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Michael J Rybak - One of the best experts on this subject based on the ideXlab platform.
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β-Lactam Combinations with Vancomycin Show Synergistic Activity against Vancomycin-Susceptible Staphylococcus aureus, Vancomycin-Intermediate S. aureus (VISA), and Heterogeneous VISA.
Antimicrobial Agents and Chemotherapy, 2018Co-Authors: Kieu-nhi Tran, Michael J RybakAbstract:Background: Increasing utilization of Vancomycin due to the high prevalence of methicillin-resistant S. aureus (MRSA) infections has lead to the emergence of Vancomycin-intermediate S. aureus (VISA) and heterogeneous VISA (hVISA). In vitro data suggest the potential for potent synergy between several beta-lactams and Vancomycin. The objective of this study is to evaluate the synergy between beta-lactams and Vancomycin against MRSA that is Vancomycin susceptible, Vancomycin susceptible Staphylococcus aureus (VSSA), hVISA, and VISA. Methods: Fifty randomly selected clinical MRSA strains with varying susceptibility to Vancomycin were evaluated for Vancomycin alone and Vancomycin in combination with varying concentrations of cefazolin (CFZ), cefepime (FEP), ceftaroline (CPT), and nafcillin (NAF) minimum inhibitory concentration (MIC). The potential for synergy was assessed by 24h time-kills. Results: Beta-lactams reduced Vancomycin MIC values against all strains (4-16 fold reduction). In time-kill studies against MRSA, CFZ, FEP, CPT, and NAF all demonstrated a similar extent of killing at 24h, and all showed synergistic activity with Vancomycin against VSSA, hVISA, and VISA. Each of these combinations was also superior to any single agent against isolates of all three phenotypes, and each was bactericidal (P Conclusions: The combination of Vancomycin and beta-lactams significantly improved antibacterial activity against VSSA, hVISA, and VISA compared to any agent alone, supporting the potential use of Vancomycin/beta-lactams combination therapy in infections caused by MRSA. Further clinical research is warranted to investigate the synergy of Vancomycin against these Staphylococcus strains.
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early use of daptomycin versus Vancomycin for methicillin resistant staphylococcus aureus bacteremia with Vancomycin minimum inhibitory concentration 1 mg l a matched cohort study
Clinical Infectious Diseases, 2013Co-Authors: Kyle P Murray, Michael J Rybak, Jing J Zhao, Susan L Davis, Ravina Kullar, Keith S Kaye, Paul LephartAbstract:Background Recent reports have described decreased effectiveness with Vancomycin treatment for methicillin-resistant Staphylococcus aureus bacteremia (MRSAB) when the Vancomycin minimum inhibitory concentration (MIC) is >1 µg/mL. Methods This matched, retrospective cohort study compared the clinical effectiveness of daptomycin with that of Vancomycin for the treatment of MRSAB with Vancomycin MICs >1 µg/mL. The primary outcome was clinical failure, defined as a composite of 30-day mortality or bacteremia persisting for ≥7 days. Results One hundred seventy patients were matched 1:1 with respect to the antimicrobial administered. In the daptomycin group, all patients received Conclusions This is the first matched study comparing early daptomycin versus Vancomycin for the treatment of MRSAB when the Vancomycin MIC is >1 µg/mL. Treatment with daptomycin resulted in significantly improved outcomes, including decreased 30-day mortality and persistent bacteremia. These results support the practice of switching early from Vancomycin to daptomycin for the treatment of MRSAB when the Vancomycin MIC is >1 µg/mL.
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novel combinations of Vancomycin plus ceftaroline or oxacillin against methicillin resistant Vancomycin intermediate staphylococcus aureus visa and heterogeneous visa
Antimicrobial Agents and Chemotherapy, 2013Co-Authors: Brian J Werth, George Sakoulas, Celine Vidaillac, K P Murray, K L Newton, Poochit Nonejuie, Joe Pogliano, Michael J RybakAbstract:We demonstrated a significant inverse correlation between Vancomycin and beta-lactam susceptibility in Vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous VISA (hVISA) isolates. Using time kill assays, Vancomycin plus oxacillin or ceftaroline was synergistic against 3/5 VISA and 1/5 hVISA or 5/5 VISA and 4/5 hVISA, respectively. Beta-lactam exposure reduced overall Vancomycin-bodipy binding but may have improved Vancomycin-cell wall interactions to improve Vancomycin activity. Further research is warranted to elucidate the mechanism behind Vancomycin and beta-lactam synergy.
