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PubMed1987

Ciprofloxacin versus vancomycin in the therapy of experimental methicillin-resistant Staphylococcus aureus endocarditis.

We compared the efficacy of ciprofloxacin with that of vancomycin by using the rabbit model of methicillin-resistant Staphylococcus aureus endocarditis. Endocarditis was treated with ciprofloxacin (25 mg/kg [body weight] intravenously every 8 h) or vancomycin (17.5 mg/kg intravenously every 6 h) for 3 days. Vancomycin and ciprofloxacin were equally efficacious in clearing bacteremia. Both reduced vegetation bacterial counts by 5 log10 CFU/g and renal and splenic bacterial counts by more than 3 log10 CFU/g as compared with untreated control rabbits after 26 h of infection (P less than 0.001). Both antimicrobial agents were able to eradicate the infectious process in an equivalent proportion of animals. No methicillin-resistant S. aureus that was recovered from ciprofloxacin-treated rabbits developed resistance to ciprofloxacin during therapy. Peak concentrations of ciprofloxacin in the sera of rabbits with endocarditis were significantly higher than those predicted by single-dose studies in uninfected rabbits. This finding was likely due to changes in the pharmacokinetics of the drug with multiple dosing and in infected versus uninfected rabbits. This study demonstrated that intravenously administered ciprofloxacin is as efficacious as vancomycin is in an in vivo model of a serious systemic methicillin-resistant S. aureus infection.

Animals↗

PubMed1987

Altered pharmacokinetic disposition of ciprofloxacin and vancomycin after single and multiple doses in rabbits.

The pharmacokinetic disposition of vancomycin and ciprofloxacin was assessed in rabbits before the efficacy of these compounds in experimental staphylococcal endocarditis was compared. Ciprofloxacin was given in single intravenous bolus doses of 25 and 35 mg/kg and also in a multiple-dose regimen of 35 mg/kg every 6 h. Vancomycin was given in a similar manner in single doses of 17.5 and 25 mg/kg and in a multiple-dose regimen of 17.5 mg/kg every 6 h. Serum was sampled frequently after injections and analyzed by microbiologic assay for drug concentration. The pharmacokinetic parameters of clearance and steady-state volume of distribution were calculated by compartment-independent methods. These studies revealed that clearance of ciprofloxacin was reduced significantly after multiple doses (7.42 +/- 0.85 [standard deviation] versus 6.09 +/- 0.71 liters/h, P less than 0.01). Although the half-life and volume of distribution increased after multiple dosing, the differences were not statistically significant. The disposition of vancomycin following single doses was significantly altered after the 25-mg/kg dose compared with the 17.5-mg/kg dose. Half-life, clearance, and volume of distribution changed from 1.27 +/- 0.2 to 1.60 +/- 0.21 h (P less than 0.05), 0.54 +/- 0.05 to 0.39 +/- 0.04 liters/h (P less than 0.01), and 0.37 +/- 0.04 to 0.31 +/- 0.03 liters/kg (P less than 0.05), respectively. The disposition of ciprofloxacin was not altered with increases in dose size, and the disposition of vancomycin was not altered after multiple doses. If such alterations in the pharmacokinetic disposition of antimicrobial agents are unanticipated, the higher and more prolonged than expected serum concentrations may have an effect on the outcome of experimental infections.

Animals↗

PubMed1990

Assessment of effects of protein binding on daptomycin and vancomycin killing of Staphylococcus aureus by using an in vitro pharmacodynamic model.

Initial clinical trials with daptomycin (2 mg/kg per day) were prematurely suspended because of unexplained treatment failures in patients with bacteremia who were treated with daptomycin, despite in vitro data indicating that the gram-positive cocci causing the infection were susceptible to daptomycin. One explanation for these clinical failures may relate to the relatively high degree of daptomycin protein binding (94%). To evaluate the impact of protein on daptomycin activity, a two-chamber in vitro pharmacodynamic model was used to study and compare the interaction between Staphylococcus aureus (clinical isolate) and either daptomycin or vancomycin, each in the presence and absence of physiologic human albumin concentrations. Low-dose (2 mg/kg) daptomycin, high-dose (6 mg/kg) daptomycin, and 10 mg of vancomycin per kg beta-phase elimination serum-concentration-versus-time curves were simulated by using this in vitro pharmacodynamic model. The bacterial kill rates by all three regimens were decreased in the presence of albumin (P less than 0.0002). The average times required for a 99% kill of the initial S. aureus inocula (approximately 5 x 10(7) CFU/ml) without albumin were 0.81 (low-dose daptomycin), 0.33 (high-dose daptomycin), and 6.18 (vancomycin) h. The average times required for a 99% kill of S. aureus with albumin were 7.66 (low-dose daptomycin), 0.95 (high-dose daptomycin), and 10.52 (vancomycin) h. These data demonstrate that, depending on the concentration of daptomycin, the presence of albumin can profoundly diminish the bactericidal activity of daptomycin.

