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PubMed2004

Synergistic activity of vancomycin and teicoplanin alone and in combination with streptomycin against Enterococcus faecalis strains with various vancomycin susceptibilities.

The synergy between two glycopeptides, vancomycin (Vm) and teicoplanin (Tec) and streptomycin (Sm) was studied by time-kill method. Five clinical vanB resistant Enterococcus faecalis (ENC) isolates with variable Vm-susceptibility were used. Different concentrations of Vm, Tec and Sm representing therapeutic concentrations were combined. Antibacterial activity was related to the concentrations of Vm and Sm, and Vm susceptibility to ENC. For strains with Vm MIC up to 64 mg/l, synergy was achieved with higher concentrations of Vm and Sm, while all combinations of Tec and Sm were synergistic against all strains except ENC 29. For ENC 29 with Vm MIC of 512 mg/l and Tec MIC of <1 mg/l, none of the combinations was synergistic. The significance of these in vitro results needs further investigation in vivo.

Anti-Bacterial Agents↗
PubMed2001

Comparative evaluation of penicillin, ampicillin, and imipenem MICs and susceptibility breakpoints for vancomycin-susceptible and vancomycin-resistant Enterococcus faecalis and Enterococcus faecium.

Although imipenem has in vitro activity against Enterococcus faecalis and Food and Drug Administration-approved indications for treatment of infections caused by this microorganism, there are no NCCLS guidelines for susceptibility testing of imipenem versus enterococci. Therefore, the in vitro activities of penicillin, ampicillin, imipenem, and vancomycin against 201 blood isolates of E. faecalis and 24 blood isolates of Enterococcus faecium were compared. The susceptibility of isolates to penicillin or ampicillin accurately predicted the in vitro activity of imipenem. Since the susceptibility of enterococci to imipenem can be predicted by the results obtained by testing of penicillin or ampicillin, testing of imipenem by clinical laboratories probably is not necessary.

Anti-Bacterial Agents↗
PubMed2002

The effect of active surveillance for vancomycin-resistant enterococci in high-risk units on vancomycin-resistant enterococci incidence hospital-wide.

BACKGROUND: Vancomycin-resistant enterococci (VRE) have become a major cause of nosocomial infections and are now endemic in many geographic areas. The aim of this study was to describe the effect of active surveillance for patients with VRE in high-risk units on the VRE incidence rate hospital-wide. METHODS: We determined 4 time periods based on the intervention of active surveillance: preactive surveillance (period 1), active surveillance (period 2), no active surveillance (period 3), and reinstutition of active surveillance (period 4). VRE incidence rates based on first clinical culture for VRE per 10,000 patient days for each of these periods and incidence rate ratios were then calculated. RESULTS: Active surveillance in high-risk units was associated with a significant reduction in VRE incidence hospital-wide in 2 of the 3 comparisons made. The incidence rate ratio when comparing the first period of active surveillance (period 2) to the preactive surveillance period (period 1) was 0.63 (95% CI, 0.38-1.1); it was 0.36 (95% CI, 0.23-0.55) when comparing the first period of active surveillance (period 2) to the subsequent period (period 3) and 0.68 (95% CI, 0.54-0.85) when comparing the second period of active surveillance (period 4) to the prior period without active surveillance periods. CONCLUSIONS: Active surveillance culturing for VRE in the high risk-units prevented further VRE transmission, as evidenced by a significant increase in hospital-wide incidence rates when active surveillance was discontinued and a significant decrease in incidence rates when it was restarted.

Baltimore↗
PubMed1999

A polyclonal outbreak of predominantly VanB vancomycin-resistant enterococci in northeast Ohio. Northeast Ohio Vancomycin-Resistant Enterococcus Surveillance Program.

We studied the molecular epidemiology of vancomycin-resistant enterococci (VRE) isolated in northeast Ohio during 1996 and examined the association between isolation of VRE from samples other than stool and antimicrobial purchases for five Cleveland hospitals. Susceptibility testing and pulsed-field gel electrophoresis were used to analyze 363 isolates from individual patients from 13 hospitals. Susceptibility testing indicated that 287 strains (79%) expressed the VanB phenotype and 76 (21%) expressed the VanA phenotype. The outbreak was polyclonal, with 30 total genotypes. Both VanA and VanB VRE demonstrated multiple genotypes. One genotype was present in all hospitals, suggesting spread between hospitals. For five teaching hospitals, rates of isolation from non-stool sources and from blood correlated positively with purchases of ticarcillin/clavulanic acid (P = .005). In summary, this outbreak demonstrates transmission of VRE between several hospitals in a geographic region and suggests that use of certain beta-lactam antibiotics may be associated with an increased prevalence of VRE.