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Nephrotoxicity of Vancomycin, alone and with an aminoglycoside
Journal of Antimicrobial Chemotherapy, 1990Co-Authors: Michael J Rybak, Lisa M. Albrecht, Steven C. Boike, Pranatharthi H. ChandrasekarAbstract:The incidence of nephrotoxicity in patients receiving Vancomycin alone or in combination with an aminoglycoside was prospectively evaluated. A total of 231 courses of antibiotic therapy in 224 patients were consecutively monitored over 28-month period. One hundred and sixty-eight patients received Vancomycin alone, 63 patients received Vancomycin with an aminoglycoside, and 103 patients received gentamicin. Nephrotoxicity was defined as an increase in serum creatinine of 0.5 mg/dl or a 50% increase above baseline, whichever was greater. Eight patients (5%) receiving Vancomycin alone, 14 patients (22%) receiving Vancomycin with an aminoglycoside, and 11 patients (11%) receiving gentamicin alone were found to have nephrotoxicity. Factors found to be associated with increased risk of nephrotoxicity in patients receiving Vancomycin were concurrent therapy with an aminoglycoside, length of treatment with Vancomycin (greater than 21 days), and Vancomycin trough serum concentration (greater than 10 mg/l). Although the incidence of Vancomycin nephrotoxicity is low, patients receiving Vancomycin therapy with the above risk factors should be closely monitored.
George Sakoulas - One of the best experts on this subject based on the ideXlab platform.
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novel combinations of Vancomycin plus ceftaroline or oxacillin against methicillin resistant Vancomycin intermediate staphylococcus aureus visa and heterogeneous visa
Antimicrobial Agents and Chemotherapy, 2013Co-Authors: Brian J Werth, George Sakoulas, Celine Vidaillac, K P Murray, K L Newton, Poochit Nonejuie, Joe Pogliano, Michael J RybakAbstract:We demonstrated a significant inverse correlation between Vancomycin and beta-lactam susceptibility in Vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous VISA (hVISA) isolates. Using time kill assays, Vancomycin plus oxacillin or ceftaroline was synergistic against 3/5 VISA and 1/5 hVISA or 5/5 VISA and 4/5 hVISA, respectively. Beta-lactam exposure reduced overall Vancomycin-bodipy binding but may have improved Vancomycin-cell wall interactions to improve Vancomycin activity. Further research is warranted to elucidate the mechanism behind Vancomycin and beta-lactam synergy.
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comparative effectiveness of nafcillin or cefazolin versus Vancomycin in methicillin susceptible staphylococcus aureus bacteremia
BMC Infectious Diseases, 2011Co-Authors: Marin L Schweizer, Jon P Furuno, Anthony D Harris, Kristie J Johnson, Michelle Shardell, Jessina C Mcgregor, Kerri A Thom, Sara E Cosgrove, George SakoulasAbstract:The high prevalence of methicillin-resistant S. aureus (MRSA) has led clinicians to select antibiotics that have coverage against MRSA, usually Vancomycin, for empiric therapy for suspected staphylococcal infections. Clinicians often continue Vancomycin started empirically even when methicillin-susceptible S. aureus (MSSA) strains are identified by culture. However, Vancomycin has been associated with poor outcomes such as nephrotoxicity, persistent bacteremia and treatment failure. The objective of this study was to compare the effectiveness of Vancomycin versus the beta-lactam antibiotics nafcillin and cefazolin among patients with MSSA bacteremia. The outcome of interest for this study was 30-day in-hospital mortality. This retrospective cohort study included all adult in-patients admitted to a tertiary-care facility between January 1, 2003 and June 30, 2007 who had a positive blood culture for MSSA and received nafcillin, cefazolin or Vancomycin. Cox proportional hazard models were used to assess independent mortality hazards comparing nafcillin or cefazolin versus Vancomycin. Similar methods were used to estimate the survival benefits of switching from Vancomycin to nafcillin or cefazolin versus leaving patients on Vancomycin. Each model included statistical adjustment using propensity scores which contained variables associated with an increased propensity to receive Vancomycin. 267 patients were included; 14% (38/267) received nafcillin or cefazolin, 51% (135/267) received both Vancomycin and either nafcillin or cefazolin, and 35% (94/267) received Vancomycin. Thirty (11%) died within 30 days. Those receiving nafcillin or cefazolin had 79% lower mortality hazards compared with those who received Vancomycin alone (adjusted hazard ratio (HR): 0.21; 95% confidence interval (CI): 0.09, 0.47). Among the 122 patients who initially received Vancomycin empirically, those who were switched to nafcillin or cefazolin (66/122) had 69% lower mortality hazards (adjusted HR: 0.31; 95% CI: 0.10, 0.95) compared to those who remained on Vancomycin. Receipt of nafcillin or cefazolin was protective against mortality compared to Vancomycin even when therapy was altered after culture results identified MSSA. Convenience of Vancomycin dosing may not outweigh the potential benefits of nafcillin or cefazolin in the treatment of MSSA bacteremia.
