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PubMed1978

Effects of binding and bactericidal action of vancomycin on Bacillus licheniformis cell wall organization as probed by 15N nuclear magnetic resonance spectroscopy.

The effects of binding and the bactericidal action of vancomycin on the arrangement and mobilities of cell wall polymers in Bacillus licheniformis were investigated by (15)N nuclear magnetic resonance spectroscopy. The bactericidal action of vancomycin led to reduced mobilities of cell wall teichoic acid and teichuronic acid in surviving cells. The decrease in teichoic acid mobility was also observed upon binding of vancomycin to B. licheniformis cells and resulted from a specific interaction between the antibiotic and teichoic acid, rather than from electrostatic contraction of the cell wall. The reduction in teichuronic acid mobility appeared to be related either to the elastic contraction of the cell wall resulting from loss of cell turgor or to separation of the cell wall from the protoplast membrane. No spectral changes associated with cell wall autolysis or alterations in cell wall composition, amidation, and cross-linking were found in vancomycin-treated B. licheniformis cells. Binding of vancomycin to Micrococcus lysodeikticus cell walls led to a decrease in mobility of C-terminal d-alanine residues but was accompanied by an increase in the mobilities of other peptidoglycan residues. The possible contributions of changes in the arrangements of cell wall polymers to the lethal action of vancomycin is discussed.

Bacillus↗

PubMed1992

In vitro pharmacodynamic effects of concentration, pH, and growth phase on serum bactericidal activities of daptomycin and vancomycin.

Clinical trials with daptomycin were halted in December 1990 because of treatment failures including two resistant Staphylococcus aureus strains. High protein binding of daptomycin (> 90%) and the lower-than-expected concentrations in serum with the dosage regimen of 3 mg/kg of body weight every 12 h may have contributed to these failures. To evaluate the effect that higher concentrations would have on bactericidal activity measured by time-kill curves, peak and trough concentrations were estimated for dosage regimens of 3, 5, and 10 mg/kg every 12 h. MICs, MBCs, and killing curves for daptomycin and vancomycin were performed by using the estimated concentrations with four S. aureus strains obtained from patients who failed daptomycin therapy for endocarditis. MICs and MBCs of daptomycin demonstrated a greater inoculum effect than those of vancomycin; MICs and MBCs of daptomycin increased three- to fourfold, but those of vancomycin increased only one- to twofold when the inoculum was increased from 5 x 10(5) to 5 x 10(7) CFU/ml. No pH-dependent effect on MICs or MBCs was seen. Strenuous experimental conditions were chosen: high inoculums (5 x 10(7) CFU/ml), extremes of pH (6.4, 7.4, and 8), and stationary and exponentially growing organisms; and all experiments completed in the presence of pooled human serum. Daptomycin exhibited concentration-dependent killing and statistically faster kill rates than vancomycin against stationary- or exponential-growth-phase organisms. A pH-dependent decrease in activity with daptomycin was also demonstrated. Daptomycin and vancomycin produced higher kill rates against exponentially growing organisms. A pH-dependent decrease in activity with daptomycin was also demonstrated. Daptomycin and vancomycin produced higher kill rates against exponentially growing organisms. The results indicate that the use of higher dosage regimens with compounds similar to daptomycin may be capable of overcoming the effects of pH, high inoculum, and protein binding.

Blood Bactericidal Activity↗

PubMed1992

Vancomycin is not an essential component of the initial empiric treatment regimen for febrile neutropenic patients receiving ceftazidime: a randomized prospective study.

The use of vancomycin as part of the initial antibiotic therapy of febrile neutropenic patients has become a controversial issue. Some studies support its incorporation in the initial regimen, and others suggest that vancomycin can be added later. We examined this issue in a prospective, randomized trial. We randomized 127 febrile neutropenic patients to receive either ceftazidime alone or ceftazidime plus vancomycin as the initial empiric antibiotic treatment. We added vancomycin to the ceftazidime arm of the study when fever persisted after 96 h of monotherapy, when new fever occurred after this time, or when a moderately ceftazidime-resistant gram-positive bacterium was isolated. Each of these regimens had similar initial response rates, similar durations of initial fever, similar frequencies of new fever during therapy, similar microbiological cure rates, similar superinfection rates, and similar survival rates. We observed more renal and cutaneous toxicities in patients receiving vancomycin and ceftazidime as initial therapy. We conclude that ceftazidime is appropriate as initial therapy for febrile neutropenic patients and that the addition of vancomycin is appropriate when fever persists after 4 days of monotherapy or when fever recurs following an initial response.