Daptomycin↗

PubMed1990

Vancomycin-induced histamine release and "red man syndrome": comparison of 1- and 2-hour infusions.

Vancomycin-induced "red man syndrome" (RMS) is mediated in part by histamine release, and its severity is correlated with the area under the plasma histamine concentration-time curve. Ten adult male volunteers participated in a randomized, double-blind, two-way crossover trial (1-week washout interval between regimens) to determine the effect of 1- and 2-h infusions of vancomycin (1.0 g) on histamine release and on the frequency and severity of RMS. The severity of RMS was classified a priori as mild, moderate, or severe from a combined score of pruritus and extent of erythema. Serial concentrations of histamine in plasma and concentrations of vancomycin in serum were measured at baseline and during and after each infusion. Of 10 subjects, 8 had evidence of RMS during the 1-h infusion (3 mild, 3 moderate, and 2 severe), whereas only 3 of the 10 subjects (all mild) had RMS during the 2-h infusion (P less than 0.05). The 1-h infusion was associated with a significantly greater peak concentration of histamine in plasma (1.8 +/- 0.7 versus 1.0 +/- 0.3 ng/ml, P = 0.004) and a greater total release of histamine (74.3 +/- 54.1 versus 36.4 +/- 22.6 ng.min/ml, P = 0.017) than was the 2-h infusion. These data suggest that administration of vancomycin over 2 h reduces the frequency and severity of RMS and the amount of histamine released compared with those after a 1-h infusion in healthy volunteers.

Adult↗

PubMed1990

Oral temafloxacin versus vancomycin for therapy of experimental endocarditis caused by methicillin-resistant Staphylococcus aureus.

We compared oral temafloxacin, a new fluoroquinolone agent, with vancomycin, each with and without rifampin, in the therapy of rats with aortic valve endocarditis caused by a clinical isolate of methicillin-resistant Staphylococcus aureus. The temafloxacin, vancomycin, and rifampin MICs and MBCs were 0.78 and 1.56, 1.56 and 3.13, and less than 0.024 and 0.78 microgram/ml, respectively. The animals were classified into the following six treatment groups: vancomycin (60 mg/kg) +/- rifampin (6 mg/kg) each intramuscularly every 12 h for 5 days; temafloxacin (100 mg/kg) orally +/- rifampin (6 mg/kg) intramuscularly every 12 h for 5 days; rifampin (6 mg/kg) intramuscularly every 12 h for 5 days; and untreated controls. All regimens with either vancomycin or temafloxacin resulted in improved survival over controls, but only temafloxacin regimens resulted in a significant reduction in bacterial counts in vegetations. These data support further investigation of the efficacy of temafloxacin in treating serious infections caused by methicillin-resistant S. aureus.

4-Quinolones↗

PubMed1990

Application of a Bayesian method to monitor and adjust vancomycin dosage regimens.

A Bayesian method for monitoring vancomycin concentrations and adjusting regimens in patients with unstable renal function by using a two-compartment population model was evaluated with a personal computer. The population model was derived from data from 12 cardiac outpatients who received single doses of vancomycin. The performance of the method was then tested in 27 acutely ill patients who received multiple doses of vancomycin. Significant renal impairment was observed in 15 patients. Renal function changed in 15 patients. The vancomycin concentrations in the patients with changing renal function were not at steady state during the observation times. Two concentrations in serum (peak and then trough, or trough and then peak) were fitted along with the population model to individualize the parameter values for each patient. All the subsequent concentrations in serum for each patient were then predicted by using the parameter values for each patient. Future concentrations of 118 serum samples were predicted. The mean absolute prediction error was 3.6 +/- 4.5 micrograms/ml, and the mean prediction error was -0.7 +/- 5.3 micrograms/ml. These results confirm that a two-compartment pharmacokinetic model can be sufficiently individualized with the knowledge of just two concentrations of drug in patient serum; it is possible to predict closely subsequent concentrations in serum, and dosing regimens for individual patients can be well adjusted to achieve the chosen therapeutic goals.