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induction of daptomycin heterogeneous susceptibility in staphylococcus aureus by exposure to Vancomycin
Antimicrobial Agents and Chemotherapy, 2006Co-Authors: George Sakoulas, Robert C Moellering, Jeff Alder, C Thauvineliopoulos, George M EliopoulosAbstract:We studied Vancomycin and daptomycin susceptibility in methicillin-resistant Staphylococcus aureus from patients exposed to Vancomycin, glycopeptide-intermediate S. aureus, and S. aureus passaged in Vancomycin-containing medium. A correlation between Vancomycin and daptomycin heteroresistance was noted in some strains, suggesting that exposure of S. aureus to Vancomycin may affect susceptibility to daptomycin.
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relationship of mic and bactericidal activity to efficacy of Vancomycin for treatment of methicillin resistant staphylococcus aureus bacteremia
Journal of Clinical Microbiology, 2004Co-Authors: George Sakoulas, Pamela A Moisebroder, Jerome J Schentag, Alan Forrest, Robert C Moellering, George M EliopoulosAbstract:We attempted to find a relationship between the microbiological properties of bloodstream isolates of methicillin-resistant Staphylococcus aureus (MRSA) and the efficacy of Vancomycin in the treatment of bacteremia. Vancomycin susceptibility testing was performed, and bactericidal activity was determined for 30 isolates from 30 different patients with MRSA bacteremia for whom clinical and microbiological outcome data were available. The majority of these patients had been previously enrolled in multicenter prospective studies of MRSA bacteremia refractory to conventional Vancomycin therapy. Logistic regression found a statistically significant relationship between treatment success with Vancomycin and decreases in both Vancomycin MICs (≤0.5 μg/ml versus 1.0 to 2.0 μg/ml; P = 0.02) and degree of killing (reduction in 1og10 CFU/milliliter) by Vancomycin over 72 h of incubation in vitro (P = 0.03). For MRSA isolates with Vancomycin MICs ≤ 0.5 μg/ml, Vancomycin was 55.6% successful in the treatment of bacteremia whereas Vancomycin was only 9.5% effective in cases in which Vancomycin MICs for MRSA were 1 to 2 μg/ml. Patients with MRSA that was more effectively killed at 72 h by Vancomycin in vitro had a higher clinical success rate with Vancomycin therapy in the treatment of bacteremia (log10 6.27 [n = 8], 50%). We conclude that a significant risk for Vancomycin treatment failure in MRSA bacteremia begins to emerge with increasing Vancomycin MICs well within the susceptible range. Elucidating the mechanisms involved in intermediate-level glycopeptide resistance in S. aureus should begin by examining bacteria that begin to show changes in Vancomycin susceptibility before the development of obvious resistance. Prognostic information for Vancomycin treatment outcome in MRSA bacteremia may also be obtained by testing the in vitro bactericidal potency of Vancomycin.
George M Eliopoulos - One of the best experts on this subject based on the ideXlab platform.
