗

PubMed2002

Clinical outcomes for patients with bacteremia caused by vancomycin-resistant enterococcus in a level 1 trauma center.

To assess the degree of morbidity and mortality attributable to vancomycin resistance in enterococcal bacteremia (EB), a matched case-control study was conducted. Patients with bacteremia due to vancomycin-resistant enterococcus (VRE) were matched to control patients with bacteremia due to vancomycin-susceptible enterococcus. During 1996--2000, 65 patients with cases of clinically significant VRE bacteremia were identified, and 53 of these patients were successfully matched. In this group of patients, VRE bacteremia was found to be an independent predictor of crude mortality (odds ratio [OR], 4.0; 95% confidence interval [CI], 1.2--13.3) and the infection-related mortality rate (OR, 5.2; 95% CI, 1.4--20.0). It was also an independent predictor of the rate of clinical failure at day 7 after the onset of EB (OR, 4.6; 95% CI, 1.2--17.3) and overall clinical failure (OR, 4.3; 95% CI, 1.3--14.5) and was associated with a longer mean length of hospitalization after the onset of EB, compared with that for control patients (22.7plus minus1.88 vs. 15.9 +/- 1.7, P=.006). These observations indicate that vancomycin resistance in EB independently affects outcomes.

Analysis of Variance↗

PubMed2003

Linezolid does not increase the risk of thrombocytopenia in patients with nosocomial pneumonia: comparative analysis of linezolid and vancomycin use.

Reports from uncontrolled studies suggest that linezolid is associated with rates of thrombocytopenia higher than those reported in clinical studies. We assessed the risk of thrombocytopenia in 686 patients with nosocomial pneumonia who received linezolid or vancomycin for > or =5 days in 2 randomized, double-blind studies and for whom follow-up platelet counts had been measured. New-onset thrombocytopenia (platelet count of <150x10(9) platelets/L) occurred in 19 (6.4%) of 295 linezolid recipients and 22 (7.7%) of 285 vancomycin recipients with baseline platelet counts of > or =150x10(9) platelets/L; severe thrombocytopenia (platelet count of <50x10(9) platelets/L) occurred in only 1 patient in each group. Platelet counts decreased to less than the baseline level in 4 (6.6%) of 61 linezolid recipients and 5 (11.1%) of 45 vancomycin recipients who had baseline counts of <150x10(9) platelets/L. No patient had a decrease to <20x10(9) platelets/L. There were no statistically significant differences between groups in these or any other platelet assessments. Clinically significant thrombocytopenia was uncommon in our analysis, and linezolid was not associated with a greater risk of thrombocytopenia in seriously ill patients than was vancomycin.

Acetamides↗

PubMed2004

Clinical features associated with bacteremia due to heterogeneous vancomycin-intermediate Staphylococcus aureus.

We assessed all episodes of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia at our hospital during a 12-month period (n=53) and compared those due to heterogeneous vancomycin-intermediate S. aureus (hVISA; n = 5, 9.4%) with those due to vancomycin-susceptible MRSA (n=48). Patients with hVISA bacteremia were more likely to have high bacterial load infections (P=.001), vancomycin treatment failure (persistent fever and bacteremia for >7 days after the start of therapy; P<.001), and initially low serum vancomycin levels (P=.006). These clinical markers of hVISA bacteremia may help focus diagnostic efforts and treatment.

Anti-Bacterial Agents↗

PubMed2006

The pharmacokinetic and pharmacodynamic properties of vancomycin.

Vancomycin is one of only a few antibiotics available to treat patients infected with methicillin-resistant Staphylococcus aureus and methicillin-resistant, coagulase-negative Staphylococcus species. Therefore, understanding the clinical implications of the pharmacokinetic and pharmacodynamic properties of vancomycin is a necessity for clinicians. Vancomycin is a concentration-independent antibiotic (also referred to as a "time-dependent" antibiotic), and there are factors that affect its clinical activity, including variable tissue distribution, inoculum size, and emerging resistance. This article reviews the pharmacokinetic and pharmacodynamic data related to vancomycin and discusses such clinical issues as toxicities and serum concentration monitoring.

Animals↗

PubMed2000

Comparison of three methods to recover vancomycin-resistant enterococci (VRE) from perianal and environmental samples collected during a hospital outbreak of VRE.