Adolescent↗

PubMed1992

[In vitro activity of vancomycin and teicoplanin against gram-positive cocci].

The activities of vancomycin and teicoplanin against 148 strains of Gram-positive cocci were tested using agar diffusion and liquid microdilution MIC determination. Tested strains included 84 staphylococci, 32 S. aureus, 52 coagulase-negative staphylococci (CNS), 52 enterococci, and 12 streptococci. Most strains (136) were susceptible to both agents, with inhibition diameters of 17 mm or more. MRSA strains exhibited lower geometric MIC means with teicoplanin (0.90 micrograms/ml) than with vancomycin (1.79 micrograms/ml); this difference was found for methicillin-susceptible S. aureus strains (1.07 and 1.38 micrograms/ml for teicoplanin and vancomycin, respectively). In contrast, methicillin-susceptible and methicillin-resistant strains of CNS exhibited similar MICs (1.60 micrograms/ml approximately). Enterococci were more susceptible to teicoplanin (MIC 0.25 micrograms/ml) than to vancomycin (MIC 1.35 micrograms/ml). Both vancomycin and teicoplanin were thus found to be consistently effective against Gram-positive cocci; however, teicoplanin proved more effective than vancomycin against enterococci and methicillin-resistant S. aureus strains and may therefore be a valuable therapeutic alternative for these multiresistant organisms.

Anti-Bacterial Agents↗

PubMed1977

Inhibition of ristocetin-induced platelet agglutination by vancomycin.

Ristocetin and vancomycin are structurally similar glycopeptide antibiotics. Both vancomycin and ristocetin in high concentrations (3.0 mg/ml) cause the precipitation of fibrinogen, plasminogen, and IgG from platelet-poor plasma (PPP). In contrast to ristocetin, vanomycin (0.5-1.5 mg/ml) does not agglutinate platelets in normal platelet-rich plasma (PRP) or formalin-treated platelets in the presence of normal PPP. Preincubation of vancomycin (0.5-1.25 mg/ml) with normal PRP, von Willebrand platelets in normal PPP, or formalinized platelets results in inhibition of platelet agglutination induced by ristocetin (0.7-1.25 mg/ml) or ristocetin and normal PPP. This inhibition can be overcome by increasing the final concentration of ristocetin in the platelet suspension. Preincubation of formalin-treated platelets with the major fraction obtained by carboxymethyl-Sephadex C-50 chromatography of commercial vancomycin also results in inhibition of agglutination induced by ristocetin and normal PPP. Incubation with vancomycin (1.25 mg/ml) does not interfere with von Willebrand factor (vWF) or factor VIII coagulant activities in normal PPP or in Sepharose 4B void volume fractions of PPP. These results indicate that vancomycin interacts with normal, von Willebrand, and formalin-treated platelets and inhibits the binding of ristocetin (or ristocetin-vWF complexes).

Binding, Competitive↗

PubMed1978

The selectivity of vancomycin and lincomycin in NYC medium for the recovery of N. gonorrhoeae from clinical specimens.

Varying concentrations of vancomycin and lincomycin were tested separately in NYC medium to determine the degree of their selectivity and sensitivity for isolation of N. gonorrhoeae from clinical specimens. Results indicate that 2 microgram/ml of vancomycin used in conjunction with colymycin, amphotericin B, and trimethoprim lactate provide adequate selectivity and reduce the possibility of losses of vancomycin-sensitive strains of gonococci seen with 3 microgram/ml of vancomycin. The same medium with concentrations of from 1 to 4 microgram/ml of lincomycin substituted for vancomycin permitted more contamination and fewer recoveries of gonococci as compared with 2 microgram/ml of vancomycin.