Adult↗

PubMed1991

Randomized study of vancomycin versus teicoplanin for the treatment of gram-positive bacterial infections in immunocompromised hosts.

Seventy-four immunocompromised patients with severe infection due to gram-positive organisms were randomized to receive either vancomycin or teicoplanin. Extensive cancer was present in 71 patients, of whom 47 died within a month. The types of infections were 46 bacteremias (39 associated with central catheters), 24 skin and soft tissue infections (3 with bacteremia), and 7 others (mainly bronchopneumonia). The most frequent pathogen was Staphylococcus epidermidis, followed by Staphylococcus aureus. Microbiological eradication was obtained in 23 of 35 evaluable patients treated with vancomycin (65.7%) and 28 of 36 patients treated with teicoplanin (77.8%) (P = 0.4). Clinical cure and improvement were obtained in 26 of 35 patients (74.3%) and 27 of 36 patients (75.0%), respectively. No significant side effects were observed with teicoplanin, in contrast to reversible increases in serum creatinine (three patients) and skin rashes (four patients) with vancomycin. Superinfection was observed in five patients treated with vancomycin and two patients treated with teicoplanin. No relation was found between peak concentration in serum (at steady state) or bactericidal titers and outcome.

Adult↗

PubMed1992

Analysis of peptidoglycan precursors in vancomycin-resistant enterococci.

Analysis by high-pressure liquid chromatography of the cytoplasmic peptidoglycan precursors of a high- and a low-level vancomycin-resistant Enterococcus spp. was performed before and after induction of resistance. This analysis showed a decrease of the D-Ala-D-Ala and UDP-MurNac-pentapeptide pools, an increase of the UDP-MurNac-tripeptide pool, and the appearance of new UDP-MurNac-containing material. These results lead us to suggest that the vancomycin-induced carboxypeptidase activity cleaves the D-Ala-D-Ala (L. Gutmann, D. Billot-Klein, S. Al-Obeid, I. Klare, S. Francoul, E. Collatz, and J. van Heijenoort, Antimicrob. Agents Chemother. 36:77-80, 1992), which in turn would prevent formation of the normal UDP-MurNac-pentapeptide and thereby of the vancomycin target. The novel UDP-MurNac-containing material is thought to correspond to peptidoglycan precursors which might be synthesized by an alternate pathway (T. D. H. Bugg, G. D. Wright, S. Dutka-Malen, M. Arthur, P. Courvalin, and C. T. Walsh, Biochemistry 30:10408-10415, 1991) and which would be unable to bind vancomycin in glycopeptide-resistant enterococci.

Cells, Cultured↗

PubMed1992

Vancomycin resistance gene vanC is specific to Enterococcus gallinarum.

Nearly all strains of Enterococcus gallinarum are resistant to low levels of vancomycin. The glycopeptide resistance gene vanC from E. gallinarum BM4174 has recently been cloned and sequenced. A probe specific for vanC hybridized with a 2.7-kb EcoRI and a 4.5-kb HindIII fragment of total DNA from the 42 strains of E. gallinarum studied. No homology was detected with DNA of strains belonging to other species intrinsically resistant to vancomycin, including Enterococcus casseliflavus, a species that expresses a vancomycin resistance phenotype similar to that of E. gallinarum. No hybridization with DNA of enterococcal strains with acquired resistance to high or low levels of vancomycin was observed. The specificity of the vanC probe allowed us to distinguish E. gallinarum from 12 other species of enterococci, indicating that this probe is a useful tool for species identification within the genus Enterococcus.

Culture Media↗

PubMed1994

Minocycline versus vancomycin for treatment of experimental endocarditis caused by oxacillin-resistant Staphylococcus aureus.

The purpose of this study was to determine the penetration of minocycline and vancomycin into cardiac vegetations and to determine their efficacy in a rabbit model of endocarditis caused by oxacillin-resistant Staphylococcus aureus. Animals were randomized into three groups: control (no antibiotic), minocycline (6 mg/kg given intravenously every 8 h), and vancomycin (50 mg/kg given intravenously every 8 h). Penetration of the antibiotics into aortic valve vegetations was determined by using the tissue/serum area under the concentration-time curve ratio. The reductions in the bacterial density of the vegetations caused by both vancomycin (4.8 +/- 1.2 CFU/g) and minocycline (5.3 +/- 1.6 CFU/g) were significantly different from that of controls (8.7 +/- 1.8 CFU/g). Although the penetration of minocycline was twice that of vancomycin, they were equally effective in reducing the bacterial density of the vegetations, since the concentrations of both agents in tissue remained above their MICs for oxacillin-resistant S. aureus. For organisms for which the MICs are higher, however, these penetration differences may result in treatment differences.