OBJECTIVE: To establish an efficient and sensitive technique for recovering vancomycin-resistant enterococci (VRE) from perianal and environmental samples collected during implementation of control measures for an outbreak of VRE. DESIGN: Perianal and environmental samples were collected in triplicate on sterile swabs. One swab was used to inoculate a selective broth medium containing 6 pg of vancomycin and 8 pg of ciprofloxacin per mL, one to inoculate Campylobacter agar containing 10 microg/mL of vancomycin, and one to inoculate Enterococcosel agar containing 8 microg/mL of vancomycin. SETTING: Samples were collected in the intensive care units of a 600-bed university hospital over a period of 2 months. SAMPLE SELECTION: Patients and their immediate environment were sampled if they resided in a ward with a patient known to be colonized or infected with VRE. RESULTS: Of the 88 perianal samples obtained from 63 patients, 37 were positive for VRE by broth culture, with 36 also recovered on both types of solid media (sensitivity, 97.3%; negative predictive value, 98.1%). Of the initial samples collected from each of the 63 patients, 20 were positive for VRE by all methods. Of the 500 environmental samples cultured, 139 were positive for VRE in broth, with only 33 recovered on Campylobacter agar (sensitivity, 23.7%; negative predictive value, 77.2%) and 22 on Enterococcosel agar (sensitivity, 15.8%; negative predictive value, 75.2%). CONCLUSIONS: Our data indicate that, when performing surveillance cultures during an outbreak of VRE, use of an enrichment broth medium is required to recover VRE contaminating environmental surfaces; however, direct inoculation to selective solid medium is adequate to recover VRE in patient perianal specimens.

Agar↗

PubMed2004

Eradication of a large outbreak of a single strain of vanB vancomycin-resistant Enterococcus faecium at a major Australian teaching hospital.

OBJECTIVE: To demonstrate that nosocomial transmission of vancomycin-resistant enterococci (VRE) can be terminated and endemicity prevented despite widespread dissemination of an epidemic strain in a large tertiary-care referral hospital. INTERVENTIONS: Two months after the index case was detected in the intensive care unit, 68 patients became either infected or colonized with an epidemic strain of vanB vancomycin-resistant Enterococcus faecium despite standard infection control procedures. The following additional interventions were then introduced to control the outbreak: (1) formation of a VRE executive group; (2) rapid laboratory identification (30 to 48 hours) using culture and polymerase chain reaction detection of vanA and vanB resistance genes; (3) mass screening of all hospitalized patients with isolation of carriers and cohorting of contacts; (4) environmental screening and increased cleaning; (5) electronic flagging of medical records of contacts; and (6) antibiotic restrictions (third-generation cephalosporins and vancomycin). RESULTS: A total of 19,658 patient and 24,396 environmental swabs were processed between July and December 2001. One hundred sixty-nine patients in 23 wards were colonized with a single strain of vanB vancomycin-resistant E. faecium. Introducing additional control measures rapidly brought the outbreak under control. Hospital-wide screening found 39 previously unidentified colonized patients, with only 7 more nonsegregated patients being detected in the next 2 months. The outbreak was terminated within 3 months at a cost of dollar 2.7 million (Australian dollars). CONCLUSION: Despite widespread dissemination of VRE in a large acute care facility, eradication was achievable by a well-resourced, coordinated, multifaceted approach and was in accordance with good clinical governance.

Cohort Studies↗

PubMed1998

Vancomycin-resistant enterococci.

Enterococci, a part of normal gut flora, are not particularly pathogenic organisms in humans. For example, they do not cause respiratory tract infections. The most frequent enterococcal infections are urinary tract infections. Despite their lack of pathogenicity, enterococci have emerged as significant nosocomial pathogens in the United States and elsewhere. Enterococci are formidable pathogens because of their resistance to antimicrobial agents. Enterococci are intrinsically resistant to beta-lactam agents and aminoglycosides and were the first bacteria to acquire vancomycin resistance. Infection control measures have been far from effective at preventing the dissemination of vancomycin-resistant enterococci in the hospital. Therapy for infections due to vancomycin-resistant enterococci presents real challenges. Most isolates remain susceptible to nitrofurantoin, but this agent is useful only for urinary tract infections. The greatest threat posed by vancomycin-resistant enterococci is the potential to transfer their resistance genes to more pathogenic gram-positive bacteria, which could produce truly frightening pathogens.

Anti-Bacterial Agents↗