Amphotericin B↗

PubMed1992

Simplified dosing and monitoring of vancomycin for the burn care clinician.

Vancomycin has excellent activity against Gram-positive bacteria and is often selected for use in the infected burn patient. Because of multiple-compartment pharmacokinetics, vancomycin serum concentrations can decrease dramatically in a short time period following the end of an intravenous infusion. This accounts for the widely divergent recommendations for serum vancomycin peak concentrations, e.g. from 15 mg/l up to 80 mg/l, when the time for blood sampling following the end of intravenous infusion is different. It is in general not necessary to monitor vancomycin peak concentrations, not only because its toxic potential is overrated but also because potential toxicity and therapeutic efficacy are correlated with trough concentrations. Post-distribution 'peak' concentrations are generally only useful for determining the optimal dosing interval for patients with impaired renal function. A dosing and monitoring paradigm for vancomycin therapy in burned adults has been devised for burn care clinicians. It provides suggested dose and dosing intervals based on body weight and creatinine clearance, with specific recommendations for regimen modification based upon the results of trough serum concentration determinations.

Adult↗

PubMed1978

Oral vancomycin for antibiotic-associated pseudomembranous colitis.

Nine patients with antibiotic-associated pseudomembranous colitis were treated with oral vancomycin. All had severe diarrhoea, tissue-culture evidence of a clostridial toxin in stool, and typical lesions on sigmoidoscopic examination, despite discontinuation of all antimicrobials for periods of 10 days to 8 weeks. Oral vancomycin was given in doses of 2 g daily. All patients showed a good clinical response with gradual resolution of diarrhoea over 7 days and a rapid decrease in concentrations of the toxin in stools. Follow-up sigmoidoscopies in seven patients showed major improvement or complete clearing of lesions after 7-10 days of vancomycin treatment. The mean concentration of vancomycin in twenty-five stools obtained during treatment was 3100 microgram/g, levels in serum being very low. These results suggest a role for oral vancomycin treatment of antibiotic-associated pseudomembranous colitis which persists for extended periods despite discontinuation of the incriminated antimicrobial.

Administration, Oral↗

PubMed1992

Vancomycin elimination during high-flux hemodialysis: kinetic model and comparison of four membranes.

Vancomycin clearance was measured in five patients during dialysis with cuprophane (CU), polysulfone (PS), cellulose triacetate (CT), and polyacrylonitrile (PAN) dialyzers. Vancomycin was significantly cleared during routine high-flux (HF) hemodialysis (HD) with the latter three membranes, but not by CU. Postdialytic rebound of serum vancomycin concentrations was noted following HF dialysis, necessitating use of a two-compartment pharmacokinetic model. Measurement of serum vancomycin concentration immediately postdialysis significantly overestimates intradialytic removal, possibly resulting in inappropriate dose adjustment. Vancomycin infusion during HF HD results in significant drug removal during its administration to the patient, complicating the calculation of an adequate dose.

Acrylic Resins↗

PubMed1992

A cluster of vancomycin-resistant Enterococcus faecium in an intensive care unit.

OBJECTIVE: To describe the epidemiology of a cluster of vancomycin-resistant Enterococcus faecium (VAREC) in a cardiothoracic surgery intensive care unit. DESIGN: A case series of patients identified through review of surveillance data on nosocomial infections, review of microbiologic records, and culture survey of patients in the unit. RESULTS: Six patients in the cardiothoracic surgery intensive care unit had VAREC with identical antimicrobic susceptibility patterns over a 6-month period. Four patients were identified with VAREC through prospective surveillance and 2 through retrospective review. Prior vancomycin use was seen more commonly in patients with VAREC (6/6, 100%) than in those without VAREC (3/12, 25%) (Fisher's exact test, p = .01). Six of the 7 patients with prior infection developed VAREC (85.7%). A prior nosocomial infection and prior exposure to vancomycin were found to be important variables in a logistic regression analysis. VAREC also was isolated from the environment. A combination of cohorting of patients and staff, and modifications of standard contact isolation practices eliminated the presence of VAREC from the cardiothoracic surgery intensive care unit. CONCLUSIONS: The results suggest that prior administration of vancomycin, especially in the patient who develops nosocomial infection, can influence the acquisition of vancomycin-resistant enterococci and that VAREC may be transmitted from patient to patient. Using a modification of the standard infection control practice of isolation, we were able to control the spread of this resistant strain of E faecium.