Animals↗

PubMed1994

Bactericidal activities of teicoplanin, vancomycin, and gentamicin alone and in combination against Staphylococcus aureus in an in vitro pharmacodynamic model of endocarditis.

We adapted an in vitro pharmacodynamic model of infection to incorporate simulated endocardial vegetations. The bactericidal activities of teicoplanin, vancomycin, gentamicin, and various combinations of these drugs were studied against a strain of methicillin-susceptible Staphylococcus aureus obtained from a patient being treated for endocarditis at Detroit Receiving Hospital. Bacteria were grown overnight, concentrated, and added to a mixture of cryoprecipitate (80%) and thrombin (10%) to achieve approximately 5 x 10(9) CFU/g. Fibrin clots (8 to 10) were suspended into the model, removed at 24, 48, and 72 h in duplicate, weighed, and homogenized in 1.25% trypsin. Control experiments were conducted to characterize the growth kinetics. The following antibiotics were administered to simulate the pharmacokinetics of the drugs in humans: teicoplanin at 3 and 15 mg/kg of body weight, vancomycin at 15 mg/kg, and gentamicin at 1 mg/kg. Fibrin clot samples used to detect resistance were plated on antibiotic-containing tryptic soy agar plates. For the teicoplanin and vancomycin regimens, protein binding to cryoprecipitate, thrombin, and fibrin clot was determined to be 32, 43, and 50% and 26, 28, and 29%, respectively. In comparison with no treatment, vancomycin or teicoplanin at 15 mg/kg or either of these regimens combined with gentamicin significantly reduced bacterial counts (P < 0.0001). Monotherapy with teicoplanin at 3 mg/kg or gentamicin resulted in no killing activity. Combination treatment with teicoplanin at 3 mg/kg and gentamicin resulted in the killing of approximately 2 log10 CFU/g by 72 h and the development of resistance to gentamicin. The results obtained with the in vitro model of endocarditis are similar to the results reported by several investigators with the rabbit model of infective endocarditis. This unique infection model is useful for designing initial drug dosage regimens and may be predictive of drug efficacy against infective endocarditis.

Blood Proteins↗

PubMed1995

Inducible and constitutive expression of resistance to glycopeptides and vancomycin dependence in glycopeptide-resistant Enterococcus avium.

A clinical isolate of Enterococcus avium, Ea1, which exhibited inducible, low-level resistance to vancomycin and teicoplanin, and two mutants selected from this strain, Ea3 and Ea31, were studied. Ea3 was vancomycin dependent and derived from Ea1, while Ea31 was not vancomycin dependent, was constitutively resistant, and was derived from Ea3. Hybridization studies revealed that vanA was present in Ea1 and suggested that it was located on a high-molecular-weight plasmid. In the absence of induction, Ea1 synthesized only the natural UDP-MurNAc-pentapeptide precursor, and after induction it synthesized an additional precursor identified as UDP-MurNAc-tetrapeptide-D-lactate. The latter was the only precursor found in Ea3 and Ea31, even after precursor accumulation. From these results, we infer that (i) the low level of resistance to glycopeptides in strain Ea1 may be in part due to the residual synthesis of the normal precursor and (ii) the vancomycin dependence of mutant Ea3 could be due to the fact that this strain does not produce any peptidoglycan precursor in the absence of induction.

Adult↗

PubMed1995

Inducible and constitutive expression of vanC-1-encoded resistance to vancomycin in Enterococcus gallinarum.