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induction of daptomycin heterogeneous susceptibility in staphylococcus aureus by exposure to Vancomycin
Antimicrobial Agents and Chemotherapy, 2006Co-Authors: George Sakoulas, Robert C Moellering, Jeff Alder, C Thauvineliopoulos, George M EliopoulosAbstract:We studied Vancomycin and daptomycin susceptibility in methicillin-resistant Staphylococcus aureus from patients exposed to Vancomycin, glycopeptide-intermediate S. aureus, and S. aureus passaged in Vancomycin-containing medium. A correlation between Vancomycin and daptomycin heteroresistance was noted in some strains, suggesting that exposure of S. aureus to Vancomycin may affect susceptibility to daptomycin.
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relationship of mic and bactericidal activity to efficacy of Vancomycin for treatment of methicillin resistant staphylococcus aureus bacteremia
Journal of Clinical Microbiology, 2004Co-Authors: George Sakoulas, Pamela A Moisebroder, Jerome J Schentag, Alan Forrest, Robert C Moellering, George M EliopoulosAbstract:We attempted to find a relationship between the microbiological properties of bloodstream isolates of methicillin-resistant Staphylococcus aureus (MRSA) and the efficacy of Vancomycin in the treatment of bacteremia. Vancomycin susceptibility testing was performed, and bactericidal activity was determined for 30 isolates from 30 different patients with MRSA bacteremia for whom clinical and microbiological outcome data were available. The majority of these patients had been previously enrolled in multicenter prospective studies of MRSA bacteremia refractory to conventional Vancomycin therapy. Logistic regression found a statistically significant relationship between treatment success with Vancomycin and decreases in both Vancomycin MICs (≤0.5 μg/ml versus 1.0 to 2.0 μg/ml; P = 0.02) and degree of killing (reduction in 1og10 CFU/milliliter) by Vancomycin over 72 h of incubation in vitro (P = 0.03). For MRSA isolates with Vancomycin MICs ≤ 0.5 μg/ml, Vancomycin was 55.6% successful in the treatment of bacteremia whereas Vancomycin was only 9.5% effective in cases in which Vancomycin MICs for MRSA were 1 to 2 μg/ml. Patients with MRSA that was more effectively killed at 72 h by Vancomycin in vitro had a higher clinical success rate with Vancomycin therapy in the treatment of bacteremia (log10 6.27 [n = 8], 50%). We conclude that a significant risk for Vancomycin treatment failure in MRSA bacteremia begins to emerge with increasing Vancomycin MICs well within the susceptible range. Elucidating the mechanisms involved in intermediate-level glycopeptide resistance in S. aureus should begin by examining bacteria that begin to show changes in Vancomycin susceptibility before the development of obvious resistance. Prognostic information for Vancomycin treatment outcome in MRSA bacteremia may also be obtained by testing the in vitro bactericidal potency of Vancomycin.
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Vancomycin-resistant Enterococcus faecium in hospitalized children.
Infection Control and Hospital Epidemiology, 1992Co-Authors: Lorry G. Rubin, Emilia Cercenado, Victor Tucci, George M Eliopoulos, Henry D. IsenbergAbstract:OBJECTIVE: Determine the epidemiology and risk factors for colonization with Vancomycin-resistant Enterococcus faecium. DESIGN: Survey; case-control study. SETTING: Children's hospital. PATIENTS: Pediatric oncology patients. INTERVENTION: Contact isolation, restriction of Vancomycin prescribing. RESULTS: There was a high prevalence of colonization with Vancomycin-resistant enterococci among pediatric oncology patients. The length of hospitalization and the administration of Vancomycin and other intravenous antibiotics was associated with colonization. Prevention of colonization was associated with restriction of Vancomycin use and contact isolation. CONCLUSIONS: Vancomycin use may predispose to colonization with Vancomycin-resistant E faecium. Vancomycin-resistant E faecium may be nosocomially spread. Contact isolation and restriction of Vancomycin use may prevent spread of Vancomycin-resistant E faecium.
Keiichi Hiramatsu - One of the best experts on this subject based on the ideXlab platform.