Cross Infection↗

PubMedDate not supplied

Treatment of bacterial endocarditis with vancomycin.

Five patients with bacterial endocarditis who were allergic to penicillin were treated successfully with vancomycin. The causative microorganisms were Streptococcus bovis, S faecalis, S agalactiae, S intermedius, and Staphylococcus aureus. Except for the strain of S faecalis, vancomycin was bactericidal against these organisms at easily achievable serum concentrations. To insure a bactericidal serum titer of 1:8 or greater, streptomycin was added in the therapy of the case caused by S faecalis. There was no toxicity from vancomycin therapy in our patients except for mild phlebitis at the infusion site. Vancomycin appears to be an effective alternative to penicillin in individuals with endocarditis due to susceptible organisms. Vancomycin in combination with an aminoglycoside may be appropriate therapy for enterococcal endocarditis.

Adult↗

PubMed1992

Chrononephrotoxicity in rat of a vancomycin and gentamicin combination.

The effect of time of administration on excretion of two brush border enzymes--alanine aminopeptidase (AAP) and gamma-glutamyl transferase (gamma GT), and a lysosomal enzyme, N-acetyl-beta-D-glucosaminidase (NAG) with a single high dose of vancomycin, gentamicin or a combination of vancomycin and gentamicin was studied in male Wistar rats and compared with elimination of a control group. The rats received vancomycin intraperitoneally (200 mg.kg-1), gentamicin intramuscularly (100 mg.kg-1) or the combination of the drugs by the same route. A control group received isotonic NaCl solution. The four groups of animals received a single injection at 8 a.m., 2 p.m., 8 p.m., and 2 a.m. and urine excretion values for AAP, gamma GT and NAG were determined 24 hr later. The results show that the nephrotoxicity of gentamicin + vancomycin is greater than that observed with gentamicin, which again is greater than that observed with vancomycin. Furthermore, circadian variations in renal toxicity were observed, the least occurring at 8 a.m.

Acetylglucosaminidase↗

PubMed1992

Teicoplanin versus vancomycin for prophylaxis of experimental Enterococcus faecalis endocarditis in rats.

Teicoplanin was compared with vancomycin for the prophylaxis of experimental Enterococcus faecalis endocarditis in rats. Single intravenous doses of teicoplanin (7 mg/kg of body weight) or vancomycin (15 mg/kg) were given 30 min before bacterial challenge. Two strains of E. faecalis (309 and 1209) isolated from patients with endocarditis were tested. Bacterial inocula ranged from 10(4) (i.e., the inoculum infecting 90% of the control rats [ID90]) to 10(7) CFU/ml. The MICs and MBCs of teicoplanin and vancomycin were, respectively, 0.25 to greater than 128 mg/liter and 2 to greater than 128 mg/liter for strain 309 and 0.5 to greater than 128 mg/liter and 0.5 to greater than 128 mg/liter for strain 1209. Vancomycin prevented endocarditis only in 60% (strain 309) and in 87% (strain 1209) of rats challenged with the smallest bacterial-inoculum size (ID90), whereas teicoplanin prevented endocarditis in 100% of rats challenged with the same inoculum (strain 309; P = 0.05), in 87% of rats challenged with 10 times the ID90 (strain 309; P = 0.02), and in 95% of rats challenged with 100 times the ID90 (strain 1209; P = 0.0003). The combination of teicoplanin plus gentamicin (4 mg/kg) extended the protection to inocula 100 times the ID90 (strain 309; 96% of sterile animals) and 1,000 times the ID90 (strain 1209; 100% of sterile animals). Prevention of endocarditis was likely to be due to a prolonged inhibition of bacterial growth by sustained levels of teicoplanin in serum and not to bacterial killing. Indeed, teicoplanin did not exhibit any bactericidal activity either in vitro (time-kill curves) or in vivo (serum bactericidal activity). Teicoplanin proved to be superior to vancomycin in the prophylaxis of experimental E. faecalis endocarditis in rats.