Disease Outbreaks↗
PubMed1991

Synergistic killing of vancomycin-resistant enterococci of classes A, B, and C by combinations of vancomycin, penicillin, and gentamicin.

Using both high and low inocula for time-kill curves, we examined the antibiotic killing of clinical isolates of glycopeptide-resistant enterococci (Enterococcus faecium, E. faecalis, and E. gallinarum) belonging to phenotypic resistance classes A, B, and C. None were resistant to high levels (greater than 500 mg/liter) of gentamicin. Vancomycin-penicillin-gentamicin resulted in 2 or more logs of killing above that of the most effective two-antibiotic combination for all strains except two of three E. gallinarum (VanC) strains and a constitutive mutant of a VanB strain. This strategy may be useful clinically.

Drug Resistance, Microbial↗
PubMed1996

Efficacy of vancomycin and teicoplanin alone and in combination with streptomycin in experimental, low-level vancomycin-resistant, VanB-type Enterococcus faecalis endocarditis.

The efficacy of vancomycin (VM) and teicoplanin (TE), alone and in combination with streptomycin (SM), against enterococci that express low-level VanB-type VM resistance was investigated in experimental endocarditis using isogenic strains of Enterococcus faecalis susceptible to glycopeptides and aminoglycosides or inducibly resistant to low levels of VM (MIC = 16 micrograms/ml). VM was significantly less active against the resistant strain than against the susceptible strain, establishing that low-level VanB-type VM resistance can influence therapeutic efficacy. By contrast, TE had equally good activity against both strains. VM or TE combined with SM was synergistic and bactericidal against the resistant strain in vitro. While both combinations were efficient in reducing bacterial density in vivo, TE plus SM was significantly superior to VM plus SM if valve sterilization was considered. These data suggest that despite the presence of low-level VanB-type resistance, combination therapy with a glycopeptide and SM (and presumably other aminoglycosides to which there is not high-level resistance) will nevertheless provide effective bactericidal activity.

Animals↗
PubMed1983

Susceptibility of 50 isolates of Clostridium perfringens to cefotaxime, fosfomycin, penicillin G and vancomycin; variable tolerance for vancomycin.

50 strains of Clostridium perfringens recovered from human fecal specimens were examined for susceptibility to cefotaxime (CTX), fosfomycin (Fosfo), penicillin G (Pen G) and vancomycin (Vanco) with the aid of a microtiter procedure. The geometric mean minimal inhibitory concentrations (MICs) of CTX, Fosfo, Pen G and Vanco were 0.81, 48.3, 0.15 and 0.33 micrograms/ml, respectively; the geometric mean bactericidal concentrations (MBCs) of the four drugs were 1.25, 109.8, 0.53 and 9.05 micrograms/ml, respectively. The geometric mean MBC:MIC ratios of CTX, Fosfo, Pen G and Vanco amounted to 1.56, 1.97, 3.64 and 27.0. It was concluded that the C. perfringens strains were not tolerant for CTX, Fosfo and Pen G; however, the strains displayed variable tolerance for Vanco.

Anti-Bacterial Agents↗
PubMed1997

Do vancomycin serum levels predict failures of vancomycin therapy or nephrotoxicity in cancer patients?

The purpose of this study was to determine if patients with high vancomycin (VAN) serum levels experience more toxicity than underdosed patients with lower (VAN) levels, and whether low VAN serum levels cause therapeutic failures in patients with gram-positive bacteremia. In 198 cancer patients trough and peak serum levels of VAN were measured. Acute toxicity (Red Man syndrome) appeared in 3 patients (1.5%). Patients previously or currently treated with other nephrotoxic compounds (134 patients) presented the same incidence of nephrotoxicity as those receiving VAN for the first time in monotherapy (64 patients). VAN did not increase the toxicity when patients were dosed simultaneously or previously with aminoglycosides or amphotericin B. Our second observation, when studying serum levels in our 198 patients was that high VAN trough serum levels (trough > 15 microg/mL) were associated with significantly more nephrotoxicity (33.3% vs. 11.1%, P < 0.03) than low levels in the subgroups of either pretreated patients or unpretreated with other nephrotoxic drugs. None of 198 patients who had trough levels below 15 microg/mL had peak levels exceeding 40 microg/mL. This suggests that only serum monitoring of trough levels may predict nephrotoxicity. A case control study was conducted to compare a group of 22 VAN failures with 22 successfully treated patients matched in underlying disease and neutropenia who were treated in the same period, under the same antibiotic policy, at the same cancer center, for gram-positive bacteremia. Persisting, enterococcal, or mixed enterococcal plus staphylococcal bacteremia were the only statistically significant risk factors which predicted therapy failure in cancer patients. Neither peak nor trough VAN serum levels predicted failure or cure of gram-positive bacteremia in cancer patients.

Aminoglycosides↗