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Vancomycin resistant staphylococcus aureus a new model of antibiotic resistance
Lancet Infectious Diseases, 2001Co-Authors: Keiichi HiramatsuAbstract:Summary Vancomycin has been the most reliable therapeutic agent against infections caused by meticillin-resistant Staphylococcus aureus (MRSA). However, in 1996 the first MRSA to acquire resistance to Vancomycin, was isolated from a Japanese patient. The patient had contracted a post-operative wound infection that was refractory to long-term Vancomycin therapy. Subsequent isolation of several Vancomycin resistant S aureus (VRSA) strains from USA, France, Korea, South Africa, and Brazil has confirmed that emergence of Vancomycin resistance in S aureus is a global issue. A certain group of S aureus , designated hetero-VRSA, frequently generate VRSA upon exposure to Vancomycin, and are associated with infections that are potentially refractory to Vancomycin therapy. Presence of hetero-VRSA may be an important indicator of the insidious decline of the clinical effectiveness of Vancomycin in the hospitals. Vancomycin resistance is acquired by mutation and thickening of cell wall due to accumulation of excess amounts of peptidoglycan. This seems to be a common resistance mechanism for all VRSA strains isolated in the world so far.
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characterization of staphylococci with reduced susceptibilities to Vancomycin and other glycopeptides
Journal of Clinical Microbiology, 1998Co-Authors: Fred C Tenover, Michael V Lancaster, Christine D Steward, Caroline M Ohara, Nancye C Clark, Gary Hancock, Sheila A Stocker, B. C. Hill, Keiichi HiramatsuAbstract:During the last several years a series of staphylococcal isolates that demonstrated reduced susceptibility to Vancomycin or other glycopeptides have been reported. We selected 12 isolates of staphylococci for which the Vancomycin MICs were ≥4 μg/ml or for which the teicoplanin MICs were ≥8 μg/ml and 24 control strains for which the Vancomycin MICs were ≤2 μg/ml or for which the teicoplanin MICs were ≤4 μg/ml to determine the ability of commercial susceptibility testing procedures and Vancomycin agar screening methods to detect isolates with reduced glycopeptide susceptibility. By PCR analysis, none of the isolates with decreased glycopeptide susceptibility contained known Vancomycin resistance genes. Broth microdilution tests held a full 24 h were best at detecting strains with reduced glycopeptide susceptibility. Disk diffusion did not differentiate the strains inhibited by 8 μg of Vancomycin per ml from more susceptible isolates. Most of the isolates with reduced glycopeptide susceptibility were recognized by MicroScan conventional panels and Etest Vancomycin strips. Sensititre panels read visually were more variable, although with some of the panels MICs of 8 μg/ml were noted for these isolates. Vitek results were 4 μg/ml for all strains for which the Vancomycin MICs were ≥4 μg/ml. Vancomycin MICs on Rapid MicroScan panels were not predictive, giving MICs of either ≤2 or ≥16 μg/ml for these isolates. Commercial brain heart infusion Vancomycin agar screening plates containing 6 μg of Vancomycin per ml consistently differentiated those strains inhibited by 8 μg/ml from more susceptible strains. Vancomycin-containing media prepared in-house showed occasional growth of susceptible strains, Staphylococcus aureus ATCC 29213, and on occasion, Enterococcus faecalis ATCC 29212. Thus, strains of staphylococci with reduced susceptibility to glycopeptides, such as Vancomycin, are best detected in the laboratory by nonautomated quantitative tests incubated for a full 24 h. Furthermore, it appears that commercial Vancomycin agar screening plates can be used to detect these isolates.