Animals↗

PubMed1992

Comparison of daptomycin, vancomycin, and ampicillin-gentamicin for treatment of experimental endocarditis caused by penicillin-resistant enterococci.

Infections with enterococci that are resistant to multiple antibiotics are an emerging clinical problem. We evaluated the antibiotic treatment of experimental enterococcal endocarditis caused by two strains with different mechanisms of penicillin resistance. Enterococcus faecalis HH-22 is resistant to aminoglycosides and penicillin on the basis of plasmid-mediated modifying enzymes; Enterococcus raffinosus SF-195 is susceptible to aminoglycosides but is resistant to penicillin on the basis of low-affinity penicillin-binding proteins. Animals infected with strain HH-22 received 5 days of treatment with the following: no treatment; daptomycin (20 mg/kg of body weight twice daily [b.i.d.], intramuscularly [i.m.]), vancomycin (20 mg/kg b.i.d., intravenously), or ampicillin (100 mg/kg three times daily, i.m.) plus gentamicin (2.5 mg/kg b.i.d. i.m.). Although vancomycin was superior to ampicillin-gentamicin (P less than 0.01), daptomycin was significantly better than all other treatment regimens (P less than 0.01) in reducing intravegetation enterococcal densities, although no vegetations were rendered culture negative by this agent. Animals infected with strain SF-195 received 5 days of no therapy, ampicillin, ampicillin-gentamicin, vancomycin, or daptomycin (all at the dosage regimens described above). Daptomycin, vancomycin, and ampicillin-gentamicin each lowered intravegetation enterococcal densities significantly better than did ampicillin monotherapy or no treatment (P less than 0.01); moreover, these three treatment regimens rendered significantly more vegetations culture negative than did ampicillin monotherapy or no treatment (P less than 0.05). Serum daptomycin levels remained above the MICs and MBCs for both enterococcal strains throughout the 12-h dosing interval used in the study. Daptomycin and vancomycin were both active in vivo in these models of experimental enterococcal endocarditis caused by penicillin-resistant strains, irrespective of the mechanism of resistance. This activity correlated with the unique cell wall sites of action of these agents (binding to lipoteichoic acid and pentapeptide precursor, respectively) compared with the sites of action of beta-lactams (penicillin-binding proteins). Beta-Lactamase production by strain HH-22 precluded in vivo efficacy with ampicillin-gentamicin combinations. In contrast, this combination was active in vivo against strain SF-195, which exhibited intermediate-level penicillin resistance (MIC, 32 micrograms/ml), likely reflecting the ability of high-dose ampicillin to achieve enough binding to low-affinity penicillin-binding proteins to cause augmented aminoglycoside uptake.

Ampicillin↗

PubMed1992

Detection of vancomycin resistance in Enterococcus species.

Enterococcus faecalis and Enterococcus faecium isolates that are resistant to vancomycin have recently been identified in North America and Europe. Of 155 clinical isolates of enterococci (113 E. faecium and 42 E. faecalis), we found that 98 were resistant, 52 were moderately susceptible, and 5 had intermediate susceptibilities to vancomycin by using broth microdilution susceptibility testing according to the National Committee for Clinical Laboratory Standards (NCCLS) (Approved Standard M7-A2). Using NCCLS disk diffusion methodology (Approved Standard M2-A4), we evaluated the NCCLS supplemental M100-S3 revisions for zone diameter interpretive standards and incubation conditions and found 5.8% minor errors. A total of 234 isolates, which included an additional 79 E. faecium isolates that were moderately susceptible to vancomycin, were used to evaluate the Vitek GPS-TA card (bioMerieux, Inc., Hazelwood, Mo.) and the Pos MIC type 6 panel (MicroScan; Baxter Health Care Corp., West Sacramento, Calif.) for the detection of vancomycin resistance. The Vitek card was 100% specific and 72% sensitive, whereas the MicroScan panel with the Walk/Away system was 98% specific, with a sensitivity of 93% which increased to 99% when readings were performed manually. An agar screen plate method was evaluated with vancomycin concentrations of 6, 8, 10, or 12 micrograms/ml; plates were inoculated so as to obtain a final concentration of 10(5) CFU per spot. This method was found to be 100% sensitive and specific at all concentrations.