Clinical isolates Enterococcus gallinarum AIB39 and E. gallinarum GS1 were studied to establish whether the expression of vanC-1-mediated resistance may be inducible or constitutive. By growth curve analysis, strain AIB39 exhibited the same lag period (i.e., 1 to 1.5 h) whether it was subcultured to unsupplemented brain heart infusion broth or broth containing 6 micrograms of vancomycin per ml, a growth pattern typical of constitutively expressed resistance. Use of high-performance liquid chromatography (HPLC) to separate peptidoglycan precursor extracts substantiated this finding because the serine-terminating pentapeptide precursor UDP-MurNAc-L-Ala-D-Glu-L-Lys-D-Ala-D-Ser was produced in the presence and absence of vancomycin, whereas no UDP-MurNAc-L-Ala-D-Glu-L-Lys-D-Ala-D-Ala was detected. In contrast, results with strain GS1 were consistent with inducible expression. GS1 demonstrated a lag time that was 3 to 4 h longer when it was subcultured to vancomycin-containing broth than when it was subcultured in unsupplemented broth. HPLC analysis showed that in the absence of vancomycin only UDP-MurNAc-L-Ala-D-Glu-L-Lys-D-Ala-D-Ala was detected, but in the presence of drug only UDP-MurNAc-L-Ala-D-Glu-L-Lys-D-Ala-D-Ala was found. Inducible expression of vanC-1-mediated resistance in E. gallinarum is consistent with recent findings suggesting the presence of at least two ligases in this species. Although vanC-1 may be intrinsic to E. gallinarum, our findings raise doubt regarding the natural mechanism of this gene's expression.

Amino Acid Sequence↗

PubMed1995

Pharmacodynamics of RP 59500 alone and in combination with vancomycin against Staphylococcus aureus in an in vitro-infected fibrin clot model.

The bactericidal activity and emergence of resistance to RP 59500 (quinupristin/dalfopristin) when it was administered alone and in combination with vancomycin against fibrin clots that have been infected with methicillin-susceptible Staphylococcus aureus ATCC 25923 or methicillin-resistant S. aureus (MRSA) 67 were evaluated in an in vitro pharmacodynamic infected fibrin clot model. Fibrin clots were infected with S. aureus to achieve an inoculum of approximately 10(9) CFU/g. Antibiotics were administered to simulate pharmacokinetics in humans: RP 59500 (7.5 mg/kg of body weight) every 8 h and vancomycin (15 mg/kg) every 12 h over 72 h. Preliminary test tube time-kill experiments with an inoculum of approximately 10(5) CFU/ml suggested that RP 59500 was more rapid in achieving a 99.9% reduction in the number of CFU per milliliter than vancomycin against ATCC 25923 (6.94 versus 24 h; P = 0.0003) and MRSA 67 (6.77 versus 17.03 h; P = 0.004). At a higher inoculum (approximately 10(8) CFU/ml), 99.9% kill was achieved only with the combination regimen against ATCC 25923 and MRSA 67 (10.9 and 10.5 h, respectively), with total reductions of 6.35 and 6.33 log10 CFU/ml over 24 h, respectively. In the fibrin clot model, RP 59500 was more effective than vancomycin in reducing organism titers over 72 h. In the fibrin clot model, the most optimal therapy was the combination regimen.

Blood Coagulation↗

PubMed1995

Use of primers selective for vancomycin resistance genes to determine van genotype in enterococci and to study gene organization in VanA isolates.

Vancomycin resistance in enterococci is an emerging therapeutic problem. Resistance is not always detected by standard microbiological methods. Oligonucleotide primers for PCR were designed to target amplification of defined regions of genes of the vanA cluster, as well as vanB and vanC1. These primers correctly identified 30 vancomycin-resistant isolates tested (17 VanA, 7 VanB, and 6 Enterococcus gallinarum). No amplification was observed with Enterococcus casseliflavus or vancomycin-susceptible strains. Using PCR and Southern blotting, we found that all 17 VanA isolates had orf-1, orf-2, vanR, vanS, vanH, vanA, and vanY genes in the same sequence and that the intergenic distances in the vanR-vanA segments were the same. The described methods should be applicable to the rapid detection of the different vancomycin resistance genotypes in enterococci.

Anti-Bacterial Agents↗

PubMed1995

Influence of dexamethasone on efficacy of ceftriaxone and vancomycin therapy in experimental pneumococcal meningitis.

Using a rabbit model of meningitis, we sought to determine whether concomitant use of dexamethasone affects the penetration and efficacy of ceftriaxone or vancomycin in cerebrospinal fluid. Rabbits were inoculated with a penicillin-sensitive strain of Streptococcus pneumoniae and treated with ceftriaxone or vancomycin with or without dexamethasone. In the ceftriaxone-treated groups, no statistically significant differences were seen between the group treated with dexamethasone and that without dexamethasone; however, in the vancomycin-treated groups we found statistically significant lower cerebrospinal fluid vancomycin levels at 2 h in the dexamethasone-treated rabbits and differences in bacterial killing.