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dissemination in japanese hospitals of strains of staphylococcus aureus heterogeneously resistant to Vancomycin
The Lancet, 1997Co-Authors: Keiichi Hiramatsu, Nanae Aritaka, Hideaki Hanaki, Shiori Kawasaki, Yasuyuki Hosoda, Satoshi Hori, Yoshinosuke Fukuchi, Intetsu KobayashiAbstract:Summary Background Since the discovery of the Vancomycin-resistant Staphylococcus aureus (VRSA) strain Mu50 (minimum inhibitory concentration [MIC] 8 mg/L), there has been concern about the potential spread of such strains throughout Japanese hospitals. Two important questions need to be answered: (1) what is the prevalence of VRSA, and (2) by what mechanism does Vancomycin resistance occur. Methods The Vancomycin susceptibilities of three methicillin-resistant S aureus (MRSA) strains (Mu50, Mu3, and H1) and the methicillin-susceptible S aureus type strain FDA209P were compared by MIC determinations and population analysis. Mu3 (MIC 3 mg/L) was isolated from the sputum of a patient with pneumonia after surgery who had failed Vancomycin therapy. H1 (MIC 2 mg/L), which is a representative Vancomycin-susceptible MRSA strain, was isolated from a patient with pneumonia who responded favourably to Vancomycin therapy. Subclones of Mu3 with increased resistance against Vancomycin were selected with serial concentrations of Vancomycin and their MICs were determined. The prevalence of VRSA and Mu3-like strains in Japanese hospitals was estimated by population analysis from 1149 clinical MRSA isolates obtained from 203 hospitals throughout Japan. The genetic traits of the Mu3 and Mu50 strains were compared with clonotypes of MRSA from around the world. Findings Mu3 and Mu50 had an identical pulsed-field gel electrophoresis banding pattern. When grown in a drug-free medium, Mu3 produced subpopulation of cells with varying degrees of Vancomycin resistance, thus demonstrating natural heterogeneity, or variability, in susceptibility to Vancomycin. In the presence of Vancomycin, Mu3 produced subclones with resistance roughly proportional to the concentrations of Vancomycin used. Selection of Mu3 with 8 mg/L or more of Vancomycin gave rise to subclones with Vancomycin resistance equal to that of Mu50 (MIC 8 mg/L) at a frequency of 1/1000000. During screening of Japanese MRSA strains, no strain of VRSA additional to Mu50 was found. The prevalence of MRSA isolates heterogeneously resistant to Vancomycin was 20% in Juntendo University Hospital, 9·3% in the other seven university hospitals, and 1·3% in non-university hospitals or clinics. Interpretation Heterogeneously resistant VRSA is a preliminary stage that allows development into VRSA upon exposure to Vancomycin. Heterogeneously resistant VRSA was found in hospitals throughout Japan. This finding could explain, at least partly, the frequent therapeutic failure of MRSA infection with Vancomycin in Japan.
Josep Mensa - One of the best experts on this subject based on the ideXlab platform.
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influence of Vancomycin minimum inhibitory concentration on the treatment of methicillin resistant staphylococcus aureus bacteremia
Clinical Infectious Diseases, 2008Co-Authors: Alex Soriano, Francesc Marco, Jose Antonio Baddini Martinez, Elena Pisos, Manel Almela, Veselka P Dimova, Dolores Alamo, Mar Ortega, J A Lopez, Josep MensaAbstract:BACKGROUND: Vancomycin treatment failure in methicillin-resistant Staphylococcus aureus (MRSA) bacteremia is not uncommon, even when MRSA is susceptible to Vancomycin. The aim of our study was to evaluate whether Vancomycin minimum inhibitory concentration has any influence on the mortality associated with MRSA bacteremia. METHODS: A total of 414 episodes of MRSA bacteremia were prospectively followed-up from 1991 through 2005. MIC of Vancomycin for the first isolate was determined by E-test. Clinical variables recorded were age, comorbidity, prior administration of Vancomycin, use of corticosteroids, prognosis of underlying disease, source of bacteremia, the need for mechanical ventilation, shock, and mortality. A "treatment group" variable was created and defined as follows: (1) receipt of empirical Vancomycin and an isolate with a Vancomycin MIC of 1 microg/mL (38 episodes), (2) receipt of empirical Vancomycin and an isolate with a Vancomycin MIC of 1.5 microg/mL (90 episodes), (3) receipt of empirical Vancomycin and an isolate with a Vancomycin MIC of 2 microg/mL (40 episodes), and (4) receipt of inappropriate empirical therapy (246 episodes). Univariate and multivariate analyses were performed. RESULTS: Episodes caused by strains with a Vancomycin MIC of 2 microg/mL were independently associated with a lower risk of shock (odds ratio [OR], 0.33; 95% confidence interval [CI], 0.15-0.75). Multivariate analysis selected receipt of empirical Vancomycin and an isolate with a Vancomycin MIC of 2 microg/mL (OR, 6.39; 95% CI, 1.68-24.3), receipt of inappropriate empirical therapy (OR, 3.62; 95% CI, 1.20-10.9), increasing age (OR, 1.02; 95% CI, 1.00-1.04), use of corticosteroids (OR, 1.85; 95% CI, 1.04-3.29), an ultimately (OR, 10.2; 95% CI, 2.85-36.8) or rapidly (OR, 1.81; 95% CI, 1.06-3.10) fatal underlying disease, high-risk (OR, 3.60; 95% CI, 1.89-6.88) and intermediate-risk (OR, 2.18; 95% CI, 1.17-4.04) sources of bacteremia, and shock (OR, 7.38; 95% CI, 4.11-13.3) as the best predictors of mortality. CONCLUSIONS: Mortality associated with MRSA bacteremia was significantly higher when the empirical antibiotic was inappropriate and when Vancomycin was empirically used for treatment of infection with strains with a high Vancomycin MIC (>1 microg/mL).