Drug Resistance, Microbial↗

PubMed1992

Stevens-Johnson-type reaction with vancomycin treatment.

OBJECTIVE: To report a case of Stevens-Johnson syndrome caused by vancomycin. CASE SUMMARY: Stevens-Johnson syndrome is an acute mucocutaneous process characterized by epidermal and mucosal desquamation. Its pathogenesis is poorly understood. Mortality rates have ranged from 30 to 100 percent. We describe a case of Stevens-Johnson syndrome related to the use of vancomycin in a 71-year-old woman with rheumatoid arthritis receiving treatment for an infected cervical fusion site. Classic "target" lesions distributed throughout the trunk and extremities along with erosive lesions involving the oral and vaginal mucosae were observed in this patient. DISCUSSION: A number of agents have been implicated in the etiology of Stevens-Johnson syndrome. Serious cutaneous reactions to vancomycin, however, have been uncommon. Cessation of vancomycin treatment in our patient led to eventual resolution of her symptoms. CONCLUSIONS: Vancomycin is a potential causative agent of Stevens-Johnson syndrome.

Aged↗

PubMed1992

Vancomycin and teicoplanin: something old, something new.

OBJECTIVE: To compare and contrast the pharmacology, activity and clinical efficacy of two glycopeptide antibiotics, vancomycin and teicoplanin. DATA SOURCES: English language literature search using MEDLINE, Index Medicus, relevant textbooks and product information literature. STUDY SELECTION: Over 200 publications were examined extending back to the period of initial Phase I trials with vancomycin. DATA EXTRACTION AND SYNTHESIS: Many publications covered similar ground and came to the same conclusions. In these instances one or two of the best pieces were chosen as cited reference material. Conflicting results and conclusions are discussed and an attempt is made to interpret the findings. CONCLUSION: Vancomycin and teicoplanin show differences in activity both in vitro and in vivo. Vancomycin is superior against coagulase-negative staphylococci and reliable dosage regimens are available. Teicoplanin, however, needs to be given in significantly larger doses than initially thought necessary to maximise clinical efficacy. Teicoplanin has a lower incidence of side effects but in clinical practice this advantage is small. Vancomycin remains the glycopeptide of choice for the treatment of infections due to Gram-positive bacteria.

Anti-Bacterial Agents↗

PubMed1992

[A comparative microbiological and pharmacokinetic activity of vancomycin and teicoplanin].

Vancomycin and teicoplanin are two commercially available glycopeptide antibiotics. They have identical spectra of activity and similar mechanisms of action, and both are complex molecules. In vitro, vancomycin is more active against coagulase-negative staphylococci, while teicoplanin is more active against enterococci and pneumococci. The activity of the two antibiotics against Staphylococcus aureus is similar. The serum pharmacokinetics of vancomycin and teicoplanin are highly different, teicoplanin having a longer elimination half-life (40 hours versus 6-8 hours for vancomycin), but a higher degree of protein binding (90% versus 55%). We compared the two antibiotics on the basis of their inhibitory quotient kinetics, using the MIC90 values for the above bacterial species as the microbiological parameters, and the total and free (non-protein bound) serum concentrations as the pharmacokinetic parameters. The inhibitory quotient kinetics of vancomycin were always more favorable in terms of the free concentrations, even against those bacteria for which the teicoplanin MIC was lower.

Dose-Response Relationship, Drug↗