Animals↗

PubMed1973

In vitro activity of ampicillin or vancomycin combined with gentamicin or streptomycin against enterococci.

Minimum inhibitory and bactericidal concentrations of four antibiotics and their combinations were determined for 38 strains of enterococci by a microtitration tube dilution technique. The drugs were ampicillin, vancomycin, gentamicin, and streptomycin; the combinations were ampicillin-gentamicin, ampicillin-streptomycin, vancomycin-gentamicin, and vancomycin-streptomycin. At achievable serum concentrations, ampicillin alone killed 60% of strains, whereas combination with streptomycin increased this to 90% and with gentamicin to 100%. Vancomycin alone showed striking inhibitory activity, but very poor bactericidal activity at achievable concentrations. Combination with one of the aminoglycosides increased the bactericidal activity substantially. When combined with ampicillin, gentamicin was both more active and showed synergistic bactericidal activity significantly more often (P < 0.01) than streptomycin.

Ampicillin↗

PubMed1996

Comparison of conventional dosing versus continuous-infusion vancomycin therapy for patients with suspected or documented gram-positive infections.

Ten patients were treated with conventional dosing (CD) and continuous-infusion (CI) vancomycin therapy in this prospective, randomized, crossover study. Patients were randomized to receive either CD or CI therapy for 2 consecutive days and then crossed over to receive the opposite regimen for 2 days. CD therapy consisted of 1 g of vancomycin every 12 h. CI therapy consisted of a 500-mg loading dose followed by 2 g infused over 24 h. Ten serum samples were obtained on the second day of each therapy for pharmacokinetic and pharmacodynamic analyses. Two clinical isolates of Staphylococcus aureus, one methicillin sensitive (MSSA 1199) and one methicillin resistant (MRSA 494), were chosen for pharmacodynamic evaluation of both regimens. The patient demographics (means +/- standard deviations [SD]) were as follows: sex, six males, four females; age, 36 +/- 11 years; and serum creatinine, 0.72 +/- 0.18 mg/dl. Mean pharmacokinetic parameters +/- SD for CD therapy were as follows: elimination rate constant, 0.16 +/- 0.07 h-1; half-life, 5.6 +/- 3.5 h; volume of distribution, 33.7 +/- 25 liters, 0.5 +/- 0.2 liters/kg; maximum concentration in serum, 53.4 +/- 19.3 micrograms/ml; and minimum concentration, 8.4 +/- 5.9 micrograms/ml. The steady-state concentration for CI was 20.2 +/- 11.1 micrograms/ml. Overall, both regimens resulted in the MIC being exceeded 100% of the time. The mean CD trough serum bactericidal titer (SBT) was 1:8, and the average CI SBTs were 1:16 for both isolates. Even though there was no statistically significant difference between CD trough and CI SBTs, the CI SBTs remained > 1:8 for 100% of the time versus 60% of the time for CD therapy. During CI therapy, 20 and 40% of the patients maintained SBTs of > 1:32 throughout the dosing interval for MSSA 1199 and MRSA 494, respectively. During CD therapy, however, only 10% of patients maintained SBTs of > 1:32 during the entire dosing interval for both isolates. The mean areas under the bactericidal titer-time curve (AUBC24s) +/- SD for MSSA 1199 were 528 +/- 263 for CD therapy and 547 +/- 390 for CI therapy. The mean AUBC24s +/- SD against MRSA 494 were 531 +/- 247 for CD and 548 +/- 293 for CI therapy. Similar to the AUBC24, the mean area under the concentration-time curve for a 24-h dosing interval divided by the MIC (AUC/MIC24) ratios +/- SD were 550.0 +/- 265.7 for CD and 552.6 +/- 373.4 for CI therapy, respectively. No statistically significant differences were found between any of the pharmacodynamic parameters for CD and CI therapy. In addition, no adverse effects with either CD or CI therapy were observed during the study. We conclude that CI and CD vancomycin therapy demonstrated equivalent pharmacodynamic activities. Although CI therapy was more likely to result in SBTs that remained above 1:8 for the entire regimen, the clinical impact of this result is unknown. Serum drug concentration variability was observed with both treatment regimens but to a lesser extent with CI administration. CI administration of vancomycin should be further evaluated to determine the clinical utility of this method of administration.

Adult↗