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influence of Vancomycin minimum inhibitory concentration on the treatment of methicillin resistant staphylococcus aureus bacteremia
Clinical Infectious Diseases, 2008Co-Authors: Alex Soriano, Francesc Marco, Jose Antonio Baddini Martinez, Elena Pisos, Manel Almela, Veselka P Dimova, Dolores Alamo, Mar Ortega, J Lopez, Josep MensaAbstract:BACKGROUND Vancomycin treatment failure in methicillin-resistant Staphylococcus aureus (MRSA) bacteremia is not uncommon, even when MRSA is susceptible to Vancomycin. The aim of our study was to evaluate whether Vancomycin minimum inhibitory concentration has any influence on the mortality associated with MRSA bacteremia. METHODS A total of 414 episodes of MRSA bacteremia were prospectively followed-up from 1991 through 2005. MIC of Vancomycin for the first isolate was determined by E-test. Clinical variables recorded were age, comorbidity, prior administration of Vancomycin, use of corticosteroids, prognosis of underlying disease, source of bacteremia, the need for mechanical ventilation, shock, and mortality. A "treatment group" variable was created and defined as follows: (1) receipt of empirical Vancomycin and an isolate with a Vancomycin MIC of 1 microg/mL (38 episodes), (2) receipt of empirical Vancomycin and an isolate with a Vancomycin MIC of 1.5 microg/mL (90 episodes), (3) receipt of empirical Vancomycin and an isolate with a Vancomycin MIC of 2 microg/mL (40 episodes), and (4) receipt of inappropriate empirical therapy (246 episodes). Univariate and multivariate analyses were performed. RESULTS Episodes caused by strains with a Vancomycin MIC of 2 microg/mL were independently associated with a lower risk of shock (odds ratio [OR], 0.33; 95% confidence interval [CI], 0.15-0.75). Multivariate analysis selected receipt of empirical Vancomycin and an isolate with a Vancomycin MIC of 2 microg/mL (OR, 6.39; 95% CI, 1.68-24.3), receipt of inappropriate empirical therapy (OR, 3.62; 95% CI, 1.20-10.9), increasing age (OR, 1.02; 95% CI, 1.00-1.04), use of corticosteroids (OR, 1.85; 95% CI, 1.04-3.29), an ultimately (OR, 10.2; 95% CI, 2.85-36.8) or rapidly (OR, 1.81; 95% CI, 1.06-3.10) fatal underlying disease, high-risk (OR, 3.60; 95% CI, 1.89-6.88) and intermediate-risk (OR, 2.18; 95% CI, 1.17-4.04) sources of bacteremia, and shock (OR, 7.38; 95% CI, 4.11-13.3) as the best predictors of mortality. CONCLUSIONS Mortality associated with MRSA bacteremia was significantly higher when the empirical antibiotic was inappropriate and when Vancomycin was empirically used for treatment of infection with strains with a high Vancomycin MIC (>1 microg/mL).
